Endocrinology Flashcards

(185 cards)

1
Q

What does the anterior pituitary gland release?

A

FSH

LH

ACTH (adrenocorticotropic hormone)

TSH

Prolactin

GH

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2
Q

What does the posterior pituitary release?

A

Oxytoxin

ADH

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3
Q

What are the components of the Thyroid axis?

A

TRH (from hypothalamus)

TSH

T3/T4 (triiodothyronine / thyroxine)

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4
Q

What are the components of the adrenal axis?

A

Diurnal variation (peak at early morning)

CRH (corticotrophin release hormone)

ACTH

Cortisol (from adrenal gland - stress hormone)

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5
Q

What are the actions of cortisol in the body?

A
  • Inhibits immune system
  • Inhibits bone formation
  • Raises blood glucose
  • Increases alertness
  • Increases metabolism
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6
Q

What are the components of the growth hormone axis?

A

GHRH (somatostatin inhibits, ghrelin promotes)

GH

Insulin-like growth factor (IGF-1) from liver

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7
Q

What is the action of growth hormone?

A
  • Stimulates muscle growth
  • Increases bone density
  • Stimulates cell regeneration and reproduction
  • Stimulates growth of internal organs
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8
Q

When is PTH released?

A

Low serum calcium and low magnesium (and high serum phosphate) to increase calcium resorption

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9
Q

What does PTH do?

A

Increases activity and number of osteoclasts in the bone, causing resorption into the blood, increasing serum calcium.

Stimulates an increase in calcium reabsoption in the kidneys

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10
Q

What is the additional function of PTH?

A

Stimulates the kidneys to convert vitamin D3 into calcitriol (active form of vit D) which promotes calcium absoption from food in small intestine

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11
Q

Where is Renin secreted from?

A

Juxtaglomerular cells in the afferent and efferent arterioles in kidbey (sense blood pressure - secrete less if BP is high)

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12
Q

What is the role of renin?

A

Enzyme converts angiotensinogen (from liver) into angiotension I

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13
Q

What are the two actions of angiotention II?

A

Acts on blood vessels to vasoconstrict and stimulates the release of aldosterone form adrenal glands

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14
Q

What does aldosterone result in?

A

Acts on nephrons to increase sodium reabsorption in distal tubules, potassium secretion in distal tubules and hydrogen secretion from collecting ducts

Hypernatraemia

Hypokalaemia

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15
Q

What is Cushing’s syndrome vs Cushing’s disease?

A

Syndrome = signs & symptoms after prolonged elevated cortisol

Disease = pituitary adenoma secreting excessive ACTH

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16
Q

What is the causality between Cushings disease and Cushing syndrome?

A

Disease can cause syndrome but syndrome isnt always caused by disease

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17
Q

What are the features of Cushing’s syndrome?

A

Moon face

Central obesity

Abdo striae

Buffalo hump

Proximal limb muscle wasting

Hypertension

Cardiac hypertrophy

Hyperglycaemia

Insomnia

Osteoporosis

Easy brusing

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18
Q

What are the other effects of high level of stress hormone?

A

Hypertension

Cardiac hypertrophy

Hyperglycaemia (type 2 diabetes)

Depression

Insomnia

Osteoporosis

Easy bruising / poor skin healing

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19
Q

What are some causes of Cushing’s syndrome?

A
  • Exogenuos steroids
  • Cushings Disease
  • Adrenal adenoma (not pituitary)
  • Paraneoplastic cushings
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20
Q

What is the most common cause of paraneoplastic Cushings?

A

SCLC (excess ACTH from cancer)

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21
Q

What is the choice of test for Cushing’s?

A

Dexamethasone Suppression Test

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22
Q

How does the dexamethasone suppression test work?

A

Patient is given low dose of dexamethosone (synthetic glucocorticoid steroid) at night and cortisol/ACTH is measured in the morning to see if its been suppressed

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23
Q

In the high dose Dexamathasone Suppression test (8mg vs 1mg - done if low dose test abnormal) what is the difference between Cushing’s Disease and an Adrenal Adenoma?

