Endo Flashcards
1
Q
What are the 3 most dangerous aspects of DKA?
A
- Dehydration
- Potassium imbalance
- Ketoacidosis
2
Q
What affect does insulin have on potassium?
A
Drives K into cells
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
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
5
Q
What is the diagnostic criteria for DKA?
A
- Hyperglycaemia (>11mmol/l)
- Ketosis (blood ketones >3mmol/l)
- Acidosis (<7.3)
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
7
Q
What can you add to IV fluids when managing DKA?
A
Potassium
8
Q
How do you prevent hypoglycaemia when treating DKA?
A
Give IV dextrose once blood glucose falls below 14mmol/l
9
Q
What are the levels of …. in DKA?
1. Bicarbonate
2. Creatinine
3. Sodium
A
- Low (HCO3 is used up trying to buffer ketones)
- Raised (sign of dehydration)
- Normal/raised (due to dehydration)
10
Q
What should you always screen new T1DM patients for? Why?
A
Coeliac disease, the conditions are often linked
11
Q
What viruses can trigger T1DM?
A
- Coxsackie B virus
- Enterovirus
12
Q
What is the management of severe hypoglycaemia?
A
IV dextrose and IM glucagon
13
Q
What is the normal range for blood glucose concentration?
A
4.4 - 6.1 mmol/l
14
Q
What blood pH would indicate mild DKA?
A
<7.3
15
Q
What blood pH would indicate moderate DKA?
A
<7.2
16
Q
What blood pH would indicate severe DKA?
A
<7.1
17
Q
When does ketogenesis occur?
A
When there is insufficient supply of glucose and glycogens stores are exhausted e.g. in prolonged fasting
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
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
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)
21
Q
What are typical symptoms of hypoglycaemia?
A
Tremor, sweating, irritability, dizziness and pallor
22
Q
What are long term macro-vascular complications of diabetes?
A
- Stroke
- CAD
- Hypertension
- Peripheral ischaemia
23
Q
What are long term microvascular complications of diabetes?
A
- Peripheral neuropathy
- Retinopathy
- Kidney disease, particularly glomerulosclerosis
24
Q
What HbA1c result indicates diabetes?
A
> 48 mmol/mol
25
What random plasma glucose result indicates diabetes?
>11 mmol/l
26
What fasting plasma glucose result indicates diabetes?
>7 mmol/l
27
What OGTT 2 hour result indicates diabetes?
>11 mmol/l
28
What's first, second and third line management of T2DM?
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
29
What 4 categories of insulin is there?
- Rapid-acting insulin
- Short-acting insulin
- Intermediate-acting insulin
- Long-acting insulin
30
What type of drug is metformin?
Biguanide
31
What type of drug is gliclazide?
Sulfonylurea
32
What type of drug is sitagliptin?
DPP-4 inhibitor
33
What is the role of DPP-4 inhibitors in the management of DM?
- 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
34
What are the 2 groups of corticosteroid hormones? Give an example for each
- Glucocorticoids (cortisol)
- Mineralcorticoids (aldosterone)
35
What is meant by Cushing's syndrome?
Features of prolonged high levels of glucocorticoids in the body
36
What is Cushing's disease?
A pituitary adenoma secreting excessive ACTH stimulated excessive cortisol release from the adrenal glands
37
What are the causes of Cushing's syndrome?
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)
38
What test is used to diagnose Cushing's syndrome?
- Dexamethasone suppression test
- Dexamethasone will normally suppress cortisol due to negative feedback
- A lack of cortisol suppression suggest Cushing's syndrome
39
What is the management of Cushing's syndrome?
- Treat underlying cause e.g. removal of troublesome tumour
- Where surgical removal is not possible -> adrenalectomy and life-long steroid replacement therapy
40
What is the difference between hyperaldosteronism and Conn's syndrome?
- Hyperaldosteronism refers to high levels of aldosterone
- Conn's syndrome refers to an adrenal adenoma producing too much aldosterone
41
Briefly outline the RAAS function in response low BP
- 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
42
What is the function of aldosterone?
Increased BP by...
- Increasing sodium reabsorption from the distal tubule
- Increasing potassium secretion from the distal tubule
- Increasing hydrogen secreting from collecting ducts
43
What is primary hyperaldosteronism? What will the serum renin level be? Give 2 causes
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
44
What is secondary hyperaldosteronism? What are 3 causes?
