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MED-Y3 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What are the symptoms of hypercalcaemia ?

A

Renal stones, painful bones, abdominal groans and psychiatric moans

  • Abdominal groans - Symptoms of constipation, nausea and vomiting
  • Psychiatric moans - Fatigue, depression and psychosis.
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2
Q

What causes primary hyperparathyroidism ?

A

Usually due to a tumour. This causes uncontrolled release of PTH.

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3
Q

What is present on blood tests in primary hyperparathyroidism ?

A

Hypercalcaemia and high PTH
Low phosphate

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4
Q

How is primary hyperparathyroidism treated ?

A

Resection of the tumour

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5
Q

What is secondary hyperparathyroidism ?

A

Insufficient vitamin D or chronic renal failure results in low absorption of calcium by the intestines, kidneys and bones. The PT glands react to the low serum vitamin D by excreting more PTH. This results in hyperplasia of the PTH.

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6
Q

What is present on blood tests on a patient with secondary hyperparathyroisism ?

A
  • High PTH and low calcium (sometimes normal) and elevated phosphate
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7
Q

How is secondary hyperparathyroidism treated ?

A

Treatment of the underlying deficiency or kidney transplant in renal failure

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8
Q

What is tertiary hyperparathyroidism ?

A

Occurs when secondary hyperparathyroisim continues for a long period of time, leading to hyperplasia of the glands. This means that baseline level of PTH will remain high. Caused by hyperplasia

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9
Q

What are the signs on blood tests of tertiary hyperparathyroidism ?

A

High PTH
High Calcium

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10
Q

How is tertiary hyperparathyroidism treated ?

A

Surgical treatment to remove part of the parathyroid tissue.

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11
Q

What are the symptoms of hyperparathyroidism ?

A

Symptoms of hypercalcaemia
Renal stones, abdominal groans, sore bones and psychiatric moans

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12
Q

What is a common cause of elevated calcium ?

A

Primary hyperparathyroidism

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13
Q

What is an important cause of secondary hyperparathyroidism ?

A

CKD

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14
Q

What medications can cause hyperthyroidism ?

A

Amiodarone and levothyroxine

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15
Q

How can excess contrast medium cause hyperthyrodism ?

A

High levels of iodine

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16
Q

What would be present on TFTs in hyperthyroidism ?

A

Increased t3/t4 and low TSH

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17
Q

What causes diabetic nephropathy ?

A

It is the most common cause of glomerular pathology and CKD in the UK. Chronic high levels of glucose passing through the glomeruli causes scarring. This is called glomerulosclerosis.

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18
Q

What is a key feature of diabetic nephropathy ?

A

Proteinuria and drop of eGFR

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19
Q

What do diabetic have regular screens of to prevent diabetic nephropathy ?

A

Via albumin:creatinine ratio (detects elevated proteins) and u and es.

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20
Q

How is diabetic nephropathy treated ???

A
  • Optimise blood sugar levels and blood pressure as well as give ACE inhibitors
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21
Q

What should all patients with diabetic nephropathy be given ?

A

ACE inhibitors, regardless of if they have normal blood pressure.

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22
Q

What can be used in symptom control in patients with hyperthyroidism and anxiety ?

A

Propanolol.

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23
Q

What will be present on blood testing in a patient with graves disease (antibodies)?

A

presence of anti TSH antibodies

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24
Q

What is normal glucose range ?

A

Between 4.4 and 6.1mmol/l

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25
Q

Briefly describe T1DM ?

A

Pancreas loses the ability to produce insulin. No insulin means calls cannot use up glucose. This causes hyperglycemia.

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26
Q

What condition of the thyroid is commonly associated with T1DM ?

A

Hyperthyroidism, this is screened for in routine thyroid tests.

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27
Q

How does T1DM present ?

A
  • weight loss
  • Polyuria
  • Polydipsia
  • DKA (10 percent of new diagnosis are based on a DKA episode)
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28
Q

What measurements is a diagnosis of T1DM based off ?

A
  • Raised blood glucose measurements (random BM > 11mmol/L)
  • Raised HbA1c
  • Urine ketones
  • Raised fasting glucose.
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29
Q

What is the first line of treatment in type 1 DM ?

A

Basal bolus insulin regimes - A basal-bolus routine involves taking a longer acting form of insulin to keep blood glucose levels stable through periods of fasting and separate injections of shorter acting insulin to prevent rises in blood glucose levels resulting from meals.

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30
Q

How do you calculate basal bolus regimes from a patient who had IV insulin ?

A

Moving from IV to SC insulin after an episode of DKA, new diagnosis. Say glucose need is 120 units per 24 hours in a day IV. 3 x fifths of this value should represent three meals and how much must be given with each mean, the rest is given as a long lasting insulin injection.

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31
Q

What is lipodystrophy ?

A

Injecting into the same spot repeatedly when using insulin. This can cause the fat to harden and hence patients do not absorb insulin properly from further injections into this spot.

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32
Q

What is lipodystrophy ?

A

Injecting into the same spot repeatedly when using insulin. This can cause the fat to harden and hence patients do not absorb insulin properly from further injections into this spot.

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33
Q

How is non severe HYPOglycaemia presenr and managed ?

A

Typical symptoms are tremor, sweating, irritability, dizziness and pallor.

Patients need to treat this with rapid acting glucose and slower acting carbs like biscuits.

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34
Q

How is severe hypoglycaemia present and managed ?

A

In severe hypoglycaemia, coma, reduced conciousness and death can occur. If this is the case, IV dextrose and IM glucagon should be administered.

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35
Q

What should be given in severe hypoglycaemia where there is impaired conciousness.

A

IV dextrose and IV glucagon.

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36
Q

What are some of the long term complications of diabetes ?

