Endocrinology Flashcards
(216 cards)
1
Q
Give 4 causes of hyperthyroidism
A
- G : Graves
- I : Inflammation
- S : Single toxic thyroid nodule
- T : Toxic multinodular goitre
1
Q
What are the general 7 symptoms of hyperthyroidism?
A
- Weight loss
- Anxiety
- Diarrhoea
- Menstrual and sexual disturbances
- Fatigue
- Sweating and heat intolerance
- Insomnia
2
Q
What are the 6 general signs of hyperthyroidism?
A
- Tachycardia
- Brisk reflexes on examination
- Hyperkinesia
- AF
- Tremor
- Dilated warm peripheries
3
Q
Define primary and secondary hyperthyroidism
A
- Primary hyperthyroidism : low TSH with raised T3/T4
- Secondary hyperthyroidism : raised T3/T4 with raised TSH
4
Q
What is the cause of Grave’s?
A
- Autoimmiune
- TSH receptor antibodies cause primary hyperthyroidism by stimulating thyroid to release T3 and T4
5
Q
Give 4 Grave’s specific signs of hyperthyroidism
A
- Exophthalmos, opthalmoplegia
- Pretibial myxoedema
- Thyroid acropachy (digital clubbing, swelling of hands and feet, periosteal new bone formation)
- Diffuse goitre = increased homogenous uptake in a radioactive iodine uptake test
6
Q
What autoantibodies are found in Grave’s?
A
- TSH receptor stimulating antibodies
- Antithyroid peroxidase antibodies
7
Q
What is the first line management of hyperthyroidism ?
A
- Carbimazole (40mg) -> blocks the action of thyroid peroxidase
8
Q
What is a risk associated with carbimazole use ?
A
- Acute pancreatitis
9
Q
If a patient presents with a sore throat and is taking carbimazole, what is the life-threatening cause ?
A
- Agranulocytosis - low white blood cell count
10
Q
What can be used 1st line for symptoms control in hyperthyroidism
A
- Propanolol -> non selectively blocks adrenalin related symtoms
11
Q
If carbimazole doesn’t control symptoms of hyperthyroid, what can be done?
A
- Radioactive iodine treatment
- CI = pregnant or breastfeeding and must not be pregnant within 6 mnths of treatment), <16, thyroid eye disease
12
Q
What is the definitive management of hyperthyroid?
A
- Thyroidectomy
13
Q
What is thyrotoxicosis and a resultant thyroid storm ?
A
- Thyrotoxicosis : effects of abnormal and excessive thyroid hormone
- Thyroid storm : life threatening complication of thyrotoxicosis often precipitated by thyroid surgery, trauma, infection of acute iodine overload.
14
Q
Features of a thyroid stome ?
A
- Fever > 38.5ºC
- Tachycardia
- Confusion and agitation
- N&V
- HTN
- HF
- Abnormal liver function test - jaundice may be seen clinically
15
Q
How is thyroid storm management
A
-1st line = IV propanolol
- Paracetamol for symptoms
- Anti-thyroid drugs (e.g. methimazole, propylthiouracil)
16
Q
what is De Quervain’s thyrodisitis and it’s 3 stages ?
A
- Subacute thyroditis
- Thyrotoxicosis
- Hypothyroidism
- Return to normal
17
Q
How does the thyrotoxic phase of de quervain’s present and how is it managed
A
- Thyroid swelling and tenderness, flu like illness and raised CRP/ESR
- Self limiting : NSAIDS for pain, BB for hyperthyroidism and levothyroxine for hypothyroidism
18
Q
Briefly explain thyroid hormone synthesis
A
- Blood supplies iodine
- Transported into follicular cells of thyroid
- Here, thyroidperoxidase converts iodine to iodide
- Iodide then attaches to tyrosine residues on thyroglobulin forming T3 and T4
19
Q
Define primary and secondary hypothyroidism
A
- Primary : thyroid produces inadequate T3 and T4, leading to raised TSH
- Secondary : inadequate TSH release leading to low T3 and T4
20
Q
Give 5 causes of primary hypothyroidism
A
- Hashimoto’s thyroiditis (most common)
- Iodine deficiency
- Lithium
- Amiodarone
- Hyperthyroidism treatment
21
Q
Give 5 causes of secondary hypothyroidism
A
- Pituitary adenomas
- Pituitary surgery
- Radiotherapy
- Sheehan’s syndrome : post-partum haemorrhage cause avascular necrosis of pituitary gland
- Trauma
22
Q
Give the general features of hypothyroidism
A
- General : weight gain, cold intolerance, fatigue
- Skin : dry skin, coarse scalp hair, loss of lateral aspect of eyebrow
- GI : constipation
- Gynae : menorrhagia
- Neuro : decreased tendon reflexes, carpal tunnel
23
Q
What is the mainstay of treatment for hypothyroidism and its SE
A
- Levothyroxine
- SE : hyperthyroid, reduced bone mineral density, worsening of angina, AF
24
What is Hashimoto's thyroiditis
- Autoimmune condition causing inflammation of the thyroid gland
- Is associated with anti-thyroid peroxidase (TPO) and anti-thyroglobulin (Tg) antibodies
25
What are the features of Hashimoto's and what is it associated with ?
