Endo for Finals Flashcards

1
Q

What affect does aldosterone have on sodium and potassium?

A

Sodium retention

Urinary potassium loss

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2
Q

What affect does aldosterone have on blood pressure?

A

Drives it up due to sodium and water retention

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3
Q

What are the causes of primary hyperaldosteronism?

A

Bilateral adrenal hyperplasia

Adrenal adenoma

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4
Q

What is Conn’s syndrome?

A

Primary hyperaldosteronism

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5
Q

What investigations might you do in suspected hyperaldosteronism?

A

U+E

Plasma aldosterone : renin ratio (will be raised)

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6
Q

What must you ensure before testing plasma aldosterone : renin ratio in suspected Conn’s?

A

Aldosterone antagonists (spironolactone and eplenerone) 6 weeks before test

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7
Q

‘Tea-coloured urine’ might lead you to be suspicious of what?

A

Rhabdomyolysis (due to myoglobinuria)

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8
Q

What might investigation results find in rhabdomyolysis?

A

Raised CK
Hyperkalaemia
Hypocalcaemia
Myoglubinuria (Dipstick +ve for blood)

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9
Q

Why might calcium be low in rhabdomyolysis?

A

Calcium is deposited in dead muscle cells so reduced in the circulation

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10
Q

What type of drug is metformin and what is it’s mechanism of action?

A

Biguanide - Increased peripheral insulin sensitivity, reduces hepatic glucose formation

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11
Q

What are the causes of a raised anion gap metabolic acidosis?

A
Methanol
Uraemia
Diabetic ketoacidosis
Paraldehyde
Isoniazid, infection, ischaemia
Lactic acidosis e.g. from Metformin
Ethalene glycol
Salicylates e.g. aspirin overdose
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12
Q

What are the causes of a metabolic acidosis with a normal anion gap?

A

Renal tubular acidosis

Diarrhoea, vomiting

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13
Q

What is the mechanism behind a normal anion gap metabolic acidosis?

A

Loss of bicarbonate which is buffered by chlorine, so more accurately termed a hyperchloraemic metabolic acidosis

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14
Q

In a patient being treated for DKA, how should you go about restarting their normal insulin?

A

If the patient was on a basal bolus regime:
- Give short acting with a meal and stop the insulin infusion 30-60 minutes later
- The long acting insulin should not have been stopped throughout the episode of DKA
If the patient was using a mixed insulin regime, give a dose with morning or evening meal, then stop the insulin infusion 30-60 minutes later

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15
Q

What is an Addisonian Crisis?

A

Acute adrenal insufficiency

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16
Q

What is the most common cause of an Addisonian Crisis?

A

Iatrogenic i.e. abrupt withdrawal of steroids

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17
Q

How might a patient with an Addisonian Crisis present?

A

Hypovolaemic shock: Tachycardia, hypotension, oliguria, weakness, reduced GCS, comatose

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18
Q

What electrolyte disturbances might be present in an Addisonian Crisis? Why?

A

Hyperkalaemia
Hyponatraemia
Steroids usually increase sodium so lack of steroids will cause low sodium and raised K+ as a consequence

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19
Q

What is the management of Addisonian Crisis?

A

DR ABCDE approach

  • Take bloods, particularly ACTH, cortisol, U+E
  • Hydrocortisone 100mg IV stat
  • Supportive i.e. fluids
  • Monitor glucose (risk of hypoglycaemia) and treat accordingly
  • Look for underlying cause e.g. infection
  • Switch to oral steroids after 72 hours if BP stabilised
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20
Q

What is the inheritance pattern of multiple endocrine neoplasia?

A

Autosomal dominant

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21
Q

What is multiple endocrine neoplasia?

A

Rare condition where there is formation of tumours in several endocrine glands - this may happen at the same time or at different times. Treatment is by removal of the tumours if possible. There are different types depending on the clinical manifestation of the tumours.

