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2a > Endo > Flashcards

Endo Flashcards

1
Q

What are the 3 most dangerous aspects of DKA?

A
  • Dehydration
  • Potassium imbalance
  • Ketoacidosis
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2
Q

What affect does insulin have on potassium?

A

Drives K into cells

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3
Q

What causes potassium imbalance in DKA?

A
  • Without insulin potassium is not driven into cells
  • The serum potassium may be high/normal as the kidneys continue to balance the amount of K in the blood and urine
  • Total body K is low as no K is stored in cells
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4
Q

What can happen to potassium when insulin treatment of DKA starts? What is a complication of this?

A
  • Severe hypokalaemia as K is driven into cells
  • Fatal arrhythmias
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5
Q

What is the diagnostic criteria for DKA?

A
  • Hyperglycaemia (>11mmol/l)
  • Ketosis (blood ketones >3mmol/l)
  • Acidosis (<7.3)
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6
Q

What is the purpose of given a fixed rate insulin infusion in DKA?

A

Allows cells to start using glucose again, in turn switching off the production of ketones

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7
Q

What can you add to IV fluids when managing DKA?

A

Potassium

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8
Q

How do you prevent hypoglycaemia when treating DKA?

A

Give IV dextrose once blood glucose falls below 14mmol/l

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9
Q

What are the levels of …. in DKA?
1. Bicarbonate
2. Creatinine
3. Sodium

A
  1. Low (HCO3 is used up trying to buffer ketones)
  2. Raised (sign of dehydration)
  3. Normal/raised (due to dehydration)
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10
Q

What should you always screen new T1DM patients for? Why?

A

Coeliac disease, the conditions are often linked

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11
Q

What viruses can trigger T1DM?

A
  • Coxsackie B virus
  • Enterovirus
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12
Q

What is the management of severe hypoglycaemia?

A

IV dextrose and IM glucagon

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13
Q

What is the normal range for blood glucose concentration?

A

4.4 - 6.1 mmol/l

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14
Q

What blood pH would indicate mild DKA?

A

<7.3

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15
Q

What blood pH would indicate moderate DKA?

A

<7.2

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16
Q

What blood pH would indicate severe DKA?

A

<7.1

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17
Q

When does ketogenesis occur?

A

When there is insufficient supply of glucose and glycogens stores are exhausted e.g. in prolonged fasting

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18
Q

What causes ketoacidosis in DKA?

A
  • As people with T1DM have low glucose stores, fatty acids are converted into ketones as a source of energy (ketogenesis)
  • Initially the kidneys produce bicarb to counteract rising levels of ketone acids
  • Overtime ketone acids use up bicarb and blood becomes more acidic
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19
Q

What causes dehydration in DKA?

A
  • Glucose in the urine draws water out with it in a process called osmotic diuresis
  • This results in polyuria and severe dehydration
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20
Q

How do you treat DKA? What is the acronym?

A

FIG PICK:
F – Fluids – IV fluid resuscitation with normal saline (e.g. 1 litre stat, then 4 litres with added potassium over the next 12 hours)
I – Insulin – Add an insulin infusion
G – Glucose – Closely monitor blood glucose and add a dextrose infusion if below a certain level (e.g. 14 mmol/l)
P – Potassium – Closely monitor serum potassium (e.g. 4 hourly) and correct as required
I – Infection – Treat underlying triggers such as infection
C – Chart fluid balance
K – Ketones – Monitor blood ketones (or bicarbonate if ketone monitoring is unavailable)

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21
Q

What are typical symptoms of hypoglycaemia?

A

Tremor, sweating, irritability, dizziness and pallor

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22
Q

What are long term macro-vascular complications of diabetes?

A
  • Stroke
  • CAD
  • Hypertension
  • Peripheral ischaemia
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23
Q

What are long term microvascular complications of diabetes?

A
  • Peripheral neuropathy
  • Retinopathy
  • Kidney disease, particularly glomerulosclerosis
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24
Q

What HbA1c result indicates diabetes?

A

> 48 mmol/mol

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25
Q

What random plasma glucose result indicates diabetes?

A

> 11 mmol/l

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26
Q

What fasting plasma glucose result indicates diabetes?

A

> 7 mmol/l

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27
Q

What OGTT 2 hour result indicates diabetes?