- Hypothyroidism, firm and non tender goitre
- Associated with : other autoimmune conditions and MALT lymphoma
26
What is the most common cause of acromegaly
- Pituitary adenoma
27
what rarely causes acromegaly
- Ectopic GHRH or GH release by cancer (lung/pancreatic)
28
What are the general features of acromegaly (6)
- Frontal bossing
- Coarse sweaty skin
- Large nose
- Macroglossia
- Large hands and feet
- Large protruding jaw
29
What are the mass effects of a pituitary adenoma causing acromegaly ?
- Headache
- Bitemporal hemianopia
30
What are the investigations for acromegaly ?
1. IGF-1 levels (produced by the liver).
2. Growth hormone suppression test - no suppression of GH to <2mu/L after 75g glucose drink
3. Pituitary MRI to determine presence of pituitary adeoma
31
What is the 1st line management of acromegaly
- Trans-sphenoidal surgery to remove a pituitary adenoma
- +/- external radiotherapy
32
What are the medical manegement options of acromegaly
1. Pegvisomant : SC injection, GH receptor antagonist.
2. Somatostatin analogue (ocreotide) - blocks GH release from pituitary.
3. Dopamine agonist (bromocriptine) : inhibits GH release from pituitary, less effect than ocreotide.
33
Give 5 complications of acromegaly
- HTN
- T2DM
- Cardiomyopathy (hypertrophic)
- Colorectal cancer
- Bilateral carpal tunnel
34
Define Cushing's syndrome and Cushing's disease
- Syndrome : features of prolonged high levels cortisol
- Disease : prolonged raised cortisol due to pituitary adenoma secreting ACTH
35
What are the possible causes of cushing's syndrome
- ACTH dependent : cushing's disease, ectopic ACTH product (SCLC)
- ACTH independent : iatrogenic steroids, adrenal adenoma/carcinoma
- Pseudo cushing's : due to alcohol excess or severe depression
36
What are the features of cushing's syndrome (7) ?
- 'Full moon' face
- 'Buffalo hump'
- Muscle wasting in the extremeties
- Easy bruising and poor skin healing
- Abdominal striae
- Central obesity
- Hyperpigmentation in Cushing's disease due to raised ACTH
37
What are the metabolic effects of Cushing's syndrome
- HTN
- T2DM
- Osteoporosis
- Cardiac hypertrophy and increased risk of CVD
- Dyslipidaemia
38
Where is cortisol released from
- Zona fasciculata in the adrenal cortex
39
How is Cushing's syndrome investigated ?
- 1st line = Low dose overnight dexamethasone suppression (screening to exclude cushing's)
- Low dose 24 hour (used in suspected cushing's)
- High dose 24 hour (used to determine cause)
40
Explain the dexamethasone suppression tests
1. Overnight : dexamethasone (1mg) given at night. Check cortisol 9am. No suppression = further assessment.
2. Low dose 24 hr : dexamethasone (0.5mg) every 6 hrs for 8 doses. Cortisol checked at 9am on day 1 and 9am day 3. No suppression = cushing's syndrome
3. High dose 24hr. Same as above but dose at 2mg. Cushing's syndrome = cortisol will be suppressed. Adrenal adenoma or ectopic ACTH = no suppression.
41
What is the primary treatment of Cushing's syndrome ?
- Treat underlying cause :
~ Trans-sphenoidal removal of pituitary adenoma
~ Surgical removal of adrenal tumour
~ Surgical removal of tumour producing ectopic ACTH
42
What is Nelson's syndrome
- Development of ACTH-producing pituitary tumour after sugical removal of both adrenal glands due to lack of cortisol and negative feedback
43
What medical treatment can be used to reduce production of cortisol in adrenals?
- Metyrapone
44
What does adrenal insufficiency result in a lack of ?
Steroid hormones - cortisol and aldosterone
45
What is the most common primary cause of adrenal insuficiency ?
- Addison's : autoimmune destruction of the adrenal glands resulting in a lack of cortisol and aldosterone
46
What is secondary adrenal insufficiency and 5 causes ?
- The pituitary produces a lack of ACTH
1. Pituitary tumour
2. Radiotherapy
3. Sheehan's
4. Surgery to pituitary
5. Trauma
47
What is tertiary adrenal insufficiency and the most common cause?