A

Cushing’s disease still shows some response to negative feedback whereas Adrenal Adenomas do not (however ACTH is supressed)

In ectopic ACTH neither cortisol or ACTH will be supressed

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24
Q

Complete the following:

A
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25
What is the other investigation for Cushing's?
**24 hour urinary free cortisol** (doesn't indicate underlying cause and cumbersome)
26
What is the imaging of choice for Cushing's syndrome? What will **blood tests** show?
**MRI brain** for pituitary adenomas **Chest CT** for small cell lung cancer **Abdo CT** for adrenal tumours _Bloods_ **FBC** (raised WCC) and **electrolytes** (potassium may be low if **aldosterone** also secreted by **adrenal adenoma**)
27
What is the treatment of Cushing's?
**Trans-sphenoidal** surgery for pituitary adenoma **Surgical removal** of adrenal tumour / tumour producing ectopic ACTH If **surgical removal** of cause not possible then can **remove both adrenal glands** and give replacement steroids for life
28
What hormones are particularily lacking in adrenal insufficiency?
**Cortisol** and **aldosterone**
29
What is Addison's **disease**?
**Specific condition** where the adrenal glands have been **damaged** resulting in a reduction of cortisol and aldosterone (mainly **autoimmune** cause) Aka **primary adrenal insufficiency**
30
What is **secondary adrenal insufficiency** commonly due to?
**Inadequate ACTH** resulting in low cortisol E.g. from **sugery to remove pituitary tumour**, **infection, loss of blood, radiotherapy**
31
What is Sheehan's syndrome?
Massive blood loss during childbirth leading to pituitary gland necrosis (causes **secondary adrenal insufficiency**)
32
What is teritary adrenal insufficiency?
Inadequate **CRH** released by the **hypothalamus** usually the result of the patient being on **long term steroids** (more than 3 weeks) causing suppression of the hypothalamus. When steroids are stopped then hypothalamus doesn't 'wake up' quick enough, so steroids shouldnt be stopped abruptly
33
What are some **symptoms** of **adrenal insufficiency**?
- Fatigue - Nausea - Cramps - Abdo pain - Reduced libido
34
What are some signs of adrenal insufficiency?
**Bronze skin** due to **ACTH** stimulating melanocytes to produce melanin ## Footnote **Postural hypotension**
35
What are some investigations for adrenal insufficiency?
**Hyponatraemia** (key clue) **Hyperkalaemia** **Early morning cortisol** (often falsely normal) **SHORT SYNACTHEN TEST** (for diagnosis)
36
What antibodies are present for autoimmune Addison's?
**Adrenal cortex antibodies** and **21-hydroxylase antibodies**
37
What imaging can be used for Adrenal insufficency?
**CT/MRI** for adrenal tumour, haemorrhage **MRI pituitary** for further info about pituitary
38
What are the **ACTH** levels in **primary adrenal failure** and **secondary adrenal failure**?
**Primary** = **ACTH high** **Secondary** = **ACTH low**
39
What is the short syntacthen test ?
Give patient **synacthen** (synthetic ACTH) in morning **Blood cortisol measured** at baseline, 30 mins, 60 mins after. Should rise, if not (at least double) then **primary adrenal insufficiency (Addison's disease)**
40
What is the treatment for adrenal insufficiency?
**Hydrocortisone** is a glucocorticoid to replace cortidol **Fludrocortisone** is a mineralcorticoid to replace aldosterone
41
What are patients with adrenal insifficiency given in addition?
**Steroid card** and **emergency ID tag** (indicate they are dependent on steroids) Doses **doubles** during **acute illness**
42
How do patients with **Addisonian crisis present** (acute presentation of severe addisons)?
- Reduced consciousness - Hypotension - Hypoglycaemia, hyponatraemia, hyperkalaemia
43
When can an Addison's crisis occur?
Long term **steroids stopped abruptly** **Infection** **Trauma** **Other acute illness**
44
What are the management options for a patient with an Addisonian Crisis?
- Intensive **monitoring** if unwell - **Parenteral steroids** (IV hydrocortisone 100mg stat then 100mg every 6 hours) - **IV fluid** resuscitation - **Correct hypoglycaemia** - Monitor **U&Es**
45
What are the TFTs in hyperthyroidism?
**TSH** is suppressed so low TSH, apart from in **pituitary adenoma** which secretes TSH
46
How are the TFTs in hypothyroidism?
**TSH is high** (exception is pituitary/hypothamic cause when TSH will be low)
47
Label the following:
48
What antibodies are present in **Grave's and Hashimoto's** disease?
