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Endocrinology Flashcards

1
Q

What are the properties of peptide hormones? How do they work?

A
  • Made from short-chain amino acids (size is anything from few AAs to small protein)
  • Pre-made and stored in cell, released and dissolved into blood when needed
  • Large, hydrophilic, charged molecules - cannot diffuse through a plasma membrane
  • Bind to receptors on cell membranes, triggering a second messenger to be released within cell - very quick
  • Examples: Insulin, growth hormone, TSH, ADH
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2
Q

What are the properties of steroid hormones? How do they work?

A
  • Synthesised from cholesterol
  • Not stored in cell, released as soon as they are made
  • Not water soluble - must be bound to transport proteins to travel in blood
  • Lipid soluble - can cross plasma membrane and bind to receptor inside cell - slow response
  • Examples: Testosterone, oestrogen, cortisol

Pregnenolone is the precursor for all steroid hormones, and its formation represents the rate-limiting step of steroid synthesis. Conversion of cholesterol to pregnenolone takes place within mitochondria.

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3
Q

Tell me about catecholamine hormones (amino acid derived)

A
  • Synthesised from the amino acid tyrosine
  • Acts same way as peptide hormone
  • Large, hydrophilic, charged molecules - cannot diffuse through a plasma membrane, so released via exocytosis
  • Examples: Adrenaline, dopamine
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4
Q

What are the cell types and their functions within the islets of langerhans in the pancreas?

A

Alpha cells - produce glucagon

Beta cells - produce insulin and amylin

Delta/D cells - produce somatostatin

PP cells - produce pancreatic polypeptide

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5
Q

What are the classes of hormones?

A
  • Steroids
  • Peptides
  • Thyroid hormones
  • Catecholamines
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6
Q

Tell me about thyroid hormones

A
  • Released via proteolysis
  • T3 = triiodothyronine, T4 = thyroxine
  • Take a day to act
  • In blood bound to thyroglobulin binding protein (produced by liver)
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7
Q

What is the blood supply to the thyroid gland?

A
  • Superior thyroid artery - off thyrocervical trunk (subclavian)
  • Inferior thyroid artery - off external carotid artery
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8
Q

Where are the thyroid and parathyroid glands located?

A
  • Thyroid gland sits at C5-T1
  • Two lobes connected by an isthmus
  • Parathyroid is 4 glands on the posterior surface of thyroid glands
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9
Q

What effect does parathyroid hormone have on the kidneys?

A
  • Increased conversion of 25-hydroxyvitamin D (inactive) to 1,25-dihydroxyvitamin D(active)
  • At the DCT: Increased Ca2+ reuptake and PO43- excretion
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10
Q

What effect does parathyroid hormone have on the gut?

A

Increased Ca2+ and PO43- absoroption

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11
Q

What hormones does the adrenal gland produce?

A

Adrenal cortex:
- Zona glomerulosa - mineralocorticoids (eg: aldosterone)
- Zona fasciculata - glucocorticoids (eg: cortisol)
- Zona reticularis - adrenal androgens

Adrenal medulla:
- Catecholamines (eg: adrenaline)

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12
Q

Draw out the process of phosphate regulation physiology

A

increased PTH:

increased phosphate—> increased FGF-23 (osteocyte)—-> less 25 dihydroxy vit D—> less inorganic phosphate absorption—-> less phosphate

increased FGF-23 then completes cycle above

Less inorganic phosphate absorption directly

PHEX leads to less phosphate

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13
Q

What can pituitary tumours do?

A
  • Press local structures - eg: optic chiasm -> bitemporal hemianopia
  • Hypopituitarism
  • Hyperpituitarism - acromegaly, Cushing’s disease, prolactinoma
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14
Q

Hormones secreted by the hypothalamus and what they stimulate from the anterior pituitary

A
  • GnRH -> FSH and LH
  • CRH -> ACTH
  • GHRH -> GH
  • TRH -> TSH
  • DA -> inhibits Prolactin
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15
Q

What is always given to unresponsive hypoglcyemic patients?

A

IM glucagon

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16
Q

Role of insulin

A
  • Increase peripheral glucose uptake
  • Glucose -> glycogen
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17
Q

Biphasic release of insulin

A
  1. Glucose binds to GLUT2 receptors of pancreas on b cells, stimulating insulin release
  2. Insulin binds to peripheral insulin receptors:
    - Activates intracellular tyrosine kinases + cascade
    - Increase of Glut-4 channel expression on CSM
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18
Q

Posterior pituitary hormones

A
  • Oxytocin (paracentricular nucleus) - milk ejection + labour induction
  • Vasopressin (supraorbital nucleus) = adh
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19
Q

What does vasopressin do?

A
  • Vasoconstricts blood vessels
  • Increased APO II (aquaporin) expression in collecting duct
  • Increased aldosterone
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20
Q

Functions of cortisol

A
  • Increases protein and carb breakdown
  • Upregulates alpha 1 receptors on arterioles -> increased BP
  • Suppresses immune response
  • Increased osteoclast activity (osteoporotic)
  • Increased insulin resistance
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21
Q

GH/IGF-I axis

A

increased GHRH + decreased SMS - from hypothalamus

Leads to pituitary releasing GH

Liver then releases IGF -I which reduces hypothalamus releases of GHRH and SMS

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22
Q

Insulin secretion by the beta cell

A
  • Glucose enters via GLUT2 transporter
  • K+ channels close and depolarise cell membrane
  • Calcium channels open and Ca2+ enters cell and stimulates insulin secretory granules
  • Insulin secreted
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23
Q

Insulin action in muscle and fat cells

A
  • Insulin enters via insulin receptors
  • Intracellular signalling cascades cause GLUT4 vesicles to integrate into plasma membrane
  • Glucose enters cell via GLUT4 transporter
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24
Q

Alpha vs beta islet of Langerhans cells

A

Alpha cells: glucagon
- Increases hepatic glucose by increasing glycogenolysis and gluconeogenesis
- Stimulates lipolysis and muscle breakdown
- Reduces peripheral glucose output
Beta cells: insulin
- Suppresses hepatic glucose by decreasing glycogenolysis and gluconeogenesis
- Suppresses lipolysis and breakdown of muscle
- Increases glucose uptake into insulin sensitive tissues

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25
Q

Thyroid axis

A

Hypothalamus releases TRH, pituitary releases TSH then thyroid releases T4 & T3 which has a neg response on TRH and TSH.

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26
Q

Physiology of thyroid hormone production

A
  • Iodine diffuses from follicular thyroid cells into the colloid (fatty empty space inbetween follicular cells)
  • Iodine binds to tyrosine residues on molecule thyroglobulin
  • Cleaved from long chains to form T3 or T4(active)
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27
Q

Physiology of thyroid hormone release-what hypothalamas nucleus?