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22
Q

Give some features of multiple endocrine neoplasia Type 1

A

All the ‘Ps’:

  • Parathyroid adenoma / hyperplasia
  • Pancreatic tumours: Gastrinoma, insulinoma, glucagonoma, somatostatinoma
  • Pituitary adenoma: Prolactin secreting, GH secreting
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23
Q

What is the most common presentation of multiple endocrine neoplasia Type 1?

A

Hypercalcaemia - This is because a parathyroid tumour is the most common tumour type in MEN1

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24
Q

Which tumour type is seen both in MEN1 and MEN2a?

A

Parathyroid adenoma

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25
Which tumour types are seen in MEN2a?
Parathyroid adenoma Thyroid medullary cancer Adrenal tumour i.e. phaeochromocytoma
26
Which type of multiple endocrine neoplasia does NOT have parathyroid adenomas as a feature?
MEN2b
27
Which type of multiple endcrine neoplasia might present with a patient with a Marfanoid appearance?
MEN2b
28
Which tumour types are seen in MEN2b?
Thyroid medullary cancer Adrenal - Phaeochromocytoma Neuromas (Patients also have Marfanoid appearance)
29
Which type(s) of multiple endocrine neoplasia are caused by the RET oncogene?
MEN2a and MEN2b
30
Give some causes of primary adrenal insufficiency (Addison's disease)
``` Autoimmune: Antibodies to 21-hydroxylase Neoplastic: Adrenal metastasis, lymphoma Infective: TB, histoplasmosis Haemorrhage: Waterhouse-Friedrichsen's Syndrome Infarction ```
31
Give some causes of secondary adrenal insufficiency
Hypothalamic or pituitary disease | Iatrogenic: Withdrawal of steroid therapy
32
What is Addison's Disease?
Adrenal insufficiency - This is usually autoimmune destruction of the adrenal cortex, which results in insufficiency of glucocorticoids and mineralocorticoids
33
List some clinical features of Addison's disease
- Insidious onset, usually with non-specific symptoms (lethargy, depression, weight loss) - Postural hypotension - Nausea, vomiting, abdominal pain, diarrhoa, constipation - Hyperpigmented skin, especially buccal mucosa and skin creases - Due to stimulation of melanocytes by excess ACTH - Vitiligo - Loss of body hair in women - Addisonian crisis
34
What initial screening tests can you do for Addison's disease? What would they show?
9am cortisol and ACTH Primary hypoadrenalism = ACTH high Secondary hypoadrenalism = ACTH low
35
What is the diagnostic test for Addison's disease?
Short Synacthen Test
36
What happens in the Short Synacthen Test?
Demonstrate's body's response to ACTH administration for investigation of Addison's Disease: Measure cortisol then administer 250ug of Synacthen (synthetic ACTH), and remeasure cortisol after 30 minutes. Cortisol should rise by more than 550umol/L. Addison's confirmed if this risk is not seen.
37
What is the treatment for Addison's?
Replace steroids: Daily hydrocortisone Replace mineralocorticoids to maintain BP and electrolyte balance: Daily fludrocortisone Investigate for causes Education about adrenal crisis i.e. don't stop steroids!
38
What class of drug are exanatide and liraglutide?
GLP-1 analogues
39
Give 2 examples of GLP-1 analogues
Exenatide | Liraglutide
40
What is the importance of GLP-1?
It stimulates insulin production in response to an oral glucose load - the 'incretin effect'. This is known to be decreased in diabetes and so increasing GLP-1 levels will help with insulin production and thus lowering glucose levels.
41
True / False: GLP-1 analogues typically cause weight gain
False - They cause no increase in weight, in fact they often cause weight loss
42
How do DPP-4 inhibitors work?