A

> 11 mmol/l

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28
Q

What’s first, second and third line management of T2DM?

A
  1. Metformin
  2. Add one of; sulfonylurea, pioglitazone, DPP-4 inhibitor or SGLT-2 inhibitor
  3. Metformin plus 2 second line drugs OR metformin plus insulin
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29
Q

What 4 categories of insulin is there?

A
  • Rapid-acting insulin
  • Short-acting insulin
  • Intermediate-acting insulin
  • Long-acting insulin
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30
Q

What type of drug is metformin?

A

Biguanide

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31
Q

What type of drug is gliclazide?

A

Sulfonylurea

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32
Q

What type of drug is sitagliptin?

A

DPP-4 inhibitor

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33
Q

What is the role of DPP-4 inhibitors in the management of DM?

A
  • DPP-4 is an enzyme that inhibits hormones called incretins
  • Incretins are good and are secreted in response to large meals to lower blood glucose
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34
Q

What are the 2 groups of corticosteroid hormones? Give an example for each

A
  • Glucocorticoids (cortisol)
  • Mineralcorticoids (aldosterone)
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35
Q

What is meant by Cushing’s syndrome?

A

Features of prolonged high levels of glucocorticoids in the body

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36
Q

What is Cushing’s disease?

A

A pituitary adenoma secreting excessive ACTH stimulated excessive cortisol release from the adrenal glands

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37
Q

What are the causes of Cushing’s syndrome?

A

CAPE
- C - cushing’s disease
- A - adrenal adenoma (adrenal tumour secreting cortisol)
- P - paraneoplastic syndrome (ACTH produced from tumour somewhere other than pituitary e.g. small cell lung cancer)
- E - exogenous corticosteroids (e.g. prednisolone or dexamethasone)

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38
Q

What test is used to diagnose Cushing’s syndrome?

A
  • Dexamethasone suppression test
  • Dexamethasone will normally suppress cortisol due to negative feedback
  • A lack of cortisol suppression suggest Cushing’s syndrome
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39
Q

What is the management of Cushing’s syndrome?

A
  • Treat underlying cause e.g. removal of troublesome tumour
  • Where surgical removal is not possible -> adrenalectomy and life-long steroid replacement therapy
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40
Q

What is the difference between hyperaldosteronism and Conn’s syndrome?

A
  • Hyperaldosteronism refers to high levels of aldosterone
  • Conn’s syndrome refers to an adrenal adenoma producing too much aldosterone
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41
Q

Briefly outline the RAAS function in response low BP

A
  • Low BP detected by juxtaglomerular cells in the kidney
  • Renin secreted
  • Renin converts angiotensinogen into angiotensin I
  • ACE converts angiotensin I into angiotensin II
  • Angiotensin II stimulates the release of aldosterone from the adrenal glands
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42
Q

What is the function of aldosterone?

A

Increased BP by…
- Increasing sodium reabsorption from the distal tubule
- Increasing potassium secretion from the distal tubule
- Increasing hydrogen secreting from collecting ducts

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43
Q

What is primary hyperaldosteronism? What will the serum renin level be? Give 2 causes

A

When the adrenal glands are directly responsible for producing too much aldosterone

Serum renin will be low as high BP suppresses release

Causes:
- Bilateral adrenal hyperplasia (most common)
- Conn’s syndrome

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44
Q

What is secondary hyperaldosteronism? What are 3 causes?

A

Excessive renin stimulating the release excessive aldosterone

High renin is a result of abnormally low BP therefore the causes are linked to causes of low BP:
- Renal artery stenosis
- HF
- Liver cirrhosis and ascites

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45
Q

What test can be used to determine the type of hyperaldosteronism?

A

Alsoderone-to-renin ration
- High aldosterone and low renin = primary
- High aldosterone and high renin = secondary

46
Q

What other investigation findings indicate high aldosterone?

A
  • Raised BP
  • Low potassium (aldosterone increases K+ secretion)
  • Alkalosis
47
Q

What is the management of hyperaldosteronism?

A
  • Management of underlying cause e.g. surgical removal of adrenal adenoma in Conn’s syndrome
  • Medical management with aldosterone antagonists e.g. eplerenone, spironolactone
48
Q

What happens in primary hyperthyroidism? What are the levels of thyroid hormones?