A

Chronic hyperglycemia causes peripheral disease as well as suppression of the immune system.
- Hyperthyroidism
- CAD/stroke/hypertension
- Glomerulosclerosis
-Renal disease
- Retinopathy
-PAD

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37
Q

How is type 1 diabeties monitored ?

A
  • HbA1C (glycated HB). It is considered to be a reflection of the average glucose level over the past 3-4 months.
  • Capillary blood glucsoe
  • Flash glucose monitoring
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38
Q

What is the target blood pressure for patients with type 2 diabetes ?

A

140/90

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39
Q

What are the risk factors for developing T2DM ?

A

Non-Modifiable

  • Older age
  • Ethnicity (Black, Chinese, South Asian)
  • Family history

Modifiable

  • Obesity
  • Sedentary lifestyles
  • High carbohydrate (particularly refined carbohydrate) diet
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40
Q

What are some of the presenting features of a patient with type 2 DM ?

A
  • Polyuria and polydipsia
  • Fatigue
  • Weight loss
  • Slow healing
  • Glucosuria.
    -Repeated infections
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41
Q

What should all patients presenting with GP with any T2DM RF have tested ?

A

HbA1c

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42
Q

What is the Oral glucose tolerance test ?

A

Patients have fasting plasma glucose taken, then given a 75mg glucose drink. Plasma glucose is then measured 2 hours later.

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43
Q

What is a diagnostic result for T2DM in the OGTT ?

A

11.1 mmol/l

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44
Q

What is a diagnostic test for patients with suspected T2DM ?

A

OGTT

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45
Q

What parameters can be used to diagnose T2DM ?

A
  • HbA1c > 48
  • Random glucose > 11
  • Fasting glucose > 7mmol
  • OGTT > 11
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46
Q

What is the first line of management in patients with T2DM ?

A

Patient education about lifestyle changes like
Diet modification
Exercise and weight loss
Smoking Cessation
Treatment for underlying CV disease

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47
Q

What complications need to be monitored in patients with T2DM ?

A
  • Diabetic retinopathy
  • Kidney disease
  • Diabetic foot
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48
Q

What are HbA1c targets in patients with new T2DM ?

A

48

53 in patients on triple therapy

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49
Q

What is the first line medical management of patients with T2DM ?

A

Metformin

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50
Q

If metformin alone has not controlled T2DM symptoms, what other medication can be added ?

A

Add in sulfonylurea, piglitazone, DPP-4 inhib or SgL2 inhib.

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51
Q

What is third line treatment for patients with T2DM ?

A

Triple therapy (metformin and two of the second line drugs combined or ….)
Add in sulfonylurea, piglitazone, DPP-4 inhib or SgL2 inhib.

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52
Q

What is an alternate treatment for patients with T2DM who are failing to respond to triple therapy ?

A

Metformin and insulin.

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53
Q

What are some of the potential side effects of metformin.

A

Diarrhoea and abdominal pain, lactic acidosis.

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54
Q

What are some of the side effects if pioglitazone (used in diabeties management) ?

A

Weight gain, fluid retention, anaemia, HF and extended use can increase risk of bladder cancer

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55
Q

What are the side effects of sulfonylurea (used in T2DM management)?

A

weight gain, hypoglycaemia and increased risk of CV disease/MI

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56
Q

What are the side effects of SGLT-2 inhibitors ( used in T2DM management) ?

A

weight gain, hypoglycaemia and increased risk of CV disease/MI

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57
Q

What is the most appropriate insulin to use in T2DM ?

A

Immediate acting insulins like insulartard, humulin I)

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58
Q

What are three common complications of T2DM ?

A
  • Sexual dysfunction
  • Gastroparesis
  • Peripheral neuropathy/neuropathic foot ulcers
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59
Q

What are the symptoms of gastroparesis ?

A

Nausea, feeling full easily, large burps that smell like eggs.

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60
Q

What is the treatment of gastropariesis ?

A

Metocloparamide

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61
Q

What are the common complication of peripheral neuropathy ?

A

Neuropathic foot ulcers

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62
Q

What are the key symptoms of peripheral neuropathy ?

A

Sensory loss in the stocking distribution

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63
Q

What is the most common causative organism of neuropathic foot ulcers ?

A

Psudomonal aeurginosa

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64
Q

What is diabetes insipidus ?

A

Lack of ADH or lack of response to ADH.

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65
Q

What is primary polydipsia ?

A

Drinking excessive quantities of water leads to excessive urine production.

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66
Q

What is nephrogenic DI ?

A

Collecting ducts of the kidney do not respond to ADH

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67
Q

What is the common drug cause of DI

A

Patients may have bipolar disorder in questions
Lithium

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68
Q

What are some causes of nephrogenic DI ?

A
  • Lithium
  • AVPR2 mutations
  • CRD
  • Hypokalaemia
  • Hypercalcamia.
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69
Q

What is cranial DI ?

A

Hypothalamus does not produce ADH to be secreted by the pituitary.

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70
Q

What are some causes of cranial DI ?

A

-idiopathic
-brain tumours
-head injury
- Brain malformations
- Meningitis/TB/Encephalitus
- SCA
- Sarcoidosis

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71
Q

How does DI present (+ biochemical findings)?

A
  • Polyuria and polydipsia
  • Dehydration
  • Postural hypotension
  • Hypernatraemia.
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72
Q

What biochemical abnormalities does DI cause ?

A

Hypernatraemia

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73
Q

What is found on investigation in patients with DI ?

A
  • Low urine osmolality
  • High serum osmolality
    -Hypernatraemia
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74
Q

What is the test of choice when diagnosing DI ?

A

The water deprivation test/Desmopressin stimulation test.

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75
Q

What is the water deprivation test ?

