Endocrine Flashcards

1
Q

What are the 5 classes of hormone? Give 2 examples of each.

A
  1. Amino acid derivatives e.g. dopamine, catecholamines 2. Small neuropeptides eg. GnRh, TRH, ADH 3. Large proteins eg. insulin, PTH 4. Steroid hormones eg. cortisol, oestrogen 5. Vitamin derivatives eg. vitamin A,D
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2
Q

What are the functions of hormones?

A

Growth Maintenance of homeostasis Reproduction

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3
Q

What is the difference between primary and secondary endocrine disease?

A

Primary - target organ dysfunction Secondary - pituitary dysfunction

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4
Q

In what zone are mineralocorticoids produced?

A

Zona glomerulosa

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5
Q

In what zone are glucocorticoids produced?

A

Zona fasciculata

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6
Q

In what zone are androgens produced?

A

Zona reticularis

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7
Q

What does the adrenal medulla produce?

A

Epinephrine, norepinephrine and dopamine

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8
Q

TSH stimulates the thyroid to produce…

A

T3 - potent T4 - converted to T3 at certain tissue sites (by deiodinisation)

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9
Q

LH stimulates the leydig cells to produce…

A

Testosterone (95% produced in tested, other 5% in adrenal)

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10
Q

LH stimulates production of…

A

Progesterone

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11
Q

FSH stimulates production of…

A

Oestrogen

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12
Q

What are the roles of progesterone?

A
  • Maintenance of uterine lining - Decreased contractility of uterine smooth muscle - Skin elasticity and bone strength
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13
Q

What are the roles of oestrogen?

A
  • Secondary sex characteristics - Inhibition of bone resorption - Altered lipid profile - Vascular endothelium
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14
Q

What is the pathology of congenital adrenal hyperplasia?

A

21 hydroxylase deficiency resulting in reduced or absent production of cortisol and aldosterone. This means that the androgen pathway, which is unaffected, is favoured.

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15
Q

What are the symptoms of congenital adrenal hyperplasia?

A

Presents with ambiguous genitalia, hyponatremia, and arrhythmias, soon after birth

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16
Q

What is the definition of hyponatremia?

A

Sodium < 135 mmol/L

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17
Q

What are the symptoms and signs of hyponatraemia?

A

Symptoms: none, lethargy, cramps, headache, N&V Signs: disorientation, cerebral oedema, seizures, death

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18
Q

What are the categories of causes of hyponatraemia?

A
  • Pseudohyponatremia
  • Sodium depletion
  • Excess water intake
  • Reduced renal free water clearance
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19
Q

What causes pseudohyponatremia?

A

Hyperglycaemia Hypertriglyceridaemia

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20
Q

What causes sodium depletion?

A

Renal loss - diuretics, salt wasting, nephropathy, hypoadrenalism

Non-renal - gut loss

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21
Q

What causes excess water intake?

A

Diabetes insipidus IV fluids

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22
Q

What causes reduced renal free water clearance?

A

Hypovolaemia - sepsis, portal HTN, renal failure, hypoalbuminaemia

Cardiac failure

Nephrotic syndrome

Hypothyroid

SIAD

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23
Q

How is hyponatremia treated?

A

Give hypertonic saline

Restrict fluid intake - this is because hyponatremia will mean there will be more water and cells will swell.

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24
Q

What is the pathology of SIADH?

A

Syndrome of Inappropriate ADH Inappropriate continued secretion of ADH from the posterior pituitary or ectopic. Symptoms of hyponatremia!!