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
45
What test can be used to determine the type of hyperaldosteronism?
Alsoderone-to-renin ration
- High aldosterone and low renin = primary
- High aldosterone and high renin = secondary
46
What other investigation findings indicate high aldosterone?
- Raised BP
- Low potassium (aldosterone increases K+ secretion)
- Alkalosis
47
What is the management of hyperaldosteronism?
- 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
What happens in primary hyperthyroidism? What are the levels of thyroid hormones?
- Thyroid produces excessive thyroid hormones
- High T3/T4, low TSH
49
What happens in secondary hyperthyroidism? What are the levels of thyroid hormones?
- Pituitary produces excessive TSH
- High TSH, high T3/T4
50
What happens in primary hypothyroidism? What are the levels of thyroid hormones?
- Thyroid produces inadequate thyroid hormones
- Low T3/T4, high TSH
51
What happens in secondary hypothyroidism? What are the levels of thyroid hormones?
- Pituitary produces inadequate TSH
- Low TSH, low T3/T4
52
What is a cause of secondary hyperthyroidism?
Pituitary adenoma
53
What is a cause of secondary hypothyroidism?
Surgical removal of the pituitary
54
What are anti-thyroid peroxidase antibodies?
Antibodies against the thyroid gland
55
What are anti-thyroglobulin antibodies?
Antibodies against thyroglobulin. A protein produced by and present in the thyroid gland
56
What are TSH receptor antibodies?
Antibodies that mimic TSH. The bind to TSH receptors and stimulate T3/T4 release
57
When is anti-TPO raised?
In autoimmune thyroid disease e.g. Graves/Hashimoto's
58
When is anti-Tg raised?
- Graves
- Hashimotos'
- Thyroid cancer
- Can be raised in individuals without thyroid disease
59
When is TSH receptor antibodies raised?
TSH receptor antibodies cause Graves disease
60
What is toxic multi nodular goitre?
- A condition where nodules develop on the thyroid gland
- These are unregulated by the thyroid axis so produce excess thyroid hormones
61
What are the causes of hyperthyroidism?
GITS
- G – Graves’ disease
- I – Inflammation (thyroiditis)
- T – Toxic multinodular goitre
- S – Solitary toxic thyroid nodule
62
Give 4 causes of thyroiditis. What is the typical disease course of thyroiditis?
- DeQuervains thyroiditis, Hashimoto’s thyroiditis, post-partum thyroiditis, drug-induced thyroiditis
- Initial period of hyperthyroidism followed by hypothyroidism
63
What features are specific of Graves disease? What is their cause?
- 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
How does thyroid storm present?
- Fever
- Tachycardia
- Delirium
65
Hyperthyroidism management:
1. First and second line anti-thyroid drugs
2. Potential adverse effects
3. How might these present?
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
How is radioactive iodine used to treat hyperthyroidism? What rules do patients undergone treatment have to follow?
- 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
What is the most common cause of primary hypothyroidism in the developed world?
Hashimoto's thyroiditis
68
What is the most common cause of primary hypothyroidism in the developing world?
Iodine deficiency
69
What 2 medications cause primary hypothyroidism?
- Lithium - inhibits the production of thyroid hormones
- Amiodarone - interferes with thyroid hormone production
70
What is the first line treatment of hypothyroidism? What is it?
- Levothyroxine
- Synthetic version of T4
71
Where is parathyroid hormone produced?
- PTH is produced by chief cell in the parathyroid glands
- 4 parathyroid glands located in the 4 corners of the thyroid
72
When is PTH normally produced?
In response to hypocalcaemia
73
How does PTH raise serum calcium?
- 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
What are the symptoms of hypercalcaemia?
- Bones (bone pain +/- fractures)
- Stones (renal)
- Abdominal groans (constipation, N + V)
- Psychiatric moans (fatigue, depression, psychosis)
75
What are the types of hyperparathyroidism?
- Primary
- Secondary
- Tertiary
76
What happens in primary hyperparathyroidism? What is the treatment?
- Uncontrolled hormone production by a tumour of the parathyroid glands
- Tx = surgical removal of tumour
77
What happens in secondary hyperparathyroidism? What is the treatment?