- Lack of CRH from the hypothalamus
- Long term oral steroid use = hypothalamus suppression. Once expogenous steroids are stopped the hypothalamus doesn't 'wake up' and leads to a lack of endogenous steroid release.
48
How does adrenal insufficiency present ?
- Fatigue
- Muscle weakness
- Weight loss
- Thirst and salt craving
- N&V
49
What is a sign of adrenal insufficiency caused by Addison's?
- Bronze hyperpigmentation of the skin, particularly in the palmar creases.
- Due to excess ACTH stimulating melanocytes to produce melanin.
50
What biochemical findinds are seen in adrenal insufficiency and why ?
- Hyponatraemia and hyperkalaemia : aldosterone increases Na+ reabsoprtion and K+ secretion. A lack of it causes this.
- Hypoglycaemia
- Raised creatinine and urea due to dehydration
- Hypercalcaemia
51
What is the investigation of choice for diagnosing adrenal insufficiency
- Short Synacthen test
52
What is the short synacthen test ?
- Synthetic ACTH is given and blood cortisol measured 30 and 60 mins after the dose
- Cotrisol level should at least double.
- Failure = adrenal insufficiency
53
Once adrenal insufficiency is established how is primary or secondary insufficiency determined?
- ACTH level
- It will be high in primary and low in secondary
54
How is adrenal insufficieny managed ?
- Replace steroids : hydrocortisone and fludrocortisone
- Give steroid carrd, ID tag and emergency letter.
- Double glucocorticoid dose in acute illness.
55
how many an adrenal crisis present ?
- Reduced consciousness
- Hyperkalaemia and hyponatraemia
- Hypoglycaemia
- Hypotension
56
How is an adrenal crisis managed ?
- Hydrocortisone 100 mg IM or IV. Then 6hrly until stable
- IV fluids (1L normal saline) over 30-60 mins or with dextrose if hypoglycaemic
57
Define hyperaldosteronism and Conn's syndrome
- Hyperaldosteronism = raised aldosterone
- Conn's = raised aldosterone due to an adrenal adenoma producing too much aldosterone
58
Explain the role of the renin-angiotensisn-aldosterone system in blood pressure
- Juxtaglomerular cells in the affterent arterioles of the kidney detect a low BP
- They release renin
- Renin converts angiotensinogen produced by the liver to angiotensin I
- ACE in the lungs converts angiotensin I to angiotensin II
- Angiotensisn II stimulates aldosterone release from the adrenal glands - zona glomerulosa
59
What is the role of aldosterone in low BP?
- Increases sodium resorption from distal tubule
- Increases potassium secretion from. distal tubule
- Increases hydrogen secretion from collecting ducts
60
What is primary hyperaldosteronism and give 3 causes
- Adrenal glands produce too much aldosterone.
- Renin is low as suppressed due to high BP.
1. Bilateral adrenal hyperplasia.
2. Conn's - adrenal adenoma
3. Familial
61
What is secondary hyperaldosteronism and 3 causes
- Excessive renin stimulates release of aldosterone
1. Renal artery stenosis
2. HF
3. Liver cirrhosis and ascites
62
What is the screening test for hyperaldosteronism
Aldosterone-to-renin ratio
~ High aldosterone with low renin = primary
~ High aldosterone with high renin = secondary
63
what investigations are used to determine underlying cause of hyperaldosteronism ?
- High resolution CT for adrenal tumour or adrenal hyperplasia and adrenal vein sampling to differentiate adenoma and bilateral hyperplasia
- Renal artery imaging for renal artery stenosis
64
what is the medical management of hyperaldosteronism ?
- Adenoma : laparoscopic adrenalectomy
- Hyperplasia :Aldosterone antagonists : eplerenone, spironolactone
65
What is SIADH ?
- Increased release of ADH (vasopressin) from the posterior pituitary
66
What is the action of ADH
- Increases water resorption form the collecting ducts of the kidneys
66
What are the 2 possible sources of excessive ADH release?
- Increased secretion by the posterior pituitary
- Ectopic ADH release by a SCLC
66
What is the result of excessive ADH release ?
- Increased water resorption
- This dilutes the blood
- Causes hyponatraemia
- Excessive fluid doesn'tm usually cause fluid overload = euvolaemic hyponatraemia
66
what is the effect on the urine in SIADH
- It becomes more concentrated
- High urine osmolality
- High urine sodium
66
If not asymptomatic how migh SIADH present ?
- Headache, fatigue, muscle aches and cramps, confusion
- Severe = seizures and reduced consciousness
66
What are 3 more common causes of SIADH
- Post operative
- Ectopic ADH release from SCLC
- Medications (SSRI's / carbamazepine)
66
What are the 5 clinical features of SIADH ?