A
  • Thyroid produces excessive thyroid hormones
  • High T3/T4, low TSH
49
Q

What happens in secondary hyperthyroidism? What are the levels of thyroid hormones?

A
  • Pituitary produces excessive TSH
  • High TSH, high T3/T4
50
Q

What happens in primary hypothyroidism? What are the levels of thyroid hormones?

A
  • Thyroid produces inadequate thyroid hormones
  • Low T3/T4, high TSH
51
Q

What happens in secondary hypothyroidism? What are the levels of thyroid hormones?

A
  • Pituitary produces inadequate TSH
  • Low TSH, low T3/T4
52
Q

What is a cause of secondary hyperthyroidism?

A

Pituitary adenoma

53
Q

What is a cause of secondary hypothyroidism?

A

Surgical removal of the pituitary

54
Q

What are anti-thyroid peroxidase antibodies?

A

Antibodies against the thyroid gland

55
Q

What are anti-thyroglobulin antibodies?

A

Antibodies against thyroglobulin. A protein produced by and present in the thyroid gland

56
Q

What are TSH receptor antibodies?

A

Antibodies that mimic TSH. The bind to TSH receptors and stimulate T3/T4 release

57
Q

When is anti-TPO raised?

A

In autoimmune thyroid disease e.g. Graves/Hashimoto’s

58
Q

When is anti-Tg raised?

A
  • Graves
  • Hashimotos’
  • Thyroid cancer
  • Can be raised in individuals without thyroid disease
59
Q

When is TSH receptor antibodies raised?

A

TSH receptor antibodies cause Graves disease

60
Q

What is toxic multi nodular goitre?

A
  • A condition where nodules develop on the thyroid gland
  • These are unregulated by the thyroid axis so produce excess thyroid hormones
61
Q

What are the causes of hyperthyroidism?

A

GITS
- G – Graves’ disease
- I – Inflammation (thyroiditis)
- T – Toxic multinodular goitre
- S – Solitary toxic thyroid nodule

62
Q

Give 4 causes of thyroiditis. What is the typical disease course of thyroiditis?

A
  • DeQuervains thyroiditis, Hashimoto’s thyroiditis, post-partum thyroiditis, drug-induced thyroiditis
  • Initial period of hyperthyroidism followed by hypothyroidism
63
Q

What features are specific of Graves disease? What is their cause?

A
  • Proptosis/exophthalmos
  • Pretibial myxoedema
  • Diffuse goitre (without nodules)
  • Thyroid acropachy (hand swelling and finger clubbing)

Features are related to the presence of TSH receptor antibodies

64
Q

How does thyroid storm present?

A
  • Fever
  • Tachycardia
  • Delirium
65
Q

Hyperthyroidism management:
1. First and second line anti-thyroid drugs
2. Potential adverse effects
3. How might these present?

A
  1. Carbimazole (first line), propylthiouracil
  2. Risk of acute pancreatitis with carbimazole, risk of severe liver reactions with propylthiouracil, risk of agranulocytosis with both
  3. Acute pancreatitis - severe epigastric pain, agranulocytosis - sore throat
66
Q

How is radioactive iodine used to treat hyperthyroidism? What rules do patients undergone treatment have to follow?

A
  • A single dose of radioactive iodine is drunk. This is taken up by thethyroid gland and the radiation destroys a number of the cell
  • Women must not get pregnant within six months of treatment
  • Men must not father children within 4 months of treatment
  • Limit contact with women and children following the dose
67
Q

What is the most common cause of primary hypothyroidism in the developed world?

A

Hashimoto’s thyroiditis

68
Q

What is the most common cause of primary hypothyroidism in the developing world?

A

Iodine deficiency

69
Q

What 2 medications cause primary hypothyroidism?

A
  • Lithium - inhibits the production of thyroid hormones
  • Amiodarone - interferes with thyroid hormone production
70
Q

What is the first line treatment of hypothyroidism? What is it?

A
  • Levothyroxine
  • Synthetic version of T4
71
Q

Where is parathyroid hormone produced?

A
  • PTH is produced by chief cell in the parathyroid glands
  • 4 parathyroid glands located in the 4 corners of the thyroid
72
Q

When is PTH normally produced?

A

In response to hypocalcaemia

73
Q

How does PTH raise serum calcium?