They prevent the breakdown of GLP-1, thus increasing it's availability and increasing insulin via the incretin effect
43
Give 2 examples of DPP-4 inhibitors
The 'gliptin's: - Sitagliptin - Linagliptin
44
By what route are GLP-1 analogues administered? By what route are DPP-4 inhibitors administered?
GLP-1 analogues = Subcutaneous injection before a meal | DPP-4 inhibitors = Orally
45
True / False: DPP-4 inhibitors cause weight gain
False - DPP-4 inhibitors do not cause weight gain
46
Give 1 example of a thiazolidinedione
Pioglitazone
47
List some side effects of thiazolidinediones e.g. pioglitazone
Weight gain Fractures Deranged LFTs Bladder cancer
48
Give an example of a sulphonylurea
Gliclazide
49
Give some side effects of sulphonylureas
Hypoglycaemia Weight gain SIADH Deranged LFTs
50
Give an example of a biguanide drug
Metformin
51
What type of drug is gliclazide?
Sulphonylurea
52
What type of drug is pioglitazone?
Thiazolidinedione
53
What type of drug are sitagliptin and linagliptin?
DPP-4 inhibitors
54
What type of drug is Metformin?
A biguanide
55
What are the key side effects of metformin?
GI upset: Diarrhoea | Lactic acidosis
56
What is the target HbA1c for patients with TIIDM on metformin only?
48mmol/L (6.5%)
57
What is the target HbA1c for patients with TIIDM on gliclazide?
53mmol/L (7.0%) due to risk of hypoglycaemia on this drug
58
What is the mechanism of SGLT2-inhibitors?
They inhibit glucose uptake in the renal tubule, thus causing renal excretion of glucose to reduce systemic levels
59
Give an example of an SGLT-2 inhibitor
Dapaglifloxin
60
What is the target HbA1c for a patient on metformin and another drug?
53mmol/L (7.0%)
61
After lifestyle modification, what is the first line for patients with TIIDM?
Metformin
62
What is the next step in the management of a patient with TIIDM on metformin who has an HbA1c greater than 58mmol/L?
``` Continue metformin and add one of the following: DPP-4 inhibitor e.g. Sitagliptin Sulphonylurea e.g. Gliclazide Pioglitazone SGLT-2 inhibitor e.g. Dapagliflozin ```
63
What is the next step in the management of a patient with TIIDM on metformin and another drug (dual therapy) who has an HbA1c greater than 58mmol/L?
Try one of the following triple therapies: - Metformin, DPP-4 inhibitor, sulphonylurea - Metformin, pioglitazone, sulphonylurea - Metformin, pioglitazone, SGLT-2 inhibitor - Metformin, sulphonylurea, SGLT-2 inhibitor
64
What is the next step in the management of a patient with TIIDM on triple therapy who has an HbA1c greater than 58mmol/L?
In patients who have BMI more than 35 or who cannot tolerate insulin, add a GLP-1 analogue. In all other patients consider insulin.
65
What is the management of patients with TIIDM who cannot tolerate metformin (or for whom it is contraindicated)?
DPP-4 inhibitor (sitagliptin) OR sulphonylurea OR pioglitazone
66
What is the diagnostic criteria for diabetes?
- One hyperglycaemic reading i.e. fasting glucose over 7mmol/L or non-fasting over 11.1mmol/L in a patient with symptoms - Two hyperglycaemia readings OR a 2 hour OGTT result over 11.1mmol/L - HbA1c more than 48mmol/L (6.5%)
67
What is the diagnostic criteria for impaired fasting glucose?
Fasting glucose more than 6.1mmol/L but less than 7mmol/L
68
What is the diagnostic criteria for impaired glucose tolerance?
Fasting glucose less than 7mmol/L but OGTT 2 hour result more than 7.8mmol/L but less than 11.1mol/L
69
What are the main complications of insulin?
Hypoglycaemia Injection site lipo-atrophy Injection site lipo-hypertrophy Weight gain
70
Is metformin discontinued peri-operatively?
It depends! - Continue pre-operatively, do not need to stop - Likely to be continued on the day of the surgery depending on the length of the surgery and how long the patient is NBM for - Continue after surgery but check U+E to ensure it's safe to restart