**anti-TPO** (antithyroid peroxidase) antibodies **anti-thyroglobulin** antibodies (limited use as present in normal individuals)
49
What antibodies are present in Grave's disease?
**TSH receptor antibodies**
50
What imaging is available for thyroid problems?
**Thyroid ultrasound** - diagnose thyroid nodules, and for biopsy guide (distinguish between **cystic** and **solid nodules**) **Radioisotope scans** - for **hyperthyroidism** and **thyroid cancers** (diffuse uptake of iodine in Graves, focal is adenomas/toxic multinodular goitre, 'cold' aka abnormally low is thyroid cancer) **gamma camera** is used to detect **gamma rays** from **radioactive iodine**
51
What is Graves' disease?
**Autoimmune condition** where **TSH receptor antibodies** (mimic TSH) cause a **primary hyperthyroidism**
52
What is toxic multinodular goitre (Plummer's disease)?
**Nodules** develop on the gland **acting independently of the normal feedback system** and continuously produce excessive thyroid hormone
53
When is exopthalmos seen?
Grave's disease
54
What is **pretibial myxoedema**?
**Specific to Grave's disease** where there are deposits of **mucin** under the skin and on the **anterior aspect of the leg** - discoloured, wavy, oedematous appearance of the skin over this area (reaction to the TSH receptor antibodies)
55
What are some **causes** of **hyperthyroid**?
**Grave's disease** **Toxic multinodular goitre** **Solitary toxic thryoid nodule** **Thyroiditis** (e.g. De Quervain's, Hashimoto's, postpartum and drug-induced thyroiditis)
56
What are some **universal features** of **hyperthyroidism**?
- Anxiety and irritabilty - Sweating and heat intolerance - Tachycardia - Weight loss - Fatigue - Losse stools - Sexual dysfunction
57
What are some **unique features** of **Grave's disease**?
- Diffuse **Goitre** (without nodules) - Graves eye disease - **Exopthalmos** - **Myxoedema**
58
What are some **unique features** of **toxic multinodular goitre**?
- **Goitre** with firm nodules - **Most patients \>50** - Second most common form of **thyrotoxicosis** (after Graves')
59
What is a **single abnomal thyroid nodule** called?
**Adenoma** (benign - treated with surgical removal)
60
What is **De Quervain's Thyroiditis**?
**Viral infection** with fever, neck pain and tenderness, **dysphagia** and features of **hyperthyroidism**. **Hyperthyroid phase** followed by a **hypothyroid phase** as the TSH levels fall due to negative **Self limiting condition** and supportive treatment is with **NSAIDs** for pain and **beta-blockers** for symptoms
61
What is a Thyroid Storm?
Rare presentation of **hyperthyroidism**'thyrotoxicosis crisis' Severe presentation of hyperthyroidism with pyrexia, tachycardia and delerium (requires **admission**)
62
What is the first line antithyroid drug?
**Carbimazole** - remission is usually achieved in 18 months of treatment **Titration block** = careful titration for normal levels **Block and replace** = blocks all production and patient take levothyroxine
63
What are the other treatments for hyperthyroidism?
**Propylthiouracil** - **second line** used in similar way to carbimazole (small risk of **severe hepatic reaction**) **Radioactive iodine treatment** - (drinking single dose of radioactive iodine) radiation destroys the thyroid cells - can be left hypothyroid after and require levothyroxine replacement **Beta blockers** (blocks adrenaline symptoms - **propanolol** is non selective so works everywhere) **Surgery** (thyroidectomy) - requires levothyroxine for life
64
What are the **'rules'** for **radioactive iodine** treatment?
- Patient must not be pregnant to allowed to get pregnancy in 6 months - No close contact with children/pregnant women 3 weeks after - Limit contact with anyone for several days after
65
What are some causes of **hypothyroidism**?
**Hashimoto's Thyroititis** (anti-TPO and antithyroglobulin antibodies - with goitre followed by atrophy of thyroid gland) **Iodine deficiency** **Secondary to treatment of hyperthyroidism** (carbimazole, propylthiouracil, radioactive iodine, thyroid surgery)
66
What **medications** can inhibit the production of thyroid hormones?
Lithium Amiodarone
67
What are some **central causes** (secondary) **hypothyroidism**?
**Pituitary gland** fails to produce enough TSH (associated with lack of ACTH) - **hypopituitarism**: * Tumours * Infection * Vascular (e.g. Sheehan syndrome) * Radiation
68
How do patients with hypothyroidism present?
- Weight gain - Fatigue - Dry skin - Coarse hair - Fluid retention (oedema, ascites) - Heavy / irregular periods - Constipation