A
  • Increases osteoclast activity in bones -> calcium reabsorption
  • Increased calcium reabsorption in the kidneys
  • Activates vitamin D in the kidneys -> Vitamin D increases calcium reabsorption in the intestines
74
Q

What are the symptoms of hypercalcaemia?

A
  • Bones (bone pain +/- fractures)
  • Stones (renal)
  • Abdominal groans (constipation, N + V)
  • Psychiatric moans (fatigue, depression, psychosis)
75
Q

What are the types of hyperparathyroidism?

A
  • Primary
  • Secondary
  • Tertiary
76
Q

What happens in primary hyperparathyroidism? What is the treatment?

A
  • Uncontrolled hormone production by a tumour of the parathyroid glands
  • Tx = surgical removal of tumour
77
Q

What happens in secondary hyperparathyroidism? What is the treatment?

A
  • Low vit D/CKD -> hypocalcaemia
  • The parathyroid glands react by excreting more PTH
  • Tx = correct underlying cause e.g. vit D deficiency or CKD
78
Q

What happens in tertiary hyperparathyroidism? What is the treatment?

A
  • Occurs when secondary hyperparathyroidism continues for an extended period
  • Hyperplasia of the parathyroid glands
  • When the underlying cause of secondary hyperparathyroidism is treated the baseline PTH production remain high
  • This results in hypercalcaemia
  • Tx = surgical removal of parathyroid tissue restore normal PTH levels
79
Q

How can investigations differentiate between the types of hyperparathyroidism?

A

PTH and calcium

  • Primary - PTH (high) Ca (high)
  • Secondary - PTH (high) Ca (low/normal)
  • Tertiary - PTH (high) Ca (high)
80
Q

How does hypoparathyroidism present?

A

Symptoms are secondary to hypocalcaemia:
- Tetany
- Perioral paraesthesia
- Trousseau’s sign (carpal spasm if the brachial artery is occluded by inflating the BP cuff
- Chvostek’s sign (tapping over parotid causes facial muscles to twitch)
- If chronic - depression, cataracts
- ECG - prolonged QT

81
Q

What blood indicate hypoparathyroidism?

A
  • Low Ca
  • High phosphate
82
Q

What’s the most common cause of acromegaly? Give one other cause?

A
  • Pituitary adenoma
  • Ectopic GH production from lung/pancreatic tumour
83
Q

Give 2 investigations for acromegaly?

A
  • Insulin-like growth factor-1 (IGF-1)
  • Growth hormone suppression test - 75g glucose drink should suppress GH level, failure to suppress this indicates acromegaly
84
Q

What is the management of acromegaly?

A
  • Surgery to remove tumour

If surgery is unsuitable:
- Pegvisomant daily SC injection - a growth hormone receptor antagonist
- Somatostatin analogues - block growth hormone release
- Dopamine agonists (e.g., bromocriptine) - block growth hormone release, less powerful than somatostatin analogues

85
Q

What happens in adrenal insufficiency?

A

The adrenal glands do not produce enough steroid hormones - cortisol and aldosterone

86
Q

How can adrenal insufficiency be categorised?

A
  • Primary adrenal insufficiency
  • Secondary adrenal insufficiency
  • Tertiary adrenal insufficiency
87
Q

What is Addison’s disease?

A
  • Primary adrenal insufficiency
  • Adrenal glands produce reduce cortisol and aldosterone
88
Q

What happens in secondary adrenal insufficiency?

A

Loss/damage of the pituitary -> inadequate ACTH -> low cortisol secretion from the adrenals

89
Q

What causes secondary adrenal insufficiency?

A

Things affecting the pituitary gland:
- Pituitary adenomas
- Surgery
- Radiotherapy
- Sheehan’s syndrome
- Trauma

90
Q

What happens in tertiary adrenal insufficiency?

A

Inadequate CRH release by the hypothalamus -> affects remaining adrenal axis

91
Q

What is the most common cause of tertiary adrenal insufficiency? How is it prevented?

A
  • Long term oral steroid use (more than 3 wks)
  • Causes suppression of the hypothalamus (via -ve feedback)
  • When exogenous steroids are withdrawn the hypothalamus does not ‘wake up’ fast enough meaning endogenous steroids are not adequately produced

Prevention:
- Long term steroids must be tapered slowly to allow the adrenal axis to regain normal function

92
Q

What are signs of adrenal insufficiency?

