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Finals > Endo > Flashcards

Endo Flashcards

1
Q

diabetes

what is Maturity onset diabetes of the young (MODY)

A

A group of inherited genetic disorders affecting the production of insulin.

Results in younger patients developing symptoms similar to those with T2DM, i.e. asymptomatic hyperglycaemia with progression to more severe complications such as diabetic ketoacidosis

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2
Q

diabetes

which antibodies are present in T1DM

A
  • anti-glutamic acid decarboxylase (anti-GAD) (80%)
  • Islet cell antibodies (ICA) 70-80%
  • Insulin autoantibodies (IAA): correlates strongly with age, found in >90% of young children with T1DM but only 60% of older patients
  • Insulinoma-associated-2 autoantibodies (IA-2A)
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3
Q

diabetes

what is Latent autoimmune diabetes of adults (LADA)

A

often misdiagnosed as having T2DM because they develop autoimmune diabetes later on in life

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4
Q

Thyroid function tests

TSH: low
T3+4: high

A

hyperthyroidism

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5
Q

Thyroid function tests

TSH: high
T3+4: low

A

hypothyroidism

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6
Q

Thyroid function tests

TSH: low
T3+4: low

A

secondary hypothyroidism (a pituitary or hypothalamic cause)

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7
Q

Thyroid function tests

TSH: high
T3+4: high

A

pituitary adenoma (secretes TSH)

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8
Q

Thyroid function tests

what antibodies are present in Grave’s disease

A

anti TPO

antithyroglobulin

TSH receptor

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9
Q

Thyroid function tests

what antibodies are present in Hashimoto’s Thyroiditis

A

anti TPO

antithyroglobulin

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10
Q

Thyroid function tests

what antibodies are present in thyroid cancer

A

antithyroglobulin

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11
Q

why should you stop taking metformin before a CT scan

A

the dye/contrast and metformin is filtered out of your blood the kidneys

in an attempt not to overload your kidneys, do not take metformin whilst body is working to eliminate the dye from body (approx 48h).

Taking both could cause metformin to build up in body

could lead to lactic acidosis in pts with decreased kidney function

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12
Q

Type 2 Diabetes

pathophysiology

A

repeated exposure to glucose + insulin makes the cells in the body become resistant to the effects of insulin

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13
Q

Type 2 Diabetes

non-modifiable RFs

A
  • older age
  • ethnicity (black, chinese, s.asian)
  • FH
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14
Q

Type 2 Diabetes

modifiable RFs

A
  • obesity
  • sedentary lifestyle
  • high carb diet (esp refined carbs)
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15
Q

Type 2 Diabetes

test to screen for diabetes

A

HbA1C

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16
Q

Type 2 Diabetes

symptoms

A
  • fatigue
  • polydipsia + polyuria
  • unintentional weight loss
  • opportunistic infections
  • slow healing
  • glucose in urine (on dipstick)
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17
Q

Type 2 Diabetes

what does the OGTT involve

A

fasting plasma glucose result

give 75g glucose drink

measure plasma glucose 2hrs later

tests the ability of the body to cope with a carb meal

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18
Q

Type 2 Diabetes

pre-diabetes diagnosis

A

any 1 of:

  • HbA1c: 42-47
  • impaired fasting glucose: 6.1 - 6.9 mmol/l
  • impaired glucose tolerance: OGTT 7.8 - 11.1 mmol/l
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19
Q

Type 2 Diabetes

diabetes dx

A

any 1 of:

  • HbA1c >48
  • Random glucose >11
    Fasting glucose >7
  • OGTT >11
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20
Q

Type 2 Diabetes

mnx (diet)

A
  • veg + oily fish
  • low glycaemic, high fibre diet
  • low carb diet
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21
Q

Type 2 Diabetes

mnx (RFs)

A
  • exercise + weight loss
  • stop smoking
  • optimise trx for other illnesses: HTN, hyperlipidaemia, CVD
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22
Q

Type 2 Diabetes

what complications to monitor

A
  • diabetic retinopathy
  • kidney disease
  • diabetic foot
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23
Q

Type 2 Diabetes

what are the HbA1c targets for someone with new T2DM

A

48mmol/mol

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24
Q

Type 2 Diabetes

what are the HbA1c targets for diabetics that have moved beyond metformin alone

A

53 mmol/mol

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25
Q

Type 2 Diabetes

1st line medical mnx

A

metformin

titrated from initially 500mg OD as tolerated

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26
Q

Type 2 Diabetes

2nd line medical mnx

A

add either of:

  • sulfonylurea
  • pioglitazone
  • DPP-4 inhibitor
  • SGLT-2 inhibitor
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27
Q

Type 2 Diabetes

3rd line medical mnx

A

triple therapy: metformin + 2 of:

  • sulfonylurea
  • pioglitazone
  • DPP-4 inhibitor
  • SGLT-2 inhibitor

or metformin + insulin

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28
Q

Type 2 Diabetes

which 2nd line medication is preferred in patients with CVD

A

SGLT-2 inhibitors

GLP-1 mimetics (e.g. liraglutide)

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29
Q

Type 2 Diabetes

what is metformin

A

a biguanide

it increases insulin sensitivity

+ decreases liver production of glucose

weight neutral: doesn’t increase or decrease body weight

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30
Q

Type 2 Diabetes

SEs of metformin

A
  • lactic acidosis

- diarrhoea + abdo pain

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31
Q

Type 2 Diabetes

advantages of metformin

A

does NOT typically cause hypoglycaemia

weight neutral

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32
Q

Type 2 Diabetes

name a sulfonylurea

A

gliclazide

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33
Q

Type 2 Diabetes

how do sulfonylureas work

A

they stimulate insulin release from the pancreas

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34
Q

Type 2 Diabetes

SEs of sulfonylureas

A
  • increased risk of CVD + MI when used as monotherapy
  • weight gain
  • hypoglycaemia
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35
Q

Type 2 Diabetes

how do Pioglitazones work

A

it’s a thiazolidinedione

it increases insulin sensitivity

and decreases liver production of glucose

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36
Q

Type 2 Diabetes

SE’s of Pioglitazone (5)

A
  • weight gain
  • fluid retention
  • anaemia
  • HF
  • extended use may increase risk of bladder cancer
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37
Q

Type 2 Diabetes

advantage of Pioglitazone

A

doe NOT typically cause hypoglycaemia

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38
Q

Type 2 Diabetes

what are incretins

A

hormones produced by the GI tract

they’re secreted in response to large meals and act to reduce blood sugar

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39
Q

Type 2 Diabetes

what 3 things do incretins do

A
  1. increase insulin secretions
  2. inhibit glucagon production
  3. slow absorption by the GI tract
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40
Q

Type 2 Diabetes

name the main incretin

A

glucagon-like peptide-1 (GLP-1)

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41
Q

Type 2 Diabetes

what enzyme inhibits incretins

A

dipeptidyl peptidase-4 (DDP-4)

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42
Q

Type 2 Diabetes

name the most common DPP-4 inhibitor

A

sitagliptin

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43
Q

Type 2 Diabetes

how do DPP-4 inhibitors work

A

they inhibit the DPP-4 enzyme

therefore increasing GLP-1 activity

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44
Q

Type 2 Diabetes

SE’s of DPP-4 inhibitors

A
  • GI tract upset
  • sx of URTI
  • pancreatitis
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45
Q

