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Year 6 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What are the classifications of Acromegaly?

A

Growth hormone releasing hormone (GHRH) independent:
- Pituitary adenoma (most common)
- Primary pituitary hyperplasia

GHRH dependent (rarer):
- Hypothalamic source = excess GHRH from he hypothalamus causes secondary pituitary hyperplasia
- Ectopic release = excess GHRH from ectopic tissue

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2
Q

Define Acromegaly

A

A disorder caused by an excessive amount of growth hormone w/ characteristic clinical features

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3
Q

What’s the difference between acromegaly and gigantism?

A

Age of onset - gigantism occurs before the epiphyseal plates close leading to excess linear growth, whilst acromegaly occurs after the plates close leading to enlargement of bones and soft tissue

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4
Q

Acromegaly pathophysiology

A
  • Excess GH results in the excess production of insulin-like growth factor 1 (IGF-1)
  • IGF-1 receptor is widely distributed across a wide range of tissues, and excess stimulation results in abnormal growth of these tissues
  • Excess GH also results in increased gluconeogenesis, lipolysis and insulin resistance
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5
Q

Acromegaly features

A

Hands:
- spade-like, large, doughy hands
- Sweaty
- Thick skin w/ large pores
- Carpal tunnel syndrome

Face:
- Interdental separation
- Prognathism
- Large ears, nose, lips
- Prominent supraorbital ride and facial creases
- Macroglossia
- Acne

Visual field defects = bitemporal hemianopia/upper quadrantanopia

Axilla:
- Acanthosis nigricans
- Skin tags

Neck:
- Acanthosis nigricans
- Goitre

Chest:
- Cardiomegaly
- Pulmonary oedema
- Gynaecomastia

Legs:
- Peripheral pitting oedema
- Proximal muscle weakness
- OA
- Large feat

Back:
- Kyphoscoliosis

Systemic:
- Secondary HTN
- Organomegaly
- Increased risk of colonic polyps and thus colorectal cancer

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6
Q

Acromegaly investigations

A

Bedside:
- Fundoscopy -=optic atrophy
- Visual fields testing
- Urine dip = glycosuria
- ECG = LVH due to HTN

Bloods:
- IGF-1 levels
- If raised, do confirmatory test = oral glucose tolerance test - fails to supress GH

Imaging:
- MRI pituitary

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7
Q

Acromegaly management

A

Medical = if surgery is contraindicated, mechanism not due to pituitary adenoma, or is refractory to surgery:
- Somatostatin analogues (1st line) = octreotide (supress GH release)
- GH antagonists = pegvisomant
- Dopamine agonist = cabergoline

Surgery (1st line):
- Transphenoidal surgery to remove pituitary adenoma (1st line)
- Transfrontalr resection of the pituitary
- +/- radiotherapy

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8
Q

Define Adrenal insufficiency

A

A clinical syndrome that arises due to the insufficient production of glucocorticoids and mineralocorticoids from the adrenal cortex

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9
Q

What are the classifications of Adrenal insufficiency?

A

Primary = Addison’s disease:
- AI destruction
- Surgical removal
- Trauma
- TB
- Haemorrhage
- Infarction
- Neoplasm
- Steroid overuse

Secondary:
- Congenital disorders
- Basal skull fractures
- Pituitary surgery
- Pituitary neoplasm
- Infiltration or infection of the brain
- Corticotrophin-releasing hormone deficiency

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10
Q

Adrenal insufficiency features

A
  • Hypotension
  • Fatigue and weakness
  • GI symptoms
  • Syncope
  • Skin pigmentation due to increased ACTH production and thus increased melanocyte stimulating hormone
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11
Q

Adrenal insufficiency investigations

A
  • U&Es and serum cortisol = hyponatraemia, hyperkalaemia and low serum cortisol
  • Hypoglycaemia
  • ABG = hyperkalaemia, hyponatraemic metabolic acidosis
  • Ab testing
  • CT adrenals
  • MRI pituitary

Short synacthen test is confirmatory:
- Measure cortisol before
- Give syacthen (syhnethtic ACTH)
- Measure cortisol 30 min later
- Cortisol should be >420, else probably Addison’s