A
  1. Patient should avoid fluids for 8 hours. Urine osmolality is measured.
  2. Desmopressin (synthetic ADH is then given) and urine osmolality is measured again.
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76
Q

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

A

After deprivation - low
After ADH - high

Remember in cranial DI, the hypothalamus does not produce ADH

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77
Q

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

A
  • After deprivation - Low
  • After ADH - Low

Remember the body still makes ADH just the CT can not respond to it

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78
Q

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

A
  • After deprivation - High
  • After ADH - High
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79
Q

How is cranial DI treated ?

A

Desmopressin
Treat underlying cause

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80
Q

Can nephrogenic DI be treated with desmopressin ?

A

In some cases yes, high doses with close monitoring. Mild cases may be managed without any intervention.

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81
Q

What group of diabetics does HHS usually occur in ?

A

Type 1 diabetics.

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82
Q

What the three key complications of DKA ?

A
  • Ketones (raised)
    -Dehydration
  • K imbalance (hypokalaemia)
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83
Q

What are some of the possible causes of DKA ?

A
  • Forgetting to inject insulin
  • First presentation in children
  • Infection (suspect if patient has fever), fasting dehydration
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84
Q

What is one of the key complications of DKA ?

A

Cerebral odema, make sure to closely monitor GCS.

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85
Q

When should you be suspicious of cerebral odema in patients with DKA ?

A

Be suspicious in patients with DKA that have headaches, altered behaviours, bradycardia or changes in consciousness.

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86
Q

How is cerebral odema managed ?

A

Slowing of IV fluids, mannitol and IV hypertonic saline.

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87
Q

How does DKA present ?

A
  • Polyuria and polydipsia
  • Nausea and vomiting with abdominal paun
  • Weight loss
  • Acetone smell to breath
  • Hypotension due to dehydration.
  • Altered consciousness
  • Symptoms of underlying trigger like sepsis.
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88
Q

What parameters are used to diagnose DKA ?

A
  • Hyperglycaemia > 11
  • Ketosis >3
  • Acidosis
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89
Q

How is DKA INITIALLY managed ?

A
  • Correct dehydration over 48 hours. Fast increases riek of cerebral odema (700mL Iv saline bolus in adults)
  • Fixed rate insulin infusion
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90
Q

Apart from the immediate management, how is DKA managed ?

A
  • Avoid fluid bolus
  • Treat underlying triggers
  • Prevent hypoglycaemia with IV dextrose if falls below 14
  • Add potassium to IV fluids
  • Monitor signs
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91
Q

What group of diabetics does HHS usually occur in ?

A

Type 2 diabetes

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92
Q

How does HHS typically present and on investigation like hypotension ?

A
  • Nausea and vomiting
  • Lethargy
  • Weakness
  • Confusion
  • Dehydration
  • Coma
  • Seizure
  • Hypovolaemia, tachycardia, hypo tension and exhaustion.
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93
Q

What are some causes of HHS ?

A
  • Infection
  • Medications that cause fluid loss or lower glucose tolerance
  • Surgery
  • Impaired renal function
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94
Q

What is the diagnostic criteria for HHS ?

A
  • severe hyperglycaemia (>=30mmol/L), more so than in DKA.
  • hypotension
  • hyperosmolality (usually >320 mosmol/kg)
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95
Q

What is the difference chemically between HHS and DKA ?

A
  • In HHS (severe hyperglycaemia) absence of ketosis
  • DKA - ketosis and hyperglycaemia.
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96
Q

How is HHS managed (and amount)?

A
  • 0.9 percent saline STAT then after an hour, add potassium (1000ml an hour)
  • Fixed rate insulin infusion at 0.05 units an hour if ketones are raised or glucose fails to fall. Correct dehydration and electrolytes before this
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97
Q

What else is important to make sure patients in HHS are given due hyperviscocity ?

A

VTE prophylaxis

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98
Q

What are the symptoms of hyperparathyroidism ?

A

Symptoms of hypercalcaemia

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99
Q

What blood tests are characteristic of primary hyperparathyroidism ?

A

Raise PTH
Raised calcium
Decreased phosphate

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100
Q

A GP performs routine blood tests on a 50 year old woman and finds a slightly raised calcium. She is on no medications and is otherwise well. The rest of her bloods are normal.

What should be considered in the differential diagnosis of hypercalcaemia?

A

Primary hyperparathyroidism

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101
Q

What mechanism causes primary hyperthyroidism ?

A

Thyroid pathology

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102
Q

What are some of the causes of primary hyperthyroidism ?

A

Graves disease
Thyroid adenoma
Multinodular goitre
De quirvains thyroiditis (painful goitre)
Silent thyroiditis

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103
Q

What mechanism causes secondary hyperthyroidism ?

A

Overstimulation of TSH receptors via pituitary/hypothalamus pathology

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104
Q

What are some of the causes of secondary hyperthyroidism ?

A

Amiodarone and lithium
TSH pituitary adenomas
Cholocarcinoma
Gestational

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105
Q

What are some of the features of hyperthyroidism ?

A
  • Irritability and anxiety
  • Sweating and fatigue
  • Tachycardia
  • Goitre
    -Muscle wasting/weakness
  • Weight loss
  • Clubbing
  • Sexual dysfunction
  • Diarrhoea
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106
Q

What is used as symptomatic relief in hyperthyroidism ?

A

BB like propanolol

107
Q

What is the first line treatment of hyperthyroidism and when is it CI ?

A

Carbimazole
First trimester of pregnancy

108
Q

What is used in second line of treatment of hyperthyroidism and when is it used in particular ?

A

propylthiuracil

109
Q

What will be present on thyroid function tests in hyperthyroidism ?