A
  • Supraventricular nucleus of hypothalamus releases TRH
  • TSH released from thyrotrophs in anterior pituitary
  • Binds to TSH-receptors on thyroid
  • Causes T3/T4 to diffuse from colloid to follicular cells then to the bloodstream
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28
Q

PTH regulation

A
  • Tightly regulated by body Ca2+ to prevent hyper/hypocalcaemia
  • Directly inhibited by calcitonin - from parafollicular C cells fo the thyroid
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29
Q

Testing gonadal axis: men

A
  • Low testosterone, high LH/FSH: Primary hypogonadism
  • Low testosterone, normal/low LH/FSH: Hypopituitarism
  • Low testosterone and low LH: Anabolic use

Measure 9hr fasted testosterone (morning) and LH/FSH in pituitary disease

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30
Q

Testing gonadal axis: women

A
  • Low oestradiol, high LH and FSH (FSH greater) = Primary ovarian failure
  • Low oestradiol, normal/low LH and FSH, oligo/amenorrhoea = Hypopituitarism
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31
Q

Normal gonadal levels in women

A

Before puberty:
- Low oestradiol
- Low LH/FSH
Puberty:
- Increased oestradiol
- Increased pulsatile LH
Post menarche:
- Monthly menstrual cycle with LH/FSH
- Mid-cycle surge in LH and FSH
- Levels of oestradiol increases through cycle

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32
Q

What does the pituitary gland control?

A
  • Thyroid
  • Adrenal cortex
  • Testis
  • Ovary

Not the adrenal medulla

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33
Q

What hormones have a circadian rhythm

A
  • Cortisol
  • Testosterone
  • DHEA
  • 17OH Progesterone

Not T4

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34
Q

Which hormones suppress appetite?

A
  • Peptide YY
  • CCK
  • GLP 1
  • Glucose
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35
Q

What is the main adipose signal to the brain?

A

Leptin

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36
Q

Typical features of hypogonadism in males

A
  • Joint and muscular aches
  • Decreased sexual appetite
  • Decreased hair growth
  • Asymptomatic
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37
Q

What is satiety?

A

The physiological feeling of no hunger

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38
Q

What does ghrelin do?

A

Stimulates hunger

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39
Q

What do long term corticosteroid medications lead to?

A
  • Suppression of the adrenal glands
  • Long term atrophy of the adrenal glands - can’t produce enough corticosteroids
  • Adrenal insufficiency if medication is stopped
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40
Q

Differential diagnoses for presentation of polyuria and polydipsia

A
  • Diabetes mellitus
  • Diabetes insipidus
  • SIAD - Syndrome of Inappropriate Antidiuretic Hormone Secretion.
  • Primary polydipsia
  • Hypercalcaemia
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41
Q

Side effects of dopamine agonists such as bromocriptine

A

Impulsiveness, so can lead to addictions

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42
Q

Link between acromegaly and prolactinoma

A

50% of acromegaly tumours are associated with prolactinoma

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43
Q

Primary adrenal insufficiency

A
  • Addison’s disease
  • Pathology is at the adrenal glands
  • Decreased producion of adrenocortical hormones (cortisol and aldosterone)
  • High ACTH, low adrenocortical hormones
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44
Q

Secondary adrenal insufficiency

A
  • Pathology is in the pituitary
  • Inadequate ACTH released from pituitary
  • Leading to low release of adrenocortical hormones from the adrenal gland
  • Low ACTH, low adrenocortical hormones
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45
Q

Why do patients with primary adrenal sufficiency present with bronzed skin?

A

High ACTH stimulates melanocytes, resulting in hyperpigmentation

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46
Q

Aetiology of primary adrenal insufficiency

A
  • Developed world: Autoimmune adrenal destruction (21-hydroxylase present in 60-90% of people)
  • Developing world: TB (+ sarcoidosis)
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47
Q

Risk factors for adrenal insufficiency

A
  • Female
  • Adrenocortical antibodies
  • Other autoimmune disease
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48
Q

Other causes of adrenal insufficiency

A
  • Adrenal metastasis (lung, liver, breast)
  • Adrenal haemorrhage (eg: meningococcal septicaemia)
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49
Q

Symptoms of adrenal insufficiency

A
  • Weight loss
  • Nausea and vomiting
  • Lethargy and generalised weakness
  • Salt cravings
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50
Q

Signs of adrenal insufficiency

A
  • Bronze hyperpigmented skin, particularly in palms (only in Addison’s)
  • Postural hypotension
  • Hypoglycaemia
  • Change in body hair distribution - Loss of pubic hair in women
  • Associated autoimmune condition
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51
Q

Signs of adrenal crisis

A
  • Hyponatraemia
  • Hyperkalaemia
  • Profound fatigue
  • Dehydration
  • Vascular collapse (low BP)
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52
Q

Treatment of Addisonian/adrenal crisis

A
  • Immediate 100mg hydrocortisone
  • IV solve + dextrose (if hypoglycaemia)
  • Without cortisol, you will die from adrenal crisis if you have an infection
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53
Q

Diagnosis of adrenal insufficiency

A
  • First line: 8-9am cortisol
  • Gold standard: ACTH stimulation test (short Synacthen test)

RESULTS
- Low cortisol, high ACTH, poor response to synacthen = Primary adrenal insufficiency
- Low cortisol, low/normal ACTH, poor response to synacthen = Secondary adrenal insufficiency OR hypopituitarism

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54
Q

Other investigations for adrenal insufficiency

A
  • U+E to test for hyponatraemia and hyperkalaemia
  • Aldosterone:renin ratio
  • Adrenal CT or MRI
  • Test bloods for 21-hydroxylase adrenal antibodies
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55
Q

Treatment for Adrenal insufficiency

A
  • Hydrocortisone - glucocorticoid to replace cortisol
  • Fludrocortisone - mineralocorticioid to replace aldosterone if necessary
  • Double the dose of hydrocortisone in trauma/infection
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56
Q

Tertiary adrenal insuffiiency

A
  • Caused by inadequate CRH released by the hypothalamus
  • Usually a result of long term oral steroids
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57
Q

Complications of adrenal insufficiency

A
  • Addisonian crisis (experiences by 40% of patients) - life-threatening situation that results in low blood pressure, low blood levels of sugar and high blood levels of potassium.
  • Cushing’s syndrome
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58
Q

What are carcinoid tumours?

A
  • Poorly malignant tumours of enterochromaffin cells which produce 5-HT/serotonin
  • Mostly in the GI tract at the appendix and terminal ileum
  • Can also be in the lungs
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59
Q

Carcinoid tumours vs syndrome

A
  • Tumours - only the neoplastic cell, no/v little symptoms
  • Syndrome - when tumour metastasises to the liver
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60
Q

Presentation of carcinoid syndrome

A
  • Diarrhoea
  • Flushing
  • Tricuspid incompetence (valve lesion)
  • Right upper quadrant pain- hepatic metasteses.
  • Bronchospasm
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61
Q

What does carcinoid syndrome tend to express?

A

Somatostatin receptors

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62
Q

Diagnosis of carcinoid syndrome

A
  • High volume of 5-hydroxyindoleacetic acid (breakdown of serotonin) in urine
  • Metabolic panel and LFTs
  • Liver ultrasound to confirm metastases
  • CT/MRI to locate primary tumour
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63
Q

Treatment for carcinoid syndrome

A
  • Surgically excise primary tumour
  • Peri-operative ocreotide (SST analogue) infusion to block tumour hormones
  • For metastases: above + radiofrequency ablation
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64
Q

Carcinoid crisis treatment

A
  • Life threatening
  • Treated with high dose SST analogue (octeotride)
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65
Q

Symptoms of HHS

A
  • Generalised weakness and leg cramps
  • Confusion, lethargy, hallucinations, headaches
  • Visual disturbance
  • Polyuria and polydipsia
  • Nausea, vomiting and abdo pain (more common in DKA)

Hyperosmolar hyperglycemic syndrome (HHS) is a clinical condition that arises from a complication of diabetes mellitus.