69
What is the management of hypothyroidism?
**Levothyroxine** (synthetic T4) which is metabolised to T3 in the body Initially measure **monthly** until stable then less frequently until symptomatic
70
What does the body want to keep blood glucose between?
4.4 and 6.1
71
Where is Insulin made?
**Beta cells** in the **Islets of Langerhans** in the pancreas
72
How does insulin reduce blood sugar?
Causes cells in the body to **absorb glucose** and causes formation of **glycogen stores** (in muscle and liver)
73
Where it glucagon made?
**Alpha cells** in the Islets of Langerhans in the pancreas
74
What does Glycogen do?
Tells the liver to break down stored glycogen into glucose (**glycogenolysis**) Also promotes **gluconeogenesis**
75
What is **Ketogenesis**?
When there is insufficient glucose and glycogen stores are depleted the liver takes **fatty acids** and turns them into **ketones** They are water soluble fatty acids which can be used as fuel (can cross BBB)
76
How can ketone levels be measured?
"Dipstick" In blood using a **ketone meter** Ketosis = acetone smell on breath
77
What happens in T1DM and why?
**Pancreas** stops being able to produce insulin, clause **unclear** may be **genetic** or triggered by viruses e.g. **Coxsackie B virus** and **enterovirus**
78
What does diabetic ketoacidosis result in?
**Metabolic acidosis** which is life threatening
79
What happens in T1DM ketoacidosis?
**Over production of ketone acids** causes metabolic acidosis
80
Why does d**ehydration** occur in T1DM?
**Glucose in the urine** draws water out with it (osmotic diuresis) causing polyuria and polydipsia
81
Why does **T1DM** result in a **potassium imbalance**?
**Serum potassium = normal** but total body potassium is low because of no stores When insulin is started all potassium is driven into cells causign severe hypokalaemia very quickly
82
How does **DKA present**?
- Hyperglycaemia - Dehydration - Ketosis - Metabolic acidosis - Potassium imbalance
83
How does a patient present with DKA?
- Polyuria - Polypdipsia - N&V - Acetone smell on breath - Dehydration - Altered conciousness
84
How is DKA diagnosed?
- Hyperglycaemia \>11 - Ketosis \>3 - Acidosis \<7.3
85
What is the treatment for DKA?
**FIG-PICK** **F**luids - IV fluid resus with normal saline (1 litre stat, 4 litres with K+ over 12 hrs) **I**nsulin - e.g. Act rapid **G**lucose - monitor and add dextrose (if below 14 mmol / L) **P**otassium - monitor and correct (infused at **no more than 10 mmol / hr**) **I**nfection - treat any infection **C**hart - fluid balance **K**etones - monitor blood ketone Establish on **normal subcut regime** prior to stopping insulin
86
What is the **long term management** of T1DM?
- Sub cut **insulin regimes** - Monitor **dietary carb intake** - Monitor **blood sugar levels on waking** - Monitoring for **complications**
87
How is insulin usually prescribed?
Combi of **background** - long acting and **Short acting** (30 mins before meal)
88
What can injecting at the same spot be called?
"**lipodystrophy**" - sub cut fat hardens, patients are told to cycle their injecting spots
89
What are some short term complications of T1DM?
Hyperglycaemia (and DKA) Hypoglycaemia
90
What are the symptoms of hypoglycaemia?
Tremor Sweating Irritability Dizziness Pallor (reduced consciousness, coma and death)
91
How is **hypoglycaemia treated**?
**Rapid acting glucose** e.g. lucozade and **slower acting** e.g. biscuits If **severe** = **IV dextrose** and **IM glucagon**
92
What are some long term complications of T1DM?
- Damage to **endothelial cells** of blood vessels (leaky / unable to regenerate) - High sugar levels causes **suppression of the immune system** providing optimal environment for infectious organisms to thrive
93
What are some macrovascular complications of T1DM?
- **Coronary artery disease** - Peripheral ischaemia and '**diabetic foot**' - **Stroke** - **Hypertension**
94
What are some **microvascular complications** of T1DM?
**Peripheral neuropathy** **Retinopathy** **Kidney disease,** particularly **glomerulosclerosis**
95
What are some **infection related complications** of T1DM?
**Urinary Tract Infections** **Pneumonia** **Skin and soft tissue infections** **Fungal infections**, particularly oral and vaginal **candidiasis**
96
How is T1DM monitored?
**HbA1c** every 3-6 months (glycated Hb - how much glucose attached) **Capillary blood glucose** **Flash glucose monitoring** (sensor measures glucose levels of **interstitial fluid** - lag of 5 mins - need "**reader**" to swipe over sensor - sensor needs replacing every 2 weeks)
97
