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Phase 4 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Which hormones does the anterior pituitary gland produce?

A 
Thyroid Stimulating Hormone (TSH)
Adrenocorticotropic Hormone (ACTH)
Follicle Stimulating Hormone (FSH) and Luteinising Hormone (LH)
Growth Hormone (GH)
Prolactin
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2
Q

Which hormones does the posterior pituitary gland produce?

A 
Oxytocin
Antidiuretic Hormone (ADH)
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3
Q

How is thyroid hormone regulated?

A

Hypothalamus –> TRH –> pituitary –> TSH –> thyroid gland –> T3 and T4 –> suppress hypothalamic and pituitary release of TRH and TSH (negative feedback).

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4
Q

How is cortisol regulated?

A

Hypothalamus –> CRH –> AP –> ACTH –> Adrenal glands –> cortisol –> suppresses hypothalamic and AP release of CRH and ACTH (negative feedback)

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5
Q

When is cortisol at its highest?

A

Early morning. Lower in evening.

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6
Q

Give 5 effects of cortisol.

A 
Inhibits the immune system
Inhibits bone formation
Raises blood glucose
Increases metabolism
Increases alertness
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7
Q

How is growth hormone regulated?

A

Hypothalamus -> GHRH –> AP –> GH –> Liver –> IGF-1

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8
Q

Give 4 effects of growth hormone.

A

Stimulates muscle growth
Increases bone density and strength
Stimulates cell regeneration and reproduction
Stimulates growth of internal organs

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9
Q

How is serum calcium regulated?

A

Low serum Ca (or low Mg, or high phosphate) –> Parathyroid glands –> PTH –> increases serum Ca –> suppresses parathyroid release of PTH.

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10
Q

Give 3 ways in which PTH increases serum calcium.

A
  1. PTH increases the activity and number of osteoclasts in bone, causing reabsorption of calcium from the bone into the blood thereby increasing serum calcium concentration.
  2. PTH also stimulates an increase in calcium reabsorption in the kidneys meaning that less calcium is excreted in the urine.
  3. stimulates the kidneys to convert vitamin D3 into calcitriol, which is the active form of vitamin D that promotes calcium absorption from food in the small intestine.
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11
Q

How is blood pressure regulated using the renin-angiotensin system?

A

Low BP –> afferent arteriole of kidney –> juxtaglomerular cells –> renin –> liver –> angiotensinogen –> ATI –> ATII (via ACE in lungs) –> vasoconstriction, adrenals –> aldosterone –> retain Na –> retain water –> increase BP –> suppresses renin secretion from kidney.

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12
Q

What are 3 effects of aldosterone?

A

Mineralocorticoid hormone. Acts on nephrons to
1. increase sodium reabsorption from the distal tubule
2. increase potassium secretion from the distal tubule
3. increase hydrogen secretion from collecting ducts.
Water follow sodium by osmosis –> high intravascular volume –> higher blood pressure.

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13
Q

What is Cushing’s syndrome? Give 5 features.

A

Signs and symptoms of prolonged elevation of cortisol:
Central obesity, moon face, abdo striae (stretch marks), buffalo hump, proximal limb muscle wasting.
Cortisol –> htn, cardiac hypertrophy, hyperglycaemia (T2DM), depression, insomnia
Osteoporosis, easy bruising, poor skin healing

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14
Q

What is Cushing’s disease?

A

Elevated cortisol due to pituitary adenoma secreting ACTH. Causes a Cushing’s syndrome.

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15
Q

What causes Cushing’s syndrome?

A
  1. Exogenous steroids (in patients on long term high dose steroid medications)
  2. Cushing’s Disease (a pituitary adenoma releasing excessive ACTH)
  3. Adrenal Adenoma (a hormone secreting adrenal tumour)
  4. Paraneoplastic - ACTH is released from a cancer (ectopic ie not of the pituitary) and stimulates excessive cortisol release. Usually small cell lung cancer.
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16
Q

How is Cushing’s syndrome diagnosed? how does the test work?