Type 2 Diabetes

what are GLP-1 mimetics

A

they mimic the action of GLP-1

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46
Q

Type 2 Diabetes

name a common GLP-1 mimetic and how is it given

A

Exenatide

SC BD by pt or once weekly in a modifiable release form

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47
Q

Type 2 Diabetes

name another GLP-1 mimetic other than Exenatide and how is it given

A

Liraglutide

OD SC

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48
Q

Type 2 Diabetes

in overweight patients, what medications may be given

A

GLP-1 mimetic + metformin + sulfonylurea

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49
Q

Type 2 Diabetes

SE’s of GLP-1 mimetics

A
  • GI tract upset
  • weight loss
  • dizziness
  • low risk of hypoglycaemia
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50
Q

Type 2 Diabetes

name some SGLT-2 inhibitors

A

____gliflozin

  • empagliflozin
  • canagliflozin
  • dapagliflozin
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51
Q

Type 2 Diabetes

how do SGLT-2 inhibitors work

A

SGLT-2 protein: reabsorbs glucose from urine into the blood in the proximal tubules of the kidneys

SGLT-2 inhibitors block the action of this protein and cause glucose to be excreted in the urine

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52
Q

Type 2 Diabetes

which SGLT-2 inhibitor has been shown to reduce the risk of CVD, HF hospitalisation and mortality

A

Empagliflozin

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53
Q

Type 2 Diabetes

which SGLT-2 inhibitor has been shown to reduce the risk of CV events such as MI, stroke and death and HF hospitalisation

A

Canagliflozin

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54
Q

Type 2 Diabetes

SE’s of SGLT-2 inhibitors

A
  • Glucoseuria (glucose in urine)
  • diabetic ketoacidosis
  • UTIs
  • weight loss
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55
Q

Type 2 Diabetes

which SE appears to be more common in pts on canagliflozin

A

lower limb amputation

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56
Q

Type 2 Diabetes

how long do rapid-acting insulins work for

A

10min - 4h

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57
Q

Type 2 Diabetes

name 3 rapid acting insulins

A
  • Novorapid
  • Humalog
  • Apidra
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58
Q

Type 2 Diabetes

how long do short-acting insulins work

A

30min - 8h

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59
Q

Type 2 Diabetes

name 3 short-acting insulins

A
  • Actrapid
  • Humulin S
  • Insuman Rapid
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60
Q

Type 2 Diabetes

how long do intermediate-acting insulins work

A

1h - 16h

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61
Q

Type 2 Diabetes

name 3 intermediate-acting insulins

A
  • Insulatard
  • Humulin I
  • Insuman Basal
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62
Q

Type 2 Diabetes

how long do long-acting insulins work for

A

1h - 24h

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63
Q

Type 2 Diabetes

name 3 long-acting insulins

A
  • Lantus
  • Levemir
  • Degludec ( lasts >40h)
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64
Q

Type 2 Diabetes

what do combination insulins contain

A

a rapid acting and an intermediate acting insulin

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65
Q

Type 2 Diabetes

name 3 combinations insulins

A

In brackets is the proportion of rapid to intermediate acting insulin:

Humalog 25 (25:75)
Humalog 50 (50:50)
Novomix 30 (30:70)
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66
Q

Adrenal Insufficiency

what is it

A

adrenal glands doesn’t produce enough cortisol and aldosterone

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67
Q

Adrenal Insufficiency

what is Addison’s disease

A

aka Primary Adrenal Insufficiency

specific condition where the adrenal glands have been damaged, resulting in a reduction in the secretion of cortisol and aldosterone

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68
Q

Adrenal Insufficiency

what is the most common cause of Addison’s disease

A

autoimmune

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69
Q

Adrenal Insufficiency

what is secondary adrenal insufficiency

A

loss or damage to the pituitary gland

inadequate ACTH stimulating the adrenal glands

low cortisol release

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70
Q

Adrenal Insufficiency

causes of secondary adrenal insufficiency

A
  • surgery to remove pituitary tumour
  • infection
  • loss of blood flow
  • radiotherapy
  • Sheehan’s syndrome
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71
Q

Adrenal Insufficiency

how does Sheehan’s syndrome cause secondary adrenal insufficiency

A

massive blood loss during childbirth leads to pituitary gland necrosis

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72
Q

Adrenal Insufficiency

what is tertiary adrenal insufficiency

A

long term PO steroids causes suppression of the hypothalamus

inadequate CRH release

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73
Q

Adrenal Insufficiency

why should long term steroids be tapered down slowly

A

to allow time for the adrenal axis to regain normal function

to avoid tertiary adrenal insufficiency

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74
Q

Adrenal Insufficiency

sx (5)

A
  • fatigue
  • nausea
  • cramps
  • abdo pain
  • reduced libido
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75
Q

Adrenal Insufficiency

signs (2)

A
  • bronze hyperpigmentation to skin

- hypotension (esp postural)

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76
Q

Adrenal Insufficiency

why is there bronze hyperpigmentation

A

ACTH stimulates melanocytes to produce melanin

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77
Q

Adrenal Insufficiency

what is the key biochemical clue

A

hyponatraemia

hyperkalaemia is also possible

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78
Q

Adrenal Insufficiency

test of choice for dx

A

short synacthen test

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79
Q

Adrenal Insufficiency

ACTH level in primary adrenal failure and why

A

high

pituitary is trying to stimulate adrenal glands without any negative feedback in the absence of cortisol

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80
Q

Adrenal Insufficiency

ACTH level in secondary adrenal failure and why

A

low

as the reason the adrenal glands are not producing cortisol is that they are not being stimulated by ACTH

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81
Q

Adrenal Insufficiency

which adrenal autoantibodies will be present in autoimmune adrenal insufficiency

A

adrenal cortex antibodies

21-hydroxylase antibodies

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82
Q

Adrenal Insufficiency

which inx if suspecting an adrenal tumour, haemorrhage or other structural pathology

A

CT / MRI adrenals

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83
Q

Adrenal Insufficiency

which inx if suspecting pituitary pathology

A

MRI pituitary

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84
Q

Adrenal Insufficiency

what does the short synacthen test involve

A

measure baseline cortisol

give synacthen (synthetic ACTH)

measure cortisol 30 + 60 min after

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85
Q

Adrenal Insufficiency

what should the cortisol level do in a healthy individual in the short synacthen test

A

at least double

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86
Q

Adrenal Insufficiency

what level cortisol in the short synacthen test indicates Addison’s

A

less than double the baseline

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87
Q

Adrenal Insufficiency

trx and why

A

hydrocortisone (glucocorticoid) replaces cortisol

fludrocortisone (mineralcorticoid) replaces aldosterone

for life

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88
Q

Adrenal Insufficiency

if pt is acutely ill, how do you manage meds

A

doses are doubled until they have recovered to match the normal steroid response to illness

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89
Q

Adrenal Insufficiency

what are pts given to alert emergency services that they are dependent on steroids for life

A

steroid card and an emergency ID tag

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90
Q

Adrenal Insufficiency

what is Addisonian Crisis

A

aka adrenal crisis

an acute presentation of severe Addisons, where the absence of steroid hormones leads to a life threatening presentation

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91
Q

Adrenal Insufficiency

Addisonian Crisis presentation

A
  • reduced consciousness
  • hypotension
  • hypoglycaemia
  • hyponatraemia
  • hyperkalaemia
  • pt very unwell
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92
Q

Adrenal Insufficiency

what can an Addisonian Crisis be triggered by

A
  • infection
  • trauma
  • acute illness
  • could be their first presentation
  • someone on long term steroids suddenly withdrawing those steroids
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93
Q