Who normally gets diabetes (due to beta cells getting fatigued)?
**Asian, Black** **Male** **Elderly \>40** **Obese** **Those with lack of exercise**
98
What are the **non-modifiable** and **modifiable** risk factors for **T2DM**?
**Non-modifiable**: * Older age * Ethnicity (black, chinese, south asian) * FH **Modifiable:** * Obesity * Sedentary lifestyles * High carb (refined) diet
99
What’s a normal HbA1c?
**\<48 mmol/L**
100
How long does a HbA1c look at?
**2 months**
101
What is the diet advice to diabetics?
​**Low glycaemic and high fibre diet** ## Footnote **Veg and oily fish**
102
How would type 2 diabetes present?
**Fatigue** **Polydipsia** and **polyuria** Unintentional **weight loss** **Opportunistic infections** **Slow healing** **Glucose in urine** (on dipstick)
103
What’s normal capillary blood glucose?
4-7
104
How is OGTT done?
**Take baseline blood sugar** before breakfast **Then measure 2 hours after sugary** drink
105
WhaWhat is HbA1c for pre-diabetes (heading towards T2DM but don't fit diabetic diagnostic criteria)?
**42-47** (48 for diabetes)
106
What is the random blood glucose/OGTT for diabetes?
\>11
107
What is the fasting blood glucose for diabetes?
\>7
108
What is the management of diabetes?
Educate (its **curable** - e.g. DiRECT study - put on 800 calories per day and remission) **Diet advice** - veg and oily fish, low glycaemic, high fibre diet **Other risk factors** - exercise and weight loss, stop smoking, optimise treatment for other illnesses e.g. HTN, hyperlipaemia, CVD
109
What complications would you look for in diabetes?
Retinopathy Kidney disease Diabetic foot
110
What is the HbA1c target for metformin treatment and further?
48 (new T2DM) and 53 (moved beyond metformin)
111
What are the 2nd line treatments after metformin?
**Any of:** Sulfonylurea DPP-4 inhibitor SGLT-2 inhibitor Pioglitazone
112
What is the **3rd line treatment** for diabetes?
**Metformin and 2 second line drugs** OR **Metformin and insulin**
113
How does **metformin** (biguanide) exert its action?
Increases **insulin sensitivity** **Decrease liver production of glucose** "weight neutral"
114
Does metformin have an effect on weight?
No
115
What are some side effects of metformin?
**Lactic acidosis** **Diarrhoea** and **abdo pain** Does NOT typically cause hypoglycaemia
116
How does pioglitazone work?
**Same as metformin** (increases insulin sensitivity / decreases liver production of glucose)
117
What are some **side effects** of **pioglitazone**?
**Weight gain** **Fluid retention** **Anaemia** **Heart failure** **Bladder cancer** NOT HYPOGLYCAEMIA
118
Name a sulfonylureas?
Gliclazide
119
How do sulfonylureas work?
**Stimulate insulin release** from pancreas
120
What are some side effects of sulphonureas?
**Weight gain** **HYPOGLYCAEMIA (only one)** Myocardial Infarction (and CVD when used as monotherapy)
121
What does **GLP-1 (an incretin)** do?
Increase insulin secretion Slows GI tract Inhibits glucagon production
122
How does a **DPP4** (enzyme which breaks down GLP-1) **inhibitors** work?
Inhibits breakdown of GLP-1
123
Name a DPP-4 inhibitor?
**Sitagliptin**
124
What a side effect DPP-4 inhibitor?
(**P**)ancreatitis GI upset Symptoms of **upper respiratory tract infection**
125
What is the most common **GLP-1 mimetic**?
Exenatide (given as subcut injection twice a day / once weekly in **modifiable form**)
126
What are some side effects of GLP-1 mimetic?
**GI upset** **Weight LOSS** **Dizziness**
127
Name a **SGLT-2 inhibitor**?
End with -gliflozin e.g. **dapagliflozin, empagliflozin**, **canagliflozin**
128
How do SGLT-2 inhibitors work?
**Block SGLT-2 transporter in proximal tubules** of kidneys (usually reabsorbs glucose from urine)
129
What are some side effects of SGLT-2 inhibitors?
**Glucoseuria** (increased UTIs) ## Footnote **Weight LOSS** **DKA**
130
Name an rapid-acting insulins? How long do they last?
**Novorapid** **Humalog** **Apidra** 10 mins - 4 hours
131
When do **rapid-acting insulins** start work?
10 mins to 4 hours
132
Name a short acting insulin?
**Actrapid** **Humulin S**
133
When do short acting insulins work?
**30mins - 8 hours**
134
Name an intermediate insulin?
**Humulin I** **Insulatard**
135
When do intermediate insulins work?
**1 hours to 16 hours**
136
Name a long acting insulin?
**Degludec** (lasts over 40 hours) ## Footnote **Levemir** **Lantus**
137
When do long acting insulins work?
1 hour - 24
138
What are some causes of GH excess?
Pituitary adenoma Lung cancer secreting GHRH
139