A

Dexamethasone suppression test - dex is a steroid so in normal people should reduce CRH and ACTH from hypothalamus and pituitary, leading to reduced cortisol from the adrenals. Dex is given at 10pm and measured at 9am.
1. Low dose test - takes 1mg dex, see if hypothalamus responds by reducing the CRH output. If this is normal (cortisol level suppressed), Cushing’s is excluded. If abnormal (cortisol remains high), go on to (2)
2. High dose test - 8mg dex.
Cushings disease (Pituitary adenoma) - cortisol and ACTH suppressed by high dose
Adrenal adenoma - cortisol is not suppressed but ACTH is suppressed, because cortisol production is independent from the pituitary.
If ectopic ACTH eg SCLC, nothing is suppressed.

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17
Q

What bloods would you do in Cushing’s syndrome and what might they show?

A

FBC - raised WCC

U+E - low aldosterone –> low K+ - indicates adrenal adenoma

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18
Q

What causes low dose dexamethasone suppression test to show high cortisol, but the high dose test shows suppressed cortisol and ACTH? What investigation would help confirm the diagnosis?

A

Indicates Cushing’s disease. MRI brain for pituitary adenoma.

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19
Q

Low dose dex test: High cortisol
High dose dex test: high cortisol and ACTH
Diagnosis and next investigation?

A

Likely ectopic ACTH production, usually small cell lung cancer so chest CT.

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20
Q

Low dose dex test: High cortisol
High dose dex test: High cortisol, low ACTH
Diagnosis and next investigation?

A

Likely adrenal adenoma so abdo CT.

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21
Q

How is Cushing’s syndrome treated?

A

Remove underlying cause eg:
Trans-sphenoidal removal of pituitary adenoma
Surgical removal of adrenal tumour
Surgical removal of tumour producing ectopic ACTH.
Or remove adrenals and replace with steroids for life.

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22
Q

What is adrenal insufficiency?

A

Adrenal glands not producing enough steroid hormones, particularly cortisol and aldosterone. Life-threatening.

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23
Q

What is Addison’s disease?

A

Primary adrenal insufficiency - adrenal glands damaged, usually autoimmune.

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24
Q

What is secondary adrenal insufficiency?

A

Inadequate ACTH stimulating the adrenal glands, resulting in low cortisol release. Caused by pituitary excision, infection, ischemia, radiotherapy.

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25
Q

What is Sheehan’s syndrome?

A

Pituitary gland necrosis due to massive blood loss during childbirth.

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26
Q

What is tertiary adrenal insufficiency?

A

Inadequate CRH release by hypothalamus. Usually due to long term oral steroids (more than 3 weeks), suppress hypothalamus, withdrawal of steroids –> not enough endogenous steroids. Hence taper slowly

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27
Q

How does adrenal insufficiency present?

A

Fatigue, nausea, cramps, abdo pain, reduced libido

Bronze hyperpigmentation to skin (ACTH stimulates melanocytes), hypotension (particularly postural)

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28
Q

What investigations would you do for suspected adrenal insufficiency and what might they show?

A

Short synacthen test
U+Es - hyponatraemia, hyperkalaemia
Morning cortisol
Short synacthen test - cortisol fails to rise
ACTH - primary adrenal failure = high, secondary adrenal failure = low
Adrenal autoantibodies - adrenal cortex abs, 21-hydroxylase abs
CT/MRI adrenals if structural cause suspected (not for AI)
MRI pituitary if indicated

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29
Q

What is the short synacthen test?

A

Synacthen = SYNthetic ACTH. Give synacthen –> measure blood cortisol at baseline, 30 mins and 60 mins. If adrenals are working, they will be stimulated to produce cortisol. If the cortisol fails to rise to double the baseline, this indicates primary adrenal insufficiency (Addison’s disease).
Done in the morning.

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30
Q

What is Addisonian crisis?

A

Aka adrenal crisis

Acute severe primary adrenal insufficiency.

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31
Q

How does Addisonian crisis present?

A

Reduced consciousness, hypotension, hypoglycaemia, hyponatraemia, hyperkalaemia

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32
Q

What causes Addisonian crisis?

A

First presentation of Addison’s, infection, trauma, acute illness, sudden withdrawal of steroids.

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33
Q

How do you manage Addisonian crisis?

A 
STEROIDS - IV hydrocortisone 100mg stat
Intensive monitoring
IV fluid resuscitation
correct hypoglycaemia
monitor electrolytes and fluid balance
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34
Q

What would TFTs show in hyperthyroidism?

