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Year 3 Medicine > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is the definitive management of tertiary hyperparathyroidism?

A

Surgery to remove the parathyroid glands

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2
Q

How will tertiary hyperparathyroidism manifest in blood tests?

A

Inappropriately high PTH levels
Increased serum calcium
Increased serum phosphate

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3
Q

Why does CKD cause secondary hyperparathyroidism?

A

In response to hypocalcemia

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4
Q

How does secondary hyperparathyroidsim lead to tertiary hyperparathyroidism?

A

Overtime gland hypertrophy causes PTH secretion to become autonomous and independent of negative feedback, leading to raised PTH and raised calcium

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5
Q

What is the order of hormone loss in pituitary hormone deficiency?

A 
Growth hormone
Gonadotrophins
TSH
ACTH
Prolactin
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6
Q

What is the first line treatment of SIADH?

A

Fluid restriction

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7
Q

What features indicated a diagnosis of SIADH?

A

Euvolaemic hyponatremia
Low serum osmolality
High urine osmolality
High urine sodium

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8
Q

What is MEN 1 syndrome?

A

Mutations in the MEN1 gene cause neoplastic mutations of pituitary, parathyroid and the pancreas?

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9
Q

What are the symptoms of hypernatremia?

A 
Thirst
Apathy
Irritability 
Weakness
Confusion
Reduced conciousness 
Seizures
Hyperreflexia 
Spasticity
Coma
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10
Q

Causes of HYPOvolemic hypernatremia?

A

Renal free water losis (osmotic diuresis (NG feed), loop diuretics, intrinsic renal losses)
Non-renal free water loses (excess sweating, burns, diarrhoea, fistulas)

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11
Q

EUvolemic hypernatremia causes?

A 
Renal losses (Diabetes insipidus, hypodispia)
Extra-renal losses (insensible, resp losses)
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12
Q

HYPERvolemic causes of hypernatremia?

A 
Primary hyperalodsteronism
Cushing's syndrome
Hypertonic dialysis
Hypertonic sodium bicarbonate
Sodium chloride tablets
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13
Q

Main differential for diabetes insipidus?

A

Psychogenic polydipsia

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14
Q

What is the urine osmolality in DI?

A

Urine osmolality <300 (dilute urine)

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15
Q

What is the sodium status of a patient with DI?

A

Hypernatermic

Or Normal

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16
Q

Causes of cranial DI?

A

Impaired release of ADH
Tumours
Trauma/post-op
Cerebral vasculitits (SLE, Wegener’s_

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17
Q

Causes of Npehrogenic DI?

A 
Resistance to ADH:
Congenital 
Drugs (lithium, amphoterecin, demeclocycline)
Hypokalaemia
Hypercalcemia
Tubulointersitial disease
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18
Q

How is hypernatremia treated?

A

Treat underlying cause

Free water

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19
Q

Symptoms of hyponatremia?

A 
Decreased perception
Gait disturbance
Yawning
Nausea 
Reversable ataxia
Headache
Apathy 
COnfusion
seizures
Coma
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20
Q

What is the plasma osmolality in hyponatremia?

A

Low

If normal or raised it is psudohyponatremia

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21
Q

Why does pseudohyponatremia occur?

A

High Lipids
Myeloma
Hyperglycemia
Uraemia

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22
Q

Causes of HYPOvoaemia hyponatraemia?

A

Renal loss
-Diuretics (thiazides)
-Osmotic diuresis (glucose, urea in recovering ATN)
Addison’s disease - mineralcortocoid deficiency
Non-renal loss
-Diarrhoea
-Vomiting
-Sweating
-Third space losses (burns, bowel obstruction pancretatitis)

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23
Q

At which rate should you correct hypovolaemic hyponatremia?

A

0.9% NaCl at 1-3ml/kg/hour

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24
Q

What will the urine sodium be in a patient with hypovoaemic hyponatraemia due to renal losses?

A

> 20mmol/L

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25
Q

What will the urine sodium be in a patient with hypovoaemic hyponatraemia due to non-renal losses?

A

<20mmol/L

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26
Q

Causes of Euvolaemic Hyponatremia?

A 
Primary polydipsia (urine osmolality <100)
Glucocorticoid deficiency - adrenal insufficiency, SIADH
Hypothyroidism
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27
Q

What is SIADH

A

Euvolaemic hyponatraemia
Low serum osmolality
Inappropriately concentrated urine - urine osmolality >100, Na>20
Not on diuretics
DIagnosis of elimintation - normal renal, thyroid, adrenal function

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28
Q

How is SIADH managed?

A

Fluid restrict <800ml/day
PO sodium chloride
May give furosemide
Demeclocycline/tolvaptan

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29
Q

Causes of hypervolaemic hyponatremia?

A

CCF
Nephrotic syndrome
Liver cirrhosis

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30
Q

How is hypervolaemic hyponatremia treated?

A

Fluid restriction

COnsider furosemide

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31
Q

What is the risk of correcting hyponatraemia too quickly, and how much should be aimed to correct each day?

A

Central pontine/osmotic myelinosis

Aim to correct <12 mmol/L/day

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32
Q

How is acute hyponatremia treated (within 48 hours) if symptomatic?

A

Given 3% hypertonic saline IV boluses +/- furosemide

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33
Q

How is symptomatic chronic (48 hours or more) hyponatermia treated?

A

Hypertonic saline boluses only if fitting

Otherwise isotonic saline and furosemide - aim for 8mmol/L in 24 hours

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34
Q

How is chronic, asymptomatic hyponatermia treated

A

Stop offending drug
Water restriction
If dehydrated, restore volume, if overloaded - Na and water restriction and diuretics

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35
Q

Causes of hyperkaelmia?

A

CKD
K rich diet (dried fruit, potatoes, oranges, tomatoes, avacados, nuts)
Drugs
Hyperalodsteronism, Addison’s disease, Acidosis, DKA, rhabdomyolysis, tumour lysis, massive haemolysis, succinylocholine use
Rarer - hyperkalaemic periodic paralysis, Gordons syndrome
Artifcat hyperkalaemia, haemolysis, leucocoytosis, thrombocytosis

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36
Q

What drugs can cause hyperkalaemia?

A 
ACEi
ARBs
Sprinolactone 
Amiloride
NSAIDs
Heparin
LMWH
CYclosporin
Calcineurin inhibitors 
High dose trimethoprim
Digoxin toxicity
B-blockers
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37
Q

How can hyperkalemia be treated?

A

Low K diet
Lopp diuretic if fluid overloaded
IV calcium gluconate
IV insulin with glucose, B2 agonist nebs

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38
Q

Less common causes of hyperkalemia?

A

Hyporeninaemic Hypoaldosteronism (Type IV RTA)
Hypochloraemic acidosis in about 50%, hyperkalaemia,
typically with increased age and reduced eGFR classically
in diabetes nephropathy, acute GN (nephritis), TIN/sickle
cell, NSAIDs, CNIs, lupus nephritis

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39
Q

What are the symptoms of hypokalaemia?

A 
Fatigue
Constipation
Proximal muscle weakness
Paralysis
Cardiac arrythmias
Worsened glucose control in diabetics
HTN
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40
Q

Causes of hypokalaemia?

A

Pseudohypokalaemia - acute leukaemia
Extra-renal losses - indadequete PO intake, gut losses (NG, vommiting, secretory diarrhoea, laxatives, VIPoma, zollinger-ellison, ileostomy , enteric fistula)
Redisribution - delerium tremens, beta agonists, insulin caffine, theophylline, alpha-blockers (doxazosin), hypokalaemic periodic paralysis
Refeeding syndrome, alkalosis, vigourous exercise,
glue sniffing
Primary hyperaldosteronism (conn’s syndrome), cushings synfrome, secondary hyperaldosteronism
Renal losses (diuretics, RTA, tubulopathies, bartters/liddles/gittlmans), liqiorice, flucocorticoids, hypomagesaemia)

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41
Q

What proportion of the basal bolus insulin regime should be short acting (so the peak corresponds to the glycemic load of each of the three daily meals)?

A

60%, across 3 doses

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42
Q

What proportion of the basal bolus insulin regime should be long acting?