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25
How is SIADH diagnosed?
Hyponatraemia \< 135mmol/L Urine Na \> 20mmol/L Urine osmol \>100mOsm/kg in absence of - adrenal failure - oedema - hypotension - non-osmotic ADH release Plasma osmol \< 280mOsm/kg Also renal AQP2 excretion
26
What causes SIADH?
Brain damage (meningitis/SAH) Malignancy (SCLC) Drugs (carbamazepine, SSRIs, amitriptylline) Infection (pneumonia) Hypothyroidism
27
How should SIADH be managed?
Fluid restriction Sodium replacement SLOW Treatment of underlying cause NB - patients can tolerate chronic low sodium but the correction needs to be slow or the patient is at risk of osmotic demyelination syndrome
28
What is osmotic demyelination syndrome?
Severe damage and necrosis of the myelin sheath from rapid correction of hyponatremia
29
What are the symptoms of osmotic demyelination syndrome?
- Quadriplegia - Opthalomoplegia - Pseudobulbar palsy - Coma
30
How can osmotic demyelination syndrome be prevented?
Dont let sodium rise more than 10mmol/L/24h
31
A patient has hyponatremia with urine \>100mOsmol/kg and urine \>30mmol Na What are your differentials?
Drugs (ACEis diuretics) SIAD Salt wasting nephropathy Hypoadrenalism Vomiting
32
A patient has hyponatremia with urine \>100mOsmol/kg and urine \<30mmol Na What are your differentials?
Low arterial volume Heart failure Cirrhosis Nephrotic syndrome Hypoalbuminaemia Third space loss GI loss
33
What is the definition of hypernatremia?
\>144 Na
34
What are the symptoms and signs of hypernatremia?
Symptoms: THIRST, confusion, weakness, appetite loss, nausea Signs - muscle twitching, spasms, seizures
35
What causes hypernatremia?
Excess sodium in IV therapy Dehydration (elderly, terminally ill)
36
What is the management of hypernatremia?
Hypotonic fluids IV If hyper\<24 hrs - rapidly If hyper \>48 hr - slowly Hypotonic means that fluid will move into the cells along a concentration gradient
37
What is the definition of hypokalemia?
\<3.5 potassium
38
What are the symptoms and signs of hypokalemia?
Symptoms: ASYMPTOMATIC, constipation, fatigue, weakness/neuromuscular, cramps, palps Signs: ARRHYTHMIA on ECG, paralysis
39
What causes hypokalemia?
Diuretics Conns syndrome Barrters syndrome Gitelmans syndrome Diarrhoea/laxative use
40
What are the complications of hypokalemia?
Cardio -arrhythmias Neuromuscular - tetany, paralysis, rhabdomyolysis Renal - decreased GFR, nephritis, metabolic alkalosis Endocrine - growth retardation, decreased insulin secretion
41
What is the definition of hyperkalemia and what causes it?
\>5 potassium Decreased excretion - renal failure, drugs, hypoaldosteronism, acidosis Increased release from cell - acidosis, tissue damage, digoxin, vigorous exercise Increased extraneous load - potassium chloride, blood transfusion
42
What are the symptoms and signs of hyperkalemia?
Symptoms: Parasthesia, weakness Signs: ARRHYTHMIA, paralysis
43
What are the complications of hyperkalemia?
Cardio - arrhythmias Neuromuscular - parasthesia, weakness Renal - decreased renal NH4 production Endocrine - increased insulin secretion
44
How is hyperkalemia managed? (think rule of 10s)
1. IV calcium gluconate 10% 10mg 2. IV actrapid (10units) and dextrose (25g) 3. IV saline 50ml 4. Salbutamol neb 10-20mg Stop potassium containing/sparing meds. Dialysis if no response
45
What is given to stabilise the membrane in hyperkalemia ?
IV calcium gluconate 10% 10ml over 10 min IV saline 50ml
46
What is given to push potassium back into the cells in hyperkalemia?
Salbutamol 10-20mg nebulised IV actrapid 10units (and IV dextrose 25g to prevent hypoglycaemia)
47
What are the ECG features of hypokalemia?
- ST depression - Flat T wave - Prominent U wave
48
What are the ECG features of hyperkalemia?
Tented T waves
49
Where is potassium primarily stored?
Muscles, liver, RBCs
50
Where is the main place of potassium reabsorption in the kidney?
Proximal convoluted tubule
51
How is hypokalemia treated?
Sando potassium tablets Mild (3-4) - TDS Moderate (2.5-2.9)- QDS Severe (\<2.5) - IV 40mmol KCL in 1L saline (1mmol/hr) If IV, give in central line as K irritates tissues Dont give bolus as risk of arrhythmia
52
What is Barrters syndrome?
A range of inherited defects in the loop of hence in TAL Na+ and Cl- transport that causes hypokalemia and metabolic alkalosis
53
What is Gitelmans syndrome?
An inherited thiazide-like defect in DCT Na+/Cl- transport that causes hypokalaemia and metabolic alkalosis
54
What hormones does the anterior pituitary produce?
ACTH TSH FSH/LH Prolactin GH
55
What hormones does the posterior pituitary produce?
ADH (vasopressin) Oxytocin
56
In general, what causes pituitary hormone deficiency?
Congenital Acquired - SOL - Trauma - Iatrogenic - Infection - Infiltrative/inflam disease - Vascular - Idiopathic
57
In general what causes pituitary hormone excess?
- Benign pituitary adenoma - Ectopic secretion
58
What are 'mass effect' symptoms when referring to pituitary disease, and what causes them?