- Euvolaemia
- Hyponatraemia
- Low serum osmolality
- High urine osmolality
- High urine sodium
67
How is SIADH managed?
- Admission (If Na+ <125)
- Tx underlying cause
- Fluid restriction (750-1000ml per day)
- Vasopression receptor antagonists (tolvaptan) -> block ADH receptors
67
Why does the sodium need to be corrected slowly in SIADH
- Risk of osmotic demyelination syndrome
68
what is the cause of T1DM?
- Pancreas unable to produce adequate insulin
69
Explain where insulin is produced and it's role
- Anabolic hormone , acts to reduce blood glucose
- Beta cells in the islets of langerhans of the pancreas
- Cells to take up glucose
- Liver and muscle to convert glucose to glycogen (glycogenesis)
70
Explain where glucagon is produced and its role
- Catabolic hormone, acts to increase blood glucose
- Alpha cells, islets of langerhans
- Causes liver to breakdown glycogen to glucose (glycogenolysis)
- Causes liver to convert protein and fats to glucose (gluconeogenesis)
71
Explain where and why ketones are produced
- Produced by the liver when there is inadequate glucose and depleted glycogen stores
- Fatty acids - ketones
- Acidic properties of ketones buffered by the kidneys
72
In what 2 ways can T1DM present ?
- DKA
- Signs of hyperglycaemia and dehydration (polyuria, polydipsia, weight loss)
73
What is the diagnostic criteria for T1DM
- If symptomatic : fasting glucose > or equal to 7.0mmol/l OR random glucose > or equal to 11.1mmol/L
- If asymptomatic, above needs to be demonstrated on 2 separate occassions.
74
When may autoantibodies or serum c-peptide be used for diagnosis of T1DM?
- When there is doubt between T1DM & T2DM.
- C peptide is a measure of inuslin production : it will be LOW in T1DM
- T1DM autoantibodies are : anti-islet cell, anti-GAD and anti-insulin
75
What is required for a diagnosis of DKA
- Hyperglycaemia (>11mol/l) or known DM
- Ketones (>3mmol/L) or +2 on dipstick
- pH <7.3 or bicarbonate <15mmol/l (metabolic acidosis )
76
How does DKA present
- Abdo pain
- Polyuria, polydipsia, dehydration
- Kussmaul respiration
- Acetone 'pear drop' smelling breath
77
why does DKA cause dehydration
- Hyperglycaemia eventually overwhelms the kidneys
- Glucose is lost in urine
- This causes water to be lost in the urine leading to polyuria and severe dehydration
78
Explain the patholphysiology behind the potassium imbalance in DKA
- Insulin is required to draw K+ into cells
- Without it, total body potassium is low
- This can lead to hypoklaemia was treatment begins
79
What are the principles of treatment in DKA
- F : fluids
- I : insulin
- G : glucose
- P : potassium
- I : infection (treat if underlying)
- C : chart fluid balance
- K : ketones
80
How are the fluids given for DKA
- IV normal saline
- 1L in first hour
- Followed 1L every 2 hours
81
How is insulin given in DKA
Fixed rate at 0.1unit/kg/hour
82
When is glucose given in DKA management
- Added to infusion when levels reach less than 14mmol/l
83
Give 4 key complications during treatment of DKA
- Hypoglycaemia
- Hypokalaemia
- Cerebral oedema (rapid fluid)
- Pulmonary oedema (sec. to fluid overload or acute resp distress)
84
what monitoring is involved for a patient with T1DM?
-HbA1c measure every 3-6 months
- Capillary blood glucose monitoring at least 4 times daily
85
what are the blood glucose targets of someone with T1DM?
- 5 to 7 mmol/l on waking
- 4 to 7 mmol/l before meals and at other times.
86
What is the basal-bolus regime for managing T1DM ?
- Background, long acting insulin injected once daily
- Short acting insulin injected 30 mins before consuming carbs
87
what needs to be considered when injected insulin
- Not injecting same site every time, can cause lipodystrophy
88
Give 2 short term complications of T1DM
- Hypoglycaemia
- HYperglycaemia and DKA
89
What are the macrovascular long term complications of T1Dm
- Coronary artery disease
- Peripheral ischaemia lading to poor skin healing and foot ulcers
- Stroke
- Hypertension
90
What are the microvascular long term complications of T1DM
- Peripheral neuropathy
- Retinopathy
- Kidney disease, esp glomerulosclerosis
91
Give 4 infection-related complications of T1DM
- UTI
- Pneumonia
- Skin and soft tissue infections, esp in the feet
- Fungal infections, es oral and vaginal candidiasis
92
Give 3 non modifiable RF for T2DM
- Older age
- FHx
- Ethnicity (black afran, caribeean, south asian)
93
Give 3 modifiabke RF for T2DM
- Obesity
- High carb diet
- Sedentary lifestyle
94
what is required for a diagnosis of T2DM
- If asymptomatic :
~ HbA1c > 48mmol/l
~ Fasting glucose greater than or equal to 7.0 mmol/l
~ Random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)
If asymptomatic the above needs demonstrating on 2 separate occasions
95
Give 6 presenting symptoms of T2DM
- Tiredness
- Polyuria and polydipsia
- Unintentional weight loss (rare)
- Opportunistic infections
- Slow wound healing
- Glucose in urine (on dipstick)
96
What skin sign can be seen in someone with T2DM?