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66
Q

Epidemiology of HHS

A
  • Less than 1% of diabetes admissions
  • 5-15% mortality

Risk factors:
- Infection
- MI
- Poor medication compliance

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67
Q

Pathophysiology of HHS

A
  • Rise in counter-regulatory hormones (glucagon, Ad, cortisol, GH)
  • Causes hyperglycaemia ans hyperosmolality
  • Electrolytes in blood overflow into urine -> excessive loss of water and electrolytes
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68
Q

Characteristics of HHS

A
  • Marked hyperglycaemia
  • Hyperosmolality
  • Profound dehydration
  • Electrolyte abnormalities
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69
Q

Diagnosis of HHS

A

Diagnostic:
- Hyperglycaemia ≥30mmol/L without a metabolic acidosis or significant ketonaemia
- Hyperosmolality ≥320mOsmol/kg
- Hypovolaemia

Other tests:
- Urine dipstick: heavy glycosuria
- U+E: low total body K+, high serum K+

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70
Q

How can HHS be differentiated from Diabetic ketoacidosis?

A

DKA
- T1DM
- Patients younger and leaner
- Ketoacidosis
- Develops over hours to a day
HHS
- T2DM
- No ketoacidosis
- Significantly higher mortality rate
- Develops over a longer time - days to a week

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71
Q

Treatment of HHS

A
  • IV fluid 0.9% saline
  • IV insulin only if there is ketonaemia or IV fluids aren’t working
  • LMWH to anticoagulate patient as they have thicker blood
  • Electrolyte loss (K+)
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72
Q

What are complications of HHS treatment with insulin?

A
  • Insulin-related hypoglycaemia
  • Hypokalaemia
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73
Q

Signs of HHS

A
  • Reduced GCS
  • Dehydration
  • Hemiparesis (can be confused for a stroke)
  • Seizures
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74
Q

Why is there no acidosis in HHS?

A
  • Small amounts of circulating insulin in T2DM
  • So lipolysis doesn’t occur
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75
Q

Complications of HHS

A
  • Cardiovascular - venous thromboembolism, arrhythmias, MI
  • Neuro - stroke and seizures
  • AKI
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76
Q

Causes of hypoglycaemia

A
  • Diabetic drugs: sulfonylureas or insulin
  • Non diabetic: oral, liver failure, Addison’s, increasing age
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77
Q

Symptoms of hypoglycaemia on the brain

A
  • Cognitive dysfunction
  • Blackouts
  • Seizures
  • Comas
  • Psychological effects
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78
Q

Treatment for hypoglycaemia

A

If not serious, food to release blood sugars

  • IV glucose or oral glucose gel
  • If no access, IM glucagon (only if alpha cells are working)
  • Check Blood sugar after 5 mins and if it’s increased give food
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79
Q

Symptoms of hypoglycaemia on the heart

A
  • Increased risk of MI
  • Cardiac arrhythmias
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80
Q

Symptoms of hypoglycaemia on the musculoskeletal system

A
  • Falls
  • Accidents (inc. driving)
  • Fractures
  • Dislocations
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81
Q

Symptoms of hypoglycaemia on circulation

A
  • Inflammation
  • Blood coagulation abnormalities
  • Haemodynamic changes
  • Endothelial dysfunction
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82
Q

Blood glucose of patient with hypoglycaemia

A

<3.5mmol/L

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83
Q

Epidemiology of Diabetic Ketoacidosis

A

4% of T1DM patients develop each year

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84
Q

Risk factors for DKA

A
  • Poorly managed/undiagnosed T1DM
  • Infection/illness
  • Characteristic in patients around 20 years old
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85
Q

Pathophysiology of DKA

A
  • Absolute immune deficiency = unrestrained lipolysis and gluconeogenesis and decreased peripheral glucose uptake
  • Not all glucose from gluconeogenesis is usable so converted to ketone bodies, which is acidic
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86
Q

Describe Kussmaul’s breathing

A

Deep and rapid breathing in acidosis to expel acidic carbon dioxide

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87
Q

Signs of DKA

A
  • Kussmaul’s breathing
  • Pear drop breath
  • Reduced tissue turgar (hypotension + tachycardia)
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88
Q

How to investigate DKA

A
  • Ketones > 3mmol/L
  • RPG > 11.1mmol/L (hyperglycemic)
  • pH < 7.3 or HCO3- < 15mmol
  • Urine dipstick glyosuria/ketonuria
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89
Q

What are common differentials of DKA?

A
  • HHS
  • Lactic acidosis - identical presentation, normal serum glucose and ketones
  • Starvation ketosis - physiologically appropriate lipolysis
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90
Q

Treatment for DKA (in order)

A
  • ABCDE
  • IV fluids FIRST 0.9% saline
  • IV insulin 0.1units/kg/hour - once glucose level <14mmol add 10% glucose
  • Restore electrolytes, eg: K+
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91
Q

Complications of DKA

A
  • Coma
  • Cerebral oedema
  • Thromboembolism
  • Aspiration pneumonia
  • Death
  • Dehydration
  • MI
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92
Q

Symptoms of DKA

A
  • Nausea and vomiting
  • Weight loss
  • Drowsy/confused
  • Abdominal pain
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93
Q

Define T1DM

A

Absolute insulin deficiency, usually resulting from autoimmune destruction of the insulin-producing beta islet cells in the pancreas
- Type 4 hypersensitivity

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94
Q

Which genes are linked with increased risk of developing T1DM?

A

HLA-DR2 and HLA-DQ3
or
HLA-DR4 and HLA-DQ8

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95
Q

Environmental factors that can increase the risk of developing T1DM

A
  • Diet
  • Vitamin D deficiency
  • Early-life exposure to viruses associated with islet inflammation (eg: enteroviruses)
  • Decreased gut-microbiome diversity
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96
Q

Epidemiology of T1DM

A
  • Young (usually between 5-15 years)
  • Lean
  • North European descent
  • 10% of diabetes is type 1
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97
Q

Macrovascular complications of T1DM

A

Atherosclerosis, which leads to:
- CVD
- Stroke
- Peripheral arterial disease

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98
Q

Microvascular complications of T1DM

A
  • Nephropathy
  • Retinopathy -> glaucoma, cataracts
  • Neuropathy -> diabetic foot disease
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99
Q

Other autoimmune conditions that can result from T1DM (most to least common)

A
  • Thyroid disease
  • Autoimmune gastritis
  • Pernicious anemia
  • Coeliac diease
  • Vitiligo
  • Addison’s disease
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100
Q

Psychological complications of T1DM

A
  • Anxiety
  • Depression
  • Eating disorders
    Also in children:
  • Behavioural and conduct disorders
  • Family/relationship difficulties
  • Risk-taking behaviour
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101
Q

Signs of T1DM

A
  • BMI < 25kg/m2
  • Failure to thrive in children
  • Glove and stocking sensory loss
  • Reduced visual acuity
  • Diabetic retinopathy
  • Diabetic foot disease
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102
Q

Symptoms of T1DM

A
  • Polyuria
  • Polydipsia
  • Weigt loss
  • Lethargy
  • Recurrent infections
  • Evidence of complications - eg: blurred vision or parasthesia
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103
Q

At what level of blood glucose can it no longer be absorbed?

A

10mmol/L

Thirsty and develop polyuria - body attempts to remove excess glucose

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104
Q

At what level of Beta cell destruction does hyperglycaemia develop?

A

80-90%

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105
Q

Diagnosis of T1DM

A

Random blood glucose ≥11mmol/L
Fasting blood glucose ≥7mmol/L

  • One abnormal value diagnostic in symptomatic patients
  • Two abnormal values diagnostic in asymptomatic patients
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106
Q

What is the most accurate test for T1DM?