71
Is gliclazide discontinued peri-operatively?
- Continue until day of surgery | - Withold on day of surgery as patient is NBM and it's a hypoglycaemic drug
72
Describe the rules about insulin administration peri-operatively
- Continue until day of surgery - Take long-acting insulin on day of surgery but omit short-acting - Recommence short-acting when the patient is eating and drinking - Consider prescribing rescue medication for hypoglycaemia in a diabetic patient peri-operatively - Start variable rate insulin infusion in: Poorly controlled DM patients, patients who are having large operations and who are likely to miss more than 1 meal, diabetic patients undergoing emergency surgery
73
What is tested at a diabetic patient's annual review?
``` Bloods: - U+E, eGFR - Cholesterol - HbA1c Urine for ACR Feet for neuropathy Compliance to medication etc. ```
74
Give examples of 2 long-acting insulins
Lantus | Levemir
75
What is the diagnostic criteria for diabetic ketoacidosis?
pH less than 7.3 ± bicarbonate less than 18mmol/L Hyperglycaemia: Blood glucose more than 11.1mmol/L Presence of ketones: 2+ ketones on urine dip, or more than 3mmol/L in blood
76
What might be the cause of diabetic ketoacidosis?
Previously undiagnosed diabetes Poor-compliance with insulin Intercurrent infection
77
What is the management of DKA?
DRABCDE approach - IV access: Take bloods for FBC, U+E, CRP, ketones - ABG - Fluid resuscitation if BP low - IV fluids...1L 0.9% sodium chloride in 1 hour, then 1L in 2 hours, 1L in 2 hours, 1L in 4 hours, 1L in 4 hours, 1L in 6 hours - Start fixed rate insulin infusion with ActRapid insulin 50 units in 50mL 0.9% NaCl at a rate of 0.1units/kg/hr added to 2nd bag of fluids - Continuous cardiac monitoring - Add K+ if levels below 5.5mmol/L - LMWH in all patients - Consider NG tube if patient vomiting, consider catheter to monitor urine output - Give 10% glucose alongside saline if glucose levels drop below 14mmol/L - Continue fixed rate insulin until ketones less than 0.3mmol/L, pH more than 7.3 and bicarbonate more than 18mmol/L
78
How do you measure the serum osmolality?
[2 x Na] + K + glucose + urea Although K+ not always included
79
What are the features of hyperosmlar hyperglycaemic state?
``` Only seen in TIIDM Hyperglycaemia Hypovolaemia Hyperosmolality (more than 320mosmol/kg) Hypernatraemia due to dehydration Normal pH Normal bicarbonate Normal pCO2 Normal K+ No (or minimal) ketones ```
80
How is hyperosmolar hyperglycaemic state treated?
Insulin infusion Rehydration LMWH
81
What is HHS?
Hyperosmolar hyperglycaemic state
82
What is the most common form of secretory pituitary adenoma?
Prolactinoma
83
What test might be done in the initial screening for acromegaly?
IGF-1 level If normal, acromegaly is unlikely
84
What is the definitive test for acromegaly?
Oral glucose tolerance test Normally, high level of glucose suppresses the production of growth hormone. If GH remains high despite high levels of glucose, this confirms acromegaly diagnosis
85
What is the definitive test for growth hormone deficiency?
Insulin tolerance test Administering insulin causes hypoglycaemia which should normally stimulate a stress response resulting in the release of cortisol and growth hormone. If GH remains low despite insulin administration, this indicates GH deficiency
86
What is the treatment for growth hormone deficiency?
Recombinant growth hormone
87
List some causes of hyperprolactinaemia
Pituitary adenoma i.e. prolactinoma Dopamine antagonists e.g. metoclopramide, domperidone, anti-psychotics (haloperidol) Compression of the pituitary stalk which reduces dopamine thus removing the inhibition of prolactin Physiological: Pregnancy, breast-feeding Acromegaly Polycystic ovarian syndrome Hypothyroidism