A

40%

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43
Q

What is Felty’s syndrome?

A

Triad of rheumatoid arthritis, splenomegaly and neutropenia

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44
Q

Notable side effects of corticosteroids?

A 
Oedema
Fluid retention
Hypokalemia
Supine HTN
Glucose intolerance
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45
Q

How does Conn’s syndrome present?

A 
Metabolic alklaosis 
Hypokalaemia
HTN
Hypernatremia 
Patients do not present with vomiting
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46
Q

How is diabetes insipidus investigated (first line test)?

A

Water deprivation test
Patients are deprived of fluids for 8 hours or until 3% loss of their body weight is reached.
Serum osmolaity, urine volume and urine osmolality are all measured hourly.
Positive if suboptimal response in urinary concentration to dehydration (urine osmolality<700mOsm/kg)
The level of concentration in urine osmolality gives and indication of renal concentrating capacity, and thus the severity of diabetic insipidus

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47
Q

Why do patients with Addisons disease not always have hyponatremia?

A

Although aldosterone normally enhances sodium reabsorption, other sodium retaining mechanisms such as the renin-angiotensin-aldosterone system are able to compensate to an extent

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48
Q

COmplication of severe hyponatremia?

A

brain herniation

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49
Q

What type of hyponatermia does SIADH cause?

A

Euvolemic hyponatremia

Urine sodium is above 40mmol/L and serum osmolality is above 100mosmol/L

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50
Q

How is acute severe hypercalcemia (>3.5) treated initially?

A

IV 0.9% saline 4L/24 hours

Agressive fluid rehydration will improve kidney function and help excess calcium be excreted

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51
Q

What is the combination of raised PTH, raided calcium and decreased phosphate charcteristic?

A

Primary hyperparathyroidism (overproduction of PTH by the parathyroid glands)

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52
Q

Most common causes of pseudohyponatremia?

A

Secondary to hyperlipidemia
Paraproteinaemia as seen in multiple myeloma
High blood glucose levels and use of mannitol or glycine

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53
Q

How to confirm a diagnosis of pseudohyponatraemia?

A

Measure serum osmolality level

Level of 275 mOsm/kg + supports the diagnosis

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54
Q

What blood test abnormalities can haemolysis of a sample before laboratory processing cause?

A

Pseudohyperkalemia due to potassium from inside red cells released into the serum
Potassium levels are significantly higher in red cells than in the serum hence significant alteration of true potassium level

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55
Q

What can cause pseudohyperkalemia?

A

Prolonged torniquet time during venepuncture (lactic acid production from temp ischema)
Haemolysis of blood sample before the lab

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56
Q

What is the first-line investigation for Addison’s disease

A

Morning serum cortisol - between 8 and 9 am when cortisol levels peak
Do not wait for result in an addisonian crisis, give IV hydrocortisone straight away

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57
Q

What paroneoplastic syndrome can cause SIADH?

A

Small cell lung cancer

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58
Q

What is the gold standard diagnostic test for a phaeochromocytoma?

A

Urine metanephrines

Plasma metanephrines

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59
Q

How is carcinoid syndrome diagnosed?

A

Urinary 5-HIAA excertion in a 24 urinary collection

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60
Q

What is Cushing’s Syndrome?

A

Signs and symptoms developing after prolonged abnormal elevation of cortisol

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61
Q

What is Cushing’s disease?

A

Subtype of cushing’s syndrome which occurs when a pituitary tumour secretes excessive ACTH.

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62
Q

Features of Cushing’s syndrome features?

A 
ROUND IN THE MIDDLE WITH THIN LIMBS
Round 'moon' face
Central obesity 
Abdnominal striate 
Buffalo Hump (fat pad on upper back)
Proximal limb muscle wasting 
HTN
Cardiac hypertrophy 
Hyperglycaemia (Type 2 Diabetes)
Depression 
Insomina 
Osteoporosis 
Easy bruising and poor skin
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63
Q

Causes of Cushing’s Syndrome?

A

Exogenous steroids - long term high dose steroid medication
Cushing’s DIsease (a pituitary adenoma releasing excessive ACTH)
Adrenal Adenoma
Paraneoplastic Cushing’s

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64
Q

What is Paraneoplastic Cushing’s?

A

Ectopic ACTH

Excess ACTH relased from a cancer (not of the pituitary) and stimulates cortisol release.

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65
Q

What is the most common cause of Paraneoplastic Cushing’s?

A

Small cell lung cancer

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66
Q

What is the gold standard investigation for Cushing’s disease?

A

Dexamethasone suppression test

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67
Q

How does the dexamethasone supression test work?

A

Initial low dose test - if normal, excludes Cushing’s syndrome
Abnormal test - perform high dose test performed
Dose of dexamethasone given at night time.
Cortisol and ACTH is measured in the morning (9AM)
Goal is to find out if dexamethasone supresses their normal morning cortisol spike.

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68
Q

Low dose dexamethasone suppression test dosage?

A

1mg

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69
Q

What is the dose for high dose dexamethasone suppression test?

A

8mg

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70
Q

What is a normal response to the low dose dexamethasone supression test (1mg)?

A

Dexamethasone supresses the release of cortisol be effecting negative feedback on the hypothalamus and pituitary.

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71
Q

What response will be shown in cushing’s disease in the high dose dexamethasone supression test?

A

Pituitary still show some response to the negative feeback and 8mg is enough to suppress the cortisol (but 1mg in the low dose test is not hence abnormal response there)

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72
Q

What is the response to the high dose dexamethasone supression test in an adrenal adenoma and why?

A

Cortisol not supressed as cortisol production is happening independent of the pituitary.
ACTH is supressed due to negative feedback on hypothalamus and pituitary gland

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73
Q

What is the response to the high dose dexamethasone suppression test where ectopic ACTH is being produced?

A

Neither cortisol of ACTH are suppressed because the ACTH production is independent of the hypothalamus or pituitary gland.

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74
Q

Why is 24 hour urinary free cortisol not the first line investigation for Cushing’s syndrome?

A

Can diagnose cushings, but
Cumbersome to carry out
And no indication of underlying cause

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75
Q

What investigations unrelated directly to cortisol and ACTH may be carried out when investigating Cushing’s

A 
FBC: raised WCC
Electrolytes: in an adrenal carcinoma, if alodsterone is also secreted there may be hypokalemia
MRI brain for pituitary adenoma
Chest CT - SCLC
Abdonminal CT - adrenal tumor
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76
Q

How is Cushing’s syndrome treated?

A

Transpehenoidal removal of pituitary adeoma
Surgical removal of adrenal tumour
Surgical removal of tumour producting ectopic ACTH

If the above are not possible: removal of adrenal glands and give the patient replacement steroid hormones for life

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77
Q

What is Addison’s disease?

A

Primary adrenal insufficiency, usually caused by an autoimmune process damaging the adrenal glands which leads them to not produce sufficient cortisol or aldosterone.

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78
Q

What is secondary adrenal insufficiency?

A

Result of inadequate ACTH stimulating the adrenal glands resulting in low cortisol release.
This is a result of loss or damage tk the pituitary gland:
Surgery
Pituitary tumour
Lack of blood to pituitary gland
Radiotherapy
Sheenans syndrome

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79
Q

What causes Sheenans syndrome?

A

Loss of blood during child birth causes necrosis of the pituitary gland

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80
Q

What is tertiary adrenal gland sufficiency?

A

Result of inadequate CRH release by the hypothalamus
Usually the result of >3 week course of steroids causing hypothalamic suppression, when the exogenous steroids are withdrawn the hypothalamus does not respond adequately and endogenous steroids are not produced

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81
Q

Why must high dose long term steroids be tapered down slowly?

A

Allow adrenal axis to regain normal function

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82
Q

Describe how the adrenal axis leads to steroid production?

A

CRH from the hypothalamus acts on anterior pituitary gland
ACTH from the AP acts on the adrenal glands
Adrenal glands release cortisol which has a negative feedback on the hypothalamus and AP

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83
Q

Signs and symptoms of adrenal insufficiency?

A 
Fatigue
Nausea
Cramps
Abdominal pain
Reduced libido
 Hyperpigmentation 
Hypotension
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84
Q

Why is early morning cortisol not the investigation of choice for Adrenal Insufficiency?