A

Increased T3/T4 and decreased TSH.

110
Q

What are some of the possible complications of hyperthyroidism ?

A
  • Thyroid storm
  • High output cardiac failure
  • Osteoporosis/osteopenia
  • Corneal ulcers/vision loss in graves
  • AF
111
Q

When is thyridectomy indicated in hyperthyroidism ?

A

If there is cancer, graves and recurrence

112
Q

What are the specific features of graves disease ?

A

Diffuse goitre (without nodules)
Graves’ eye disease, including exophthalmos
Pretibial myxoedema (It gives the skin a discoloured, waxy, oedematous appearance over this area)
Thyroid acropachy (hand swelling and finger clubbing)

113
Q

What causes graves disease ?

A

TSH receptor antibodies

114
Q

What is thyroid storm ?

A

A more serious presentation of hyperthyroidism.
Presents with fever, tachycardia and delerium.

115
Q

How is thyroid storm treated ?

A

IV digoxin
IV propanolol
Propulthiuracil IV followed by iodine 6 hours later (NG)
Prednisolone

116
Q

When is radioactive iodine indicated in hyperthyroidism?

A

Multinodular goitre/adenoma

117
Q

What antibodies are present in graves disease

A

Anti TSH receptor antibodies

118
Q

What is a key side effect of carbimazole used to treat hyperthyroidism ?

A

Agranulocytosis which can lead to neutropenia and severe sepsis. A sore throat but non specific sign of infection.

119
Q

A 34 year old man with a past medical history of vitiligo attends the endocrinology clinic with signs and symptoms of weight loss. He has lost 5 kg over the last 2 months without dieting or making any changes to his lifestyle. He feels generally anxious and has been getting intermittent palpitations. There is no family history of note.

Thyroid blood tests:

Free T3 9.9 (normal range: 3.5 – 7.8 pmol/L)

Free T4 31.2 (normal range: 9 – 24 pmol/L)

TSH 0.02 (normal range: 0.4–4.0 mU/L²)

What would the most appropriate initial step in management be for this patient?

A

commence propanolol and carbimanazole

120
Q

How would a patient presenting to A and E with addisons present ?

A
  • Hypotension
  • Hypoglycaemia
  • Fatigue (tired every day)
  • Abdominal pain and vomiting
  • Dehydration
    -Hypopigmentation
121
Q

What is waterhouse friderichsen syndrome ?

A

Adrenal gland failure due to bleeding into the arenal gland. Usually caused by severe meningiococcal infection or other severe bacterial infection. MENINGITIS
Symptoms - Acute adrenal gland insufficiency and profound shock.

122
Q

What does a low cortisol level at 9am indicate ?

A

Adrenal insufficiency

123
Q

What is the most common cause of addisons disease ?

A

Autoimmune adrenalitis ( adrenal glands are damaged)

124
Q

What will be ACTH/cortisol levels in addisons disease ?

A

High ACTH
Low cortisol.

125
Q

What are some causes of secondary adrenal insufficiency ?

A
  • Usually due to loss/damage of the pituitary resulting in decreased ACTH release
  • Common causes include trauma, removal of tumour, infection, loss of blood flow or massive blood loss.
126
Q

What will be present on blood tests in secondary adrenal insufficiency ?

A

Low ACTH
Low cortisol

127
Q

What causes tertiary adrenal insufficiency ?

A

Inadequate CRH release in the hypothalamus usually caused by taking patients on long term steroids off suddenly.

128
Q

What are the symptoms of adrenal insufficiency ?

A
  • Fatigue
  • Nausea
  • Abdo cramps and weakness.
  • Craving salt.
  • Increased thirst
  • Abdominal pain
  • Reduced libido
  • Weight loss.
129
Q

What are the signs of adrenal insufficiency ?

A
  • Bronze hyper-pigmentation to skin due to excessive ACTH production.
  • Hypo-tension (postural) with a drop of more than 20mmHg on standing.
130
Q

What is the key biochemical finding in addisons disease ?

A

Hyponatraemia

131
Q

What are the key biochemical findings in addisons ?

A

Hyponatraemia
Hyperkalaemia
Hypoglycaemia
Raised creatinine and urea

132
Q

What does failure for cortisol levels to double in the SST indicate ?

A

Primary adrenal insufficiency
or adrenal atrophy after a prolonged absence of ACTH in secondary adrenal insufficiency.

133
Q

How is adrenal insufficiency treated medically ?

A
  • Hydrocortisone (glucorticoid) used to replace cortisol.
  • Fludrocortisone (mineralocortricoid) to replace aldosterone.
134
Q

How is adrenal insufficiency treated non medically ?

A
  • Steroid card, ID tag and emergency letter.
  • Doses are doubled during an acute illness to match the normal steroid response to illness.
  • Taught to give IM hydrocortisone in an emergency.
135
Q

What should happen to steroid doses in acute illness ?

A

They should be doubled.

136
Q

How does adrenal crisis present ?

A

Acute presentation of severe addisons, where the absence of steroid hormones leads to a life threatening presentation.

It can be the first presentation of addisons disease, but also can be triggered by infection, trauma or other acute illnesses.

137
Q

How does adrenal crisis present ?

A
  • Reduced conciousness
  • Hypo-tension
  • Hypoglycemia, hyponatramia and hyperkalemia.
  • Very unwell
138
Q

How is adrenal crisis managed ?

A
  • ABCDE approach
  • Parental steroids - IV hydrocortisone 100mg STAT then 100mg every 6 hours
  • IV fluid resus
  • Correction of hypoglycaemia (IV dextrose)
  • Careful monitoring of electrolytes and fluid balance
139
Q

What type of adrenal insufficiency causes hyperpigmentation ?