Adrenal Insufficiency

mnx of Addisonian Crisis

A
  • intensive monitoring
  • IV hydrocortisone 100mg stat then 100mg every 6hr
  • IV fluid resus
  • correct hypoglycaemia
  • monitor electrolytes and fluids
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94
Q

Hyperparathyroidism

which cells produce parathyroid hormone

A

chief cells in the parathyroid glands

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95
Q

Hyperparathyroidism

when is parathyroid hormone released

A

in response to hypocalcaemia

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96
Q

Hyperparathyroidism

how does parathyroid hormone act to raise blood calcium levels

A
  • increases osteoclast activity in bones
  • increases calcium absorption from the gut
  • increases calcium absorption from the kidneys
  • increases Vit D activity
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97
Q

Hyperparathyroidism

how does vit D raise blood calcium levels

A

parathyroid hormone acts on vit D to convert it to its active form

which acts to increase Ca absorption from the intestines

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98
Q

Hyperparathyroidism

symptoms of hypercalcaemia

A

renal stones

painful bones

abdominal groans: constipation, N+V

psychiatric moans: fatigue, depression, psychosis

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99
Q

Hyperparathyroidism

cause of primary hyperparathyroidism

A

uncontrolled parathyroid hormone produced directly by a tumour of the parathyroid gland

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100
Q

Hyperparathyroidism

what are the serum calcium levels in primary hyperparathyroidism

A

hypercalcaemia

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101
Q

Hyperparathyroidism

trx of primary hyperparathyroidism

A

surgically remove tumour

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102
Q

Hyperparathyroidism

cause of secondary hyperparathyroidism

A
  • insufficient vit D

or

  • Chronic renal failure

leads to low absorption of Ca from the intestines, kidneys and bones

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103
Q

Hyperparathyroidism

what are the serum calcium levels and PTH levels in secondary hyperparathyroidism

A

hypocalcaemia or normal

high PTH

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104
Q

Hyperparathyroidism

pathophysiology of secondary hyperparathyroidism

A

parathyroid glands react to low serum Ca by excreting more PTH

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105
Q

Hyperparathyroidism

why is there hyperplasia in the parathyroid gland in secondary hyperparathyroidism

A

over time the total number of cells in the parathyroid gland increases as they respond to the increased need to produce parathyroid hormone

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106
Q

Hyperparathyroidism

trx of secondary hyperparathyroidism

A
  • correct vit D deficiency

- if in renal failure: renal transplant

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107
Q

Hyperparathyroidism

what is tertiary hyperparathyroidism

A

when secondary hyperparathyroidism continues for a long period of time

when the cause of the secondary hyperparathyroidism is treated the PTH level remains inappropriately high

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108
Q

Hyperparathyroidism

what is the cause of tertiary hyperparathyroidism

A

hyperplasia

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109
Q

Hyperparathyroidism

what are the PTH and calcium serum levels in tertiary hyperparathyroidism

A

high PTH

hypercalcaemia

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110
Q

Hyperparathyroidism

why is there hypercalcaemia in tertiary hyperparathyroidism

A

high PTH in the absence of pathology of secondary hyperparathyroidism leads to high absorption of Ca in the intestines, kidneys and bones

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111
Q

Hyperparathyroidism

trx of tertiary hyperparathyroidism

A
  • surgery: remove part of the parathyroid tissue to return the PTH to an appropriate level
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112
Q

Hyperaldosteronism

which cells sense BP in the afferent arteriole in the kidney

A

juxtaglomerular cells

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113
Q

Hyperaldosteronism

what do the juxtaglomerular cells secrete in response to low BP

A

renin (hormone)

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114
Q

Hyperaldosteronism and Conn’s Syndrome

what does the liver secrete in response to low BP

A

angiotensinogen

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115
Q

Hyperaldosteronism

what converts angiotensinogen into angiotensin I

A

renin

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116
Q

Hyperaldosteronism

what converts angiotensin I to angiotensin II

A

ACE (angiotensin converting enzyme)

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117
Q

Hyperaldosteronism

where is angiotensin I converted to angiotensin II

A

in the lungs

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118
Q

Hyperaldosteronism

what does angiotensin II do

A

stimulates the release of aldosterone from the adrenal glands

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119
Q

Hyperaldosteronism

what kind of steroid is aldosterone

A

a mineralocorticoid

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120
Q

Hyperaldosteronism

how does aldosterone act on the kidneys

A
  • increase Na reabsorption from the distal tubule
  • increase K secretion from the distal tubule
  • increase hydrogen secretion from the collecting ducts
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121
Q

Hyperaldosteronism

what is Conn’s syndrome

A

primary hyperaldosteronism

the adrenal glands are directly responsible for producing too much aldosterone

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122
Q

Hyperaldosteronism

what levels will the serum renin be in Conn’s syndrome and why

A

low as it is suppressed by the high blood pressure from high levels of aldosterone

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123
Q

Hyperaldosteronism

what does aldosterone do to BP

A

it increases it

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124
Q

Hyperaldosteronism

causes of Conn’s syndrome (primary hyperaldosteronism)

A
  • adrenal adenoma secreting aldosterone (most common)
  • bilateral adrenal hyperplasia
  • familial hyperaldosteronism type 1 and type 2 (rare)
  • adrenal carcinoma (rare)
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125
Q

Hyperaldosteronism

what is secondary hyperaldosteronism

A

excessive renin stimulate the adrenal glands to produce more aldosterone

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126
Q

Hyperaldosteronism

what are the serum renin levels in secondary hyperaldosteronism

A

high

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127
Q

Hyperaldosteronism

secondary: when do high renin levels occur

A

when the BP in the kidneys is disproportionately lower than the BP in the rest of the body:

  • renal artery stenosis
  • renal artery obstruction
  • heart failure
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128
Q

Hyperaldosteronism

secondary: which inx is used to confirm renal artery stenosis

A

doppler US , CT angiogram or magnetic resonance angiography (MRA)

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129
Q

Hyperaldosteronism

what is the best screening tool for someone that you suspect has hyperaldosteronism

A

check the renin and aldosterone levels and calculate the renin/aldosterone ratio

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130
Q

Hyperaldosteronism

what does a high aldosterone and low renin indicate

A

primary hyperaldosteronism

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131
Q

Hyperaldosteronism

what does a high aldosterone and high renin indicate

A

secondary hyperaldosteronism

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132
Q

Hyperaldosteronism

what inx relate to the effects of aldosterone

A
  • BP (hypertension)
  • serum electrolytes (hypokalaemia)
  • blood gas analysis (alkalosis)
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133
Q

Hyperaldosteronism

if a high aldosterone is found, what inx nexts?