A

HbA1C - measures glycated haemoglobin

> 48 mmol/mol or >6.5% suggest hyperglycaemia over 3 months

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107
Q

Optimal targets for glucose self monitoring

A
  • FBG: 5-7mmol/L on waking
  • Plasma glucose 4-7mmol/L before meals at other times of the day
  • If testing after meals: 5-9mmol/L at least 90 minutes after
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108
Q

How can T1DM be differentiated from Latent Autoimmine Diabetes in Adults (LADA)?

A
  • In LADA age of onset is >30 yrs
  • Low to normal C-peptide
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109
Q

How can T1DM be differentiated from Neonatal diabetes?

A

In neonatal diabetes:
Genetic testing shows mutation in genes coding ATP K+ channel and insulin gene

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110
Q

How can T1DM be differentiated from Monogenic diabetes?

A

In monogenic diabetes:
- C-peptide present
- Autoantibodies absent

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111
Q

First line treatment for T1DM

A

Basal-Bollus regimen

Basal - Long acting (either given twice or once daily)
Bollus - Short before meals

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112
Q

Pathophysiology of T1DM

A
  • Beta islet cell destruction
  • Hyperglycemia
  • Low cellular glucose (increased lypolysis and gluconeogenesis)
  • Hyperkalemia even though there is a low body K+ (enters cells via Na+/K+ ATPases)
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113
Q

NICE diagnostic criteria for T1DM

A
  • Clinical features and evidence of hyperglycaemia
  • Ketosis
  • Rapid weight loss
  • < 50 years
  • BMI < 25 kg/m2
  • Personal and/or family history of autoimmune disease
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114
Q

Other treatments for T1DM after basal-bollus

A
  • Mixed insulin regimen
  • Continuous insulin infusion
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115
Q

Mixed insulin regimen

A
  • A mixture of short or rapid acting and intermediate-acting insulin
  • Twice daily
  • For those who can’t tolerate multiple injections for basal bollus
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116
Q

Continuous insulin infusion

A
  • If patient has disabling hypoglycaemia
  • or persistently hyperglycaemic (HbA1c > 69mmol/mol) on multiple injection insulin therapy
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117
Q

Pathophysiology of T2DM

A
  • Peripheral insulin resistance with partial insulin deficiency
  • Decreased GLUT4 expression - impaired insulin secretion
  • Lipid and beta amyloid deposits in pancreas, progressive b cell damage
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118
Q

Epidemiology of T2DM

A
  • Presents later on in life (usually 30+ years)
  • Males > females
  • People of Asian, African and Afro-Carribean ethnicity are 2-4x more likely to develop T2DM than white people
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119
Q

Clinical presentation of T2DM

A
  • Obese hypertensive older patient
  • Polydipsia
  • Nocturia
  • Polyuria
  • Glycosuria
  • Recurrent thrush
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120
Q

Diagnosis of T2DM

A
  • Same as T1DM
  • fbg and random
  • Prediabetes exists this time
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121
Q

Risk factors for T2DM

A
  • Genetic link (stronger than T1DM)
  • Obesity
  • Alcohol excess
  • Hypertension
  • Gestational diabetes
  • PCOS
  • Drugs: corticosteroids, thiazides
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122
Q

Last line of treatment for T2DM if all else fails

A

Insulin treatment

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123
Q

Treatment for T2DM

A

Initial: Biguanide (metformin)

Second line: Carry on Metformin and add either:
- DPP-4 inhibitor
- Pioglitazone
- Sulfonylurea
- SGLT-2 inhibitor

124
Q

Prediabetic states

A

FBG: 6.1-6.9
2nd post prandial: 7.8-11.0
HbA1c: 42-47 (6.0-6.4%)

125
Q

First treatment for Type 2 diabetes and prediabetes before drugs

A

Lifestyle change - diet, exercise, modify RFs

126
Q

Main complication of T2DM

A

Hyperosmolar hyperglycaemic state

127
Q

Types of Insulin

A
  • Rapid: aspart, lisporo, novorapid, glulisine
  • Short: regular insulin
  • Intermediate: NPH (half a day)
  • Long: detemir, lantus, glargine
128
Q

How can you get ketoacidosis in T2DM?

A
  • Happens later on in the disease
  • Because initially, micro secretions of insulin are sometimes still present, inhibiting glucagon
129
Q

Why are thiazolidinediones (pioglitazone) not commonly given as a diabetic drug?

A
  • Increase weight
  • Increase risk of heart failure
  • Increase risk of fractures
130
Q

Advantages of basal insulin in T2DM

A
  • Patient adjusts insulin themselves, based on fasting glucose measurements
  • Carries on with oral therapy, combination therapy is common
  • Less risk of hypoglycaemia at night
131
Q

Advantages of premixed insulin in diabetes

A
  • Both basal and prandial together
  • Can cover insulin requirements though most of the day
132
Q

Disadvantages of pre-mixed insulin

A
  • Requires consistent meal and exercise pattern
  • Cannot seperately titrate individual insulin components
  • Increased risk of nocturnal and fasting hypoglycaemia
133
Q

Disadvantages of basal insulin in T2DM

A
  • Doesn’t cover meals
  • Best used with long-acting insulin analogues (expensive)
134
Q

Signs of T2DM

A
  • Acanthosis nigricans
  • Glove and stocking sensory loss
  • Diabetic retinopathy
  • Diabetic foot disease
135
Q

Side effects of other diabetic medication

A
  • SGLT-2 inhibitor - genitourinary infections
  • GLP-1 analogue - weight loss
  • Thiazide diuretics - weight gain
136
Q

Two types of diabetes insipidus

A
  • Cranial - Low ADH secretion
  • Nephrogenic - Low response to ADH
137
Q

Aetiology of cranial diabetes insipidus

A
  • ADH gene mutation
  • Pituitary adenomas
  • Brain infections
  • Idiopathic
138
Q

Aetiology of nephrogenic diabetes insipidus

A
  • Renal tubular acidosis
  • ADH-R mutation
  • Drugs (lithium)
  • Electrolyte disturbance
139
Q

Presentation of diabetes insipidus

A
  • Polyuria
  • Polydipsia
  • Hypernatremia
  • Lethargy confusion coma
  • Severe dehydration
140
Q

How much urine a day will make you suspect diabetes insipidus?