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12
Q

Adrenal insufficiency management

A

Chronic:
- Replace glucocorticoids (w/ hydrocortisone - 10mg in the morning, 5mg at noon, 5mg at night- or prednisolone)
- Replace mineralocorticoids (w/ fludrocortisone)
- Education on sick day riles (doubling steroid dose when ill)

Addisonian crisis:
- Aggressive fluid resuscitation
- IV/IM hydrocortisone STAT
- Glucose if hypoglycaemia

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13
Q

Define Addisonian crisis

A

A life-threatening condition due to an acute deficiency in cortisol and aldosterone

Presents w/:
- Hypotension
- Hyperkalaemia
- Hyponatraemia
- Metabolic acidosis

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14
Q

What are the side effects of amiodarone?

A
  • Hypothyroidism
  • Hyperthyroidism (rarer - amiodarone thyrotoxicosis)
  • Corneal deposits
  • SJS
  • Grey discoloration of the skin
  • Liver failure
  • Pneumonitis and pulmonary fibrosis
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15
Q

Define Amiodarone induced thyrotoxicosis

A

A side effect of amiodarone which is rich in iodine, presents w/ symptoms of thyrotoxicosis

Manifests in 2 types:
- AIT 1 = pt has underlying thyroid nodules, amiodarone increases thyroid hormone production due to high iodine content
- AIT 2 = pt has normal function gland, amiodarone triggers destructive thyroiditis

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16
Q

Amiodarone induced thyrotoxicosis investigations

A
  • TFTs
  • Thyroid uptake scan - AIT 1 = normal uptake, AIT 2 = decreased uptake
  • Doppler US - AIT 1 = increased vascularity, AIT 2 = reduced vascularity
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17
Q

Amiodarone induced thyrotoxicosis management

A
  • AIT 1 = carbimazole
  • AIT 2 = corticosteroids
  • Consult w/ cardio about stopping amiodarone
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18
Q

What are the causes of vasopressin deficiency?

A
  • Head trauma
  • Inflammatory conditions e.g. sarcoidosis
  • Cranial infections e.g. meningitis
  • Vascular conditions e.g. sickle cell
  • Rare genetic causes
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19
Q

What are the causes of vasopressin resistance?

A
  • Drugs e.g. lithium
  • Metabolic disturbances e.g. hypercalcaemia, hypokalaemia and hyperglycaemia
  • Chronic renal disease
  • Rare genetic causes
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20
Q

Vasopressin disorders (diabetes insipidus) features

A
  • Large volumes of dilute urine (> 3L in 24 hrs and urine osmolality of <300 mOsm/kg)
  • Nocturia
  • Excessive thirst
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21
Q

Vasopressin disorders (diabetes insipidus) investigations

A
  • U&Es = sodium normal/raised
  • Urine dip
  • Paired serum and urine osmolality (raised serum osmolality w/ inappropriately dilute urine w/ a low osmolality)

Water deprivation test is diagnostic and can distinguish from primary polydipsia:
- Deprive pt of fluids and monitor urine osmolality and weight changes (stop if pt loses >5% body weight)
- In vasopressin disorders, urine osmolality wont decrease
- In vasopressin deficiency, urine osmolality will decrease on administration of ADH
- In vasopressin resistance, urine osmolality wont change w/ administration of ADH

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22
Q

Vasopressin deficiency management

A
  • Desmopressin
  • Monitor sodium levels
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23
Q

Vasopressin resistance management

A
  • Correct underlying metabolic abnormalities
  • Stop any offending drugs
  • High dose desmopressin has varying results
  • Thiazide diuretics and NSAIDs can reduce urine volume
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24
Q

Define Carcinoid tumour

A

A slow-growing, neuroendocrine tumour which secretes hormones (usually serotonin) - most often occur in the appendix, lungs and small intestine

Can become malignant

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25
Q

What’s the difference between Carcinoid tumours and Carcinoid syndrome?