Headaches, nausea and visual disturbances You get a mixture of hormone excess and deficiency - hard to diagnose Large pituitary adenomas (functioning/non-functioning)
59
What is pituitary apoplexy?
Infarction/haemmorhage of the anterior pituitary causing headache, collapse, visual loss (bitemporal quadrantopia) and death.
60
How is pituitary apoplexy managed?
1. Resus with fluids and IV steroids 2. MRI to diagnose 3. Surgical decompression 4. Replace deficient hormones
61
What are the primary causes of hypoadrenalism?
Addisons disease (autoimmune) Glucocorticoid + mineralocorticoid deficiency
62
What are the secondary causes of hypoadrenalism?
ACTH pituitary deficiency Only glucocorticoid deficiency as mineralocorticoids are controlled by RAAS
63
What are the clinical features of hypoadrenalism?
Malaise Weight loss N&V Abdo pain Postural hypotension Hypoglycaemia Adrenal crisis
64
What electrolyte disturbance do you get in hypoadrenalism?
Low sodium, high potassium
65
How can you distinguish between a primary and secondary cause of hypoadrenalism?
Do synacthen test (synthetic form of ACTH) Measure baseline cortisol, give 250mcgrams synachten IM, measure cortisol at 0,30,60 mins Healthy - cortisol levels should double Primary - subnormal response to ACTH as the problem lies within the adrenal gland Secondary - dramatic increase in cortisol levels as problem lies with pituitary ACTH deficiency
66
Which individuals would get pigmented skin and salt cravings?
Primary adrenal insufficiency Skin - due to increased ACTH Salt cravings - mineralocorticoid deficiency
67
How is adrenal insufficiency managed?
Primary - hydrocortisone + fludrocortisone Secondary - hydrocortisone
68
What are the features of a patient with Addisons Disease
Lean, TANNED, tired, tearful, dizzy, faints, mood disorders - very non-specific
69
What causes an adrenal crisis?
Severe stress - accident/infection
70
What are the features of an adrenal crisis?
Hypovolaemic shock, abdo pain, vomiting, hypoglycaemia, confusion (severe low na) and fever
71
How is an adrenal crisis managed?
1. 1 litre 0.9% saline STAT 2. 100mg IV hydrocortisone STAT, then 200mg/24hr 3. Correct hypoglycaemia
72
What is the role of aldosterone?
Promotes sodium and water retention Lowers plasma potassium levels
73
What are the exogenous causes of Cushing's syndrome (adrenal excess)?
Steroids (RA, asthma)
74
What are the endogenous causes of Cushing's syndrome?
Adrenal tumour (benign/malignant) Pituitary tumour that secretes ACTH (Cushings disease) Ectopic ACTH secreting tumours (SCLC, carcinoid)
75
What are the symptoms and signs of Cushings syndrome?
Moon face, plethora, buffalo hump, thin hair/skin/nails, striae, central wasting, acne, hirsutism, malaise, depression, bruising, DM
76
How is Cushings syndrome investigated?
24 hour urinary free cortisol excretion AND Overnight dexamethasone suppression test (levels will be \>280 and no cortisol suppression respectively) If tumour is suspected, do CT/MRI to investigate. If ectopic suspected, administer metyrapone - if cortisol is still high, the ACTH is coming from an ectopic source
77
How can you localise the cause of Cushing's syndrome?
Do plasma ACTH levels Low ACTH = adrenal tumour (due to feedback mechanism) --\> do CT High ACTH = pituitary or ectopic High dose dexamethasone test: \<90% drop in urinary cortisol - ectopic ACTH \>90% drop - pituitary adenoma (cushings disease) Then do corticotrophin releasing test, cortisol will rise with pituitary disease but not ectopic (as it is not connected)
78
How is Cushings syndrome managed: a) Adrenal tumour b) Cushings disease c) Ectopic secretion
a) removal of adrenals, radiotherapy b) resection of pituitary adenoma, metyrapone c) surgery, radiotherapy For all, treat comorbidites and stop exogenous steroids
79
What is the role of aldosterone?
Stimulation of sodium and water absorption Removal of potassium from circulation
80
What are the 3 ways in which aldosterone secretion is managed?
1. RAAS - levels rise in response to low BP and renin release 2. Potassium - directly stimulated aldosterone secretion 3. ACTH - this is minor!!
81
What are the symptoms of hyperaldosteronism?
Hypertension!! Usually asymptomatic other than this
82
What does biochem show for hyperaldosteronism?
Decreased K and Mg Metabolic Alkalosis Primary - decreased renin Secondary - increased renin
83
What are the primary causes of hyperaldosteronism?
Conn's syndrome - adrenal adenoma Bilateral adrenal hyperplasia (MOST COMMON) Adrenal carcinoma
84
What are the secondary causes of hyperaldosteronism?
Any condition which increases renin production!! eg. renal artery stenosis, HF, liver failure, nephrotic syndrome Barrters syndrome Gitelmanns syndrome
85
How is Conn's syndrome managed?
Laparoscopic adrenelectomy Spironolactone (aldosterone antagonist) to control BP/K before op
86
What are the causes of primary hypothyroidism?
Hashimoto's thyroiditis (autoimmune) Surgery (eg. for hyperthyroid) Radiotherapy Iodine deficiency Drugs (amiodarone, lithium, iodine)