A

Often falsely normal

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85
Q

What viruses may trigger T1DM?

A

Coxsakie B virus

Enterovirus

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86
Q

Pathophysiology of T!DM?

A

Pancreatic B cell loss in the Islets of Langerhans in the pancrea due to T cell mediated destruction
No production of insulin (anabolic hormone)
Cells of the body can not take up glucose, muclse and liver cells don’t take up glucose and store it as glycogen
Cells cannot take up glucose
Blood glucose rises - hyperglycemia

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87
Q

What blood sugar does the body aim to maintain?

A

4.4-6.1 mmol/L

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88
Q

What is glucagon?

A

Catabolic homrone that increases blood sugar levels
Produced by alpha cells in the Islets of Langerhans in the pancrea
Causes liver to break down glycogen stores into glucose - glycoenolysis
Causes liver to convert proteins and fats in to glucose - gluconeogensis

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89
Q

What is ketogenesis and when does it occur?

A

Production of ketones - water soluble acids that can be used as fuel and are able to cross the blood brain barrier
Insufficient supply of glucose and glycogens stores are exchausted (prolonged fasting state)
Liver converts fatty acids to ketones
Normal in fasting conditions or on a very low carbohydrate, high fat diet

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90
Q

Presentation of DM?

A

Hyperglycemia triad - polyuria, polydipsiya, weight loss
Secondary enuresis
Reccurent infections
TYPE 1 - DKA

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91
Q

Investigating suspected diabtetes?

A

Baseline bloods including FBC, renal profile (U&E) and a formal laboratory glucose
Blood cultures should be performed in patients with suspected infection (i.e. with fever)
HbA1c can be used to get a picture of the blood sugar over the previous 3 months. This gives an idea of how long they have been diabetic prior to presenting.
Thyroid function tests and thyroid peroxidase antibodies (TPO) to test for associated autoimmune thyroid disease
Tissue transglutaminase (anti-TTG) antibodies for associated coeliac disease
Insulin antibodies, anti-GAD antibodies and islet cell antibodies to test for antibodies associated with destruction of the pancreas and the development of type 1 diabetes

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92
Q

What HbA1c indicates diabetes?

A

48 mmol/mol or higher

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93
Q

Situations where HbA1c must not be used as the sole test to diagnose diabetes?

A

Symptomatic children and young people <19 years
Symptoms suggesting T1DM
Short duration (<2 months)
Patients at high risk of diabetes who are acutely ill
Taking medication that may cause rapid glucose increase (steroids, antipsychotics)
Acute pancreatic damage/pancreatic surgery
In pregnancy
Presence of genetic, haematologic and illness related factors that influence HbA1c and its measurement
NOTE repeat readings same lab within 2 weeks if asymtomatic

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94
Q

Patients with what HbA1c should be monitored annually?

A

42-47 mmol/mol

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95
Q

Long term management of T1DM?

A

Subcutaneous insulin regimes
Monitoring dietary carbohydrates
Monitoring blood sugar levels on waking, before each meal and before bed
Monitoring for and managing complications

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96
Q

Describe a basal bolus insulin regime

A

Basal - long acting insulin such as Lantus - gives a constant background of insulin throughout that day. Typically given OD at night
Bolus - short acting insulin such as Actrapid - given three times a day before meals - also injected as per the number of carbohydrates consumed every time the patient has a snack.

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97
Q

What are the two types of insulin pump?

A

Tethered pump - devices with replaceable infusion sets and insulin
Patch pump - sits directly on the skin, controlled by a seperate remote. Disposable

Both constantly insfuse insuling via a cannula, site changed every 2-3 days to prevent lipodystrophy

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98
Q

Advantages of insulin pump?

A

Better blood sugar control
More flexability with eating
Less injections

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99
Q

Disadvantages of an insulin pump?

A

Difficulties learning to use it
Having it attatched at all times
Blockages in the infusion set
Small risk of infection

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100
Q

Short term complications of T1DM?

A

Hypogylcemia

Hyperglycemia and DKA

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101
Q

What causes hypoglycemia?

A 
Too much insulin
Not enough carbohydrates
Not processing carbohydrates correctly - malabsorbtion, diarrhoea, vomitting, sepsis
Hypothyroidism
Glycogen stoarge disorders
Growth hormone deficicency 
Liver cirrhosis 
Alcohol 
Fatty acid oxidation defects such as MCADD
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102
Q

Symptoms of hypoglycemia?

A 
Hunger
Tremor
Sweating
irritablility 
Dizziness 
Pallor 
Reduced conciousness
Coma
Death
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103
Q

How should hypoglycemia be treated?

A

No impairment of consciousness - rapid acting glucose such as lucozade and slower acting carbohydrates such as biscuits or toast to maintain the blood sugar level when the rapid acting glucose is used up
Impairment of conciousness - IV dextrose (10% - 2mg/kg bolus followed by 5mg/kg/hour infusion) and intramuscular gulcagon

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104
Q

What is nocturnal hypoglycemia and how can it be treated?

A

Hypoglycemia overnight
Child may be sweaty overnight
Morning blood glucose levels may be raised
Diagnosis made by continuous glucose monitoring
Alter bolus insulin regime and give snacks at bedtime

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105
Q

Why do patients with DM experience complications?

A

Chronic exposure to hyperglycemia causes
1. Damage to the endothelial cells of blood vessels
This leads to leaky, malfunctioning vessels that are unable to regenerate
2. Supression of the immune system and creates an optimal environement for microorganisms to thrive

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106
Q

Macrovascular complications of diabetes?

A

Coronary artery disease
Peripheral ischemia (poor healing, diabetic foot)
Stroke
HTN

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107
Q

Microvascular complications of diabetes?

A

Urinary tract infections
Pneumonia
Skin and soft tissue infections -particularly in the feet
Fungal infections - particularly oral and vaginal candidiasis

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108
Q

What is HbA1c considered to reflect?

A

Count of glycated Hb with is how much glucose is attatched to the haemoglobin molecules inside the RBC
Average blood glucose level over the last 3 months (RBC lifespan around 3-4 monthhs)

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109
Q

How can blood sugar be monitored?

A

HbA1c - 3 to 6 months
CBG with glucose meter - daily
Flash Glucose monitoring (FreeStyle Libre) - daily

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110
Q

How does the FreeStyle Libre machine work?

A

This uses a sensor on the skin that measures the glucose level of the interstitial fluid in the subcutaneous tissue
There is a 5 min lag behind blood glucose
Sensor records the glucose readings at short intervals
Swipe over reader with a sensor - this needs replacing every 2 weeks

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111
Q

Pathophysiology of DKA?

A

Patient not producing adequete insulin and not injecting adequete insulin to compensate for this. Not enough insulin to use and process glucose. Cells of the body interperit this as a state of starvation and initiates the process of ketogenesis
Glucose increases, ketones increase
Initially the kidneys produce bicarbonate to counteract the ketone acids in the blood and maintain a normal pH
Over time the ketone acids use up the bicarbonate and the blood becomes acidic - ketoacidosis

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112
Q

Why does DKA cause polydipsia and polyuria?

A

Hyperglycemia overwhelms the kidenys and glucose starts being filtered into the urine
The glucose in the urine draws water out with it (osmotic diuresis). This leads to polyuria, which leads to severe dehydration which stimulates the thirst centre in the hypothalamus, hence polydipsia.

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113
Q

Why can DKA cause arrhythmia?

A

Insulin normally drive potassium into the cells
Serum potassium and be high or normal as the kidneys continue to balance blood potassium excreted in the urine - however total body potassium is low
Without treatment patients can develop severe hypokalaemia very quickly
This can lead to fatal arrythmias

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114
Q

How does DKA presents?

A 
Hyperglycaemia 
Dehydration 
Ketosis
Metabolic acidosis (with a low bicarbonate)
Potassium imbalance 
Polyuria and polydipsia 
N&V
Acetone smell to their breath
Dehdration and subsequent hypotension
Altered conciousness
Symptoms of an underlying trigger (sepsis)
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115
Q

Most dangerous aspects of DKA?