A

Over 3L

141
Q

Water deprivation test for diabetes insipidus

A
  • No fluid for 8 hours
  • Normally serum osmolality stays normal, urine osmolality increase
  • DI = serum osmolality rises while urine osmolality unchanged
142
Q

Desmopressin test for diabetes insipidus

A

Cranial urine osmolality:
After deprivation: Low
After desmopressin: High
Nephrogenic urine osmolality:
After deprivation: Low
After desmopressin: Low
Primary polydipsia
After deprivation: High
After ADH: High

143
Q

Treatment for diabetes insipidus

A

Cranial - Desmopressin
Nephrogenic - Thiazides (+ treat underlying cause)

144
Q

High and low values for urine osmolality

A

< 300 = low
>800 = high

145
Q

Aetiology of hypercalcaemia (90% of cases)

A

90%:
- Hyperparathyroidism
- Malignancy: bone mets, myeloma, PTHrP, lymphoma

146
Q

ECG in hypercalcaemia

A

Short QTc

147
Q

Symptoms of hypercalcaemia and hyperparathyroidism

A
  • Bones - excess resorption, ostopoenia
  • Stones - kidney
  • Groans - abdominal pain, constipation
  • Psychedelic moans - confusion, depression, anxiety
  • Thrones - polyuria and polydipsia
148
Q

How does hypercalcaemia affect muscles

A

Low muscle tone and contractions as Ca2+ inhibits fast Na+ influx

149
Q

What happens to PTH in hypercalcaemia

A

It will decrease due to negative feedback
(except in hyperparathyroidism)

150
Q

Other causes of hypercalcaemia (other than top 90%)

A
  • Multiple myeloma
  • Granulomatous diseases (eg: TB and sarcoidosis)
  • Dehydration
  • Drugs
151
Q

Drugs that can cause hypercalcaemia

A
  • Thazides
  • Diuretics
  • Lithium
  • Excessive Vit D or A intake
152
Q

Treatment of hypercalcaemia

A
  • Aggressive IV fluids
  • Consider IV bisphosphonates if no response
  • Treat underlying cause
153
Q

Definition of hyperkalaemia and hypokalaemia

A

Hyper ≥ 5mmol/L
Emergency hyper = ≥ 6.5mmol/L
Hypo < 3.5mmol/L

154
Q

Presentation of hyperkalaemia

A
  • Muscle weakness and cramps
  • Parasthesia
  • Palpitations
  • Tachycardia (arrhythmias)
155
Q

Aetiology of hyperkalaemia

A

Increased intake of potassium

  • IV therapy
  • Increased dietary intake

Decreased excretion of potassium

  • AKI and CKD
  • Drugs (NSAIDs, spironolactone, ACE inhibitors)
  • Renal tubular acidosis (T4)
  • Addison’s disease

Potassium shifted to extracellular

  • Metabolic acidosis/DKA
  • Rhabdomyolysis

Other: trauma and burns

156
Q

Effect of hyperkalaemia on types of muscle

A
  • Smooth muscle cramping
  • Skeletal mucle weakness due to overcontraction
  • Cardiac arrythmias and arrest
157
Q

Effect of hyperkalaemia on Insulin, pH and Beta 2 receptors

A
  • Insulin deficiency as not enough K+ flows into the cell
  • Acidosis (H+ in and K+ out)
  • Beta blocker - inhibits pumping of K+ into cell
158
Q

Complications of hyperkalaemia + ecg

A

Cardiac arrhythmias and arrest
- Hyperkalaemia is associated with broadening QRS complex

159
Q

Pathophysiology of hyperkalaemia

A
  • High K+ decreases action potential
  • Easier depolarisation
  • Abnormal heart rhythms
160
Q

Diagnosis of hyperkalaemia

A
  • High K+ on U+Es
    ECG:
  • Absent P waves
  • Prolonged PR
  • Tall tented T waves
  • Wide QRS
  • Bradycardia
161
Q

Treatment for hyperkalaemia

A

If urgent: Calcium gluconate to stabilise cardiac membrane if there are heart problems, then insulin dextrose
Non-urgent: Insulin (+dextrose)

162
Q

Aetiology of hypocalcaemia

A
  • CKD (due to decreased Vit D activation)
  • Severe Vit D deficiency
  • Primary hypoparathyroidism
  • Acute pancreatitis
163
Q

Symptoms of hypocalcaemia and hypoparathyroidism

A

Parasthesia
- Tetany (involuntary muscle contractions)
- Chvostek sign -face twitch
- Trousseau sign - forearm wrist twitch

164
Q

How does hypocalcaemia affect muscle?

A

Muscle spasms: hands, feet, larynx, premature labour

165
Q

How does hypocalcaemia affect PTH?

A
  • Always increases
  • Except in hypoparathyroidism
166
Q

How to calculate corrected calcium levels

A

total serum calcium + (0.02* (40-serum albumin))

167
Q

Why may serum calcium levels be inaccurate?

A
  • Low serum albumin causes a low total serum calcium
  • But this is not a low ionised calcium
  • Need to do corrected calcium equation
168
Q

Drugs that can cause hypocalcaemia

A
  • Bisphosphonates
  • Phenytoin
  • Loop diuretics
  • Cinacalcet
169
Q

Treatment of hypocalcaemia

A
  • Oral calcium replacement or IV calcium gluconate
  • Treat the cause
170
Q

ECG in hypocalcaemia

A

Longer QTc and ST segment

171
Q

Presentation of hypokalaemia

A
  • Hypotonia
  • Hyporeflexia
  • Arrhythmias (especially AF)
  • Muscle paralysis and rhabdomyolysis
172
Q

Aetiology of hypokalaemia

A

Decreased intake of potassium

Increased excretion of potassium

  • Thiazides + loop diuretics
  • Renal disease
  • GI loss
  • Increased aldosterone (Conn’s syndrome)

Potassium shifted to intracellular

  • Insulin
  • Salbutamol
  • (other drugs)
173
Q

Treatment for hypokalaemia

A
  • K+ replacement
  • Aldosterone antagonist (spironolactone)
  • Treat underlying cause
  • Other electrolyte defficiencies
174
Q

Diagnosis of hypokalaemia

A
  • Low K+ in U+E
    ECG:
  • Small inverted T waves
  • Prominent U waves
  • ST depression
  • PR prolongation
175
Q

Effect of hypokalaemia on types of muscle

A
  • Smooth muscle constipation
  • Skeletal muscle weakness and cramps
  • Cardiac arrythmias and palpitations
176
Q

Effect of hypokalaemia on insulin, pH and beta 2 receptors

A
  • Excess insulin as too much K+ flows into cell
  • Alkalosis (H+ out and K+ in)
  • B2 agonist - Increase B2 pumping of K+ into cell
177
Q

Aetiology of hyperaldosteronism

A

2/3 - Adrenal adenoma (Conn’s)
1/3 - Bilateral adrenal hyperplasia

Also (rare):
- Familial hyperaldosteronism type 1 and 2
- Adrenal carcinoma

178
Q

Secondary hyperaldosteronism

A

Excessive renin stimulates the adrenal glands to produce more aldosterone

Causes:
- Renovascular disease
- Renin-secreting tumour

179
Q

Pathophysiology of hyperaldosteronism

A
  • Excess aldosterone(😱)
  • Increased sodium and water reabsorption and potassium excretion in kidneys
  • Hypertension and hypokalaemia
180
Q

Symptoms of hyperaldosteronism

A
  • Resistant hypertension (unfixable with ACE inhibitors or beta blockers)
  • Hypokalaemia (lethargy mood disturbance, parasthesia, muscle cramps)
  • Polydipsia + polyuria
181
Q

Diagnosis of hyperaldosteronism

A

1st line: Aldosterone:renin ratio
High ratio = Primary (do CT)
Low rato = Secondary

Diagnostic: High serum aldosterone not suppressed with 0.9% IV saline or fludrocortisone

Also: Hypokalaemic on U+E and ECG

182
Q

Treatment of hyperaldosteronism

A
  • Single benign adrenal tumour -> unilateral adrenalectomy
  • Bilateral adrenal hyperplasia -> Aldosterone antagonist (spironolactone)
183
Q

How to determine if hyperaldosteronism is unilateral or bilateral

A

Adrenal venous sampling
- Measures the amount of corticosteroid secreted from each adrenal gland

184
Q

Primary hyperparathyroidism

A
  • Usually caused by a parathyroid adenoma
  • Causes hypercalcaemia
185
Q

Secondary hyperparathyroidism

A
  • Caused by parathyroid hyperplasia
  • Secondary to CKD + Vit D deficiency
186
Q