A
  • CT/MRI to look for an adrenal tumour

- renal doppler US, CT angiogram or magnetic resonance angiography (MRA) for renal artery stenosis or obstruction

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134
Q

Hyperaldosteronism

medical mnx

A

aldosterone antagonists:

  • Eplerenone
  • Spironolactone
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135
Q

Hyperaldosteronism

mnx to treat underlying cause

A
  • adenoma: surgical removal

- renal artery stenosis: percutaneous renal artery angioplasty via the femoral artery

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136
Q

what is the most common cause of secondary hypertension

A

hyperaldosteronism

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137
Q

pt with high BP that is not responding to trx and perhaps a low K level

what do you do

A

consider screening for hyperaldosteronism with a renin:aldosterone ratio

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138
Q

Syndrome of Inappropriate Anti-Diuretic Hormone

where is ADH produced

A

hypothalamus

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139
Q

Syndrome of Inappropriate Anti-Diuretic Hormone

where is ADH secreted

A

posterior pituitary gland

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140
Q

Syndrome of Inappropriate Anti-Diuretic Hormone

what is ADH aka

A

vasopressin

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141
Q

Syndrome of Inappropriate Anti-Diuretic Hormone

what does ADH do

A

stimulates water reabsorption from the collecting ducts in the kidneys

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142
Q

Syndrome of Inappropriate Anti-Diuretic Hormone

what is it

A

where there is inappropriately large amounts of ADH

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143
Q

Syndrome of Inappropriate Anti-Diuretic Hormone

2 general causes

A
  • posterior pituitary producing too much ADH

- ADH secreted from elsewhere: small cell lung cancer

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144
Q

Syndrome of Inappropriate Anti-Diuretic Hormone

what does excessive ADH result in

A

excessive water reabsorption in the collecting ducts

this water dilutes the Na in the blood

hyponatraemia

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145
Q

Syndrome of Inappropriate Anti-Diuretic Hormone

what kind of hyponatraemia do you get and why

A

euvolaemic hyponatraemia

because the excessive water reabsorption is not significant enough to cause fluid overload

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146
Q

Syndrome of Inappropriate Anti-Diuretic Hormone

what will the urine osmolality and sodium be and why

A

high urine osmolality
high urine sodium

the urine becomes more concentrated as less water is excreted by the kidneys

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147
Q

Syndrome of Inappropriate Anti-Diuretic Hormone

symptoms

A
  • severe hyponatraemia: seizures, reduced consciousness
  • headache
  • fatigue
  • muscle aches and cramps
  • confusion
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148
Q

Syndrome of Inappropriate Anti-Diuretic Hormone

causes (6)

A
  • post-op
  • infection: atypical pneumonia + lung abscesses
  • head injury
  • medications
  • malignancy: small cell lung cancer
  • meningitis
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149
Q

Syndrome of Inappropriate Anti-Diuretic Hormone

what medications can cause SIADH

A
  • thiazide diuretics
  • carbamazepine
  • vincristine
  • cyclophosphamide
  • antipsychotics
  • SSRIs
  • NSAIDs
150
Q

Syndrome of Inappropriate Anti-Diuretic Hormone

how to establish diagnosis

A 
diagnosis of exclusion 
\+ 
clinical exam: euvolaemia 
U+E: hyponatraemia 
high urine Na + osmolality
151
Q

Syndrome of Inappropriate Anti-Diuretic Hormone

when establishing diagnosis, what needs to be excluded

A
  • adrenal insufficiency: -ve short synacthen test
  • no diuretic use
  • no diarrhoea, vomiting, burns, fistula, XS sweat
  • no XS water intake
  • no CKD or AKI
152
Q

Syndrome of Inappropriate Anti-Diuretic Hormone

mnx

A
  • stop causative medication
  • fluid restriction: 500ml-1L
  • Tolvaptan (ADH receptor blocker)
  • Demeclocycline (tetracycline abx)
153
Q

Syndrome of Inappropriate Anti-Diuretic Hormone

what is Tolvaptan

A

an ADH receptor blocker

v. powerful, can cause a rapid increase in Na

close monitoring: 6 hourly sodium levels

154
Q

Syndrome of Inappropriate Anti-Diuretic Hormone

what is demeclocycline

A

a tetracycline abx

inhibits ADH

it was used prior to vaptans and is now rarely used

155
Q

Syndrome of Inappropriate Anti-Diuretic Hormone

what is a complication of severe hyponatraemia (<120 mmols/l) being treated too quickly (>10 mmol/l increase over 24hrs)

A

central pontine myelinolysis (CPM)

aka osmotic demyelination syndrome

156
Q

Syndrome of Inappropriate Anti-Diuretic Hormone

how does the brain adapt to low blood Na

A

as blood Na falls, water will move across the BBB by osmosis

brain swells

brain adapts by reducing solutes in brain cells so water is balanced across the BBB. Takes a few days

157
Q

Syndrome of Inappropriate Anti-Diuretic Hormone

why does the brain cells have a low osmolality in severe or long time hyponatraemia

A

as blood Na falls, water will move across the BBB by osmosis

brain swells

brain adapts by reducing solutes in brain cells so water is balanced across the BBB. Takes a few days

158
Q

Syndrome of Inappropriate Anti-Diuretic Hormone

CPM: what happens when
the blood Na suddenly rises

A

water will rapidly shift out of the brain cells and into the blood causing 2 phases of sx

159
Q

Syndrome of Inappropriate Anti-Diuretic Hormone

CPM: what are the 1st phase symptoms

A

encephalopathic and confused

headache, N+V

due to electrolyte imbalance

160
Q

Syndrome of Inappropriate Anti-Diuretic Hormone

CPM: what are the 2nd phase symptoms

A
  • spastic quadriparesis
  • pseudobulbar palsy
  • cognitive and behavioural changes

due to demyelination of neurones

161
Q

Syndrome of Inappropriate Anti-Diuretic Hormone

CPM: mnx

A

prevention is essential as trx is only supportive

162
Q

T2DM

whom is metformin CI’d in

A

those with an eGFR<30 due to lactic acidosis

use gliclazide instead

163
Q

what recreational drug is known to deplete B12 reserves

A

laughing gas (NO)

164
Q

Diabetes Insipidus

what is it

A

a lack of ADH or a lack of response to ADH

this prevents the kidney from being able to concentrate the urine leading the polyuria + polydipsia

165
Q

Diabetes Insipidus

what can it be classified into

A

nephrogenic or cranial

166
Q

Diabetes Insipidus

what is primary polydipsia

A

when the pt has a normally functioning ADH system but they are drinking excessive quantities of water leading to excessive urine production

they don’t have diabetes insipidus

167
Q

Diabetes Insipidus

what is nephrogenic diabetes insipidus

A

when the collecting ducts of the kidneys do not respond to ADH

168
Q

Diabetes Insipidus

what are the causes of nephrogenic diabetes insipidus (4)

A
  • lithium
  • mutations in the AVPR2 gene on the X chromosome that codes for the ADH receptor
  • intrinsic kidney disease
  • electrolyte disturbance (hypokalaemia and hypercalcaemia)
169
Q

Diabetes Insipidus

mutation in which gene can cause nephrogenic diabetes insipidus

A

AVPR2 gene on the X chromosome that codes for the ADH receptor

170
Q

Diabetes Insipidus

what is cranial diabetes insipidus

A

when the hypothalamus does not produce ADH for the pituitary gland to secrete

171
Q

Diabetes Insipidus

cranial causes (6)

A
  • idiopathic
  • brain tumours
  • head injury
  • brain malformations
  • brain infections: meningitis, encephalitis, TB)
  • brain surgery or radiotherapy
172
Q

Diabetes Insipidus

presentation (5)

A
  • polyuria
  • polydipsia
  • dehydration
  • postural hypotension
  • hypernatraemia
173
Q

Diabetes Insipidus

what will the urine osmolality be

A

low

174
Q

Diabetes Insipidus

what will the serum osmolality be

A

high

175
Q

Diabetes Insipidus

what is the diagnostic inx

A

water deprivation test

176
Q

Diabetes Insipidus

what is the water deprivation test aka

A

the desmopressin stimulation test

177
Q

Diabetes Insipidus

describe the method for the water deprivation test

A
  • fluid deprivation for 8h
  • measure urine osmolality
  • administer desmopressin (synth ADH)
  • measure urine osmolality 8h later
178
Q

Diabetes Insipidus

what are the results of urine osmolality in cranial DI after fluid deprivation

A

low

179
Q

Diabetes Insipidus

what are the results of urine osmolality in cranial DI after desmopressin (ADH)?