A

Addisons disease due to high ACTH

140
Q

What is cushings syndrome ?

A

Features of prolonged high levels of glucocorticoids in the body (cortsol).

141
Q

What is cushings disease ?

A

Pituitary adenoma secreting excessive ACTH, stimulating excessive cortisol from the adrenal glands.

142
Q

What are the features of a patient with cushings disease ?

A
  • Round moon face
  • Central obesity
  • Abdominal striae
  • Enlarged fat pad on the upper back.
  • Proximal limb wasting.
  • Male pattern facial hear in women
  • Hyperpigmentation due to high ACTH like in addisons.
  • Easy bruising and poor skin healing.
143
Q

What are the metabolic effects of cushings disease ?

A
  • Hypertension
  • Cardiac hypertrophy
  • Type 2 diabeties
  • Raised cholesterol and triglycerides
144
Q

Mental health effects of cushings disease ?

A
  • Anxiety
  • Depression
  • Insomnia
  • Psycosis
145
Q

What are the main causes of cushings syndrome (CAPE) ?

A
  • Cushings disease like pituitary adenoma
  • Adrenal adenoma
  • PNP syndrome like small cell lung cancer
    E - Exogenous steroids
146
Q

What type of cancer most commonly causes cushings ?

A

SCLC

147
Q

What are the three types of dexamethasone supression tests when diagnosing cushings syndrome ?

A
  • Low-dose overnight test(used as a screening test to exclude Cushing’s syndrome). 1mg dex is given at night and cortisol is checked the following morning. Normal = supressed cortisol. Could indicate cushings disease
  • Low-dose 48-hour test(used in suspected Cushing’s syndrome). 0.5 mg is given every 6 hours for 8 doses starting at 9am. Cortisol is checked at (9am on day 1 before the first dose and 9am on the 3rd day after the last dose). Failure to supress on day 3 could indicate cushings syndrome.
  • High-dose 48-hour test(used to determine the cause in patients with confirmed Cushing’s syndrome). Same way as low dose but 2mg. The higher dose should be enough to supress cortisol in cushings syndrome caused by a pituitary adenoma but not by adrenal adenoma/ectopic ACTH.
  • ACTH can be measured directly. It is supressed in an adrenal tumour or endogenous steroids and increased in a pituitary tumour/ectopic ACTH.
148
Q

What cause of cushings syndrome is not investigated with dexamethasone supression tests ?

A

Exogenous steroid use

149
Q

What causes of cushings disease cause hyperpigmentation?

A

Due to excess ACTH release
- Cushings disease
- PNP ectopic ACTH

150
Q

What will be present on cortisol testing in an adrenal adenoma ?

A
  • Low 24 hour (not suppressed)
  • High 24 hour ( not supressed)
  • ACTH will low
151
Q

What will be present on cortisol testing in a pituitary adenoma ?

A

Low 24 hour (not suppressed)
- High 24 hour (supressed)
- ACTH will be high

152
Q

What will be present on cortisol testing in ectopic ACTH release due to PNP ?

A

Low 24 hour (not suppressed)
- High 24 hour (not supressed)
- ACTH will be high

153
Q

What is the only cause of cushings syndrome that will react to high 24 hour test ?

A

Pituitary adenoma, the rest do not have any supression.

154
Q

What is the main treatment option in cushings disease ?

A

Remove the underlying cause
- Trans-sphenoidal (through the nose) removal ofpituitary adenoma
- Surgical removal ofadrenal tumour
- Surgical removal of thetumour producingectopic ACTH (e.g.,small cell lung cancer ), if possible

155
Q

What is nelsons syndrome ?

A

Involves the development of ACTH producing pituitary tumour after the surgical removal of both adrenal glands due to adrenal adenoma causing cushings disease due to lack of cortisol and negative feedback. Causes skin pigmentation, bitemporal heminopia and lack of other pituitary hormones.

156
Q

What can be used pharmacologically to reduce the amount of cortisol in the body ?

A

Metryapone

157
Q

What are the symptoms of nelsons syndrome ?

A
  • Skin hyperpigmentation
  • Bitemporal heminopia
  • Lack of pituitary hormones.
158
Q

A 64 year old man with an extensive smoking history arrives to clinic with new chronic cough. You note he has clubbing and he informs you that he has had several cases of haemoptysis. He has increasingly found it difficult to rise from the sitting position and has noted easy bruising with purple striae of the skin.

Which of the following is the most likely cause of his skin changes?

A

ectopic ACTH release as a result of SCLC

159
Q

If a patient presents with cushings syndrome as a result of chronic steroid use, what is the first line in managing the condition ?

A

Wean the steroid therapy

160
Q

What is sub-clinical hypothyroidism ?

A

elevated TSH but no fall in T3/T4 and no symptoms of thyroid disease.

161
Q

How is a patient with asymptomatic sub-clinical hypothyroidism managed ?

A

Repeat TFT in 2-4 months

162
Q

When are patients with subclinical hypothyroidism treated ?

A

With raised TSH … symptomatic, positive autoantibodies, TSH is greater than 10 or patient is pregnant/planning to get pregnant.

163
Q

What blood tests are indicative of primary hypothyroidism ?

A

High TSH and low T3 and T4

164
Q

What blood tests are indicative of secondary hypothyroidism ?

A

Low TSH and Low T3/T4

165
Q

What are some of the causes of primary hypothyroidism (thyroid) ?

A
  • Hasimitos thyroiditis (anti TPO) and anti-Tg, iodine deficiency, hyperthyroidism treatments, lithium and amiodarone.
166
Q

What auto-antibody will be raised in hasimotos thyroidis ?

A

Anti TPO and anti Tg

167
Q

What causes of primary hypothyroidism will cause goitre ?