A

Carcinoid tumour = NET secreting serotonin

Carcinoid syndrome = occurs when the serotonin enters the blood stream, usually when the tumour has spread to the liver which allows the serotonin to be released to the systemic circulation w/out being broken down

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26
Q

Carcinoid tumour symptoms

A
  • Abdo pain
  • Diarrhoea
  • Flushing
  • Wheeze
  • Pulmonary stenosis

Pts only have symptoms if they have liver mets which allow serotonin to enter circulation

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27
Q

Carcinoid tumour investigations

A
  • 5-HIAA urine levels = breakdown product of serotonin
  • CT, MRI or octreotide scans to locate the tumour
  • Tissue biopsy for definitive diagnosis
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28
Q

Carcinoid tumour management

A

Medical:
- Octreotide (somatostatin analogue) to inhibit serotonin production
- Chemo/radiotherapy

Surgical:
- Tumour resection
- Emobliation
- Radiofrequency ablations

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29
Q

Define Cushing’s syndrome

A

Excess glucocorticoids (cortisol)

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30
Q

What are the causes of Cushing’s syndrome?

A

ACTH-dependent disease:
- Pituitary tumour (Cushing’s disease)
- Ectopic ACTH-production = lung/thymic carcinoid tumours

ACTH-independent disease:
- Primary adrenal disease = adrenal adenomas, adrenal carcinomas
- Exogenous steroid overuse

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31
Q

Cushing’s syndrome features

A
  • Proximal myopathy
  • Striae and easy bruising
  • Osteoporosis and fractures
  • Glucose intolerance and DM
  • Truncal obesity
  • HTN
  • Hypokalaemia
  • Facial changes = moon face, acne
  • Hirsutism in women
  • Supraclavicular fat pads
  • Thin extremities due to muscle wasting
  • Thin skin
  • Erectile dysfunction
  • Depression or cognitive dysfunction
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32
Q

Cushing’s syndrome investigations

A
  • 24-hr urinary free cortisol test
  • Plasma ACTH levels to distinguish between ACTH-dependent and independent
  • Inferior petrosal sinus sampling for suspecting pituitary causes
  • MRI pituitary
  • CT chest abdo

Low dose dexamethasone suppression test to confirm and distinguish:
- Measure cortisol levels, then administer 1mg oral dex and remeasure cortisol levels 24 hrs later
- Normal response = a significant decrease in cortisol levels (<1.8)
- Cushing’s disease = not supressed by low-dose, but supressed by high dose (8mg of dex)
- Cushing’s syndrome = not supressed by low or high-dose dex

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33
Q

Cushing’s syndrome management

A

Medical:
- Metyrapone = inhibitor of cortisol synthesis
- Ketoconazole = adrenolytic agent
- Mifepristone = glucocorticoid receptor antagonist
- Pasireotide = somatostatin analogue

Surgical (1st line):
- Resection of the tumour
- If its Cushing’s disease pt will need exogenous steroids for life

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34
Q

Define Delayed puberty

A

Absence of pubertal development by 14 in boys and 13 in girls

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35
Q

What are the causes of Delayed puberty?

A

Constitutional delay (most common)

Low gonadotrophin secretion:
- Craniopharyngiomas
- Kallmann syndrome
- Panhypopituitarism
- Isolated gonadotrophin deficiency
- CF
- Crohn’s disease

High gonadotrophin secretion:
- Turners XO
- Klinefelter’s XXY
- Congenital adrenal hyperplasia
- Acquired hypogonadism e.g. post chemo

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36
Q

Delayed puberty investigations

A
  • Clinical assessment
  • Hand-wrist X-ray = to determine bone age, which is typically delayed in constitutional growth delay as the epiphyseal plates are late to fuse
  • Hormone testing = FSH, LH, thyroid hormones, sex hormones - can help distinguish between causes
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37
Q

Delayed puberty management

A

Depends on the cause:
- Constitutional delay = monitor growth
- Low gonadotrophin secretion = hormone replacement therapy, surgery for tumours, management of underlying disease
- High gonadotrophin secretion = hormone replacement therapy, supportive care

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38
Q

T1DM features

A
  • Polyuria
  • Polydipsia
  • WL (distinguishes it from T2DM)
  • DKA
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39
Q

Define Maturity onset diabetes of the young (MODY)

A

A rare form of diabetes that presents in adolescence or early adulthood (<25)

It is due to impaired insulin secretion, however, this is not due to AI destruction like T1DM but instead 1 of 5 mutations which impair the beta cells ability to produce insulin

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40
Q

Maturity onset diabetes of the young (MODY) management

A
  • Sulfonylureas to stimulate insulin production
  • Insulin therapy (less common)
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41
Q