A

Low TSH. Except pituitary adenoma which secretes TSH

Raised T3 and T4

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35
Q

What would TFTs show in hypothyroidism?

A

High TSH. Except secondary hypothyroidism when the low TSH is driving the hypothyroidism (pituitary/ hypothalamic cause)
Low T3 and T4

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36
Q

What do antithyroid peroxidase (anti-TPO) antibodies indicate?

A

Grave’s Disease

Hashimoto’s thyroiditis

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37
Q

What do antithyroglobulin antibodies indicate?

A

May be normal or present in Grave’s disease, Hashimoto’s thyroiditis or thyroid cancer.

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38
Q

What do TSH receptor antibodies indicate?

A

Grave’s disease.

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39
Q

What is the function of thyroid ultrasound?

A

Diagnose thyroid nodules
Distinguish between cystic (fluid-filled) and solid nodules
Guide thyroid lesion biopsy

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40
Q

What is the function of a radioisotope scan?

A

Investigation of hyperthyroidism and thyroid cancers.
Involves giving radioactive iodine PO/IV –> more iodine taken up if more active thyroid cells.
Gamma camera detects the gamma rays emitted from the iodine. More rays = more iodine = more activity.

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41
Q

What would be seen on radioisotope scan in Grave’s disease?

A

Diffuse high uptake.

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42
Q

Focal high uptake on radioisotope scan indicates what conditions?

A

Toxic multinodular goitre

Adenomas

43
Q

What would be seen on radioisotope scan in thyroid cancer?

A

Low uptake, called ‘cold areas’.

44
Q

What is the difference between hyperthyroidism and thyrotoxicosis?

A 
Hyperthyroidism = too much thyroid hormone being produced by the thyroid gland
Thyrotoxicosis = too much thyroid hormone in the body
45
Q

What are the causes of hyperthyroidism?

A

Primary:
Grave’s disease. AI, most common cause
Toxic multinodular goitre (Plummer’s disease) - nodules on thyroid act independently to produce thyroid hormones.
Solitary toxic thyroid nodule
Thyroiditis: De Quervain’s. Hasimoto’s, postpartum, drug-induced
Secondary: Hypothalamus/pituitary produce too much TSH

46
Q

How does hyperthyroidism present?

A 
Anxiety and irritability
Sweating and heat intolerance
Tachycardia
Weight loss
Fatigue
Frequent loose stools
Sexual dysfunction
Exophthalmos (Grave's) due to inflamation, swelling and hypertrophy of tissue behind the eyeball
Pretibial myxoedema (Grave's) - mucin under skin, looks waxy.
47
Q

Give 4 features unique to Grave’s disease.

A

Diffuse goitre (without nodules)
Graves eye disease
Bilateral exophthalmos
Pretibial myxoedema

48
Q

What would cause a goitre with firm nodules in patients over 50, and symptoms of thyrotoxicosis?

A

Toxic multinodular goitre - most common cause after Grave’s.

49
Q

What is the most common type of toxic thyroid nodule?

A

Benign adenoma. Treated with surgical removal

50
Q

What is De Quervain’s thyroiditis?

A

Viral infection with fever, neck pain and tenderness, dysphagia, and:
1. hyperthyroid phase
2. hypothyroid phase as the TSH level falls due to negative feedback.
Self-limiting condition
Rx: Supportive treatment with NSAIDs for pain and inflammation and beta-blockers for symptomatic relief of hyperthyroidism

51
Q

What is a thyroid storm?

A

Aka thyrotoxic crisis. Severe presentation of hyperthyroidism with pyrexia, tachycardia and delirium
Admit, monitor, may need supportive care with fluids, anti-arrythmics and beta blockers

52
Q

What is the first like medication for hyperthyroidism?

A

Carbimazole.

53
Q

How is hyperthyroidism managed?

A
  1. Carbimazole
    - Titration-block to normal levels
    - Block and replace with levothyroxine
    Usually stop taking by 18 months
  2. Propylthiouracil - slightly increased risk of hepatic reactions
  3. Radioactive iodine to destroy some thyroid cells.
  4. Beta blockers for relief of symptoms driven by adrenaline.
  5. Thyroidectomy/ removal of toxic nodules. Will need levothyroxine for life
54
Q

What can’t you do if you have radioactive iodine treatment?