87
What are the causes of secondary hypothyroidism?
Pituitary deficiency
88
What are the symptoms of hypothyroidism?
Weight gain Hair loss (particularly lateral part of eyebrow) Cold intolerance Depression Fatigue Menorrhagia Constipation Dry Ataxia Ascites Bradycardia
89
How is hypothyroidism diagnosed?
Primary - increased TSH, low T3/T4 Secondary - normal TSH, low T3/T4
90
How is hypothyroidism treated?
Levo-thyroxine NB only use TSH to guide treatment in primary
91
What is Hashimotos Thyroidits? Describe typical presentation What anitbodies would be present?
A type of primary hypothyroidism, due to autoimmune attack of the thyroid, that is associated with T1DM, Addison's or Pernicious anaemia. It may cause transient thyrotoxicosis in the acute phase. It often presents as a goitre in women aged 60-70 years old. Anti-TPO
92
What are the causes of secondary hyperthyroidism?
Pituitary TSH, usually due to a TSHoma (very rare)
93
What are the causes of primary hyperthyroidism?
Graves disease Toxic nodule/goitre
94
What are the symptoms of hyperthyroidism?
Weight loss Intolerance to heat Ammenorhea Fatigue Anxiety Palps Diarrhoea Brisk reflexes Pretibial myxoedema
95
Name 3 specific signs to Graves What autoantibody would be present?
Orbitopathy Thyroid associated dermopathy Thyroid acropachy (clubbing) TRab
96
How is hyperthyroidism diagnosed?
Primary - low TSH, high T3/T4 Secondary - normal TSH, high T3/T4 NB - patients may have a thyroid bruit
97
How is a TSHoma managed?
Use somatostatin analogues (methimazole) Remove TSHoma with transphenoidal surgery
98
How is hyperthyroidism managed?
Inhibit fT4 to fT3 - Carbimazole, propylthioruracil Symptom control - B blockers (propanolol) Radioiodine (but will lead to hypothyroidism) Remember - if pt gets a sore throat on carbimazole go to A&E as it might be agranulocytosis
99
What is a thyroid storm and what are the features?
Severe hyperthyroidisim causing tachycardia, fever, encephalopathy, fits, stroke, hypertension, D&V, circulatory collapse and death. It is a medical EMERGENCY.
100
How is a thyroid storm treated?
Propylthiouracil Iodine Steroids(hydrocortisone) Beta-blockers (propanolol) IV fluids
101
What is a myxoedema coma?
Severe hypothyroidism causing hypothermia, bradycardia, coma, seizures, cyanosis, decreased BP and heart failure
102
How is a myxoedema coma treated?
Tri-iodothyronine Steroids (hydrocortisone) IV fluids Active warming for hypothermia
103
What is subclinical thyroid disease? Why is it clinically significant?
When TSH levels are changed but T3/T4 are normal Increased risk of CVS disease and osteoporosis
104
What is sick euthyroidism?
This is the derangement of TFTs in any systemic illness - typically everything will be low. DO NOT TREAT
105
What is Graves Eye Disease
Eye discomfort, grittiness, photophobia, afferent pupillary defect and expothalmous. This is associated commonly with Graves' disease but can be present in any thyroid disorder.
106
What would a normal thyroid uptake scan show?
Diffuse, even uptake of radioactive iodine
107
What would a graves thyroid uptake scan show?
Diffuse, increased uptake of iodine as the entire gland is overactive
108
What would a hashimotos thyroid uptake scan show?
Diffuse, decreased uptake of iodine as entire gland is underactive
109
What would a multinodular goitre show on thyroid uptake scan?
Focal areas of increased and decreased uptake
110
What is a hot/cold nodule?
An area which shows a small bit of increased/decreased uptake of radioactive iodine This requires investigation with USS FNA as it could be malignant (particularly cold) If hot it may require ablation, resection or medication
111
Name 3 causes of diffuse neck lumps
Simple goitre Thyroiditis Iodine deficiency
112
Name 4 causes of nodular neck lumps
Multinodular goitre Solitary toxic nodule Cysts Fibrosis
113
Name 2 causes of miscellaneous goitre/neck lumps
Sarcoidosis TB
114
Name 4 causes of neck tumours
Benign adenoma Carcinoma (papillary, follicular, medullary, anaplastic) Lymphoma Mets
115
What is De Quervains Thyroiditis (subacute)? Describe the stages of its development.
POST INFECTION thyroiditis 1. Initial follicular destruction 2. Release of thyroid hormones causing hyperthyroidism 3. Temporary hypothyroidism 4. Resolution or progression to longterm hypothyroid Patients will be post infection, and may have a painful neck.
116
What is acute thyroiditis?
Thyroiditis following a suppurative infection
117
What is silent thyroiditis?
Similar progression to subacute but NO PAIN and common in post-partum period
118
What are some congenital causes of primary hypogonadism?
Klinefelters syndrome (47XXY) Cryptorchidism (absence of testes) Turners syndrome (45X) Gonadal dysgenesis
119
Describe a patient with Klinefelters syndrome
Tall, gynaecomastia, reduced body hair, low libido, osteoporosis
120
What are some acquired causes of primary hypogonadism?