A

high

180
Q

Diabetes Insipidus

what are the results of urine osmolality in nephrogenic DI after fluid deprivation

A

low

181
Q

Diabetes Insipidus

what are the results of urine osmolality in nephrogenic DI after desmopressin (ADH)?

A

low

182
Q

Diabetes Insipidus

what are the results of urine osmolality in primary polydipsia after fluid deprivation

A

high

183
Q

Diabetes Insipidus

what are the results of urine osmolality in primary polydipsia after desmopressin (ADH)?

A

high

184
Q

Diabetes Insipidus

mnx in mild cases

A
  • treat underlying cause

- manage conservatively

185
Q

Diabetes Insipidus

mnx in cranial DI

A

desmopressin (synthetic ADH)

186
Q

Diabetes Insipidus

mnx in nephrogenic DI

A

desmopressin in higher doses (under close monitoring)

187
Q

Phaeochromocytoma

where is adrenaline produced

A

by the chromaffin cells in the adrenal medulla of the adrenal glands

188
Q

Phaeochromocytoma

what is it

A

a tumour of the chromaffin cells that secretes unregulated and excessive amounts of adrenaline

189
Q

Phaeochromocytoma

what is adrenaline

A

a catecholamine hormone and neurotransmitter that stimulates the sympathetic nervous system and responsible for the fight or flight response

190
Q

Phaeochromocytoma

why are there periods of worse symptoms followed by more settled periods

A

adrenaline tends to be secreted in bursts

191
Q

Phaeochromocytoma

25% are familial and associated with what?

A

multiple endocrine neoplasia type 2 (MEN2)

192
Q

Phaeochromocytoma

what is the 10% rule to describe the patterns of tumour

A

10% bilateral
10% cancerous
10% outside the adrenal gland

193
Q

Phaeochromocytoma

inx

A
  • 24h urine catecholamines

- plasma free metanephrines

194
Q

Phaeochromocytoma

why is measuring catecholamines unreliable

A

they naturally fluctuate and so will be difficult to interpret the result

195
Q

Phaeochromocytoma

what is metanephrines

A

a breakdown product of adrenaline

196
Q

Phaeochromocytoma

what is the half life of adrenaline

A

a few minutes

197
Q

Phaeochromocytoma

why are metanephrine levels a more diagnostic tool

A

metanephrines have a longer half life than adrenaline so less prone to dramatic fluctuations

198
Q

Phaeochromocytoma

presentation

A
  • peaks and troughs
  • anxiety
  • sweating
  • headache
  • HTN
  • palpitations, tachyardia + paroxysmal AF
199
Q

Phaeochromocytoma

mnx initially

A

Phentolamine IV (short acting alpha blocker) - to initially control BP

Phenoxybenzamine (longer acting alpha blocker) - to control BP before surgery can be arranged

200
Q

Phaeochromocytoma

mnx once established on alpha blockers

A

beta blockers

201
Q

Phaeochromocytoma

what is the definitive mnx

A

adrenalectomy

202
Q

trx of symptomatic prolactinomas

A

dopamine agonists (e.g. cabergoline, bromocriptine) which inhibit the release of prolactin from the pituitary gland

trans-sphenoidal surgery if medicine failed

203
Q

Cushing Syndrome definition

A

the signs and sx that develop after prolonged abnormal elevation of cortisol

204
Q

Cushing’s Disease definition

A

the specific condition where a pituitary adenoma secretes excessive ACTH

205
Q

Cushing syndrome presentation

A
  • round in the middle with thin limbs
  • high levels of stress hormones
  • extra effects
206
Q

Cushing syndrome presentation (round in the middle with thin limbs)

A
  • round moon face
  • central obesity
  • abdominal striae
  • buffalo hump
  • proximal limb muscle wasting
207
Q

Cushing syndrome presentation (high levels of stress hormone)

A
  • HTN
  • cardiac hypertrophy
  • hyperglycaemia (T2DM)
  • depression
  • insomnia
208
Q

Cushing syndrome presentation (extra effects)

A
  • osteoporosis

- easy bruising and poor skin healing

209
Q

Cushing syndrome

causes

A
  • exogenous steroids
  • cushing’s disease
  • adrenal adenoma
  • paraneoplastic cushing’s
210
Q

Cushing syndrome

what is paraneoplastic cushing’s

A

excess ACTH is released from a cancer (not the pituitary) and stimulates excessive cortisol release (ectopic ACTH)

211
Q

Cushing syndrome

what is the most common cause of paraneoplastic Cushing’s

A

Small Cell Lung Cancer

212
Q

Cushing syndrome

test of choice for dx

A

dexamethasone suppression test

213
Q

Cushing syndrome

what can be used as an alternative to the dexamethasone suppression test to dx but not indicate underlying cause

A

24 hr urinary free cortisol

214
Q

Cushing syndrome

trx

A

surgically remove tumour- trans-sphenoidal (pituitary adenoma)

215
Q

Cushing syndrome

mnx if surgical removal is not possible

A

remove both adrenal glands and give replacement steroid hormones for life

216
Q

Cushing syndrome

describe what happens in the dexamethasone test

A

give low dose dexamethasone at 10pm

measure cortisol and ACTH at 9am

then repeat but with high dose

217
Q

Cushing syndrome

normal response to low dose dexamethasone

A
  • suppresses CRH
  • supresses ACTH
  • LOW CORTISOL
218
Q

Cushing syndrome

Result of low dose dexamethosone if pt has Cushing’s syndrome

A
  • CORTISOL REMAINS HIGH as a little bit of dexamethasone makes no difference to axis
219
Q

Cushing syndrome

result of high dose dexamethasone if someone has cushing’s disease (pituitary adenoma)

A
  • high enough to suppress ACTH

- LOW CORTISOL

220
Q

Cushing syndrome

Result of high dose dexamethasone if pt has an adrenal tumour

A
  • suppresses CRH
  • suppresses ACTH
  • but no effect on adrenal gland and is still pumping out cortisol
  • HIGH CORTISOL
221
Q

Cushing syndrome

Result of high dose dexamethasone on an ectopic ACTH tumour

A
  • suppresses CRH
  • but ectopic still releasing high ACTH
  • so HIGH CORTISOL
222
Q

pt had thyroidectomy, then tingling of face and hands and spasms. what is it

A

Iatrogenic hypocalcaemia

The parathyroids may be damaged during thyroidectomy causing post-operative hypocalcaemia

223
Q

Hyperthyroidism

define hyperthyroidism

A

over-production of thyroid hormone by the thyroid gland.

224
Q

Hyperthyroidism

define thyrotoxicosis

A

an abnormal and excessive quantity of thyroid hormone in the body

225
Q

Hyperthyroidism

define primary hyperthyroidism

A

the thyroid itself that is behaving abnormally and producing excessive thyroid hormone

226
Q

Hyperthyroidism

define Secondary hyperthyroidism

A

thyroid is producing excessive thyroid hormone as a result of overstimulation by TSH. The pathology is in the hypothalamus or pituitary.