88
What effect does dopamine have on prolactin levels?
Dopamine inhibits prolactin
89
List some features of hyperprolactinaemia
Females: Oligo/Amenorrhoea, galactorrhoea, reduced libido, weight gain, vaginal dryness, infertility Males: Impotence, galactorrhoea May present late e.g. osteoporosis or mass effect from tumour (headache, visual disturbances)
90
What is the treatment for hyperprolactinaemia
Remove drugs which might be causing it Correct thyroid dysfunction Dopamine agonist e.g. Bromocriptine Specialist input regarding surgery
91
Give some causes of Cushing's
Exogenous i.e. steroid use Cushing's disease i.e. ACTH-producing tumour Ectopic ACTH secretion: Small cell lung cancer, carcinoid tumour Ectopic CRH production in thyroid cancer Adrenal causes: Adrenal adenoma, adrenal nodular hyperplasia
92
What might be a useful initial investigation in Cushing's?
ACTH level If high, continue to the dexamethasone suppression test. If low, this indicates an 'ACTH independent' cause of Cushing's i.e. an adrenal cause
93
What is the definitive investigation in Cushing's?
Dexamethasone suppression test On administration of dexamethasone, cortisol levels should fall. Pituitary causes of Cushing's = Suppression Ectopic causes of Cushing's = No suppression
94
Give some side effects of steroids
Weight gain: Central distribution of weight, buffalo hump, moon face Hypertension Raised glucose Oral / vaginal candidiasis Skin atrophy, easy bruising Osteoporosis Cataracts Psychiatric symptoms: Depression, insomnia Addisonian crisis on abrupt withdrawal of steroids
95
What is a phaeochromocytoma?
A rare catecholemine producing tumour of the sympathetic nervous system (chromaffin cells), usually found in the adrenal medulla
96
Give some familial causes of phaeochromocytoma
von Hippel Lindau MEN2 Neurofibromatosis
97
Give some features of a phaeochromocytoma
``` Palpitations Tremor Sweating Anxiety Headache Nausea Weight loss Uncontrolled hypertension ```
98
What investigations would you do in phaeochromocytoma?
Plasma metanephrines 24 hours urinary metanephrines, catecholamines, VMA (a metabolite of adrenaline) CT abdomen
99
What is the management of phaeochromocytoma?
Surgical excision of the tumour Needs medical stabilisation before surgery: - Alpha blocker e.g. phenoxybenzamine - Beta blocker e.g. propranolol
100
Why is it important to block alpha action before beta in the management of a phaeochromocytoma
It prevents there from being unopposed alpha action which would lead to refractory hypertension
101
Why is there no dynamic testing for thyroid function?
Thyroid hormones have a half life of 7 days so static testing is sufficient
102
Which is a more potent suppressor of TSH...T3 or T4?
T3
103
Low TSH, high T4 indicates what underlying pathology?
Primary hyperthyroidism: - Grave's disease - Toxic multinodular goitre - Solitary toxic adenoma
104
What antibodies are present in Grave's disease?
TSH-receptor antibodies...which act to STIMULATE the thyroid
105
Why is T4 a preferred test for thyroid function than T3?
T4 is a precursor to T4
106
What is the treatment for Grave's disease?
Propranolol may help symptoms e.g. tremor Carbimazole: Give for 18/12, in which time 50% will be in remission Radio-iodine Surgery: Considered for those whom carbimazole was ineffective
107
What are the indications for surgery of a thyroid goitre?
Failure of medical management Patient choice Large goitre - These are more likely to relapse
108
What is the key side effect of carbimazole and what should patients be advised?