Infection (mumps/HIV) Autoimmune (premature ovarian failure/PCOS) Iatrogenic (chemo) Infiltrative (haemochromatosis) Drugs (ketoconazole)
121
What are some causes of secondary hypogonadism?
Pituitary deficiency
122
What are the clinical features of hypogonadism?
Libido loss Osteoporosis (low oestrogen) Amennhorea Erectile dysfunction
123
How is hypogonadism treated?
Replacement of sex steroids (give testosterone if \<8nmol/l, with 12 weekly injections or daily gels) --\> keep an eye on the haematocrit Address fertility issues (exogenous gonadotrophin - only works in secondary)
124
How are prolactin levels normally regulated?
Dopamine pathway, dopamine suppresses prolactin
125
What are the physiological causes of raised prolactin?
Pregnancy Stress
126
What are the pathological causes of raised prolactin?
- Drugs (metoclopramide, TCAs, antipsychotics, methyldopa) - Prolactin secreting pituitary adenomas - Stalk hyperprolactinaemia (non functioning tumour) - Hypothyroidism - Cirrhosis - Renal failure - Sarcoid
127
What are the symptoms of raised prolactin?
Men - erectile dysfunction, visual defects, headache, osteopenia Women - galactorrhoea, infertility, menstrual changes
128
How is raised prolactin treated?
Dopamine agonists eg. bromocriptine, cabergoline, quinagolide
129
What causes acromegaly?
Pituitary MACROadenoma (nearly always)
130
What are the features of acromegaly?
Coarse features Sweating Organomegaly Carpal Tunnel Osteoarthritis Visual field defects from macroadenoma OSA HTN CVS disease Slightly increased cancer risk
131
How is acromegaly diagnosed?
Failure of oral glucose tolerance test
132
How is acromegaly managed?
Transphenoidal surgery Somatostatin/dopamine agonists Pegvisomant (v expensive!!)
133
What is diabetes insipidus?
Deficiency in vasopressin causing polyuria, nocturia thirst and dehydration
134
What are the central (secondary) causes of DI?
Congenital Idiopathic Head injury Pituitary adenoma Infection and inflammation
135
What are the nephrogenic (primary) causes of DI?
Kidney tubules don't respond to ADH
136
What electrolyte abnormality is seen in DI?
Hypernatremia Increased serum osmolality
137
How is DI managed?
Desmopressin
138
When should a neck USS be done?
Non-functioning nodules
139
What is the 1st line treatment for Cushings disease?
Transphenoidal surgery
140
How can Conns syndrome be screened for? What measures should be taken before doing the test?
Aldosterone:renin ratio - Higher the ratio, more likely the diagnosis Make sure potassium is normal Stop diuretics, b blockers, NSAIDs, ACEis, ARBs Do CT/MRI to diagnose adenoma
141
What test is used to investigate DI?
Water deprivation test - despite this patient will still produce dilute urine
142
What are the indications for total thyroidectomy?
Rapid control needed Severe Graves eye disease
143
What is T3 toxicosis?
Autonomous nodule low TSH, normal T4, high T3
144
How is a dexamethasone test carried out?
1mg dexamethasone administered at midnight, cortisol checked at 9am If cortisol \<50, unlikely to be bushings
145
What is a phaeochromocytoma?
Adrenomedullary catecholamine secreting tumour
146
What are the symptoms of phaeochromocytoma?
HTN General systemic 'anxiety' symptoms Headache Cardiovascular (chest pain, palps)
147
What investigations should be done for pheochromocytoma?
Plasma mets (suspcious if 3x the norm) 24hr urine metadrenalines CT scan IMIBG scan - exclude multiple tumours
148
What is a potential complication of phaeo?
- Prone to haemmorhage and necrosis - Fatal hypertensive crisis
149
How is phaeo treated: a) conservatively b) medically c) surgically?
a) high salt and fluid diet b) a blockers c) laparoscopic removal
150
Which endocrine conditions give you HTN?
Adrenal - cushings, phaeo, conns Parathyroid - hyperparathyroidism Pituitary - cushings, acromegaly Thyroid - both can
151
What are the functions of calcium ?
- Transmits nerve impulses - Maintains cell wall permeability - Activates clotting - Heart muscle contraction - Bones and teeth
152
What are the functions of phosphorus?
- Bone formation - Energy production - Carb/protein/fat metabolism - Maintains acid base balance
153
What is the function of PTH?
Regulates calcium and phosphorus - when serum ca is low, PTH increases calcium resorption from the bone and calcium reabsorbtion from the kidney. It causes phosphate excretion by blocking its reabsorption in the kidney
154
What are the causes of hyperparathyroidism?
Parathyroid hyperplasia/adenoma/carcinoma
155
What are the complications of primary hyperparathyroidism?
Kidney stones Osteoporosis Osteitis fibrosis cystica Brown tumours Corneal calcification HTN 'stones, bones, groans and moans'
156
How is primary hyperparathyroidism managed?
Surgical neck exploration Conservative Calcimimetic drugs
157
What causes hypercalcemia?
- Malignancy (ectopic, bone erosion) - Drugs - Hyperparathyroidism - Vit D and calcium intake - Sarcoidosis
158
How is severe hypercalcemia managed?
1. Do baseline PTH (if low = cancer, if high = primary PTH) 2. IV saline 3. IV bisphosphonates