A
  • Bronze hyperpigmentation of skin - particularly skin creases
  • Hypotension/postural hypotension
93
Q

What are symptoms of adrenal insufficiency?

A
  • Fatigue
  • Muscle weakness/cramps
  • Dizziness and fainting
  • Weight loss
  • Abdo pain
  • Reduced libido
94
Q

What causes bronze hyperpigmentation of skin in adrenal insufficiency?

A

Excessive ACTH -> stimulating melanocytes to produce melanin

95
Q

What is the diagnostic test for adrenal insufficiency?

A

Short Synacthen test (aka ACTH stimulation test)

96
Q

What bloods results do you see in adrenal insufficiency? Which of these is key

A

Hyponatraemia (may be the only presenting feature)

Others:
- Hyperkalaemia
- Hypoglycaemia
- Raised creatinine and urea (due to dehydration)
- Hypercalcaemia

Note: bloods can be normal

97
Q

Outline the short Synacthen test for adrenal insufficiency

A
  • The test involves giving a dose of Synacthen, which is synthetic ACTH
  • Blood cortisol is checked before and 30 and 60 minutes after the dose
  • Synthetic ACTH will stimulate healthy adrenal glands to produce cortisol
  • The cortisol level should at least double
98
Q

How do you differentiate between primary/secondary adrenal insufficiency following a +ve short Synacthen test?

A
  • Cortisol remains low in primary
  • Cortisol increases in secondary
99
Q

What is the management of adrenal insufficiency? How does the management change when the pt is unwell?

A
  • Steroid replacement
  • Hydrocortisone is used to replace cortisol
  • Fludrocortisone is used to replace aldosterone (not always required)
  • Doses are doubled during an acute illness to match the normal steroid response to illness
100
Q

What is Addisonian crisis?

A
  • AKA adrenal crisis
  • An acute presentation of severe adrenal insufficiency where the absence of steroid hormones leads to a life-threatening emergency
101
Q

How can Addisonian crisis present?

A
  • Reduced consciousness
  • Hypotension
  • Hypoglycaemia
  • Hyponatraemia and hyperkalaemia
102
Q

What is the management of Addisonian crisis?

A
  • ABCDE
  • IM/IV hydrocortisone (the initial dose is 100mg, followed by an infusion or 6 hourly doses)
  • IV fluids
  • Correct hypoglycaemia (IV dextrose)
  • Careful monitoring of electrolytes
103
Q

What happens in SIADH?

A
  • Increased ADH -> increased water reabsorption in the collecting ducts
  • The extra water in not enough to cause fluid overload -> results in euvolaemic hyponatraemia
  • Urine becomes more concentrated -> high urine osmolality and high sodium
104
Q

Where are the potential sources of too much ADH in SIADH?

A
  • Increased secretion by the posterior pituitary
  • Ectopic ADH - most commonly by small cell lung cancer
105
Q

How does SIADH present?

A
  • Symptoms relate to hyponatraemia
  • Depending on sodium level they may be asymptomatic or have non-specific symptoms e.g. headache, fatigue, muscle aches, confusion
  • Severe hyponatraemia can present with seizures and reduced consciousness
106
Q

What are the top three causes of SIADH?

A
  • Post-operative
  • SSRIs
  • Small cell lung cancer
107
Q

How do you diagnose SIADH?

A

Diagnosis is based on clinical features:
- Euvolaemic hyponatraemia
- High urine osmolality
- High urine sodium

108
Q

What is the management of SIADH?

A
  • Treat underlying cause
  • Manage acute severe hyponatraemia
  • Fluid restriction (750-1000ml/24hrs)
  • Vasopressin receptor antagonists e.g. tolvaptan
109
Q

What is important when correcting sodium levels? What is a key complication?

A
  • Sodium should not change by more than 10 mmol/L in 24 hrs
  • Due to risk of osmotic demyelination syndrome
110
Q

How does osmotic demyelination syndrome present?

A
  • Initially: confusion/encephalopathy - due to electrolyte imbalance
  • Second phase: spastic quadriparesis, pseudo bulbar palsy, cognitive/behavioural changes - due to demyelination of neurones (particularly in pons)
111
Q
A

2a (12 decks)

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