A

Dehydration
Potassium imbalance
Acidosis

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116
Q

Diagnostic criteria for DKA?

A

Hyperglycemia (CBG > 11 mmol/L)
Ketosis (blood ketones > 3 mmol/l)
Acidosis (ie. pH < 7.3)

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117
Q

How is DKA treated?

A

Fluids
Insulin (infusion, e.g. actrapid at 0.1 unit/kg/hour)
Glucose - closely monitor, add a dextrose infusion if below a certain level (e.g. 14 mmol/l)
Potassium - closely monitor serum potassium (e.g. 4 hourly) and correct as required - no more than 10 mmol per hour
Infection - treat underlying triggers such as infection
Chart - fluid balance
Ketones - monitor blood ketones (or bicarbonate if ketone monitoring)

Establish the patient on their normal subcut insulin regime prior to stopping the insulin fluid infusion

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118
Q

Non-modifiable risk factors?

A

Older age
Ethnicity (black, chinese, south asian)
Family history

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119
Q

Modifiable risk factors for type 2 DM?

A

Obesity
Sedentary lifestyles
High carbohydrate (particularly refined carbohydrate) diet

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120
Q

How might T2DM present?

A 
Fatigue
Polydipsia and polyuria (thirsty and urinating a lot)
Unintentional weight loss
Opportunistic infections
Slow healing
Glucose in urine (on dipstick)

Usually in patients with risk factors

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121
Q

How is the OGTT performed?

A

Take baseline fasting plasma glucose result
Give 75g glucose drink
Measure plasma glucose 2 hours later

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122
Q

How can pre-diabetes be diagnosed?

A

HbA1c 42-47 mmol/mol
Impaired fasting glucose 6.1-6.9 mmol/mol
Impaired glucose tolerance - plasma glucose at 2 hours - 7.8 - 11.1 mmol/l on an OGTT

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123
Q

How can diabetes be diagnosed?

A

HbA1c > 48 mmol/mol
Random Glucose > 11 mmol/l
Fasting Glucose > 7 mmol/l
OGTT 2 hour result > 11 mmol/l

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124
Q

Management of T2DM?

A

Dietary Modification

Vegetables and oily fish
Typical advice is low glycaemic, high fibre diet
A low carbohydrate may in fact be more effective in treating and preventing diabetes but is not yet mainstream advice

Optimise Other Risk Factors

Exercise and weight loss
Stop smoking
Optimise treatment for other illnesses, for example hypertension, hyperlipidaemia and cardiovascular disease

Monitoring for Complications

Diabetic retinopathy
Kidney disease
Diabetic foot

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125
Q

What is the first line medical management of T2DM?

A

Metformin titrated from initially 500mg once daily as tolerated

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126
Q

What s the second line medical management of T2DM?

A

Metformin +

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

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127
Q

What is the third line medical management of T2DM?

A

Metformin + 2 of:
sulfonylurea/pioglitazone/DPP-4 inhibitor/SGLT-2 inhibitor

OR

Metformin+insulin

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128
Q

What do SIGN Guidelines 2017 reccommend for the prefential use in medical management for patients with T2DM in patients with CVD?

A

SGLT-2 inhibiotrs and GLP-1 mimetics

129
Q

What are the HbA1c targets for type 2 diabetes?

A

48 mmol/mol for new type 2 diabetics

53 mmol/mol for diabetics that have moved beyond metformin alone

130
Q

What drug class is metformin?

A

Biguanide

131
Q

Notable side effects of metformin?

A

Diarrhoea and abnominal pain (dose dependent)
Lactic acidosis (rare)
Doesn’t cause hypoglycemia
Weight neutral

132
Q

How does metformin work?

A

Increases insulin sensitivity

Decreases liver production of glucose

133
Q

What drug class is pioglitazone?

A

Thiazolidinedione

134
Q

How does pioglitazone work?

A

Increases insulin sensitivity

Decreases liver production of glucose

135
Q

Side effects of pioglitazone?

A 
Weight gain
Fluid retention
Anaemia
Heart failure
Extended use may increase the risk of bladder cancer
Does NOT typically cause hypoglycemia
136
Q

What drug class is glicazide?

A

Sulfonylurea

137
Q

How do sulfonylureas such as glicazide work?

A

Stimulate insulin release from the pancreas

138
Q

Notable side effects of sulfonylureas such as glicazide?

A

Weight gain
Hypoglycemia
Increased risk of CVD and MI when used as monotherapy

139
Q

What are incretins? What do they do?

A

Hormones produced by the Gi tract secreted in response to large meals and act to reduce blood sugar by:
Increase insulin secretions
Inhibit glucagon production
Slow absorption by the GI tracts

Main incretin is glucagon-like peptide 1
Incretins are inhbited by DPP-4

140
Q

What drug class is sitagliptin?

A

DPP-4 inhibitor

141
Q

How do DPP-4 inhibitors/gliptins work?

A

Inhibit DPP-4
Therefore reducing the inhibiton of incretins
Therefore increaseing insulin secretions, inhibiting glucagon production, slowing absorption by the Gi tract

142
Q

Notable side effects of DPP-4 inhibitors?

A

Gi tract upset
Symptoms of URTI
Pancreatitis

143
Q

What drug class is exenatide? How is it given?

A

GLP-1 mimic

Subcut injection either twice daily or modifiable release once weekly

144
Q

What drug class is liraglutide and how is it administered?

A

GLP-1 mimic

Subcut injection once a week

145
Q

Notable side effects of GLP-1 mimics?

A

GI tract upset
Weightloss
Dizziness

Low risk of hypoglycemia

146
Q

What drug class is empagliflozin (and other drugs ending in -gliflozin)?

A

SGLT-2 inhbitor

147
Q

How does SGLT-2 inhibitors such as empagliflozin work?

A

Inhibition of SGLT-2, the protein responsible for reabsorbing glucose from the urine into the blood in the proximal tubules of the kidneys
Increase excretion og glucose into urine

148
Q

Side effects of SGLT-2 inhbiitors?

A 
Glucoseuria
Increased rate of UTI
Weight loss
Diabetic ketoacidosis 
Lower limb amputation associated with canagliflozin
149
Q

Example of rapid acting insulins?

A

Novorapid
Humalog
Apidra

150
Q

Short acting insulins?

A

Actrapid
Humulin S
Insuman rapid

151
Q

How long do rapid-acting insulins take to start working and how long do they last?

A

10 mins

4 hours

152
Q

How long do short acting insulins take to work and how long do they last?

A

30 mins

8 hours

153
Q

Examples of intermediate-acting insulins?

A

Insulatard
Humulin I
Insuman basal

154
Q

How long do intermidiate acting insulins take to work and how long do they last?

A

1 hour

16 hours

155
Q

How long do long acting insulins take to work and how long do they last?

A

1 hour

24 hours

156
Q

Examples of long acting insulins?

A

Lantus
Levemir
Degludec (last over 40 hrs)

157
Q

Examples of combination insulins (rapid+intermediate)

A 
Humalog 25 (25:75  rapid:inter)
Humalog 50 (50:50 rapid:inter)
Novomix 30 (30:70 rapid:inter)
158
Q

Hyperthyroidism vs thyrotoxicosis?

A

Hyperthyroidism - over-production of thyroid hormone by the thyroid glsnd
Thyrotoxicosis - refers to an abnormal and excessive quantity of thyroid hormone int he body

159
Q

What is Grace’s disease?

A

A type of primary hyperthyroidism

Due to thyroid pathology - it is the thyroid itself that is behaving abnormally and producing excessive quantity of thryoid hormone.

Graves disease is an autoimmune condition in which TSH receptor antibodies (abnormal antibodies which mimic TSH and stimulate TSH receptors on the thyroid) cause hyperthryoidsism

160
Q

Where is the pathology in secondary hyperthyroidism?

A

Overstimulation bt TSH, pathology in hyporthalamus or piuitary

161
Q

What is Plummer’s disease

A

Toxic multinodular goitre
Coniditon where nodules develop on the thyroid gland that act independently of the normal feedback system and continuously produce excessive thyroid hormone

162
Q

|n what thyroid disorder is exopthalmos seen? What is it? Why does it happen?