- Acanthosis nigricans - thickening and darkening of the skin at the neck, axilla and groin.
- Associated within insulin resistance
97
what HbA1c level suggest pre diabetes
42-47
98
What is the first line management of T2DM ?
metformin
99
what is the first line management of T2DM if :
- There is a high risk of CVD or established CVD or chronic HF
Metformin :
Once established add SGLT-2 inhibitor (e.g. dapagliflozin)
100
what is second line management of T2DM ?
Metformin +
- sulfonylurea, pioglitazone, DPP-4 inhibitor or SGLT-2 inhibitor (if NICE criteria met)
101
What is the third line management of T2DM?
- Triple therapy with metformin + second line drugs
OR
- Insulin therapy (initiated by specialist diabetic nurse)
102
what is the HbA1c target for someone being managed for T2Dm
- Just lifestyle : 48mmol/mol
- Lifestyle + metformin : 48 mmol/l
- Any drug which may cause hypoglycaemia : 53mol/mol
103
what is the HbA1c target for someone already on medication but HbA1c still rising
- Already on one drug, but HbA1c has risen to 58 mmol/mol : target is now 53mmol/mol
104
What kind of medication is metformin and how does work ?
- Biguanide
- Increases insulin sensitivity and decreases glucose production by the liver.
105
Does metformin cause weight gain or hypoglycaemia ?
- No weight gain
- No hypoglycaemia
106
What are the notable side effects of metformin ?
- GI symptoms : pain, nausea and diarrhoea
- Lactic acidosis (secondary to AKI)
- Modified release metformin can be used in people with GI side effects.
107
How do SGLT-2 inhibitors work ?
- They act on the sodium-glucose co-transporter 2 protein in the proximal tubules of the kidney.
- By blocking it, it causes more glucose to be excreted in the urine.
108
Doe SGLT-2 inhibitors cause weight gain or hypoglycaemia ?
- Causes hypoglycaemia and WEIGHT LOSS
109
Give 2 notable SE of SGLT-2 inhibitors
- Increased frequency of UTI's and genital thrush due to glucose passing through urine.
- DKA
110
what kind of medication is pioglitazone and how does it work ?
- Thiazolidinedione
- Increases insulin sensitivity and decreases liver production of glucose
111
Does pioglitazone cause hypoglycaemia or weight gain?
- Causes WEIGHT GAIN
- Not typically hypoglycaemia
112
Give 4 SE of pioglitazone
- Weight gain
- HF
- Increased risk of bone fractures
- Small increased risk of bladder cancer
113
Give an example of a sulfonylurea and how does it work ?
- Gliclazide
- Stimulate insulin release from the pancreas
114
Does gliclazide cause weight gain or hypoglycaemia ?
BOTH
115
What are incretins and how do they reduce blood sugar ?
- Hormones produced by GI tract
- Secreted in response to large meals and :
-Increase insulin secretion
- Inhibit glucagon production
- Slow absorption by GI tract
116
How do DPP-4 inhibitors work ?
They inhibit dipeptidyl, an enzyme which inhibits incretins
117
Give 2 examples of DPP-4 inhibitors and their 2 most notable SE
- Sitagliptin and alogliptin
- Headaches and a low risk of pancreatitis Does
118
Do DPP-4 inhibitors cause hypoglycaemia
NO
119
How do GLP-1 mimetics work and give 2 example
- Glucagon-like peptide (GLP-1) is an incretin
- exenatide and liraglutide mimic the incretin action
- They as SC injections
120
Give 3 notable SE of GLP-1 mimetics
- WEIGHT LOSS
-Reduced appetite
- GI symptoms
121
What is HHS
- HYperosmolar hyperglycaemia state
- Complication of T2DM in which there is hyperosmolality, hyperglycaemia but absence of ketones
122
Hoes HHS present
- Polyuria and polydipsia
- Weight loss
- Dehydration
- Tachycardia
- Hypotension
- Confusiojn
123
How is HHS managed ?