How does **acromegaly** present?
**Headaches**, **bitemporal hemianopia** **Overgrowth of tissue**: frontal bossing, large nose, large tongue "macroglossia", large hands and feet, large jaw
140
What organ dysfunction can GH excess cause?
**Hypertrophic heart** **Hypertension** **Type 2 diabetes** **Colorectal** cancer
141
What are the investigations for suspected acromegaly?
**IGF-1** inital screening (GH not useful - fluctuates) **OGTT** whilst measuring GH **MRI brain** for pituitary tumour **Refer to opthalmology**
142
What are the treatment options for acromegaly?
Transphenoidal surgery to **remove pituitary tumour** Medication
143
What **medications** are available for **acromegaly**?
**Pegvisomant** (GH antagonist given subcut and daily) **Somatostatin analogues** (ocreotide) Dopamine agonist to block GH release (**bromocriptine**)
144
Which cells of the parathyroid gland release PTH?
**Chief cells**
145
How does PTH act to raise blood calcium?
- Increases **osteoclast** activity - Increases absoption of calcium from gut/kidneys - Increases **vitamin D** activity
146
What are the **symptoms** of **hypercalcaemia**?
**Stones, bones, groans, moans** Renal stones Painful bones Abdo groans (constipation, nausea and vomiting) Psychiatric moans (fatigue, depression, psychosis)
147
How does secondary hyperparathyroidism come about? How is it treated?
**Insufficient vitamin D/chronic renal failure** leading to low absorption of calcium from the intestines, kidneys and bones causing hypocalcaemia - **low calcium in blood** PTH responds by raising **Correct vit D deficiency** or perform **renal transplant** to treat failure
148
What is tertiary hyperparathyroidism?
When the cause of 2ndary hyperparathyroidism is treated then the PTH remains inappropriately high - due to parathyroid gland hyperplasia and treated with surgery
149
What is primary hyperaldosteronism? (Conn's syndrome)
Adrenal glands produce too much aldosterone (**renin will be low**)
150
What can cause primary hyperaldosteronism?
- Adrenal **adenoma** - Adrenal **hyperplasia** - Familial **hyperaldosteronism** - Adrenal carcinoma (rare)
151
What is **secondary hyperaldosteronism**?
**Excessive renin** stimulates the adrenal glands to produce more **aldosterone**
152
What can cause secondary hyperaldoseronism?
**Renal artery stenosis** Renal artery obstruction Heart failure
153
When is Renal Artery Stenosis typically a result of?
Atherosclerosis
154
How can the diagnosis of renal artery stenosis be confirmed?
Doppler ultrasound CT angiogram MRA (magnetic resonance angiography)
155
What are the investigations for hyperaldosteronism?
Renin/aldosterone levels High aldosterone: Low renin = primary High aldosterone : High renin = secondary
156
What are some other investigations related to the effect of aldosterone?
**Blood pressure** (hypertension) **Serum electrolytes** (hypokalaemia) **Blood gas** (alkalosis)
157
What investigations can be done for the cause of hyperaldosteronism?
**CT/MRI** to look for adrenal tumour **Renal doppler ultrasound / CT angiogram** for RAS
158
What is the management for hyperaldosteronism?
**Aldosterone antagonist:** Eplerenone, spironolactone Treat **underlying cause**: Remove of adenoma, percutaneous renal artery angioplasty **via femoral artery** for RAS
159
What is ADH also known as?
Vasopressin
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What is the result of excessive ADH?
Excessive water reabsorption in the **collecting ducts** cauing dilution of sodium in the blood
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What is the result of SIADH?
Euvolaemic hyponatraemia (urine becomes more concentrated as less water is excreted = high urine osmolality / high urine sodium)
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What happens to the urine in SIADH?
Urine is more concentrated as less water is passed out so there is: ## Footnote **"high urine osmolality"** **"high urine sodium"**
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What are the symptoms of SIADH?
**- Headache** **- Fatigue** **- Muscle aches and cramps** **- Confusion** **- Severe hyponatraemia** causes seizures and reduced consciousness
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What are some causes of SIADH?
- Post op from major surgery - Infection (atypical pneumonia) - Head injury - Medications (thiazide diuretics, carbamazepine, vincristine, cyclophosphamide, antipsychotics, SSRIs, NSAIDs) - Malignancy e.g. SCLC - Meningitis
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How is SIADH diagnosed?