227
Q

Hyperthyroidism

what is Grave’s disease

A

an autoimmune condition where TSH receptor antibodies cause a primary hyperthyroidism

228
Q

Hyperthyroidism

Grave’s: what are TSH receptor antibodies

A

abnormal antibodies produced by the immune system that mimic TSH and stimulate the TSH receptors on the thyroid

229
Q

Hyperthyroidism

what is the most common cause

A

Grave’s disease

230
Q

Hyperthyroidism

what is Toxic multinodular goitre aka

A

Plummer’s disease

231
Q

Hyperthyroidism

what is Toxic multinodular goitre

A

nodules develop on the thyroid gland that act independently of the normal feedback system and continuously produce excessive thyroid hormone

232
Q

Hyperthyroidism

what is exophthalmos caused by

A

Grave’s disease

inflammation, swelling and hypertrophy of the tissue behind the eyeball that forces the eyeball forward

233
Q

Hyperthyroidism

what is Pretibial myxoedema

A

deposits of mucin under the skin on the anterior aspect of the leg (the pre-tibial area).

discoloured, waxy, oedematous appearance to the skin over this area

234
Q

Hyperthyroidism

cause of Pretibial myxoedema

A

specific to Grave’s disease and is a reaction to the TSH receptor antibodies.

235
Q

Hyperthyroidism

causes (4)

A
  • Grave’s disease
  • Toxic multinodular goitre
  • Solitary toxic thyroid nodule
  • Thyroiditis (e.g. De Quervain’s, Hashimoto’s, postpartum and drug-induced thyroiditis)
236
Q

Hyperthyroidism

unique features of Grave’s (all relate to presence of TSH receptor antibodies)

A
  • Diffuse goitre (without nodules)
  • Graves eye disease
  • Bilateral exophthalmos
  • Pretibial myxoedema
237
Q

Hyperthyroidism

unique features of Toxic Multinodular Goitre

A
  • Goitre with firm nodules
  • Most patients are >50
  • 2nd most common cause of thyrotoxicosis (after Grave’s)
238
Q

Hyperthyroidism

mnx of
Solitary Toxic Thyroid Nodule

A

surgical removal of the nodule.

nodules are usually benign adenomas

239
Q

Hyperthyroidism

presentation of De Quervain’s Thyroiditis

A
  • viral infection with fever, neck pain and tenderness
  • dysphagia
  • features of hyperthyroidism
240
Q

Hyperthyroidism

why is there a hyperthyroid phase followed by a hypothyroid phase in De Quervain’s Thyroiditis

A

the TSH level falls due to negative feedback

241
Q

Hyperthyroidism

mnx of De Quervain’s Thyroiditis

A

supportive treatment with NSAIDs for pain and inflammation

BB for symptomatic relief of hyperthyroidism

242
Q

Hyperthyroidism

presentation of a thyroid storm/thyrotoxic crisis

A
  • hyperthyroidism
  • pyrexia
  • tachycardia
  • delirium
243
Q

Hyperthyroidism

mnx of thyroid storm

A
  • same for thyrotoxicosis

+ fluid resus, anti-arrhythmic med + BB

244
Q

Hyperthyroidism

1st line mnx

A

carbimazole

245
Q

Hyperthyroidism

carbimazole: what is titration-block

A

The dose is carefully titrated to maintain normal levels

246
Q

Hyperthyroidism

carbimazole: what is block and replace

A

The dose is sufficient to block all production and the patient takes levothyroxine titrated to effect

247
Q

Hyperthyroidism

2nd line mnx

A

Propylthiouracil

248
Q

Hyperthyroidism

what is the risk with Propylthiouracil

A

small risk of severe hepatic reactions

249
Q

Hyperthyroidism

how does radioactive iodine work as mnx

A

drinking a single dose of radioactive iodine

taken up by the thyroid gland and the emitted radiation destroys a proportion of the thyroid cells.

250
Q

Hyperthyroidism

what are the strict rules with radioactive iodine

A
  • Must not be pregnant and are not allowed to get pregnant within 6m
  • Avoid close contact with children and pregnant women for 3w
  • Limit contact with anyone for several days after receiving the dose
251
Q

Hyperthyroidism

what are BB used for

A

to block the adrenalin related symptoms of hyperthyroidism

esp in a thyroid storm

252
Q

Hyperthyroidism

what is the BB of choice for mnx of sx and why

A

Propranolol

it non-selectively blocks adrenergic activity as opposed to more “selective” beta blockers the work only on the heart

253
Q

important safety info for carbimazole

A
  • Neutropenia and agranulocytosis: signs of infection
  • increased risk of congenital malformations
  • risk of acute pancreatitis
254
Q

when first starting carbimazole trx, how often should bloods be taken

A

every 6w

255
Q

Once your hormone levels are stable on carbimazole, how often should bloods be taken

A

every 3m

256
Q

Hypothyroidism

what is the most common cause of hypothyroidism in the developed world

A

Hashimoto’s Thyroiditis

257
Q

Hypothyroidism

what autoantibodies is Hashimoto’s Thyroiditis associated with

A

antithyroid peroxidase (anti-TPO) antibodies

and antithyroglobulin antibodies

258
Q

Hypothyroidism

does Hashimoto’s Thyroiditis cause a goitre

A

yes

259
Q

Hypothyroidism

what is the most common cause of hypothyroidism in the developing world

A

iodine deficiency

260
Q

Hypothyroidism

which foods is iodine added to to prevent iodine deficiency

A

table salt

261
Q

Hypothyroidism

which treatments can cause it

A

All of the treatments for hyperthyroidism:

  • carbimazole
  • propylthiouracil
  • radioactive iodine
  • thyroid surgery
262
Q

Hypothyroidism

which medications can cause it (not the hyperthyroid treatments)

A

lithium: inhibits the production of thyroid hormones and can cause a goitre and hypothyroidism.
amiodarone: interferes with thyroid hormone production and metabolism. Usually can cause hypothyroidism but also thyrotoxicosis

263
Q

Hypothyroidism

what does it mean by central causes

A

secondary hypothyroidism

the pituitary gland is failing to produce enough TSH

hypopituitism

264
Q

Hypothyroidism

central causes

A
  • tumours
  • infection
  • vascular (Sheehan Syndrome)
  • radiation
265
Q

Hypothyroidism

presentation and features

A
  • weight gain
  • fatigue
  • dry skin
  • coarse hair + hair loss
  • Fluid retention (oedema, pleural effusions, ascites)
  • Heavy or irregular periods
  • Constipation
266
Q

Hypothyroidism

what is primary hypothyroidism caused by

A

thyroid gland insufficiency

267
Q

Hypothyroidism

primary hypothyroidism TSH, T3 + T4 results

A

high TSH

low T3 + T4

268
Q

Hypothyroidism

what is secondary hypothyroidism caused by

A

pituitary pathology

269
Q

Hypothyroidism

secondary hypothyroidism TSH, T3 + T4 results

A

low TSH

low T3 +T4

270
Q

Hypothyroidism

mnx

A

PO levothyroxine

271
Q

Hypothyroidism

how does levothyroxine work

A

synthetic T4, and metabolises to T3 in the body.