A

Buldging of the eyeball out of the socket cause by Graves Disease (primary hyperhtyroidism)
Due to inflammation, swelling and hypertrophy of the tissue behind the eyeball that forces the eyeball forward

163
Q

Which thyroid disorder is pretibial myxoedema specific to? What is it? Why does it happen?

A

Dermatological condition where there are depositis of mucin under the skin on the anterior aspect of the leg (pre-tibial area)
Gives discoloured, waxy, oedmatous apparence to the skin ober this area.
Reaction to TSH receptor antibodies

163
Q

Which thyroid disorder is pretibial myxoedema specific to? What is it? Why does it happen?

A

Dermatological condition where there are depositis of mucin under the skin on the anterior aspect of the leg (pre-tibial area)
Gives discoloured, waxy, oedmatous apparence to the skin ober this area.
Reaction to TSH receptor antibodies

164
Q

Causes of hyperthyroidism?

A

Grave’s disease
Toxic multinodular goitre
Solitary toxic thyroid nodule
Thyroiditis (De Quervain’s, Hashimotos, postpartum, drug-induced)

165
Q

Universal features of hyperthyroidism?

A 
Anxiety
Irritability
Sweating
Heat intolerance
Tachycardia
Weight loss
Fatigue
Frequent loose stools
Sexual dysfunction
166
Q

Unique features of Grave’s disease (ie. features causes by presence of TSH antibodies)?

A

Diffuse goitre (without nodules)
Graves eye disease
Bilateral exopthalmos
Pretibial myxoedema

167
Q

Unique features of toxic multinodular goitre?

A

Goitre with firm nodules
Patients almost always over 50
Second most commmon cause of thyrotoxicosis (after Grave’s)

168
Q

What is a solitary toxic thyroid nodule and how is it treated?

A

Single abnormal thyroid nodule is acting alone to release thyroid hormone.
Normally benign adenomas. Treated with surgical removal of the nodule.

169
Q

What is De Quervain’s Thyroiditis?

A

Presentation of a viral infection with fever, neck pain and tenderness, dysphagia and features of hyperthyroidism.
There is a hyperthyroid phase followed by a hypothroid phase as the TSH levels fall due to negative feedback.
Self limiting, symptoms can be managed by NSAIDs and beta blockers

170
Q

What is a thyroid storm?

A

Rare presentation of hyperthyroidism - AKA thyrotoxic crisis.
Presents with pyrexia, tachycardia and delirium.
Patients may require supportive care with fluid resuccitation, anit-arrhythmic medication and beta-blockers.

171
Q

What is the first line anti-thyroid drug?

A

Carbimazole
Will leave patients with Grave’s disease with normal thyroid function after 4-8 weeks.
Once the patient has normal thyroid hormone levels, they continue on maintenance carbimazole and either:
The dose is titrated to maintain normal levels (titration block)
Or the dose is sufficient to block all production and patient takes levothyroxine tirated to effects (block and replace)
Complete remission and the ability to stop taking carvimazole is usually achieved within 18 months of treatment

172
Q

What is the second line anti-thyroid drug?

A

Propylthiouracil

173
Q

Risks associated Propylthiouracil?

A

Small risk of severe heaptic reactions, including death

174
Q

What strict rules should be followed after a patient is treated with radioactive iodine?

A

Must not be pregnant, patient is not allowed to get pregnant within 6 months
Must avoid close contact with children and pregnant women for 3 weeks
Limit contact with anyone for several days after receiving the dose

175
Q

How is radioactive iodine used to treat hyperthyroidism?

A

Single dose of raidoactive iodine drunk
Taken up by thyroid glands and the emmited radiation destorys a proportion of the thyroid cells
Reduction in functioning cells results in a decrease of thyroid hormone production and thus remission
Remission can take up to 6 months
Patients can be left hypothyroid and requiring levothyroxine replacement

176
Q

Beta blockers are used to block the adrenaline related symptoms of hyperthroidism, particullary in thyroid storm, which is the best choice?

A

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

177
Q

What is the disadvantage of surgery to remove the whole thyroid or toxic thyroid nodules in hyperthyroidism?

A

Patient will be left hypothyroid post thyroidectomy and require levothyroxine replacement for life

178
Q

Causes of hypothyroidism?

A

Hashimotos thyroiditis (most common in developed world)
Iodine (most common in developing world)
Secondary to treatment of hyperthyroidism: Carbimazole, Propylthiouracil, Radioactive iodine, Thyroid surgery
Medications
Secondary causes: tumours, infection, radiation, vascular (Sheehan syndrome)

179
Q

What medications can cause hypothyroidism?

A

Lithium - inhibits production of thyroid hormone, can cause goitre
Amiodarone - interferes with thyroid hormone production and metabolism, can also cause thyrotoxicosis

180
Q

Presentation and features of hypothyroidism?

A 
Weight gain
Fatigue
Dry skin
Coarse hair and hair loss
Fluid retention
Heavy or irregular periods 
Constipation
181
Q

Thyroid function test results in primary hypothyroidism vs secondary hypothyroidism?

A

Primary: thyroid gland insufficiency therefore T3+T4 are low, TSH will be high as no negative feedback to the bran (so increase production of TSH in the pituitary gland)
Secondary: pituitary pathology, resulting in low production of TSH. This, in turn, means T3 and T4 will be low

182
Q

What thyroid hormone is used to manage the dose of levothyroxine?

A

TSH

183
Q

What is levothyroxine?

A

Synthetic T4

Also metabolised T3 in the body

184
Q

How often should TSH be checked when starting levothyroxine?

A

Monthly, until stable

185
Q

What TSH would you expect in hyperthyroidism and why?

A

TSH is supressed by high T4 and T3

186
Q

In which case of hyperthyroidism would TSH be high?

A

Pituitary adenoma which secrets TSH

187
Q

What antibodies can cause thyroid disorder? What disorders are each found in?

A 
Antithyroid peroxidase (anti-TPO) antibodies - most relevant. Present in Grave;s disease and Hashimoto's thyroiditis.
Antithyroglobulin antibodies - antibodies against thyroglobulin (a protein produced and extensively present in the thyroid gland). Present in Graves disease, Hashimotos Thyroiditis and thyroid cancer.
TSH receptor antibodies are autoantibodies that mimic TSH and bind to its receptor - they are ALWAYS present in Graves disease
188
Q

How can USS of the thyroid be utilised?

A

DIagnosing thyroid nodules
Distinguishing between cystic (fluid filled) and solid nodules.
Ultrasound can also be used to guide biopsy of a thyroid lesion.

189
Q

How radioisotope scans used to investigate the thyroid?

A

Radioisotope scans are used to investigates hyperthyroidism and thyroid cancers.

190
Q

What happens in radioisotope scans of the thyroid?

A

Radioactive iodine is given orally or IV and travels to the thyroid where it is taken up by the cells.
The more active the thyroid cells, the faster the radioactive iodine.
The more gamma rays that are emitted from an area the more radioactive iodine has been taken up.
This gives really useful functional information about the thyroid gland

191
Q

Radioactive iodine uptake in Grave’s disease?

A

Diffuse high uptake

192
Q

What will be seen in multinodular goitre and adenomas on a radioisotope scan?

A

Focal high uptake is found in toxic multinodular goitre and adenomas

193
Q

What indicates thyroid cancer on radioisotope scan?

A

‘Cold’ areas (ie. abnormally low uptake)

194
Q

What is Hashimoto’s thyroiditis?

A

Autoimmune inflammation of the thyroid gland
Associated with antithyroid peroxidase (anti-TPO) antibodies and anythyroglobulin antibodies.
It initially causes goitre, then atrophy of the thyroid gland

195
Q

Why is iodine deficiency uncommon in the UK?

A

Iodine is added to foods such as table salts

196
Q

What investigations are important when suspecting adrenal insufficiency?

A

U&Es- hyponatremia may be the only presenting feature of adrenal insufficiency. Hyperkalemia may be present
Short synacthen test - test of choice
ACTH (high in primary adrenal failure, low in secondary)
Adrenal cortex antibodies and 21-hydroxylase antibodies - autoimmune antibodies
CT/MRI adrenals is suspecting an adrenal tumour, haemorrhage or other structual pathology
MRI pituitary give further information about pituitary pathology

197
Q

How is the short synacthen test performed?