Tertiary hyperparathyroidism

A
  • After many years of secondary
  • Most common cause is CKD
  • Glands act autonomously and release PTH regardless of Ca conc.
187
Q

Malignant causes of hyperparathyroidism

A
  • Neoplasms
  • (Squamous cell lung cancer, breast, renal)
  • Secrete PTHrP, ectopically mimics PTH
188
Q

Diagnosis of primary hyperparathyroidism

A
  • High PTH
  • Very high calcium
  • Low phosphate
  • High ALP- due to high bone turn over.
189
Q

Diagnosis of secondary hyperparathyroidism

A
  • High PTH
  • Low Calcium- Secondary hyperparathyroidism is when the glands are fine but a condition, like kidney failure, lowers calcium levels and causes the body to react by producing extra parathyroid hormone.
  • High phosphate - In kidney disease, your blood phosphate level can be high because your kidneys cannot remove phosphate in your urine.
  • High ALP
190
Q

Diagnosis of tertiary hyperparathyroidism

A
  • High PTH
  • High Calcium
  • High phosphate
  • High ALP
191
Q

Other tests for hyperparathyroidism

A
  • Xr KUB for kidney stones
  • DEXA scan for bone density
  • U+E to assess renal function
  • Short QT on ECG
192
Q

Treatment for hyperparathyroidism

A
  • Primary: Removal of PTH adenoma/parathyroidectomy of all 4 glands :( (most definitive)
  • Secondary and tertiary: Treat cause
  • Tertiary: Removal of parathyroid glands
  • Malignant: Remove tumour!
193
Q

Complication of hyperparathyroidism

A
  • Acute severe hypercalcaemia
  • Give IV fluids + bisphosphonates
194
Q

Diagnosis of pseudohyperparathyroidism

A
  • High PTH
  • Low calcium
  • High phosphate
195
Q

What does hypercalcaemia of malignancy do to PTH and phosphate levels?

A
  • PTH levels decrease
  • Phosphate levels stay the same
196
Q

Epidemiology and risk factors of hyperparathyroidism

A
  • Female
  • Radiation therapy to neck
  • Severe Vit D or Calcium deficiences
  • Familial rare conditions: MEN1 and 2A
197
Q

Primary vs secondary hypoparathyroidism

A

Primary: PTH gland failure, a number of causes
Secondary: After surgery (parathyroid/thyroid ectomy)

198
Q

Causes of primary hypoparathyroidism

A
  • Di George syndrome
  • Genetic
  • Radiation
  • Autoimmune
  • Infiltration
  • Magnesium deficiency
199
Q

Pseudohypoparathyroidism pathophysiology and what it’s associated with?

A
  • Very rare
  • End-organ PTH resistance due to defect in G protein signalling

Associated with:
- Low IQ
- Short stature
- Small 4th/5th metacarpals
- Obesity

200
Q

What is the Chvostek sign?

A

Twitching of facial muscles when facial nerve is trapped over parotid

201
Q

What is the Trousseau sign?

A

Carpopedal spasm when tourniquet is applied to forearm

202
Q

Diagnosis of hypoparathyroidism

A
  • Low PTH
  • Low Calcium
  • High phosphate
  • ECG = longer QTc
203
Q

Treatment for hypoparathyroidism

A

Calcium and Vitamin D suppements (AdCalD3)

204
Q

Diagnosis of pseudohypoparathyroidism

A
  • High PTH
  • Low Calcium
  • High Phosphate

Pseudopseudohypoparathyroidism also exists, but levels for everything are normal

205
Q

What is a phaeochromocytoma?

A

An adrenal medullar tumour of chromaffin cells that secrete catecholamines (NAd, Ad)

206
Q

Aetiology of phaeochromocytomas

A
  • 25% familial and associated with MEN 2a+2b
  • Neurofibromatosis 1 (tumours deposited along myelin sheath)
  • Von-Hippel Lindau disease
207
Q

Tumour patterns in phaeochromocytomas

A
  • 10% bilateral
  • 10% cancerous
  • 10% familial
  • 10% extra-adrenal (mc location: organ of Zuckerkandl at aortic bifurcation)
208
Q

Signs of phaeochromocytomas

A
  • Hypertension (90%)
  • Hypertensive retinopathy
  • Tachycardia
209
Q

Symptoms of phaeochromocytomas

A
  • Episodic headache
  • Profuse sweating
  • Palpitations
  • Anxiety
210
Q

Diagnosis of phaeochromocytoma

A
  • 24 hour urine metanephrine collection
  • Plasma free metanephrines
  • CT abdomen and pelvis
211
Q

Why are metanephrines measured to diagnose pheochromocytoma?

A
  • Adrenaline has a very short half life in blood (only a few minutes)
  • Metanephrines are a breakdown product of adrenaline and have a longer half life
212
Q

Treatment of phaeochromocytoma

A

Peri-operative
- Alpha blocker first (eg: phenoxybenzamine)
- Then beta blocker (eg: atenolol, propanolol)
- This prevents reactive vascoconstriction
Surgical
- Laproscopic adrenalectomy

213
Q

Pheochromocytoma hypertensive crisis

A
  • BP higher than 180/120
  • Causes: XR contrast, TCA, opiates
  • First line treatment: phentolamine (alpha blocker)
214
Q

Acromegaly in children

A
  • Called gigantism
  • Occurs before epiphyseal fusion
  • Hypopituitarism causes inhibition of puberty as gonadotrophs cannot be released
215
Q

Aetiology of acromegaly

A

Functional pituitary adenoma

216
Q

Pathophysiology of acromegaly

A
  • Excess GHRH
  • GHRH -> GH -> High IGF-1 (produced by liver)
217
Q

Signs of acromegaly caused by space occupying lesion

A
  • Bitemporal hemianopia
  • Headaches
218
Q

Signs of acromegaly to do with overgrowth of tissues

A
  • Prominent forhead and brow
  • Large nose, tongue, hands and feet
  • Large, protruding jaw
  • Arthritis
219
Q

Signs of acromegaly to do with GH causing organ dysfunction

A
  • Hypertrophic heart
  • Hypertension
  • Impaired glucose tolerance
  • Colorectal cancer
220
Q

Other symptoms suggesting active raised growth hormone

A
  • Development of new skin tags
  • Profuse sweating
221
Q

Diagnosis of acromegaly

A
  • 1st line: IGF-1 serum levels (high)
  • Gold standard: OGTT: Oral glucose tolerance test (failure of GH suppression 2 hours post 75g glucose load)
222
Q

First line treatment for acromegaly

A

Transsphenoidal resection of pituitary adenoma

223
Q

Other treatments for acromegaly

A
  • Somatostatin analogue to block GH (eg: ocreotide)
  • Dopamine agonist (eg: bromocriptine)
  • GH antagonist (eg: pegvisomant)
  • Radiotherapy
224
Q

Complications of acromegaly

A
  • T2DM caused by impaired glucose tolerance
  • Obstructive sleep apnoea
  • Cardiomyopathy
  • Hypertension
  • Arthropathy
  • Carpal tunnel syndrome
225
Q

Why can acromegaly cause sleep apnoea?