272
Q

Hypothyroidism

monitoring with levothyroxine

A

TSH levels monthly until stable, then once stable it can be checked less frequently

273
Q

which abx can cause diabetes insipidus

A

Demeclocycline

274
Q

what is Waterhouse-Friderichsen syndrome

A

adrenal gland failure due to bleeding into the adrenal gland

usually caused by severe meningococcal infection or other severe, bacterial infection

275
Q

symptoms of Waterhouse-Friderichsen syndrome

A

acute adrenal gland insufficiency, and profound shock

276
Q

1st line mnx for steroid induced hyperglycaemia

A

Gliclazide

277
Q

Type 1 Diabetes

what is a normal blood glucose conc

A

4.4 - 6.1 mmol/l

278
Q

Type 1 Diabetes

where is insulin produced

A

beta cells in the Islets of Langerhans in the pancreas

279
Q

Type 1 Diabetes

how does insulin reduce blood sugar

A
  • causes cells in the body to absorb glucose from the blood and use it as fuel
  • causes muscle and liver cells to absorb glucose from the blood and store it as glycogen
280
Q

Type 1 Diabetes

where is glucagon produced

A

by the alpha cells in the Islets of Langerhans in the pancreas.

281
Q

Type 1 Diabetes

what does glucagon do

A
  • glycogenolysis: tells the liver to break down stored glycogen into glucose.
  • gluconeogenesis: tells the liver to convert proteins and fats into glucose
282
Q

Type 1 Diabetes

when does ketogenesis occur

A

when there is insufficient glucose supply and glycogens stores are exhausted

283
Q

Type 1 Diabetes

what happens in ketogenesis

A

The liver takes fatty acids and converts them to ketones

they can be used as fuel

284
Q

Type 1 Diabetes

how can ketones levels be measured

A

in the urine by “dip-stick” and in the blood using a ketone meter

285
Q

Type 1 Diabetes

what is it

A

a disease where the pancreas stops being able to produce insulin

286
Q

Type 1 Diabetes

who does DKA occur in and why

A

occurs in Type 1 Diabetes

body does not have enough insulin to use and process glucose

287
Q

Type 1 Diabetes

what are the main problems

A
  • ketoacidosis
  • dehydration
  • potassium imbalance
288
Q

Type 1 Diabetes

why is there dehydration in DKA

A

glucose starts being filtered into the urine.

which draws water out with it (osmotic diuresis).

patient urinates more and drinks more

289
Q

Type 1 Diabetes

why is there hypokalaemia in DKA

A
  • Insulin normally drives potassium into cells
  • Without insulin potassium is not added to and stored in cells
  • Serum potassium can be high or normal
  • total body potassium is low because no potassium is stored in the cells
  • when trx with insulin starts, patients can develop severe hypokalaemia
290
Q

Type 1 Diabetes

signs of DKA

A
  • Hyperglycaemia
  • Dehydration
  • Ketosis
  • Metabolic acidosis (with a low bicarbonate)
  • Potassium imbalance
291
Q

Type 1 Diabetes

sx of DKA

A
  • Polyuria, Polydipsia
  • N + V
  • Acetonic breath
  • Dehydration –> hypotension
  • Altered consciousness
  • sx of underlying trigger (i.e. sepsis)
292
Q

Type 1 Diabetes

diagnosis of DKA

A
  1. Hyperglycaemia (BG > 11 mmol/l)
  2. Ketosis (blood ketones > 3 mmol/l)
  3. Acidosis (pH < 7.3)
293
Q

Type 1 Diabetes

mnx of DKA

A
  • IV fluid resus (1 litre stat)
  • Insulin infusion (Actrapid at 0.1 Unit/kg/hour)
  • potassium replacement (no more than 10mmol/hr
294
Q

Type 1 Diabetes

how is the insulin prescribed

A

combination of

  • background, long acting insulin OD
  • short acting insulin injected 30 min before meals
295
Q

Type 1 Diabetes

what can injecting in the same spot cause

A

lipodystrophy: SC fat hardens and do not absorb insulin properly

296
Q

Type 1 Diabetes

short term complications

A
  • hypoglycaemia

- hyperglycaemia (and DKA)

297
Q

Type 1 Diabetes

typical sx of hypoglycaemia

A
  • tremor
  • sweating
  • irritability
  • dizziness
  • pallor

severe:

  • reduced consciousness
  • coma
  • death unless treated
298
Q

Type 1 Diabetes

why are there vascular long term complications

A

Chronic exposure to hyperglycaemia causes damage to the endothelial cells of blood vessels.

This leads to leaky, malfunctioning vessels that are unable to regenerate

299
Q

Type 1 Diabetes

why are there infection related complications

A

High levels of sugar in the blood also causes suppression of the immune system

and provides an optimal environment for infectious organisms to thrive

300
Q

Type 1 Diabetes

macrovascular complications

A
  • Coronary artery disease: a major cause of death
  • Peripheral ischaemia: poor healing, ulcers and “diabetic foot”
  • Stroke
  • Hypertension
301
Q

Type 1 Diabetes

microvascular complications

A
  • Peripheral neuropathy
  • Retinopathy
  • Kidney disease, particularly glomerulosclerosis
302
Q

Type 1 Diabetes

infection related complications

A
  • UTIs
  • pneumonia
  • skin + soft tissue infections esp in feet
  • candidiasis
303
Q

Type 1 Diabetes

what is HbA1c

A

glycated haemoglobin: how much glucose is attached to Hb molecule

the average glucose level over the last 3 months because red blood cells have a lifespan of around 3-4 months

304
Q

Type 1 Diabetes

what is capillary blood glucose

A

used for self monitoring glucose

gives immediate result

305
Q

Type 1 Diabetes

what is Flash Glucose Monitoring (e.g. FreeStyle Libre)

A

sensor on the skin that measures the glucose level of interstitial fluid

a lag of 5 minutes behind blood glucose

306
Q

Acromegaly

what is it

A

the clinical manifestation of excessive growth hormone (GH)

307
Q

Acromegaly

where is GH produced

A

by the anterior pituitary gland

308
Q

Acromegaly

what is the most common cause

A

unregulated growth hormone secretion by a pituitary adenoma.

309
Q

Acromegaly

what is a rare cause

A

cancer (lung or pancreatic) secreting ectopic growth hormone releasing hormone (GHRH) or growth hormone

310
Q

Acromegaly

how can the presentation be separated into

A
  • space occupying lesion
  • overgrowth of tissues
  • organ dysfunction
  • sx suggesting active raised GH
311
Q

Acromegaly

presentation (space occupying lesion)

A
  • headaches

- bitemporal hemianopia

312
Q

Acromegaly

presentation (overgrowth of tissues)

A
  • frontal bossing: prominent forehead and brow
  • large nose, tongue, hands, feet
  • large protruding jaw (prognathism)
  • arthritis from imbalanced growth of joints
313
Q

Acromegaly

presentation (organ dysfunction)

A
  • hypertrophic heart
  • HTN
  • T2DM
  • colorectal cancer
314
Q

Acromegaly

presentation (sx suggesting active raised GH)

A
  • new skin tags

- profuse sweating

315
Q

Acromegaly

why is a random GH level not a helpful inx

A

it will fluctuate, giving false positives and false negatives

316
Q

Acromegaly

what is the initial screening test

A

Insulin-like Growth Factor 1 (IGF-1)

raised

317
Q

Acromegaly

other inx (apart from IGF-1)

A
  • OGTT whilst measuring GH (high glucose normally suppresses GH)
  • MRI brain for pituitary tumour
  • formal visual field testing: refer to opth
318
Q

Acromegaly

definitive mnx of acromegaly secondary to pituitary adenoma

A

trans-sphenoidal surgical removal of the pituitary tumour

319
Q

Acromegaly

what medications can block GH

A
  • Pegvisomant (GH antagonist OD, SC)
  • Somatostatin analogues to block GH release (e.g. ocreotide)
  • Dopamine agonists to block GH release (e.g. bromocriptine)
320
Q

Acromegaly

what is one of the functions of somatostatin

A

block GH release from the pituitary gland.