159
What are the symptoms of hypercalcemia?
Lethargy, fatigue Bone/kidney pain (kidney stones) Depression Anorexia Constipation HTN
160
What would an ECG of someone with severe hypo/hypercalcemia look like?
hyper - short QT interval hypo - long QT interval
161
What causes hypocalcemia?
- Hypoparathyroidism - Vit D defieciency - Drugs (bisphos, chemo) - Renal failure - Severe illness
162
What are the symptoms of hypocalcemia?
TINGLING, TWITCHING, TETANY, TROUSSEAS CHVOSTEKS AND SEIZURES
163
What are the complications of hypocalcemia?
- Osteoporosis - Arrhythmia
164
How is severe hypocalcemia treated?
ACUTE - calcium chloride DONT DO IF CHRONIC
165
What is Trousseas sign?
Forearm muscle spasm following cuff inflation, sign of tetany
166
What is Chvosteks sign?
Hyper excitability of facial nerve, sign of tetany
167
What investigations should be done for someone with bone disease?
Calcium, phosphate, PTH Xray, DEXA?
168
What is osteoporosis? How is it diagnosed?
Low bone density (T score -2.5 on BMD)
169
What are the RF for osteoporosis?
Smoking Steroids Early menopause Calcium intake Fam hx Endocrine problems Renal disease
170
What is osteomalacia? How is it diagnosed?
Softening of bones due to low calcium, phosphate and vit D, elevated PTH, ALP
171
What are the RF for osteomalacia?
Low calcium, vit D sunlight Renal hepatic disease Drugs
172
What are the X-ray appearance of osteomalacia?
Cupped epiphyses Loosers zones Rachitic rosary
173
What are the symptoms of hypomagnesia?
Tremors, tachycardia, confusion
174
What are the symptoms of hypermagnesia?
Vasodilation, hypotension, vomiting
175
What causes hypomagnesia?
Alcoholism Malnutrition
176
What causes hypermagnesia?
Renal failure Untreated DKA
177
How is T2DM diagnosed (3 ways)
Random blood glucose \>11.1 in presence of symptoms OR Random blood glucose \>11.1 on two occasions with no symptoms HbA1c \> 6.5% (48mmol/mol) (39-46mmol/mol = pre-diabetes) - this is better for checking degree of diabetes control rather than diagnosis
178
What factors can affect HbA1c, and make it invalid as a diagnostic tool?
- Conditions with increased red cell turnover eg. acute blood loss, pernicious anaemia, haemolytic anaemia, malaria, haemoglobinopathies - Pregnancy - Liver and renal disease - Ethnic variations
179
Describe the pathophysiology behind Type 1 diabetes
Insulin deficiency due to autoimmune attack of beta cells in the pancreas Linked to HLA D3/4
180
Describe the pathophysiology behind Type 2 diabetes
Acquired insulin resistance due to the body being unable to meet the requirement for insulin.
181
What conditions can cause secondary diabetes?
- Acromegaly - Cushing's syndrome - Haemochromatosis - Pancreatitis
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Describe the pathophysiology behind gestational diabetes
Excessive production of counter-insulin hormones (cortisol,oestrogen), produced during pregnancy, leading to a state of insulin resistance in the mother
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Which patients are prone to ketoacidosis?
Type 1
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Which patients usually are diagnosed through the complications that have arisen as a result of their diabetes?
Type 2
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Who gets screened for T2 diabetes?
- Women with previous gestational diabetes - People aged 65 and over - Afro caribbean and south asians aged 35 and over - People over 50 who have BMI\>30, T2DM first degree relative or hypertension - People with clinical cardiovascular disease - Women who are obese and have polycystic ovary syndrome
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What measures can reduce microvascular complications of diabetes?
Tight blood glucose control (FBG\<5.5)
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What measures can reduce macrovascular complications of diabetes?
Tight blood pressure control (\<130/80)
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What measures can decrease the incidence of cardiovascular events in diabetes?
Control of lipids (T.chol\<4)
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What are the microvascular changes seen in diabetes?
Retinopathy, nephropathy, neuropathy, erectile dysfunction, absent foot pulses, ischaemic skin chances
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What are the macrovascular changes seen in diabetes?
Ischaemic heart disease, cerebrovascular disease, peripheral vascular disease
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How can diabetic foot be managed?
1. Examine feet of all those with diabetes 2. Suspect: infection, fracture, ulceration, Charcot 3. Investigations: WBC, CRP, ESR, U&E, Swab, X-ray 4. Treatment: bed rest, IV abx, refer
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What does infection cause DKA?
1. Infection leads to high cortisol and catecholamines 2. These cause gluconeogenesis