A

Test of choice for adrenal insufficiency
Performed in AM
Give syncathen (synthetic ACTH)
Measure blood cortisol at baseline, 30 mins and 60 mins after administration
The synthetic ACTH will stimulate healthy adrenal glands to produce cortisol and cortisol should at least double
A failure in cortisol to rise less than x2 the baselin indicates primary adrenal insufficiency

198
Q

What is the long synacthen test?

A

The long synacthen test is rarely used anymore because we can now measure ACTH levels. It was used to distinguish between primary adrenal insufficiency and adrenal atrophy secondary to prolonged under stimulation in secondary adrenal insufficiency. It involves giving an infusion of ACTH over a long period.

In primary adrenal failure there is no cortisol response as the adrenals no longer function.
In adrenal atrophy (secondary adrenal insufficiency), the prolonged ACTH eventually gets the adrenals going again and cortisol rises.
Now we can simply measure ACTH and this indicates the underlying cause.

199
Q

How is adrenal insufficiency treated?

A

Replacement steroids titrated to signs, symptoms and electrolytes
Hydrocortisone (cortisol def) and/or fludrocortisone (aldosterone)

200
Q

What is hydrocortisone?

A

Glucocorticoid hormone used to replace cortisol

201
Q

What is fludrocortisone?

A

Mineralcorticoid hormone used to replace aldosterone

202
Q

How does an Addisonian crisis present?

A 
Reduced conciousness
Hypotension
Hypoglycemia
Hyponatremia
Hyperkalemia
203
Q

Triggers of an Addisonian crisis?

A

Infection
Trauma
Sudden withdrawal of long term steroids

204
Q

How is an Addisonian crisis managed?

A

Intensive monitoring if unwell
Parenteral steroids (IV hydrocrotisone 100mg stat, then 100mg every 6 hours)
IV fluid resusitation
Correction of hypoglycemia
Careful monitoring of electrolytes and fluid balance

205
Q

What is acromegaly?

A

Clinical manifestation of excessive growth hormone

206
Q

Where is growth hormone produced?

A

Anterior pituitary gland

207
Q

What is the most common cause of unregulated growth hormone secretion?

A

Pituitary adenoma - microscopic or macroscopic (causes compression of local structures)

207
Q

What is the most common cause of unregulated growth hormone secretion?

A

Pituitary adenoma - microscopic or macroscopic (causes compression of local structures)

208
Q

Rarely acromegaly can be secondary to a cancer, such as what?

A

Lung of pancreatic cancer secreting ectopic growth hormone releasing hormone (GHRH) or growth hormone (GH)

209
Q

Why might a patient with acromegaly have loss of vision in the outer half of both eyes?

A

Optic chiasm sits just above the pituitary gland
Optic chiasm is the point at which the optic nerves cross
A pituitary tumour of sufficient size can cause bitemporal hemianopia

210
Q

How does acromegaly present?

A

If SOL: Headaches, visual field defects
Overgrowth of tissues: prominent forehead and brow (frontal bossing), large nose, large tongue (macroglossia), large hands and feet, large protuding jaw ‘prognathism’, arthritis from imbalanced growth of joints
Organ dysfunction: hypertrophic heart, HTN, type 2 diabetes, colorectal cancer
Symptoms suggesting active raised growth hormone: development of new skin tags, profuse sweating

211
Q

How do you investigate suspect acromegaly?

A

Insulin-like growth factor (IGF-1) is the initial screening test
Oral glucose tolerance test whilst measuring growth hormone (high glucose normally)
MRI brain for the pituitary tumour
Refer to opathalmology for formal visual feild testing

212
Q

Definitive treatment of acromegaly secondary to pituitary adenoma?

A

Transphenoidal removal of pituitary adenoma

213
Q

What medications can be used to block GH?

A

Pegvisomant (GH antagonist, s/c, OD)
Somatostation analogue (blocks GH release) e.g. ocreotide
Dopamine agonists to block GH release e.g. bromocriptine

214
Q

Somatostain is known as growth hormone inhibiting hormone, where is it normally secreted from?

A 
The brain,
GI tract
Pancreas
Released in response to complex triggers
(note dopamine also inhibits GH but less potent)
215
Q

Which cells release parathyroid hormone?

A

Cheif cells of the parathyroid gland

216
Q

How does parathyroid hormone related to serum calcium?

A

Produced in response to hypocalcemia

Acts to raise blood calcium

217
Q

How does PTH act to raise serum calcium?

A

Increases osteoclast activity in the bones (reabsorbing calcium from bones)
Increases calcium absorption from the gut
Increasing calcium absorption from the kidneys
Increases vitamin D activity - converts it to its active form

218
Q

How does vitamin D increase serum calcium?

A

Increases calcium absorption from the intestines

219
Q

Symptoms of hypercalcemia?

A

Renal stones
Painful bones
Constipation, N&V
Depression, psychosis, fatugue

220
Q

What causes primary hyperparathyroidism?

A

Primary hyperparathyroidism is caused by uncontrolled parathyroid hormone produced directly by a tumour of the parathyroid glands

221
Q

How is primary hyperparathyroidism treated?

A

Surgical removal of the tumour

222
Q

What will the serum calcium abnormality be in primary hyperparthyroidism?

A

Hypercalcemia (bones, stones, groans, moans)

223
Q

What causes secondary hyperparathyroidism?

A

Insufficient vit D or chronic renal failure leads to low absorption of calcium.
Parathyroidglands react to hypocalcemia, by excereting more parathyroid hormone - hyperplasia.

224
Q

How is secondary hyperparathyroidism treated?

A

Renal transplant or correct vitamin D deficiency

225
Q

What will the serum calcium be in secondary hyperparathyroidism?

A

Low or normal

226
Q

What causes tertiary hyperparathyroidism?

A

Prolonged secondary hyperparathyroidism (vit d def or renal failure), leads to hyperplasia of the parathyroid gland.
The baseline level of PTH increases dramatically, so when secondary hyperparathyroidism is treated the parathyroid hormone remains inappropriately high.

227
Q

How is tertiary hyperparathyroidism treated?

A

Surgical removal of part of the parathyroid tissue to return PTH to an appropriate level

228
Q

How does low BP lead to secretion of aldosterone?

A

Juxtaglomerular cells in the afferent arteriole of the kidney sense blood pressure
Low BP: Juxtaglomerular cells secrete renin
Renin allow angiotensin (secreted by the liver) to be converted in to angiotensin I
In the lungs Angiotensin I is converted to Angiotensin II by ACE
Angiotensin II stimulates the release of aldosterone from the ADRENAL GLANDS

229
Q

How does aldosterone act on the kidney?

A
  1. Increases sodium reabsorption from the DISTAL TUBULE
  2. Increases potassium secretion from the DISTAL TUBULE
  3. Increases hydrogen secretion from the COLLECTING DUCTS
230
Q

What is primary hyperaldosteronism?

A

Adrenal glands are directly responsible for producing too much aldosterone

231
Q

What level is serum renin in hyperaldoseronism?

A

Low, as suppressed by high BP

232
Q

What are the causes of primary hyperalodsteronism?

A

Bilateral adrenal hyperplasia
Adrenal adenoma secreting aldosterone - CONNS SYNDROME
Famililal hyperaldosteronism type 1 and type 2 (rare)
Adrenal carcinoma

233
Q

What is secondary hyperaldosteroism?

A

Adrenal glands are stimulated to produce more aldosterone by excessive renin

234
Q

What causes secondary hyperaldosteronism?

A

Renal artery stenosis
Renal artery obstruction
Heart failure

235
Q

Best screening tool for hyperaldosteronism?

A

Check renin and aldosterone levels.
Check ratio to determine cause if aldosterone high
Low renin - primary
High renin - secondary

236
Q

What investigations may you want to undertake in relation to the effects of aldosterone?

A

Blood pressure
Serum electrolytes (hypokalemia)
Blood gas analysis (alkalosis)

237
Q

How would you further investigate a high aldoserone level with imaging?