A

Get pregnant within 6 months/be pregnant
Contact with children and pregnant women for 3 weeks
Contact with anyone for several days after dose

55
Q

What are the most common causes of primary hypothyroidism a) in the uk and b) globally?

A

a) Hashimoto’s thyroiditis

b) Iodine deficiency

56
Q

What is Hashimoto’s thyroiditis?

A

Autoimmune inflammation of thyroid gland.

57
Q

How does Hashimoto’s present?

A

Goitre followed by thyroid gland atrophy

58
Q

Give 5 iatrogenic causes of hypothyroidism.

A 
Treatments for hyperthyroid: 
Carbimazole
Propylthiouracil
Radioiodine
Thyroid surgery
Other:
Lithium
Amiodarone
59
Q

What is secondary hypothyroidism? Give 3 causes.

A

Pituitary gland not producing enough TSH (hypopituitarism). May be associated with lack of other pituitary hormones eg ACTH.
Causes: Tumours, Infection, Vascular (eg Sheehan syndrome), Radiation

60
Q

How does hypothyroidism present? (5 signs/symptoms)

A 
Weight gain
Fatigue
Dry skin
Coarse hair/hair loss
Fluid retention (oedema, effusions, ascites)
Heavy/irregular periods
Constipation
61
Q

How is hypothyroidism treated?

A

Levothyroxine (synthetic T4 which metabolises in the body to T3).
Titrate to TSH level - the higher the TSH, the more levothyroxine is needed.

62
Q

What is ideal blood glucose concentration?

A

4.4-6.1 mmol/l

63
Q

How does insulin reduce blood sugar?

A
  1. Causes cells to absorb glucose from blood and use it as fuel
  2. Causes muscle and liver cells to absorb glucose from blood and store it as glycogen.
    Without insulin, cells cannot take up glucose.
64
Q

How does glucagon increase blood sugar?

A
  1. Increases glycogenolysis in the liver (convert glycogen into glucose)
  2. Increases gluconeogenesis in the liver (converting proteins and fats into glucose)
65
Q

Which hormone is a catabolic hormone produced by alpha cells in the pancreas?

A

Glucagon

66
Q

Which hormone is an anabolic hormone produced by beta cells in the pancreas?

A

Insulin

67
Q

What is ketogenesis and what causes it?

A

Insufficient glucose/glycogen stores (eg fasting) –> liver converts fatty acids to ketones which can be used as fuel.

68
Q

When is ketosis dangerous?

A

Not in healthy fasting/dieting people because the acid is buffered.
However in T1 diabetes, hyperglycaemic ketosis causes metabolic acidosis which is life threatening.

69
Q

What is type 1 diabetes?

A

Type 1 diabetes mellitus (T1DM) is a disease where the pancreas stops being able to produce insulin. May be genetic, triggered by viruses such as the Coxsackie B virus and enterovirus. When there is no insulin being produced, the cells of the body cannot take glucose from the blood and use it for fuel. Therefore the cells think the body is being fasted and has no glucose supply. Meanwhile the level of glucose in the blood keeps rising, causing hyperglycaemia.

70
Q

What are the key complications of DKA?

A 
Hyperglycaemia
Dehydration
Ketosis
Potassium imbalance
metabolic acidosis
71
Q

How does DKA present?

A 
Polyuria
Polydipsia
Nausea and vomiting
Acetone smell to their breath
Dehydration and subsequent hypotension
Altered consciousness
Symptoms of an underlying trigger (i.e. sepsis)
72
Q

How is DKA managed?

A

F – Fluids – IV fluid resuscitation with normal saline (e.g. 1 litre stat, then 4 litres with added potassium over the next 12 hours)
I – Insulin – Add an insulin infusion (e.g. Actrapid at 0.1 Unit/kg/hour)
G – Glucose – Closely monitor blood glucose and add a dextrose infusion if below a certain level (e.g. 14 mmol/l)
P – Potassium – Closely monitor serum potassium (e.g. 4 hourly) and correct as required
I – Infection – Treat underlying triggers such as infection
C – Chart fluid balance
K – Ketones – Monitor blood ketones (or bicarbonate if ketone monitoring is unavailable)

73
Q

How is DKA managed acutely?