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How is DKA diagnosed?
Glucose \> 11 mmol/l Ketones \> 3 mmol/l Acidosis \<7.3 pH
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What is the pathophysiology behind DKA?
1. Glucose cannot be broken down as there is no insulin 2. The body breaks down fatty acids to get ketones for energy 3. This causes acidosis
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What are the signs and symptoms of DKA?
SYMPTOMS: Polyuria, polydipsia, weight loss, weakness, drowsiness, coma SIGNS: dehydration, hypovolaemia, increased respiration
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What is the protocol for DKA?
ABCDE 1. IV fluids 2. IV fluids + potassium 3. IV insulin infusion 4. Investigations to see what causes DKA, treat cause 5. Establish monitoring regimen 6. Once insulin in normal range, switch to glucose-insulin infusion to prevent hypos
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What are the pros and cons of the oral glucose tolerance test?
Pros - sensitive, early marker of impairment Cons - affected by short term lifestyle changes, expensive, takes time and effort
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What are the pros and cons of the glycated haemoglobin concentration (HbA1c)
Pros - reflects long term glucose, unaffected by acute change, convenient, high correlation with risks of complication Cons - lower sensitivity, expensive, not recommended for rapidly progressing diabetes
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What is metabolic syndrome?
Central obesity + 2 of: - High triglycerides - High BP - Low HDL - High fasting glucose - DM This can cause vascular events
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How can glucose control be monitored?
HbA1c, finger prick test (if on insulin)
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What is the definition of hypoglycaemia?
Plasma glucose \<3
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What are the symptoms of hypoglycaemia?
AUTONOMIC - sweating, anxiety, hunger, tremor, palpitations NEUROGLYCOPENIC - confusion, drowsy, seizures, coma
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What causes hypoglycaemia EXPLAIN?
EXogenous drugs (insulin) Pituitary insufficiency Liver failure Addison's disease Islet cell tumours Non-pancreatic neoplasms
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How is a hypoglycaemic attack managed?
ABCDEFG (dont ever forget glucose) Conscious - oral glucose Unconscious - IV dextrose, glucogel, IM glucagon - monitor BMs every 15 min - give long acting carbohydrate - review medication
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What is impaired awareness of hypoglycaemia?
Normally the autonomic symptoms of a hypo will kick in before the neuroglycopenic ones. In long term diabetics, this will not happen so you wont get the usual warning signs
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What are the features of background diabetic retinopathy?
Dots, blots and deposits
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What are the features of pre-proliferative diabetic retinopathy?
Cotton-wool spots, haemorrhages and venous beading
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What are the features of proliferative diabetic retinopathy?
New vessel formation
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How can diabetes affect the eyes?
Retinopathy, maculopathy, blurred vision, cataracts, rubeosis iridis
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What is rubeosis iris?
New vessel formation on the eye, leading to glaucoma
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What are the signs of neuropathy in the feet?
Decreased sensation, absent ankle jerks, deformity
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What is Charcot's foot?
A condition in which sugar damages the bones of the foot, causing weakness
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What is a hyperosmolar hyperglycaemic state?
T2DM - extremely high blood glucose causing severe dehydration, dry skin, confusion, coma
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How is hyperosmolar hyperglycaemic state diagnosed?
Glucose \>30mmol/l and ABSENCE OF DKA FEATURES (vomiting)
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How is HH state managed?
IV fluids slowly and electrolyte replacement (potassium)
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What is the relevance of a C-peptide level under 0.51mg/ml?
It could indiate T1DM - C-peptide is a surrogate marker for endogenous insulin as C-peptide and insulin both originate from pro-insulin
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Which antibodies can be used in T1DM diagnosis, when clinical diagnosis is uncertain?
GAD IA-2 ICA
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What are the diagnostic criteria for gestational diabetes?
- Fasting plasma \> 5.6mmol/L - 2hr plasma glucose \>7.8mmol/L