A

CT/MRI to look for an adrenal tumour
Renal doppler ultrasound
CTA angiogram or MRA for renal artery stenosis of obstruction

238
Q

What pharmacological threapy can be used to treat hyperaldosteronism?

A

Aldosterone antagonists such as eplerenone and spironolactone

239
Q

What is the most common cause of secondary HTN?

A

Hyperaldosteronism

You should consider screening if high blood pressure without response to treatment or with hypokalemia

240
Q

Management of hyperalodsteronism - treatment of underlying cause?

A

Surgical removal of adenoma (Conns syndrome, adrenal carcinoma)
Percutaneous renal artery angioplasty via the femoral artery to treat in renal artery stenosis

241
Q

What is ADH secreted?

A

posterior pituitary gland

242
Q

Where is ADH produced?

A

Hypothalamus

243
Q

What does ADH/vasopressin do?

A

Stimulates water reabsorption from the collecting ducts in the kidneys

244
Q

What is the pathophysiology of hyponatremia in SIADH

A

Excessive ADH results in excessive water reabsorption in the collecting ducts, which dilutes serum sodium resulting in hyponatermia.

245
Q

What wiil the urine of patients with SIADH be like and why?

A

High sodium
High osmolality

(concentrated as kidneys excreting less urine)

246
Q

Symptoms of SIADH?

A 
Headache
Fatigue
Muscle aches and cramps
Confusion
Seizures and reduced conciousness (severe hyponatremia)
247
Q

Causes of SIADH?

A

Either the posterior pituitary secretes too much ADH or the ADH may be coming from somwehere else

Post-operative (major surgery)
Infection, particularly atypical pneumonia and lung abscesses
Head injury
Medications (thiazide diuretics, carbamazepine, vincristine, cyclophosphamide, antipsychotics, SSRIs, NSAIDS)
Mallignnacy, particularly small cell lung cancer
Menigitis

248
Q

How is SIADH diagnosed?

A

DIagnosis of exclusion
Clinical examination will show euvolaemia
U&Es (hyponatremia)
Urine sodium and osmolality (high)
Rule out
1. adrenal insufficiency (short synacthen test)
2. history of diuretic use
3. diarrhoea, vommiting, burns, fistula, excessive sweating
4. excessive water intake
5. history of chronic kidney disease or AKI

249
Q

How might you establish the cause of SIADH?

A

History: new medication, chest infection, recent surgery
CXR: lung abscess, pneumonia, lung cancer
If mallignancy suspected CT thorax/abdomen/pelvis and brain MRI

250
Q

When would you suspect mallignancy in someone with persistent hypernatremia?

A

No clear cause

Hx of smoking, weight loss or other features of mallignancy

251
Q

How is SIADH treated?

A

Withdraw any offending medication
Fluid restriction
Tolvaptan (ADH receptor blocker) by specialist with close monitoring as it can cause a rapid increase in sodium levels (risk of CPM)

252
Q

What is central pontine myelinolysis/ osmotic demyelination syndrome and what is its pathophysiology ?

A

Complication of severe hyponatremia (<120) (long term) being treated too quickly (>10 mmol/L increase over 24hrs).

Sodium levels fall: water moves by osmosis across BBB into cells of brain from an area of low conc. to high conc.
This causes the brain to swell.
Brain adapts to this by reducing the solutes in the brain cells so that water is balanced across the BBB and the brain does not become oedematous.
This adaptation takes a few days so if severe hyponatremia is present for a long time, the brain cells will also have a low osmolality,
When sodium levels suddenly increase water will rapidly shift out of the brain cellls into the blood

253
Q

What are the two phases of CPM?

A
  1. Due to electrolyte imbalance patient presents encepalopathic and confused. May have new headache, N&V. Often resolves prior to the onset of phase 2.
  2. Dymyelination of the neurones, particularly in the pons, occurs a few days after the rapid correction of sodium. Presents as spastic quadriparesis, pseudobubular palsy and congitive and behavioural changes. Significant risk of death
254
Q

What is diabetes insipidus?

A

Lack of or lack of response to ADH, preventing the kidneys from being able to concentrate urine.

255
Q

What is primary polydipsia?

A

Primary polydipsia is when the patient 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.

256
Q

Nephrogenic DI is when the collecting ducts of the kidneys do not respond to ADH. What may cause this?

A

Drugs, particularly lithium
Mutations in the AVPR2 gene on the X chromosome that codes for the ADH receptor
Intrinsic kidney disease
Electrolyte disturbance (hypokalemia, hypercalcaemia)

257
Q

Crania diabetes insipidus occurs when the hypothalamus does not produce ADH for the posterior pituitary gland to secrete. What might cause it?

A 
Brain tumour
Head injury
Brain malformations
Brain infection (meningitis, encephalitis, TB)
Brain surgery or raidotherapy
258
Q

How does DI present?

A 
Polyuria
Polydipsia
Dehydration
Postural hypotension
Hypernatremia
259
Q

How is DI investigated?

A 
Urine osmolality (low)
Serum osmolality (high)
Water deprivation test
260
Q

What is the test of choice for diagnosing DI?

A

Desmopressin stimulation test/water deprivation test

261
Q

How is the water deprivation test performed?

A

No fluids for 8 hour
Measure urine osmolality
Administer synthetic ADH (desmopressin)
Measure urine osmolality after 8 hours

262
Q

What will the results of the water deprivation test be in nephrogenic DI?

A

Urine osmolality initially low (as it continues to be diluted by excessive water secretion in the kidneys) and remains low after desmopressin administered

263
Q

What will the results of the water deprivation test be in cranial DI?

A

Kidneys are capable of responding to ADH, so urine osmolality will be low at the beginning and high 8 hours after desmopressin is administered

264
Q

What will the results of the water deprivation test be in primary polydipsia?

A

Urine osmolality will be high before (8 hours with no water) and 8 hours after desmopressin administered.

265
Q

How is DI managed?

A

Treat underlying cause where possible
Conservatively if mild
Desmopressin in cranial DI to replace ADH
Desmopressin in nephrogenic ADH in HIGHER doses under close monitoring

266
Q

Which cells produce adrenaline?

A

Chromafinn cells in the adrenal medulla of the adrenal glands

267
Q

What is a phaeocytoma?

A

Tumour of the chromaffin cells that secretes unregulated and excessive amounts of adrenaline

268
Q

What is adrenaline?

A

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

269
Q

Why do patients with a phaeochromocytoma tend to have periods of worse symptoms and periods of more settled symptoms?

A

Adrenaline tends to be secreted by the tumour in bursts

270
Q

25% of phaeochromocytomas are familial, associated with which condition?

A

MEN 2

Multiple endocrine neoplasia type 2

271
Q

Why is phaeochromocytoma diagnosed using 24 hour urine catecholamines and plasma free metanephrines?

A

Serum catecholamines would be unreliabe as these naturally fluctuate - 24 hour urinary gives an idea of secretion over 24 hrs
Adrenaline has a short half life in the blood (few mins) where as metanephrines (their breakdown product) have a longer half life, therefore are less prone to dramatic fluctuations

272
Q

How does a phaeochromocytoma present?

A 
Anxiety
Sweating
Headache
HTN
Palpitations, tachycardia, paroxmysal AF
273
Q

How is phaeochromocytoma managed?

A

Initially medically:
1. Alpha blockers ie. phenoxybenzamine
2. Beta blockers once alpha blockers established
Once managed medically (to reduce risks of anesthetic and surgery):
Adrenalectomy

274
Q

Hormones released by the anterior pituitary?

A 
TSH
ACTH
FSH
LH
Prolactin
Growth hormone
275
Q

What hormones are released by the posterior pituitary gland?

A

Oxytocin

ADH (antidiuretic hormone)

276
Q

Describe the thyroid axis

A

TRH: thyrotropin-releasing hormone released from the hypothalamus
Stimulates AP to release TSH
Stimulates thyroid gland to release T3 and T4
Hypothalamus and AP sense T3 and T4 levels (negative feedback) supressing release of TRH and TSH

277
Q

Describe the adrenal axis

A

Hypothalamus releases corticotrophin releasing hormone (CRH) which
Stimulates AP to release ACTH
Which stimulates adrenal glands to release cortisol
Cortisol secreted by (2) adrenal glands
(Released in pulses in response to stress stimuli
Diurnal variation)
Cortisol sensed by hypothalamus and AP supressing the release of CRH and ACTH - negative feedback

278
Q

What are the actions of cortisol in the body?