A

FIGPICK
F – Fluids – IV fluid resuscitation with normal saline (e.g. 1 litre stat, then 4 litres with added potassium over the next 12 hours)
I – Insulin – Add an insulin infusion (e.g. Actrapid at 0.1 Unit/kg/hour)
G – Glucose – Closely monitor blood glucose and add a dextrose infusion if below a certain level (e.g. 14 mmol/l)
P – Potassium – Closely monitor serum potassium (e.g. 4 hourly) and correct as required. No more than 10mmol/hr
I – Infection – Treat underlying triggers such as infection
C – Chart fluid balance
K – Ketones – Monitor blood ketones (or bicarbonate if ketone monitoring is unavailable)
Put them back on their normal insulin regime before stopping insulin

74
Q

How is type 1 diabetes managed?

A

Patient education
Monitoring of carb intake, blood sugar and complications
SC Insulin:
Usually a background long acting OD + short acting 30 mins before carb intake.

75
Q

What are the short term complications of T1DM

A

Hypoglycaemia

Hyperglycaemia and DKA

76
Q

How does hypoglycaemia present?

A

Typical symptoms are tremor, sweating, irritability, dizziness and pallor. More severe hypoglycaemia will lead to reduced consciousness, coma and death unless treated.

77
Q

How is hypoglycaemia managed?

A

Rapid acting glucose such as lucozade + slower acting carbohydrates such as biscuits and toast for when the rapid acting glucose is used up. Options for treating severe hypoglycaemia are IV dextrose and intramuscular glucagon.

78
Q

How is hyperglycaemia managed?

A

Insulin cautiously

Monitor for DKA - admit if meet criteria

79
Q

What are the long term complications of T1DM?

A
  1. Endothelial cell damage - macrovascular complications - CAD, peripheral ischemia, stroke, htn
    microvascular complications - Retinopathy
    Kidney disease, particularly glomerulosclerosis
    Infection Related Complications, peripheral neuropathy
  2. Immunosuppression
    Urinary Tract Infections
    Pneumonia
    Skin and soft tissue infections, particularly in the feet
    Fungal infections, particularly oral and vaginal candidiasis
80
Q

How is glucose monitored?

A
  1. HbA1c = glycated hb = how much glucose is attached to hb. Reflects glucose level over last 3 months (lifespan of RBCs).
  2. Capillary blood glucose. (sometimes called BM as that is the machine that used to be used)
  3. Flash glucose monitoring eg FreeStyle Libre - sensor on the skin, measures glucose level of the interstitial fluid, 5 min lag behind blood glucose.
81
Q

What is type 2 diabetes and how does it occur?

A

Repeated exposure to glucose and insulin causes insulin resistance. Beta cells of the pancreas increase insulin production, become fatigued/damaged and produce less glucose. Leads to chronic hyperglycaemia.

82
Q

Give 3 non-modifiable and 3 modifiable risk factors for type 2 diabetes.

A

Non-Modifiable
Older age
Ethnicity (Black, Chinese, South Asian)
Family history

Modifiable
Obesity
Sedentary lifestyles
High carbohydrate (particularly refined carbohydrate) diet

83
Q

How does type 2 diabetes present?

A 
Fatigue
Polydipsia and polyuria (thirsty and urinating a lot)
Unintentional weight loss
Opportunistic infections
Slow healing
Glucose in urine (on dipstick)
84
Q

What is an OGTT and how does it work?

A

Oral glucose tolerance test.
Baseline fasting plasma glucose –> 75g glucose drink –> measure plasma glucose 2 hours later. Tests ability to body to cope with carbs

85
Q

What is pre-diabetes and how is it defined?

A

High risk of diabetes.
HbA1C 42-47mmol/mol
Fasting glucose 6.1-6.9mmol/l
OGTT at 2 hours 7.8-11.1mmol/l

86
Q

How is diabetes diagnosed? Give cut-off values

A

HbA1c >48mmol/mol
Random glu >11
Fasting glu >7
OGTT at 2 hours >11

87
Q

What is the management for type 2 diabetes?