A

Hashimotos thyroiditis (goitre then atrophy)
Iodine deficiency

168
Q

What are some of the causes of secondary hypothyroidism ?

A
  • Tumours, surgery, sheenans syndrome, radiotherapy, trauma ….
169
Q

How does hypothyroidism present ?

A

Weight gain
* Fatigue
* Dry skin
* Coarse hair and hair loss.
* Fluid retention (oedema, pleural effusions and ascities)
* Constipation.
* Goitre in iodine deficiency
* Hashimotos thyroiditis can initially cause a goitre followed by a period of atrophy. ALSO loss of lateral third of the eyebrow and is classicly seen in hypothyroidism ( hertoghe sign)

170
Q

What is the treatment of hypothyroidism ?

A

Oral levothyroxine

171
Q

What is sub-clinical hyperthyroidism ?

A

T3 and T4 are normal but TSH is low

172
Q

What are the two subdivisions of hyperthyroidism ?

A
  • Primary - Due to thyroid pathology. Excessive thyroid hormone production.
  • Secondary - Hypothalamus/pituitary pathology. Pituitary produces too much TSH
173
Q

Generally, what are the most common causes of hyperthyroidism ?

A

graves disease
Inflammation (thyroiditis)
Solid toxic thyroid nodule.
Toxic multinodular goitre

174
Q

What autoantibody will be raised in graves disease ?

A

TSH receptor antibodies

175
Q

What are the distinctive features of graves disease ?

A
  • Exophthalamos (proptosis) - bulging of the eyes caused by graves disease. This is due to inflammation, swelling and hypertrophy of the tissue, causing them to bulge out of the sockets.
  • Pretibial myxoedema - Deposits of glycosaminoglycans under the skin on the anterior leg. This gives the skin a discoloured, waxy, oedematous apperance over the area. Specific to graves disease.
  • Painless goitre
  • TSH receptor antibodies
  • Thyroid acropachy (hand swelling and finger clubbing)
176
Q

What is the main risk factor for thyroid eye disease ?

A

smoking

177
Q

What are the different causes of thyroiditis (cause of hyperthyroidism ?)

A
  • De quervains (sub acute)
  • Post partum
  • Drug induced
  • Hashimotos
178
Q

What is De Quervains thyroiditis (cause of hyperthyroidism) and symptoms/management ?

A

Sub-acute. Temporary inflammation of the thyroid gland (thyrotoxicosis, hypothyroidism then return to normal)

The initial thyrotoxic phase involves - excessive thyroid hormones, thyroid swelling and tenderness, flu like illness and raised inflammatory markers.

Treatment - NSAIDS, BB for hyperthyroidism symptoms like palpitations and levothyroxine for hypothyrodism.

179
Q

What antibodies will be raised in Hashimotos thyroidis (autoimmune condition) ?

A

Anti TPO antibodies

180
Q

Does Hasimotos cause hyper/hypothyroidism ?

A

Both
Period of hyperthyroidism (goitre) followed by hypothyroidism (atrophy)

181
Q

What is a solitary toxic thyroid nodule ( cause of hyperthyroidism) and how is it treated ?

A

Single abnormal thyroid nodule acts alone to reduce excessive TH. Usually benign adenomas and treatment includes surgical removal of the nodule

Commonly presents in patients over 50 with numerous firm nodules in the goitre

182
Q

What is toxic multinodular goitre (cause of hyperthyroidism ) ?

A

Thyroid gland with multiple nodules.

183
Q

How does hyperthyroidism present ?

A
  • Anxiety and irritability
  • Sweating and heat intolerance
  • Tachycardia
  • Weight loss
  • Fatigue
  • Insomnia
  • Frequent loose stools
  • Sexual dysfunction
  • Brisk reflexes on examination
184
Q

What is the first line of treatment for hyperthyroidism ?

A

Carbimazole (inhibits TPO)- 1st line, usually taken 12 to 18 months. Once the patient has normal thyroid hormone levels, they continue on maintenance values until it is maintained at one level (titration block) or at higher doses, given with levothyroxine and titrated to effect (block and replace).

185
Q

What are patients taking carbimazole at a higher risk of ?

A

Pancreatitis

186
Q

What is the second line treatment for hyperthyroidism ?

A

Propylthiouracil - 2nd line. Risk of severe liver reactions that is why 1st line is preferred. Preffered in first trimester of pregnancy,

187
Q

What is one of the possible side effects of medications used to treat hyperthyroidism ?

A

Note : Both of the above can cause agranylocytosis (very low WCC). This means that patients are very succeptable to having infections. Sore throat in exams. Patients need an urgent FBC and aggressive treatment of any infections. Stop the carbimazole.

188
Q

What are some of the other methods of treatment in hyperthyroidism ?

A
  • Radioactive iodine
  • Surgery (thyroidectomy)
  • BB - propanolol for symptomatic relief.
189
Q

What is the management of nephrogenic DI ?

A

Thiazides and low protein/salt diet

190
Q

What is the management of cranial DI ?

A

Desmopressin.

191
Q

In diabeties, what distribution is peripheral neurpathy commonly ?

A

Sensory loss to the legs in a glove and stocking distribution. The legs are usually effected first.

192
Q

What is the management of diabetic neuropathy ?

A
  • First line - Amitriptyline, duloxetine, gabapentin or pregabalin. If one of these treatments does not work, try another.
  • Tramadol may be used as a rescue therapy for exacerbations of neuropathic pain.
  • Topical capsaicin can be used for localised neuropathic pain
193
Q

Patients with diabeties can also develop gastroparesis (delayed gastric emptying). What are the symptoms of this and how is it managed ?