A

Pressure around the neck due to enlargement

226
Q

Peak ages craniopharyngiomas occur

A
  • 5 to 14 years
  • 50 to 74 years
227
Q

Pathophysiology of craniopharyngioma

A
  • Squamous epithelial remnants of Rathke’s pouch
  • Benign, slow growing tumour infiltrates to surrounding structures
  • Mixed solid and cystic parts
  • Doesn’t spread to other parts of the body but puts pressure on suprasellar region of skull
228
Q

Adamantinous vs squamous papillary craniopharyngioma

A

Adamantinous: Cyst formation and calcification
Squamous papillary: Well circumscribed

229
Q

Presentation of craniopharyngioma

A
  • Raised ICP
  • Visual disturbances (bitemporal hemianopia)
  • Growth failure
  • Pit. hormone deficiency
  • Weight increase
230
Q

Pathophysiology of Cushing’s syndrome

A

Chronic excess of cortisol released by the adrenal glands

231
Q

Aetiology of Cushing’s syndrome

A

ACTH dependent causes
- Cushing’s disease
- Ectopic ACTH production
- ACTH treatment

ACTH independent causes
- Iatrogenic (steroid use) - mc
- Adrenal adenoma

232
Q

What is Cushing’s disease?

A

Pituitary adenoma secreting excess ACTH

233
Q

Signs of Cushing’s syndrome

A
  • Hypertension
  • Moon face
  • Central obesity
  • Abdominal striae
  • Buffalo hump (fat pad on upper back)
  • Proximal limb muscle wasting
  • Ecchymoses and fragile skin
234
Q

Symptoms of Cushing’s syndrome

A
  • Bloating and weight gain
  • Mood change
  • Increased susceptibility to infection
  • Menstrual irregularity
  • Reduced libido
  • Hyperglycaemia
235
Q

Pseudo-Cushing’s

A
  • Cushingoid features and abnormal cortisol levels, but not associated with HPA pathology
  • Common causes: alcohol excess, severe depression, obesity, pregnancy
  • Results in a false positive dexamethasone suppression test and 24hr free cortisol
  • Differentiated using an insulin stress test
236
Q

Diagnosis of Cushing’s syndrome

A
  • Dexamethasone suppression test OR midnight salivary cortisol
  • If positive, test plasma ACTH to see if ACTH dependent
  • If independent, see if it is pituitary or ectopic GH release
237
Q

How to do dexamethasone suppression test

A
  • Measure cortisol at 12am, before giving dexamethasone
  • Measure cortisol 8 hours later, at 8am
  • Non-Cushing’s -> suppression >50nmol/L
  • Cushing’s -> little/no suppression
238
Q

Plasma ACTH test

A
  • Test at 9am
  • High = ACTH dependent cause -> Do high dose dexamethasone suppression test
  • Low = ACTH independent cause -> CT adrenals to look for pathology
239
Q

Treatment for Cushing’s syndrome caused by Cushing’s disease

A

Transsphenoidal resection or bilateral adrenalectomy

240
Q

Complication of bilateral adrenalectomy

A

Nelson’s syndrome
- Pituitary tumour will continue to enlarge with no negative feedback from adrenals
- High ACTH and skin hyperpigmentation

241
Q

Treatment for Cushing’s syndrome caused by adrenal adenoma

A

Tumour resection or unilateral adrenalectomy

242
Q

Treatment for Cushing’s syndrome caused by ectopic ACTH

A

Treatment of underlying cancer, such as surgical removal of SCLC
small cell lung cancer

243
Q

Complications of Cushing’s syndrome

A
  • Osteoporosis
  • T2DM
  • Hypertension and ischaemic heart disease
244
Q

Risk factors for hyperprolactinaemia

A
  • Females
  • High serum prolactin (released from lactotrophs in the ant. pituitary)
245
Q

Aetiology of hyperprolactinemia

A
  • Prolactinoma
  • Drugs (ecstacy)
246
Q

Symptoms of hyperprolactinoma

A
  • Secondary amenorrhoea
  • Galactorrhoea 🪐🌌
  • Sexual dysfunction (M+F)
  • Gynecomastia, low testosterone
247
Q

Diagnosis of hyperprolactinemia

A
  • High serum prolactin
  • > 1000mIU/L
  • or 500-1000mIU/L on two occasions
248
Q

Best treatment for hyperprolactinemia

A
  • Dopamine agonists
  • eg: cabergoline or bromocriptine
  • Massively shrinks prolactinoma (tumour) as dopamine is an inhibitor of prolactin
249
Q

How common are meningiomas?

A

Most common tumour of region after pituitary adenoma

250
Q

Cause of meningiomas

A

Complication of radiotherapy

251
Q

Complications of meningioma

A
  • Loss of visual acuity
  • Visual field defects
  • Endocrine dysfunction
252
Q

What is SIAD?

A
  • Overdiagnosed cause of hyponatremia
  • Inappropriately released ADH, dilute euvolemia
  • Excess ADH = more water retention = compensatory Na+ excretion to maintain euvolemia

Syndrome of Inappropriate Antidiuretic Hormone Secretion.

253
Q

Aetiology of SIAD

A
  • Cancers - SCLC and others
    -Infection/immunosuppression, eg: TB, pneumonia, meningitis
  • Abscesses
  • Drugs: SSRIs, carbamazepine, sulfonylureas
  • Head trauma
254
Q

Pathophysiology of SIAD

A
  • High ADH independent of RAAS
  • Increased vasoconstriction
  • APO-II expression of collecting duct
  • Lead to high BP
  • Excess H2O retained means more dilute blood and more Na+ loss
255
Q

Symptoms of hyponatremia

A
  • Vomiting
  • Headache
  • Decreased GCS
  • Muscle weakness
256
Q

Symptoms of extreme hyponatremia

A
  • Seizures
  • Neurological complications
  • Brainstem herniation
257
Q

Diagnosis of SIAD

A
  • Decrease in serum Na+ and normal serum K+
  • High urine osmolality
  • Skin turgor and jugular venous pressure test
258
Q

Differential diagnosis of SIAD

A

Na+ depletion
- Give 0.9% saline
- Na+ depletion -> serum will normalise
- SIAD -> serum fails to normalise

259
Q

Treatment for hyponatraemia secondary to SIAD

A
  • Asymptomatic/mild symptoms: Fluid restrict; vaptans (vasopressin antagonist)
  • Severe symptoms: 3% hypertonic saline to concentrate blood
260
Q

Which conditions do you need to rule out before confirming SIAD?

A
  • Hypothyroidism
  • Hypervolaemia
  • Adrenal insufficiency
  • Diuretic use
261
Q

Treatment of chronic cases of SIAD

A
  • Furosemide
  • Vasopressin antagonist (tolvaptan)
  • Demeclocycline (inhibits ADH)
262
Q

Cancers that can cause SIAD

A
  • SCLC (small cell carcinoma)
  • Prostate cancer
  • Pancreatic cancer
  • Lymphomas
  • Cancer of the thymus
263
Q

Normal water sodium distribution vs SIADH

A

equal na+ and h20 = normal

siadh= lots of h20 not much na+
euvolemia with hyponatremia

264
Q

How can hyponatremia cause brain stem herniation?

A
  • Low Na+ means high compensatory H2O
  • Enters skull, high ICP
  • Causes hyponatremic encephalopathy
  • Risk of brainstem herniating through foramen magnum (tentorial herniation)
265
Q

Signs of thyroid storm

A
  • Hyperpyrexia, often >40°C
  • Tachycardia, often >140bpm, with or without atrial fib
  • Reduced GCS
266
Q

Diagnosis of thyroid storm

A
  • TFTs: High T3 and T4, suppressed TSH
  • ECG
  • Blood glucose (perform in all patients with reduced consciousness)
267
Q

Treatment of thyroid storm

A

High dose propylthiouracil and KI

268
Q

What is thyroid storm/thyrotoxic crisis?