321
Q

Acromegaly

where is somatostatin secreted

A

by the brain, GI tract and pancreas in response to complex triggers

322
Q

Acromegaly

which has a more of an inhibitory effect on GH release: somatostatin or dopamine

A

somastostatin

323
Q

In which part of the adrenal gland is the mineralocorticoid produced?

A

The zona glomerulosa produces mineralocorticoids (e.g aldosterone)

324
Q

In which part of the adrenal gland is glucocorticoid produced?

A

The zona fasciculata produces glucocorticoids (e.g. cortisol)

325
Q

what is a complication of DKA

A

cerebral oedema

326
Q

when should 5% glucose be added in mnx in DKA

A

until blood glucose is <14 mmol/L

327
Q

what is the first line treatment of primary hypogonadism in men.

A

testosterone therapy

328
Q

is TB adrenalitis is a well recognised cause of Addison’s disease

A

yes

329
Q

what is a carcinoid tumour

A

rare, slow growing malignant tumours that develop in the neuroendocrine system

330
Q

what hormone do 5-10% of carcinoid tumours secrete

A

serotonin

331
Q

clinical features of carcinoid tumours

A
  • Abdominal pain
  • Diarrhoea
  • Flushing
  • Wheeze
  • Pulmonary stenosis
332
Q

mnx of carcinoid tumours

A
  • octreotide: an analogue of Somatostatin in order to inhibit tumour products
  • surgical resection
333
Q

when to inform the DVLA and stop immediately driving if patient has hypoglycaemia

A

> 1 severe episode of hypoglycaemia whilst awake

or 1 episode of severe hypoglycaemia whilst driving

334
Q

what is classed as severe hypoglycaemia

A

an episode the patient required help from another person to manage

335
Q

what is impaired fasting glucose

A

a pre-diabetic state defined as:

  • Fasting glucose 6.1-7mmol/L
  • 2h glucose <7.8mmol/L
336
Q

when is metformin CI’d

A

if eGFR <30 ml/min

337
Q

definition of Impaired glucose tolerance is a pre-diabetic state

A

Fasting glucose <7mmol/L

2h glucose 7.8-11mmol/L

338
Q

why does Hypoglycaemia unawareness occur

A

due to a blunting of the body’s autonomic and stress responses because of recurrently low blood glucose levels

339
Q

1st line approach to hypoglycaemia unawareness

A

Reduce the patients insulin doses and set higher than normal blood glucose targets.

340
Q

According to NICE guidelines, gestational diabetes mellitus is diagnosed if the woman has either:

A
  • fasting plasma glucose level of ≥5.6 mmol/L;

or
- 2 hour post-oral glucose tolerance test plasma glucose level of ≥7.8 mmol/L.

341
Q

what are 1st line medications for diabetic neuropathic pain

A

duloxetine, gabapentin, pregabalin or amitriptyline.

342
Q

TSH normal
T4 elevated

what could this be

A

Subacute (De Quervain’s) Thyroiditis.

starts with hyperthyroidism followed by a hypothyroid phase following depletion of TSH

343
Q

what do medullary thyroid cancers secrete

A

cancer of the parafollicular cells and so secrete calcitonin

344
Q

why is there abdo pain in DKA

A

theories:

  • acidosis
  • hyperglycaemia increasing gastric motility
  • rapid expansion of the hepatic capsule
  • mesenteric ischaemia due to volume depletion (secondary to dehydration)
345
Q

what is pseudohypoparathyrodism

A

a rare genetic condition resulting in failure of target organs to respond to normal levels of parathyroid hormone

346
Q

how is pseudohypoparathyroidism different to hypoparathyroidism

A

hypoparathyroidism: PTH deficiency
pseudo: failure to respond to PTH

347
Q 
15 year old 
low Ca
high phosphate 
high PTH 
no kidney disease 
blunting of the 4th and 5th knuckles

what could this be

A

Pseudohypoparathyroidism - Type 1a

348
Q

low Ca
low phosphate
normal PTH

what could this be

A

Vitamin D deficiency

349
Q

what is Psuedopseudohypoparathryoidism

A

the patient has the phenotypic appearance of a patient with Pseudohypoparathyroidism but has no biochemical abnormality

350
Q

clinical presentation of hypocalcaemia

A
  • Numbness/tingling of fingers and toes
  • Muscle cramps
  • Carpopedal spasm
  • Seizures
  • Chvostek’s sign
  • Trousseau’s sign
351
Q

hypocalcaemia: what is Chvostek’s sign

A

tapping the facial nerve results in twitching of the face

352
Q

hypocalcaemia: what is Trousseau’s sign

A

inflation of a blood pressure cuff results in carpopedal spasm

353
Q

what modifications would you make to someone’s diabetic medication if on end of life care

A
  • stop PO hypoglycaemic agents in T2DM
  • Insulin: convert to OD long-acting, at a 25% dose reduction.
  • Metformin is safe unless eGFR < 30 ml/L/1.73m2.
354
Q

why stop PO hypoglycaemic agents in end of life care

A

carry a significant risk of precipitating hypoglycaemia in patients at the end of their lives, due to their reduced oral intake

355
Q

Which type of thyroid cancer carries the worst prognosis?

A

Anaplastic

356
Q

how does a thyroid lymphoma present as

A
  • rapidly expanding mass in the neck
  • hoarseness
  • difficulty swallowing
  • difficulty breathing
357
Q

is Hashimoto’s Thyroiditis a RF for developing thyroid lymphoma

A

yes

358
Q

What is the most common type of thyroid cancer?

A

Papillary thyroid cancer

359
Q

what is the gold standard test for establishing the diagnosis of insulinoma

A

A 72 hour fast

360
Q

what is a by product of insulin production

A

serum c-peptide

361
Q

what does a high insulin and high c-peptide indicate

A

excessive endogenous production of insulin

362
Q

what does a high insulin and low c-peptide indicate

A

exogenous administration of insulin

363
Q

features of MEN-1

A
  • pituitary tumours
  • parathyroid hyperplasia
  • pancreatic tumours
364
Q

features of MEN-2

A
  • medullary thyroid cancer
  • Adrenal: pheochromocytoma
  • Parathyroid: hyperplasia/adenomas
365
Q

Which of the 6 anterior pituitary hormones tends to stop first?

A

Go Look For The Adenoma

growth hormone -> LH -> FSH -> thyroid -> ACTH

366
Q

The most important initial treatment for symptomatic hypercalcaemia

A

aggressive intravenous fluid therapy.

367
Q

what would you expect to see in the WBC of someone with an Addisonian crisis

A

raised WBC esp eosinophilia

368
Q

consequences if you start her on too high a dose of levothyroxine

A
  1. Hyperthyroidism –>thyroid storm
  2. MI, arrythmias (AF)
  3. sweating, palpitations, N+V, diarrhoea, coma, psychosis
369
Q

2 commonest causes of hypercalcaemia

A

Primary hyperparathyroidism

Malignancy: bony mets, myeloma

370
Q

mnx of hypercalcaemia

A
  • aggressive IV fluids typically 3-4 litres/day.
  • Bisphosphonates
  • calcitonin
  • furosemide
371
Q

ECG findings of hypokalaemia

A
  • small/inverted T waves
  • U waves
  • prolonged PR interval
  • ST-segment depression
372
Q

If the patient is unwell due to their hyponatraemia (e.g. having seizures, or is comatose), how do you manage

A

hypertonic (3%) saline

Finals (47 decks)

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