A
  • Erratic Blood glucose control, bloating and vomiting.
  • Management - metrocloparamide, domperidone and erythromycin (prokinetic agents)
194
Q

What mechanism causes diabetic nephropathy ?

A

Chronic high levels of glucose passing through the glomeruli causes scarring. This is called glomerulosclerosis.

195
Q

What is a key biochemical finding in diabetic nephropathy ?

A

Proteinuria

196
Q

What is the screening programme for diabetic nephropathy ?

A
  • Annual screening of ACR (early morning specimine)
  • More than 2.5 = microalbuminuria.
197
Q

What is the general management of diabetic nephropathy ?

A
  • Diabetic protein restriction
  • Tight glycaemic control
  • BP control (aim for less than 130/80)
  • ACE/ARB if urinary ACR is more than 3.
  • Control dyslipidaemia like statins.
198
Q

When should an ACE/ARB be commenced in diabetic nephropathy ?

A

If the ACR (albumin creatinine ratio) is more than 3

199
Q

What are the diagnostic glucose levels in T1DM ?

A
  • Fasting glucose over or equal to 7
    Random glucose over 11

Low C peptide, ketosis, symptomatic and Fhx

200
Q

What screening is offered in diabetics ?

A

HbA1c testing every 3-6 months
ACR annually (nephropathy)

201
Q

What are the target HbA1c levels in type 1 diabetics ?

A

Below 48

202
Q

How much potassium should be given if potassium levels are 3.5-5.5 ?

A

40 mmol/l

203
Q

What is the management of DKA ?

A
  • 0.9 percent saline (1L bolus)
  • Insulin IV infusion at 0.1 unit/kg an hour. Once more than 14, 10 percent dextrose infusion
  • Correction of electrolyte disturbance (hypokalaemia after insulin). If 3.5-5.5 40 mmol/l of K should be given. Any lower than this = specialist input.
  • Long acting insulin continued, short acting stopped.
204
Q

What type of diabeties is HHS most common in ?

A

Type 2 DM

205
Q

What is the diagnostic criteria for HHS ?

A
  • severe hyperglycaemia (>=30mmol/L), more so than in DKA.
  • hypotension
  • hyperosmolality (usually >320 mosmol/kg)
  • Not accompanied by significant acidosis. Endogenous insulin production is enough to prevent ketosis.
206
Q

What is the general management of HHS ?

A
  • IV 0.9 percent sodium chloride solution usually at 0.5-1L/hour depending on clinical assessment.
  • K levels monitored
  • Insulin should NOT be given unless blood glucose stops falling while giving fluids
207
Q

How is hypertension initially managed in diabetics ?

A

ACE(pril)/ARB (sartan)

208
Q

What is the management of hypertension in patients under 55 ?

A

ACE(pril)/ARB (sartan)

209
Q

What is the management of hypertension in patients over 55 or of black african/carribean origin ?

A

CCB

210
Q

Levothyroxine used in the treatment of hypothyroidism can cause ??

A

Osteoporosis and cardiac arrhythmias

211
Q

What is the treatment of prolactinomas ?

A

Carbeigoline ( dopamine agonist)
HRT is no features of galactorrhoea

Transphenoidal resection ( the same in a adenoma)

212
Q

What is the imaging method in suspected adenomas/prolactinomas ?

A

MRI brain.

213
Q

What are the symptoms of a pituitary adenoma ?

A

Headache and visual field loss

214
Q

What are the general symptoms of a prolacinoma ?

A
  • W = Oligomenorrhoea, galactorrhoea, infertility and vaginal dryness
  • M = Erectyle dysfunction, reduced facial hair

In both !!!

Headache-visual field defect

215
Q

What is the diagnostic criteria for T2DM ?

A
  • Random blood glucose more than 11.1
  • Fasting blood glucose more than 7
  • 2 he OGTT more than 11.1
  • HbA1c more than 48

symptomatic only need one
asymptomatic need 2

216
Q

What is a phaeochromocytoma ?

A

Catecholamine tumor (think adrenaline/dopamine — RISE IRRITABLE) that arises in the adrenal medulla.

217
Q

What are the symptoms of a phaeochromocytoma ?

A
  • Episodic hypertension
  • Anxiety and weight loss
  • Fatigue
  • Palpitations and sweating
  • Headaches
  • FLUSHING and ABDO pain
  • Pyrexia and Dyspnoea.
218
Q

What are the signs OE of a phaeochromocytoma ?

A
  • Hypertension
  • Tremor
  • Postural hypotension
  • Hypertensive retinopathy.
219
Q

What is the initial investigations in a phaeochromocytoma ?

A
  • Plasma metanephrines followed by urinary metanehprines have the best diagnostic accuracy.
  • Adrenal imaging after confirmed by the above (CT ABDO and CHEST)
220
Q

What is the definitive management of a phaeochromocytoma ?

A

definitive is tumor resection. Pre-op alpha blockade is required by phenoxybenzamine started first followed by BB.

221
Q

What are the symptoms of thyroid storm ?

A

Patients with marked hyperthyroid symptoms after an acute stress event.

222
Q

What is the management of thyroid storm ?

A

Iv propanolol/digoxin
NG propyluracil followed by iodine
Pred/hydro

223
Q

Levothyroxine (used in the treatment of hypothyroidism) has a SE of ?

A

OP

224
Q

Long term pred use can increase the risk of ?

A

T2DM

225
Q

What us the most common cause of diabetic foot ulcers/ infection ?

A

Pseudomonas aerginosa (water spreading)

226
Q

What is a key biochemical finding in DI ?

A

Hypernatraemia

227
Q

What is used in the treatment of gastroparesis (T2DM complication) ?

A

Promotility drugs like metrocloparamide/domperidone.

228
Q

What drug can cause both hyper/hypothyroidism ?