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How are diabetics managed during: a) pregnancy? b) labour?
a) folic acid 5mg, monitor BM/ketones b) GKI infusion to maintain blood glucose 4-7 during labour. Monitor BM every 30-60 mins during this period. Reduce insulin rate post partum.
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What are the indications for GD screening?
- BMI\>30 - Previous macrosomic baby \>4.5kg - Previous GD - Family history - High risk ethnic minority
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What is MODY? What are the two main types?
Maturity Onset Diabetes of the Young This is diabetes caused by a inherited mutation in a gene involved in insulin production. The two main types are: - Glucokinase - Transcription factor
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What are the key diagnostic features in MODY?
- Diagnosis under the age of 25 - Two or more generation family hx of diabetes - Residual insulin secretion over 3yrs after supposed T1DM diagnosis - Lack of metabolic syndrome in supposed T2DM diagnosis
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What is the pathology of glucokinase MODY?
Mutation in glucokinase leading to a higher threshold for glucose stimulated insulin secretion, so blood glucose levels are slightly higher than normal
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How does glucokinase MODY present and how should it be treated?
It is asymptomatic so usually only picked up through routine testing (eg. in pregnancy) Only treat in pregnancy
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What is the pathology of transcription factor MODY?
Mutation in one of the transcription factors involved in pancreatic development, causing impaired insulin secretion\> Factors affected: HNF1a HNF1b HNF4a
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How does transcription factor MODY present and how is it treated?
HNF1a/4a - normoglycemic in childhood, develop symptoms of diabetes at 12-30yrs Treat with low dose sulphonylureas HNF1b - may present with pancreatic atrophy/renal cysts/genitourinary abnormalities Treat with insulin
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What is a lipodystrophy syndrome? What are the two main types and their features?
Complete or partial absence of adipose tissue, with associated insulin resistance. Diagnose clinically. Congenital generalised - develop DM in 10-20yrs, big appetite, autosomal recessive Familial partial - loss of fat in lower body and arms, excess fat in face and trunk
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A patient presents with a chubby face and trunk and very thin legs and arms. What is the diagnosis?
Familial partial lipodystrophy syndrome
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Describe 3 clinical features of insulin resistance
- Persistent hyperglycaemia despite large doses of insulin - Acanthosis nigricans - PCOS
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Name 5 heritable conditions that have associations with diabetes mellitus
Turners Klinefelters Downs Prader Willi PCOS Lawrence-moon
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Describe the features of temporary and permanent neonatal diabetes
Presents before 6 months with high glucose levels or DKA, low birth weight and low C-peptide This may progress to permanent, in which you would start to see added neurological features
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What is the pathophysiology of neonatal diabetes?
GOF mutation in beta cell K ATP channel - K channel cannot respond to ATP so is permanently open. This means there is no beta cell depolarisation and no insulin release. Eg. KCNJII/ABCC8 genes
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Why do HIV treated patients have a 4 fold risk of DM?
Protease inhibitors (component of HAART) cause increased insulin resistance Indanavir increases hepatic glucose production
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What is central salt wasting syndrome?
A rare endocrine condition featuring low serum Na and dehydration in response to brain injury
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What is latent autoimmune diabetes?
Presents with features of T1DM in adulthood Symptoms persist despite diet and medication Presence of islet cell antibodies
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What is a side effect of insulin injection?
Lipohypetrophy
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What is Kallman syndrome?
Hypogonadism + infertility + hypo-anosmia
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How do you calculate the anion gap?
(sum of all positive ions) - (sum of all negative ions) Normal = 8-10 (diarrhoea, renal tubular acidosis, hyperparathyroidism) High = lactic acidosis, ketoacidosis, salicylate overdose
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What is the best way of investigatin a pituitary tumour?
MRI scan
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