- 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
What happens in tertiary hyperparathyroidism? What is the treatment?
- 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
How can investigations differentiate between the types of hyperparathyroidism?
PTH and calcium
- Primary - PTH (high) Ca (high)
- Secondary - PTH (high) Ca (low/normal)
- Tertiary - PTH (high) Ca (high)
80
How does hypoparathyroidism present?
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
What blood indicate hypoparathyroidism?
- Low Ca
- High phosphate
82
What's the most common cause of acromegaly? Give one other cause?
- Pituitary adenoma
- Ectopic GH production from lung/pancreatic tumour
83
Give 2 investigations for acromegaly?
- 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
What is the management of acromegaly?
- 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
What happens in adrenal insufficiency?
The adrenal glands do not produce enough steroid hormones - cortisol and aldosterone
86
How can adrenal insufficiency be categorised?
- Primary adrenal insufficiency
- Secondary adrenal insufficiency
- Tertiary adrenal insufficiency
87
What is Addison's disease?
- Primary adrenal insufficiency
- Adrenal glands produce reduce cortisol and aldosterone
88
What happens in secondary adrenal insufficiency?
Loss/damage of the pituitary -> inadequate ACTH -> low cortisol secretion from the adrenals
89
What causes secondary adrenal insufficiency?
Things affecting the pituitary gland:
- Pituitary adenomas
- Surgery
- Radiotherapy
- Sheehan's syndrome
- Trauma
90
What happens in tertiary adrenal insufficiency?
Inadequate CRH release by the hypothalamus -> affects remaining adrenal axis
91
What is the most common cause of tertiary adrenal insufficiency? How is it prevented?
- 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
What are signs of adrenal insufficiency?
- Bronze hyperpigmentation of skin - particularly skin creases
- Hypotension/postural hypotension
93
What are symptoms of adrenal insufficiency?
- Fatigue
- Muscle weakness/cramps
- Dizziness and fainting
- Weight loss
- Abdo pain
- Reduced libido
94
What causes bronze hyperpigmentation of skin in adrenal insufficiency?
Excessive ACTH -> stimulating melanocytes to produce melanin
95
What is the diagnostic test for adrenal insufficiency?
Short Synacthen test (aka ACTH stimulation test)
96
What bloods results do you see in adrenal insufficiency? Which of these is key
Hyponatraemia (may be the only presenting feature)
Others:
- Hyperkalaemia
- Hypoglycaemia
- Raised creatinine and urea (due to dehydration)
- Hypercalcaemia
Note: bloods can be normal
97
Outline the short Synacthen test for adrenal insufficiency
- 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
How do you differentiate between primary/secondary adrenal insufficiency following a +ve short Synacthen test?
- Cortisol remains low in primary
- Cortisol increases in secondary
99
What is the management of adrenal insufficiency? How does the management change when the pt is unwell?
- 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
What is Addisonian crisis?
- AKA adrenal crisis
- An acute presentation of severe adrenal insufficiency where the absence of steroid hormones leads to a life-threatening emergency
101
How can Addisonian crisis present?
- Reduced consciousness
- Hypotension
- Hypoglycaemia
- Hyponatraemia and hyperkalaemia
102
What is the management of Addisonian crisis?
- 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
What happens in SIADH?
- 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
Where are the potential sources of too much ADH in SIADH?
- Increased secretion by the posterior pituitary
- Ectopic ADH - most commonly by small cell lung cancer
105
How does SIADH present?
- 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
What are the top three causes of SIADH?
- Post-operative
- SSRIs
- Small cell lung cancer
107
How do you diagnose SIADH?
Diagnosis is based on clinical features:
- Euvolaemic hyponatraemia
- High urine osmolality
- High urine sodium
108
What is the management of SIADH?
- Treat underlying cause
- Manage acute severe hyponatraemia
- Fluid restriction (750-1000ml/24hrs)
- Vasopressin receptor antagonists e.g. tolvaptan
109
What is important when correcting sodium levels? What is a key complication?
- Sodium should not change by more than 10 mmol/L in 24 hrs
- Due to risk of osmotic demyelination syndrome
110
How does osmotic demyelination syndrome present?
- 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