A

Amiodarone

229
Q

What is a key biochemical finding in addisons ?

A

Hypernataemia (due to decreased cortisol and increased renal Na loss)

230
Q

What will be present om C.diff infection on colonoscopy ?

A

Yellow plaques and mucosal inflammation.

231
Q

What is the treatment of cholera infection ?

A

Oral doxycyline

232
Q

What is the characteristic feature of typhoid fever ?

A

Vomiting and diarrhoea associated with a red macolopapular rash that blanches on pressure

233
Q

What is the treatment of H.pylori ?

A

7 day course of Amoxicillin, clarithromycin and omeprazole.

234
Q

What medications are used in alcohol withdrawal ?

A
  • Chlordiazepoxide (long acting benzo)
  • Seizure IV lorazepam
  • Pabrinex - to reduce risk of wernikes encephalopathy
  • Delerium tremens (oral or perentral lorazapam)
235
Q

In a patient that is taking metformin, when should you consider adding a second agent (HbA1c) ?

A

Rises to 58

236
Q

What is the immediate management of sudden onset sensioneural hearing loss ?

A

Same day ENT refferal

237
Q

What causes hyperaldosteronism ?

A

May be primary or secondary and is caused by excess aldosterone.

238
Q

What is the biochemical picture in patients with hyperaldosteronism ?

A

Hypertension/Hypokalaemia/metabolic alkalosis

239
Q

What are the common causes of hyperalsosteronism ?

A
  • Adrenal adenoma (Conns)
  • Bilateral adrenal hyperaldosteronism
  • Familial hyperaldosteronism
  • Adrenal carcinoma.
240
Q

What are the clinical features of hyperalsosteronism ?

A

Polyuria, polydipsia, lethargy and headaches and osteoporosis.

241
Q

How is hyper-aldosteronism managed ?

A
  • Identify the underlying cause.
  • Surgical removal of the effected adrenal gland.
  • Bilateral adrenal disease use K sparing diuretics like amiloride/spirinolactone and eplerenone.
242
Q

What are the clinical features of hypogonadism ?

A
  • Lethargy and weakness
  • weight gain
  • Loss of libido
  • Erectile dysfunction
  • Gynaecomastia
  • Depression
  • Infertility and OP
243
Q

What is the mainstay of treatment in hypo-gonadism ?

A

HRT is the mainstay of treatment in those with persistent/symptomatic hypo-gonadism.

244
Q

What is the characteristic presentation of SIADH ?

A

Euvolaemic hyponatraemia causing inappropriate release of ADH causing water retention.

245
Q

What are the common causes of SAIDH ?

A
  1. Hypoxia - Pneumonia, COPD and TB.
  2. CNS disease - Meningitis, stroke, SAH, head injury, brain tumours and acute psychosis.
  3. Malignancy - SCLC, pancreatic cancer, prostate cancer, thymoma and lymphoma and glioma
  4. Drugs - Carbamazepine, SSRIs, Opiates, Anti-psychotics
  5. Other - Acute intermittent polyphyria, trauma, major abdominal or thoracic surgery and symptomatic HIV.
246
Q

How is SIADH managed ?

A
  • Fluid restriction and identify underlying cause
  • ADH antagonist - tovaptan/deomeclucycline
    -Oral sodium and furosemide.
247
Q

What drug can cause hyperthyroidism and hypothyroidism ?

A

Amiodarone

248
Q

When is metformin contraindicated ?

A

In eGFR less than 45.

249
Q

High blood pressure, headache, sweating and anxiety in a young patient should raise suspicion of ..

A

Pheaochromocytoma

250
Q

what is a pheaochromocytoma ?

A

Benign tumor that develops in the adrenal gland.

251
Q

What is the test of choice in phaeochromocytoma ?

A

Plasma metanephrines.

252
Q

What is multiple endocrine neoplasia ?

A

Group of genetic conditions characterized by formation of hormone producing tumors in multiple endocrine organs.

253
Q

What are the features of MEN1 ?

A

Caused by a mutation of the MEN-1 gene
PT hyperplasia/adenomas
Gastrinoma/insuloma
Prolactinoma

254
Q

What are the features of MEN 2a ?

A
  • Mutation in RET gene
  • Medullary thyroid cancer
  • Phaeochromocytoma
  • PT hyperplasia/adenomas
255
Q

What are the features of MEN-2b ?

A
  • Medullary thyroid cancer
    Phaeochromocytoma
    PT hyperplasia/adenomas
    Mucosal neuromas.
256
Q

A patient with familial medullary cancer is likely to have …

A

MEN-2

257
Q

Screening vs diagnosis in patients with acro-megaly ?

A
  • Screening serum IGF
  • Diagnosis = OGGT
258
Q

Symptoms of thyrotoxicosis ?

A
  • Palpitations and tachycardia
  • Sweating
    -Pretibial myxodema
  • Diarrhoea
    -Anxiety and tremor
259
Q

What drug causes thyrotoxicosis ?

A

Amiodarone

260
Q

How does diabetic retinopathy present on fundoscopy ?

A

Mild - Dots and exudates as well as blot haemorrhage
Severe - Engorged tortous veins, cotton wool spots and large blot haemorrhages

261
Q

what is the initial investigation in hyperaldosteonism ?

A

renin aldosterone ratio

262
Q

What is whipples triad ?

A

symptomatic hypoglycaemia, glucose levels of 2.2 or lower and resolution of symptoms with glucose

Insuloma

263
Q

What is whipples triad ?

A

symptomatic hypoglycaemia, glucose levels of 2.2 or lower and resolution of symptoms with glucose

Insuloma

264
Q

What is the gold standard of diagnosis in insuloma ?

A

72 hour fast

MED-Y3 (24 decks)

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