Agranulocytosis Advise patient if symptoms of rash, sore throat, fever, stop the medication and consult medical help. Check FBC.
109
Normal to high TSH, with high T4, indicates what underlying pathology?
Secondary hyperthyroidism: - TSH secreting tumor (TSHoma) - Ectopic thyroid tissue e.g. follicular thyroid cancer - Exogenous thyroid production e.g. iodine excess - Drugs e.g. amiodarone, too much thyroxine!
110
Which patients are not suitable for radio-iodine treatment?
Thyroid eye disease patients - Radioiodine can make symptoms worse due to antigen release
111
What investigation results would you expect in subclinical hypothyroidism?
High TSH, normal T4
112
High TSH, Low T4 indicates what underlying pathology?
Primary hypothyroidism - Hashimoto's thyroiditis - Post-treatment for hyperthyroidism - Primary atrophic hypothyroidism
113
Which antibodies are present in Hashimoto's thyroiditis?
Anti-TPO antibodies (thyroid peroxidase)
114
A patient is started on levothyroxine for hypothyroidism. 6/52 later their thyroid is checked and the TSH levels are low, while T4 is towards the upper limit of normal. What is the cause?
Likely over-treatment. Consider reducing thyroxine replacement.
115
A patient has a painful thyroid goitre - what is the likely cause?
Subacute (de Quervain's) thyroiditis
116
List some complications of thyroid surgery
Acute / rare: Bleeding into thyroid bed (leads to airway compromised), thyroid crisis Damage to local structures: Hypoparathyroidism, recurrent laryngeal nerve palsy Late complications: Hypothyroidism, recurrent hyperthyroidism
117
List 2 drugs which might cause hypothyroidism
Lithium | Amiodarone
118
What are they types of thyroid tumours?
``` Benign: Follicular adenoma Malignant: - Papillary carcinoma - Medullary carcinoma - Anaplastic carcinoma ```
119
What is the most common type of thyroid cancer?
Papillary carcinoma
120
Which thyroid cancer has the worst response to treatment?
Anaplastic carcinoma
121
Which thyroid cancer is associated with a tumour marker? What is it?
Medullary carcinoma - Produces calcitonin so useful marker of the disease
122
Which thyroid cancer might be seen in MEN2?
Medullary carcinoma
123
What are the differentials for a midline neck swelling?
Thyroid goitre Thyroiglossal cyst Thyroid cancer
124
What are the differentials for a lateral neck lump?
``` Lymph node Solitary thyroid nodule Vascular cause: Carotid aneurysm, carotid body tumour Sebaceous cyst Lipoma Cystic hygroma Branchial cyst Salivary glands Neurofibroma ```
125
How might you differentiate a sebaceous cyst from a lipoma?
Sebaceous cyst = Attached to skin at punctum | Lipoma = Mobile, no punctum
126
Give 2 differences between a cystic hygroma and a branchial cyst
Cystic hygroma = Posterior triangle, present from birth | Branchial cyst = Anterior triangle, generally appears in teenage / young adulthood
127
What investigation results would you expect to see in primary hyperparathyroidism?
High PTH High calcium Low phosphate High ALP
128
What investigation results would you expect to see in secondary hyperparathyroidism?
High PTH Normal or low calcium High phosphate in CKD, low phosphate in Vitamin D deficiency
129
What investigation results would you expect to see in tertiary hyperparathyroidism?
High PTH High calcium High PTH High ALP
130
What are the causes of primary hyperparathyroidism?
Parathyroid adenoma / hyperplasia Drugs: Thiazide diuretics, lithium Pancreatic neuroendocrine tumours
131
What is the cause of secondary hyperparathyroidism?
Chronic kidney disease | Vitamin D deficiency
132
What is the treatment for tertiary hyperparathyroidism?
Parathyroidectomy
133
What is the treatment for primary hyperparathyroidism?
IV fluids Avoid drug causes e.g. thiazide diuretics Parathyroidectomy