A

Curable eg with extreme low calorie diet
Conservative: diet - low glycaemic, high fibre, veg, oily fish; exercise, wt loss, smoking cessation, control comorbidities, monitor for complications.
Medical:
1. Metformin from 500mg OD
2. + Sulfonylurea/ pioglitazone/ DPP4i/ SGLT2i.
3. Triple therapy OR metformin + insulin

Target HbA1C 48mmol/mol or 53 if on more than just metformin

88
Q

How would you counsel a patient starting metformin? (ATHLETIC)

A

Action - Biaguanide, increases sensitivity of cells to insulin and decreases liver production of glucose –> allows body to make better use of lower insulin levels.
Time - OD with breakfast (may be BD)
How - Tablet with meals same time each day
Length - lifelong if it works
Effect - help move glucose from blood into cells
Tests - U+Es before starting then annually; HBA1c
Indications - diabetes, PCOS
Important SEs - nausea, diarrhoea, abdo pain, wt loss
CI - renal impairment, ketoacidosis, low BMI, within 3 days of general anaesthetic/contract (lactic acidosis)
Supplementary information:
If you miss a dose, take as soon as remember unless its close to next dose time.
Diabetes.org.uk

89
Q

Give 5 side effects of pioglitazone.

A 
Weight gain
Fluid retention
Anaemia
Heart failure
Extended use may increase the risk of bladder cancer
90
Q

Give 3 side effects of sulfonylureas and name a common sulfonylurea.

A

Gliclazide. Stimulates INSULIN release from pancreas
HYPOGLYCAEMIA
Wt gain
Increased risk CVD and MI

91
Q

How do incretins work?

A

Hormones secreted in response to large meals –> increase insulin secretion, inhibit glucagon production, slow GI absorption.
Main one is GLT-1.

92
Q

Give 3 side effects of DPP4 inhibitors and name the most common DPP4i.

A

Sitagliptin
SI tract upset
URTI symptoms
Pancreatitis

93
Q

How does exenatide work? Give 3 side effects.

A

GLP1 mimetic.
GI upset
Wt LOSS
dizziness

94
Q

Give 2 SGLT2 inhibitors and 3 side effects.

A

Empagliflozin, canagliflozin, dapagliflozin.
SGLT2 reabsorbs glucose from urine into blood in PT of kidney –> SGLT2i blocks this so more glucose EXCRETED –>
SEs - glucoseuria, UTIs, wt loss
DKA - more likely to be euglycaemic
Lower limb amputation more common in canagliflozin
Reduce risk of CVD and heart failure

95
Q

Give 2 rapid acting insulins. and give their timeline of action.

A

Start working around 10 mins, last 4 hours
Novorapid
Humalog
Apidra

96
Q

Give 2 short acting insulins and their timeline of action.

A

Start working in around 30 mins and last 8 hours
Actrapid
Humulin S
Insuman Rapid

97
Q

Give 2 intermediate acting insulins and their timeline of action.

A

Start working in 1 hour and last 16 hours
Insulatard
Humulin I
Insuman Basal

98
Q

Give 2 long acting insulins and their timeline of action.

A

Start working in 1 hour and last 24 hours
Lantus
Levemir
Degludec (40 hours)

99
Q

What is Humalog?

A

Combination insulin - rapid acting + intermediate acting.

Eg Humalog 25:75 = 25% rapid, 75% intermediate

100
Q

What is acromegaly?

A

Excessive growth hormone (GH) resulting in clinical symptoms and signs.

101
Q

Give 3 causes of acromegaly.

A

Usually due to pituitary adenoma but can be due to ectopic GH production by lung or pancreatic cancer.

102
Q

How does acromegaly present?

A

Excessive GH: frontal bossing, large nose, tongue (macroglossia), hands and feet, jaw (prognathism), arthritis
Organ dysfunction - cardiac hypertrophy, htn, T2dm, colorectal cancer
New skin tags, sweating
Pituitary adenoma - bitemporal hemianopia
SOL - headache

103
Q

How is acromegaly diagnosed? Give 3 investigations.

A

GH fluctuates so can’t just measure that once
IGF-1 raised
OGTT while measuring GH - high glucose usually suppresses GH
MRI brain for tumour
Formal visual field testing

104
Q

How is acromegaly managed?

A

Surgical: Pituitary adenoma –> trans-sphenoidal surgical removal; treat other cancer if ectopic
Medical (if cant operate):
SC pegvisomant (GH antagonist)
Somatostatin analogue eg ocreotide (somatostatin = GH inhibiting hormone)
Dopamine agonist eg bromocriptine

Phase 4 (11 decks)

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