A 
Inhibits immune system
Inhibits bone formation
Raises blood glucose
Increases metabolism
Increases alertness
279
Q

What is the action of growth hormone?

A

Stimulates insulin-like growth factor 1 from the liver
GH works indirectly and directly on almost all body cells:
Stimulates muscle growth
Increases bone density and stregth
Stimulates cell regeneration and reproduction
Stimulates growth of internal organs

280
Q

Where is GHRH released from?

A

Hypothalamus

acts on AP to release GH

281
Q

Where is GH released from?

A

Anterior pituitary gland

282
Q

What criteria must be fufilled for patients who are treated with insulin for diabetes to be allowed to drive?

A

All patients with diabetes who are treated with insulin must notify the DVLA. For the DVLA to license an insulin-treated individual with a Group 1 licence, they must meet all the following criteria:
Adequate hypoglycaemia awareness
No more than 1 episode of severe hypoglycaemia while awake in the preceding 12 months AND the most recent episode occurred more than 3 months ago
Practises appropriate glucose monitoring
Not regarded as a likely risk to the public while driving
Meets the visual standards for acuity and visual field
Under regular review

283
Q

Patients with T1DM who are likely to miss a meal or more due to surgery should have what changes made to their insulin regime?

A

Reduce sub cut insulin basal dose by aprox 1/3
Omit morning insulin
Commence VRII

284
Q

How should a patient be taken off of VRIII and back onto their sc insulin regime?

A

At the first oral meal, overlap the VRIII and start normal SC insulin regimes.
Rapid acting should be given aprox 20 mins prior to meal
VRIII can be stoped 30 mins to an hour after eating

285
Q

What does corneal involvement in Grave’s disease suggest?

A

Severe eye pathology

286
Q

In Sick euthyroid syndrome what will the TFTs be?

A

TSH normal

T3 and T4 low

287
Q

What condition is Bromocriptine used to manage medically?

A

Prolactinoma

288
Q

Why might a splenectomy mean a patients HbA1C result is innacurate?

A

Splenectomy can give a falsely high HbA1c level due to the increased lifespan of RBCs

289
Q

What features suggest subacute thyroiditis?

A

Subacute thyroiditis is suggested by the tender goitre, hyperthyroidism and raised ESR. The globally reduced uptake on technetium thyroid scan is also typical

290
Q

Likely outcome of papillary thyroid cancer?

A

Papillary thyroid cancer shows excellent prognosis, despite the tendency to spread to cervical lymph nodes early

291
Q

What is the most common type of thryoid cancer?

A

Papillary

292
Q

Sick day rules for patients with Addison’s

A

Addison’s patient with intercurrent illness → double the glucocorticoids, keep fludrocortisone dose the same

293
Q

How does multiple endocrine neoplasia type I typically present?

A

Galactohorrea
Peptic ulceration
Hypercalcemia

294
Q

Symptoms of hypoparathyroidism?

A

a tingling sensation (paraesthesia) in your fingertips, toes and lips
twitching facial muscles
muscle pains or cramps, particularly in your legs, feet or tummy
tiredness
mood changes, such as feeling irritable, anxious or depressed
dry, rough skin
coarse hair that breaks easily and can fall out
fingernails that break easily

295
Q

Blood test results in hypoparathyroidism?

A

low parathyroid hormone levels
low calcium levels
high phosphoate levels

296
Q

Medical management of hypoparathyroidism?

A

Calcium carbonate and vitamin D supplements – usually calcitriol (Rocaltrol) or alfacalcidol (One-Alpha)

297
Q

Causes of hypocalcemia?

A 
1. Vitamin D deficiency
Malnutrition (i.e. osteomalacia)
Malabsorption (e.g. gastrectomy, short bowel syndrome, Coeliac disease, chronic pancratitis)
CKD
2. Hypoparathyroidism
Post-parathyroidectomy
Inherited
Pseudohypoparathyroidism
3. Hyperphosphataemia
Tumour lysis syndrome
Rhabdomyolysis
Phosphate administration
4. Acute pancreatitis
5. Hypomagnesaemia
6. Acute alkalosis
298
Q

Clinical features of hypocalcemia?

A

SPASMODIC:

S – Spasms (Trousseau's sign)
P – Perioral parasthaesia
A – Anxiety/Irritability
S – Seizures
M – Muscle tone increase (colic, dysphagia)
O– Orientation impairment (i.e. confusion)
D – Dermatitis
I – Impetigo herpetiformis
C – Chvostek's sign
299
Q

Assesment of hypocalcemia?

A 
ECG (looking for arrhythmia)
Bone profile (calcium, phosphate, albumin, total protein, ALP)
PTH
Magnesium
Vitamin D
Amylase (if suspected pancreatitis)
X-rays (if suspected osteomalacia)
300
Q

How is hypocalcemia managed?

A

Management of acute hypocalcaemia:
Mild: oral calcium supplementation
Severe (spasms or ECG changes): IV calcium gluconate repeated as needed

Long term management:
Treat cause
Encourage good dietary calcium and Vitamin D intake
Calcium and Vitamin D supplementation
Alphacalciferol if CKD
Magnesium supplements if concurrent hypomagnesaemia

301
Q

What type of anaemia is associated with autoimmune thyroid disease?

A

Macrocytic, non-megaloblastic

e.g. pernicious anaemia

302
Q

Triad of symptoms associated with phaeochromocytoma?

A

headache
sweating
tachycardia

303
Q

Initial screening for acromegaly?

A

Level of serum IGF-1 do not fluctuate much and is therfore a fairly stable indicator

304
Q

What pathopysiological mechanism is impliacted in the devlopment of diabetic neuropathy?

A

Advanced glycation end products resulting from hyperglycemia act on specific receptors, including monocytes and endothelial cells to increase the production of cytokines and adhesion molecules.
Advanced glycation end products have an effect on metalloproteinases which damage efferent nerve fibers

305
Q

What is the most common cause of mortality in elderly patients?

A

Heart and circulation problems

306
Q

Which diabetic drug can increase the risk of Fourniers gangrene

A

SGLT-2 inhibitors (e.g. canagliflozin) are a risk factor for Fournier’s gangrene as they increase the urinary excretion of glucose, which increases the risk of a UTI and progression to necrotising fasciitis.

307
Q

Endocrine abnormalities in Kallman’s syndrome?

A

Kallman’s syndrome - LH & FSH low-normal

Testosterone

308
Q

How many units of insulin is 1ml?

A

In 1ml of (most standard) insulin, there are 100 units

309
Q

Biochemical abnormalities in congenital adrenal hyperplasia?

A

Increased plasma 17-hydroxyprogesterone levels
Increased plasma 21-deoxycortisol levels
Increased urinary adrenocorticosteroid metabolites

310
Q

What causes congenital adrenal hyperplasia syndrome?

A

It is inherited via an autosomal recessive pattern.

The condition is due to a deficiency of the 21-hydroxylase enzyme (responsible for biosynthesis of aldosterone + cortisol)

311
Q

Why is the risk of osmotic demylination syndrome low when treating acute hyponatremia?

A

Cerebral neurons have not had adequete time to lose organic osmoles to compensate for the hyponatremia

Major concern is risk of brain herniation

312
Q

Half life of thyroxine?

A

4-6 weeks

313
Q

Why should alpha blocker such as phenoxybenzamine be given in phaoechromocytoma before beta blocker added?

A

B blocker alone may precipitate a hypertensive crisis

314
Q

Why does postural hypotension occur in addisons?

A

Aldosterone insufficiency

315
Q

Low urine osmolality after fluid deprivation, but high after desmopressin

A

Cranial DI

316
Q

Low urine osmolality after both fluid deprivation and desmopressin

A

Nephrogenic DI

317
Q

What is the cut off for true hyponatremia (serum osmolality)

A

The maximum osmolality level cut-off for true hyponatraemia is 275 mOsm/kg

Year 3 Medicine (8 decks)

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