Diagnosis of exclusion - **U&Es** = hyponatraemia - **Urine sodium and osmolality** will be high
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How can other causes of hyponatraemia be rulled out?
- **Negative short synacthen test** to exclude adrenal insufficiency - No history of diuretic use - No diarrhoea, vomiting/burns - No excessibe water intake - No CKD / AKD
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How can a cause for SIADH be established?
**CXR** as first line for pneumonia, lung abscess, lung cancer
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Why should sodium in hyponatraemia be corrected slowly?
Due to risk of central pontine myelinolysis
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What are the management steps of SIADH?
Treat cause (typically medications) **Fluid restriction** (to 500ml - 1 litre) **Tolvaptan** - ADH receptor blocker **Demeclocycline** is a **tetracycline abx** that inhibits ADH (used prior to development of vaptans)
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What is central pontine myelinolysis?
Due to **rapid correction** of hyponatraemia Long standing hyponatraemia causes brain to reduce solutes to prevent oedema - rapidly correcing causes brain cells to burst as water rapidly moves out, presenting: **First phase** (due to electrolyte imbalance) headache, nausea and vomiting **Seconds phase** (due to demyelination) spastic quadriparesis, cognitive/behavioural changes
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What is diabetes insipidus?
Lack of ADH or lack of a response (classified as **nephrogenic** / **cranial**)
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What is **primary polydipsia**?
Patient has a normally functioning ADH system but they are drinking excessive water leading to **excessive urine production** don't have diabetes insipidus
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What is nephrogenic diabetes insipidus?
Collecting ducts in the kidneys do not respond to ADH, caused by: - **Drugs** e.g. lithium - Intrinsic **kidney disease** - Electrolyte disturbance (hypokalaemia / hypercalcaemia)
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What is **cranial diabetes insipidus**?
**Hypothalamus doesn't produce ADH** for pituitary gland to secrete Idiopathic or caused by: - Brain tumours - Brain malformations - Head injury - Brain Infections e.g. meningitis, encephalitis
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How does diabetes insipidus present?
**Polyuria** **Polydispsia** **Dehydration** **Postural hypotension** **Hypernatraemia**
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What is the test of choice for diagnosing diabetes insipidus?
**Water deprivation test** **Initial fluid deprevation** (8 hours) then urine osmolality is measured, **synthetic ADH** (desmopressin) is given and 8 hours **later urine osmolality is measured** again In **cranial diabetes** insipidus the kidneys will respond and urine osmolality will rise In **nephrogenic diabetes insipidus** patient is unable to respond to ADH - urine osmolality will be low and remain low
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Label the following:
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How is diabetes insipidus managed?
**Desmopressin** (synthetic ADH) used in: **Cranial diabetes insipidus** to replace ADH and nephrogenic diabetes insipidus in higher doses
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Where is adrenaline produced?
**Chromaffin** cells of the **adrenal glands** in adrenal medulla
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What type of hormone is adrenaline?
Catecholamine
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What is a phaeochromocytoma?
Tumour of the chromaffin cells secreting unregulated and excessive adrenaline
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How is a phaeochromocytoma diagnosed?
**24 hour urine catecholamines** Plasma free metanephrines (break down product of adrenaline - has longer half life as adrenaline only lasts few mins so fluctuates)
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How does a phaeochromocytoma present?
- Anxiety - Sweating - Headache - HTN - Palpitations, **paroxysmal AF**
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What is the management of a phaeochromocytoma?
**Alpha blockers** (phenoxybenzamine) **Beta blockers** **Adrenalectomy** Symptoms need controlling medically before surgery
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