A
  • Endocrine emergency often seen in patients with Graves’ disease or toxic multinodular goitre
  • Secondary to precipitating factor such as infection or trauma
  • 10-20% mortality
269
Q

Treatment for DeQuervain’s thyroiditis

A
  • NSAIDs for pain and inflammation
  • Beta blockers for symptomatic relief
270
Q

Difference between primary and secondary hyperthyroidism?

A
  • Primary: Pathology is in the thyroid
  • Secondary: Pathology is in the hypothalamus/pituitary
271
Q

TFTs for hyperthyroidism

A
  • Low TSH, high T4 = primary hyperthyroidism (Graves’)
  • High TSH, high T4 = secondary hyperthyroidism OR thyroid hormone resistance
272
Q

Graves’ specific hyperthyroid signs

A
  • Exophithalmos or ephthalmoplegia - eye issues
  • Pretibial myxedema due to deposits of mucin under the skin (may also be seen in Hashimoto’s)- scaly skin, leg swelling
  • Thyroid acropachy
273
Q

Epidemiology and risk factors of hyperthyroidism

A
  • Middle aged women
  • Family history
  • Autoimmune diseases
274
Q

Pathophysiology of Graves’ disease

A
  • Immune system produces TSH receptor antibodies that mimic TSH and stimulate the TSH receptors on the thyroid
  • Increased T3 increases metabolic rate, CO, bone resorption and activates the sympathetic nervous system
275
Q

Symptoms of hyperthyroidism

A
  • Heat intolerance and sweating
  • Weight loss
  • Palpitations
  • Oligomenorrhoea
276
Q

What is toxic multinodular goitre? (also known as Plummer’s disease)

A

Nodules develop on the thyroid gland and produce excessive thyroid hormone

277
Q

Symptoms of thyroid storm

A
  • NDV
  • Abdo pain
  • Jaundice
  • Confusion, delirium or coma
278
Q

Diagnosis of hyperthyroidism

A

First line: TFT (thyroid function test)

  • Anti-TSH receptor antibodies positive in Graves’
  • Anti TPO antibodies in 80% of cases (but much more in hypo)
  • Thyroid ultrasound
279
Q

First line treatment for hyperthyroidism

A
  • Carbimazole
  • Blocks synthesis of T4
  • Normal thyroid function after 4-8 weeks (euthyroidism)
  • SE: agranulocytosis, presents as sore throat/mouth ulcers
    • beta blocker (eg: propanolol) alongside for rapid symptom relief
280
Q

Second line treatment for hyperthyroidism

A
  • Propylthiouracil
  • Prevents T4->T3 conversion
  • Small risk of severe hepatic reaction, including death
281
Q

Radioactive iodine treatment for hyperthyroidism

A
  • First line definitive treatment for Grave’s disease and toxic multinodulae goitre
  • Destroys excess thyroid tissue
  • Remission can take 6 months
  • Patient must not be pregnant or planning to get pregnant within 6 months, must also avoid close contact with children and pregnant women for 3 weeks
  • Also limit contact with anyone for several days after receiving the dose
282
Q

Last resort treatment for hyperthyroidism

A

Surgery or radioactive iodine

283
Q

How to stop patients from becoming hypothyroid after hyperthyroidism treatment

A

Give them levothyroxine

284
Q

Who would you not want to give carbimazole to?

A

Women wanting to get pregnant as it’s teratogenic (causes fetal abnormalities)

285
Q

What to do after euthyroidism is achieved in hyperthyroid treatment

A

Maintenance carbimazole using either:
- Titration block regimen
- Block and replace regimen
Complete remission achieved after 18 months of treatment (remission rate 50%)

286
Q

Risk factors of hyperthyroidism

A
  • Smoking
  • Stress
  • HLA-DR3
  • Female 20-40 years
  • Other autoimmune diseases
287
Q

General signs of hyperthyroidism

A
  • Postural tremor
  • Palmar erythema
  • Hyperreflexia
  • Goitre
  • Lid lag and retraction
288
Q

Most common cause of hypothyroidism in the developed world

A
  • Hashimoto’s thyroiditis
  • Autoimmune inflammation of the thyroid gland - initially cause a goitre
  • Associated with anti-TPO antibodies and antithyroglobulin antibodies
289
Q

Most common cause of hypothyroidism in the developing world

A

Iodine deficiency

290
Q

What is postpartum thyroiditis

A
  • Same mechanism as Hashimoto’s
  • Acute: presents during pregnancy
  • Resolves by itself within 1 year of symptoms
291
Q

Other causes of hypothyroidism

A
  • DeQuervain’s thyroiditis
  • Post-thyroidectomy or post-radioiodine
  • Drugs; amiodarone, lithium, carbimazole
292
Q

Causes of secondary hypothyroidism (pathology at pituitary gland)

A
  • Compression from a pituitary tumour
  • Sheehan syndrome
  • Drug: cocaine, steroids, dopamime (all inhibit TSH secretion)
293
Q

Symptoms of hypothyroidism

A
  • Cold intolerance
  • Constipation
  • Weight gain
  • Lethargy
  • Menorrhagia
294
Q

Signs of hypothyroidism

A
  • Hair loss, dry and cold skin
  • Bradycardia
  • Goitre
  • Decreased deep tendon reflexes
  • Carpal tunnel syndrome
295
Q

Diagnosis of hypothyroidism

A
  • TFT (thyroid function test)
  • Anti-TPO antibodies high
  • Tyically anaemic (any type)
296
Q

TFTs for hypothyroidism

A
  • High TSH, low T4 = primary hypothyroid
  • Low TSH, low T4 = secondary hypothyroid
  • Normal/low TSH, Low T4 = hypopituitarism
297
Q

Treatment for hypothyroidism

A
  • Levothyroxine (T4)
  • Titrate dose so you don’t induce iatrogenic hyperthyroidism
298
Q

Complication of hypothyroidism

A

Myxedema coma
- Often infection precipitated
- Rapidly drops T4
- Loss of consciousness, heart failure

299
Q

Treatment for myxedema coma

A
  • Levothyroxine
  • Antibodies
  • Hydrocortisone
300
Q

Epidemiology of hypothyroidism

A
  • Mainly >40 years
  • F>M 6:1
301
Q

Types of thyroid carcinoma

A
  • Papillary - 70%
  • Follicular - 25%
  • Anaplastic (worst prognosisas as it metastasises the most)
  • Lymphoma
  • Medullary cell
302
Q

Most common metastasis sites for thyroid carcinoma

A
  • Lung - 50%
  • Bone - 30%
  • Liver - 10%
  • Brain - 5%
303
Q

How does thyroid carcinoma usually present?

A
  • As hard and irregular thyroid nodules
  • May have local compression (eg: hoarse voice)
304
Q

Treatment for thyroid carcinoma

A
  • Papillary and follicular = thyroidectomy or radioactive iodine
  • Anaplastic = mostly palliative :(
305
Q

Diagnosis of thyroid carcinoma

A
  • Fine needle aspiration biopsy
  • TFTs
  • Thyroid ultrasound
306
Q

De Quervain’s thyroiditis

A
  • Follows a viral prodrome and can also present with a transient thyrotoxic state
  • Painful goitre with raised inflammatory markers. Usually self limiting

Haroon flashcards (10 decks)

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