Fluids
124
Give 8 complications of T2DM
- Infections (e.g., periodontitis, thrush and infected ulcers)
- Diabetic retinopathy
- Peripheral neuropathy
- Autonomic neuropathy
- Chronic kidney disease
- Diabetic foot
- Gastroparesis (slow emptying of the stomach)
- Hyperosmolar hyperglycemic state
125
what is used 1st line for management of HTN in any patient with T2DM
- ACE inhibitors
126
what advice is given to people with T2DM during ramadan ?
- Try and and eat a meal containing long-acting carbohydrates prior to sunrise.
- Given a blood glucose monitor to allow them to check their glucose levels, particularly if they feel unwell
- For patients taking metformin the expert consensus is that the dose should be split one-third before sunrise (Suhoor) and two-thirds after sunset (Iftar)
- Expert consensus also recommends switching once-daily sulfonylureas to after sunset.
- For patients taking twice-daily preparations such as gliclazide it is recommended that a larger proportion of the dose is taken after after sunset
- No adjustment is needed for patients taking pioglitazone
127
what are the 3 sick days rules for patients with diabetes ?
- Increase frequency of blood glucose monitoring to four hourly or more frequently.
- Encourage fluid intake aiming for at least 3 litres in 24hrs.
- Struggling to eat may need sugary drinks to maintain carbohydrate intake
128
Explain the 3 types of hyperparathyroidism
1. Primary : tumour of parathyroid leads to excess secretion. Most likley solitary adenoma
2. Secondary : insufficient vit D or CKD leads to low Ca2+. As a result, more parathyroid is secreted.
3. Tertiary : prolonged secondary hyperparathyroidism leads to hyperplasia of parathyroid gland.
129
Give the levels of PTH and calcium in each type of parathyroidism.
1. Primary : Ca2+ and PTH high. (PTH could be normal)
2. Secondary : PTH high, calcium low or normal
3. Tertiary : Both high.
130
Where is PTH produced and in response to what ?
- Chief cells in the 4 parathyroid glands
- Released in response to low blood calcium
131
Give 3 actions of PTH
1. Increase osteoclast activity in the bones (resorbing calcium)
2. Increasing calcium absorption in the kidneys.
3. Increasing vit D activity, resulting in increased Ca2+ absorption in intestines.
132
How does parathyroid act on vitamin D
- Converts it into its active form, vitamin D then increases calcium absorption from. the intestines
133
Give 4 symptoms of hypercalcaemia
STONES, BONES, GROANS, MOANS
- Kidney stones
- Painful bones
- Abdominal groans (constipation, N&V)
- Psychiatric moans (fatigue, depression, psychosis).
- Polydipsia, polyuria
134
Other than hyperparathyroidism, what else can cause hypercalcaemia
- Malignancy
- calcium will be high, PTH is low but parathyrpid hormone related peptide may be raised
135
give 3 causes of primary hypoparathyroidism
- Decrease PTH secretion
e.g. secondary to thyroid surgery*
- Low calcium, high phosphate
Treated with alfacalcidol
136
Give 5 signs of hypoparathyroidism
MOSTLY SECONDARY TO HYPOCALCAEMIA
- Tetany: muscle twitching, cramping and spasm
- Perioral paraesthesia
- Trousseau's sign: carpal spasm if the brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic
- Chvostek's sign: tapping over parotid causes facial muscles to twitch
- If chronic: depression, cataracts
137
what is seen on ECG in hypocalcaemia ?
Prolonged QT interval
138
What is pseudohypoparathyroidism
- Target cells are insensitive to PTH
due to abnormality in a G protein.
- Associated with low IQ, short stature, shortened 4th and 5th metacarpals
- Low calcium, high phosphate, high PTH
- Diagnosis is made by measuring urinary cAMP and phosphate levels following an infusion of PTH.
- In hypoparathyroidism this will cause an increase in both cAMP and phosphate levels. In pseudohypoparathyroidism type I neither cAMP nor phosphate levels are increased whilst in pseudohypoparathyroidism type II only cAMP rises.
139
What are the two causes of diabetes insipidus
- Cranial : lack of ADH secretion
- Nephrogenic : insensitivity to ADH in collecting duct of kidney.
140
What are the causes of cranial diabetes insipidus
- Brain tumours
- Brain injury
- Brain surgery
- Brain infections (e.g., meningitis or encephalitis)
- Genetic mutations in the ADH gene (autosomal dominant inheritance)
- Wolfram syndrome (a genetic condition also causing optic atrophy, deafness and diabetes mellitus)
- Haemochromatosis
141
What are the cause of nephrogenic diabetes insipidus
- Genetic:
more common form affects the vasopression (ADH) receptor
less common form results from a mutation in the gene that encodes the aquaporin 2 channel
electrolytes
- Hypercalcaemia
- Hypokalaemia
- Medications : lithium
- Demeclocycline
- Tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis
142
what are the features of DI and why ?
- Polyuria
- Polydipsia
- Dehydration
- Postural hypotension
- Lack of ADH = lack of water resoprtion in the kidneys.
143
What do the investigations show in DI
- Low urine osmolality (lots of water diluting the urine)
- High/normal serum osmolality (water loss may be balanced by increased intake)
- More than 3 litres on a 24-hour urine collection
144
what is the investigation of choice for diagnosing DI
- Water deprivation test
145
what is the water deprivation test ?
- Pt avoids fluids for 8 hours.
- Urine osmolality measured.
- Desmopression is given and urine smolality measured 2-4 hrs later
146
what is the result of the water deprivation test in cranial DI?
- Low prior to desmopression, high after
147
what is the result of the water deprivation test in nephrogenic DI?
- Low prior to desmopression, low after
148
what is the result of the water deprivation test in primary polydipsia
High urine osmolality, therefore desmopression not given
149
How is cranial DI managed ?
desmopression : vasopressin V2 receptor agonist
150
How is nephrogenic DI managed ?
- Ensuring access to plenty of water + low salt/protein diet
- Thiazide diuretics
- NSAIDs
- High-dose desmopressin
151
How is BMI calculated
weight (kg) / height (m)
152
what are the classifications based on BMI/
- Underweigh : < 18.49
- Normal : 18.5 - 25
- Overweight : 25 - 30
- Obese class 1 : 30 - 35
Obese class 2 : 35 - 40
Obese class 3 : > 40
153
what is the stepwise management of obesity
- Conservative: diet, exercise
- Medical : orlistat, liraglutide
- Surgical
154
what is the criteria for orlistat use in obesity
- BMI of 28 kg/m^2 or more with associated risk factors, or
BMI of 30 kg/m^2 or more
- Continued weight loss e.g. 5% at 3 months
- orlistat is normally used for < 1 year
155
How does orlistat work and what are it's SE
-Pancreatic lipase inhibitor.
- SE : faecal urgency/incontinence and flatulence
156
what is liraglutide and how is it used
- (GLP-1) mimetic
- SC injection
157
what is the criteria for liraglutide use
- Person has a BMI of at least 35 kg/m²
- Prediabetic hyperglycaemia (e.g. HbA1c 42 - 47 mmol/mol)
- Can be given as an adjuncr to orlistat
158
What is the definitive management of hyperparathyroidism
Total parathyroidectomy
159
What is the conservative management of hyperparathyroidism
- Cinacalcet
- A calcimimetic
160
what is seen on a blood gas in cushing's?
hypokalaemic metabolic alkalosis
161
What is a phaeochromocytoma ?
Tumour of the adrenal glands -> leading to excessive release of catecholamines (adrenaline)
162
Where is adrenaline produced
- Chromaffin cells in the medullla of the adrenal gland
163
what 3 genetic conditions are associated with phaeochromocytomas ?
- Multiple endocrine neoplasia type 2 (MEN 2)
- Neurofibromatosis type 1
- Von Hippel-Lindau disease
164
How does a phaeochromocytoma present ?
Intermittent episodes related to bursts of adrenaline release :
- Anxiety
- Sweating
- Headache
- Tremor
- Palpitations
- Hypertension
- Tachycardia
165
How is phaeochromocytoma investigated ?
- Initial : 24 hr urine metanephrines
- CT/MRI for tumour
- Genetic testing
166
How is a phaeochromocytoma managed ?
- Initially establish patient on an alpha blocker (phenoxybenzamine) then BB (propanolol)
- Then surgery to remove adrenal adenoma
- Surgery is then definitive management
167
How is hypercalcaemia managed
- Initially rehydrate with normal saline
- Following rehydration, bisphosphonates
168
- Vitamin D deficiency (osteomalacia)
- CKD
- Hypoparathyroidism
-
Pseudohypoparathyroidism
- Magnesium deficiency
- Massive blood transfusion
- Acute pancreatitis
169
how is severe hypocalcaemia managed
IV calcium gluconate, 10ml of 10% solution over 10 minutes
170
what is seen on ECG in hypercalcaemia ?
Shortened QT interval
171
Give 6 causes of hyperkalaemia
- AKI
- Drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers, spironolactone, ciclosporin, heparin**
- Metabolic acidosis
- Addison's disease
- Rhabdomyolysis
- Massive blood transfusion
172
what is seen on ECG in hyperkalaemia ?
- Peaked or 'tall-tented' T waves (occurs first)
- Loss of P waves
- Broad QRS complexes
- Sinusoidal wave pattern
- Ventricular fibrillation
173
what are the stages of hyperkalaemia ?
- Mild: 5.5 - 5.9 mmol/L
- Moderate: 6.0 - 6.4 mmol/L
- Severe: ≥ 6.5 mmol/L
174
what is management of severe hyperkalcaemia
- IV calcium gluconate: to stabilise the myocardium
- Insulin/dextrose infusion: short-term shift in potassium from ECF to ICF
175
what causes hypokalaemia with alkalosis ?
- Vomiting
- Thiazide and loop diuretics
- Cushing's syndrome
- Conn's syndrome (primary hyperaldosteronism)
176
what causes hypokalaemia with acidosis ?
- Diarrhoea
- Renal tubular acidosis
- Acetazolamide
- Partially treated diabetic ketoacidosis
177
what are the features of hypokalaemia ?
- Muslce weakness, hypotonia
178
what are. 4ECG features of hypokalaemia ?
- U waves
- small or absent T waves
- Prolonged PR interval
- ST depression
- Long QT
179
what are carcinoid tumours ?
- A neuroendocrine tumour
180
what is carcinoid syndrome
- A collection of symtpoms that occur when people have a neuroendocrine tumour
181
what are the most common causes of carcinoid syndrome ?
1. Metastases in the liver releasing serotonin into the systemic circulation.
2. Lung carcinoid
182
Give 7 features of carcinoid syndrome
- Flushing (often the earliest symptom)
- Diarrhoea
- Bronchospasm
- Hypotension
- Right heart valvular stenosis (left heart can be affected in bronchial carcinoid)
- Other molecules such as ACTH and GHRH may also be secreted resulting in, for example, Cushing's syndrome
- Pellagra can rarely develop as dietary tryptophan is diverted to serotonin by the tumour
183
what investigations are done in carcinoid syndrome
- Urinary 5-HIAA
- Plasma chromogranin A y
184
what is the management of carcinoid syndrome
- Somatostatin analogues e.g. octreotide
- Diarrhoea: cyproheptadine may help
185
what can be seen on routine bloods on someone taking steroids (e.g. prednisolone)
Neutrophilia
186
When is gradual withdrawal of systemic corticosteroids (over weeks, not days) indicated ?
- Received more than 40mg prednisolone daily for more than one week
- Received more than 3 weeks of treatment
- Recently received repeated courses
187
How should a patient with addisons adjust medications when suffering from an intercurrent illness ?
Double the glucocorticoids, keep fludrocortisone dose the same
188
What kind of diuretic can cause hypercalcaemia ?
- Thiazides (e.g. bendroflumethiazide)
189
Explain the difference in goitre seen in hashimotos and de Quervain's thyroiditis
- Hashimoto's = firm and non tender
- De Quervain's = tender
190
what is a risk of opver replacement in hypothyroidism ?
osteoporosis
191
what side effect can occur in men taking digoxin ?
- Drug induced gynaecomastia
192
What changes need to be made in pregnancy in women with hypothyroidism ?
- Increase their thyroid hormone replacement dose by up to 50% as early as 4-6 weeks of pregnancy
193
First line management of hyperhidrosis
Topical aluminium chloride
194
Low T3/T4 and normal TSH in the context of acute illness
Sick euthyroid syndrome
Repeat TFTs in sick weeks at GP
195
what metabolic abnormalities are seen in cushing's
Hypokalaemia
Hypernatraemia
196
Most important modifiable risk factor for development of thyroid eye disease
Stop smoking
197
Treatment of choice for toxic multinodular goitre
Radioactive iodine therapy
198
4 features of DKA
- Abdominal pain
- Polyuria, polydipsia, dehydration
- Kussmaul respiration (deep hyperventilation)
- Acetone-smelling breath ('pear drops' smell)
199
Initial management of DKA
IV 0.9% sodium chloride
200
Following initial fluids, management of DKA
- Insulin infusion at 0.1 unit/kg/hr
- Once blood glucose is < 14 mmol/l an infusion of 10% dextrose should be started at 125 mls/hr in addition to the 0.9% sodium chloride regime
201
Important complication of fluid resuscitation in DKA
Cerebral oedema
202
Effect of excess parathyroid hormone on calcium and phosphate
EXCESS PARATHYROID + EXCESS PHOSPHATE EXCRETION
= High calcium
= Low phosphate
203
hypothyroidism in pregnancy
Increase dose by up to 50% in first 4-6 wks of pregnancy
204
Acromegaly increases the risk of what cancer
colorectal
205
Management of prolactinoma
- Dopamine agonists (bromocriptine, cabergoline)
- Surgery for those who can't tolerate of fail to repsond.
206
Excess prolactin in women
Amenorrhoea
Galactorrhoea
Infertility
207
Excess prolactin in men
Impotence
Loss of libido
Galactorrhoea
208