T1DM investigations

A
  • Random blood glucose > 11.1 or fasting plasma gluocse > 7
  • 2-hour glucose tolerance > 11.1
  • HbA1C > 48

If pt is symptomatic then only needs one of those results

If pt is asymptomatic then they need 2

Can confirm w/ C-peptide levels (will be low)

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42
Q

T1DM management

A

Insulin therapy:
- Long actin insulin given at night time
- Short acting insulin given after meals and snacks

Tight glycaemic control:
- Pre-meal BM = 4-7
- Bedtime BM = 6-10
- HbA1c < 53

Regular BM’s

Hypoglycaemic management

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43
Q

What are the sick day rules for T1DM?

A
  • Monitor BM every 3-4 hours and adjust insulin doses
  • Monitor ketones, seek help if levels > 3mmol
  • Maintain normal meal patterns
  • If unable to eat, replace meals w/ carbohydrate-containing drinks e.g. fruit juice
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44
Q

T2DM investigations

A
  • Random blood glucose > 11.1
  • Fasting plasma gluxose > 7
  • 2 hour glucose toelrance test > 11.1
  • HbA1c > 48

Need 1 if symptomatic

Need 2 on different days if asymptomatic

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45
Q

T2DM management

A

Conservative:
- Dietary advice
- Regular exercise
- Smoking cessation

Medical:
- Initial management = metformin
- If HbA1c > 58 on monotherapy, add pioglitazone, DDP-4 inhibitors or a sulfonylurea
- If dual therapy not working than add a 3rd agent from the list
- Always add an SGLT-2 inhibitor if pt has HF
- If triple therapy not working then switch to insulin (start w/ intermediate acting, then switch to long/short acting regime)
- If pt obese, consider a GLP-1 agonist
- ACEi if HTN (renoprotective)

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46
Q

What are examples of sulfonylureas?

A

Gliclazide, tolbutamide

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47
Q

What are examples of DDP-4 inhibitors?

A

Sitagliptin, linagliptin

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48
Q

What are examples of GLP-1 agonists?

A

Semaglutide, dulaglutide

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49
Q

What are examples of SGLT-2 inhibitors?

A

Empagliflozin, dapagliflozin

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50
Q

What are the complications of T2DM?

A

Macrovascular:
- CVD
- PAD
- Cardiac complications

Microvascular:
- Diabetic retinopathy
- Diabetic neuropathy
- Diabetic nephropathy (+ diabetic foot)
- Autonomic neuropathy (gastroparesis)
- Sexual dysfunction

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51
Q

What are the T2DM medication sick day rules?

A
  • Metformin = stop if risk of dehydration (vomit/diarrhoea) to lower risk of lactic acidosis
  • Sulfonylureas = may cause hypoglycaemia if reduced oral intake
  • SGLT-2 inhibitors = stop if dehydrated as can cause euglycemic DKA
  • GLP-1 agonists = stop if risk of dehydration to decrease risk of AKI
  • Insulin = don’t stop, adjust based on recommendations of diabetic team
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52
Q

Define Diabetic ketoacidosis

A

A medical emergency consisiting of the triad of:

  • Hyperglycaemia (BM > 11)
  • Ketosis (blood ketones > 3, or urinary ketones ++)
  • Acidosis (pH <7.2 or bicarb <15)
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53
Q

What parameters classify a DKA as severe?

A

One of:

  • Blood ketones > 6
  • Bicarb < 5
  • Blood pH < 7
  • Anion gap > 16
  • Hypokalaemia on admission
  • GCS < 12
  • O2 sats <92% on air
  • Systolic BP < 90
  • Brady or tachycardia
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54
Q

DKA features

A

Symptoms:
- N&V
- Abdo pain
- Polyuria
- Polydipsia
- Weakness

Signs:
- Dry mucous membranes
- Hypotension
- tachycardia
- Altered mental state
- Kussmaul breathing (deep, sighing breaths to compensate for metabolic acidosis by b lowing of CO2)
- Fruit-like smelling breath

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55
Q

What are common triggers for DKA?

A
  • Infection
  • Dehydration and fasting
  • Missing dose of insulin
  • Steroids
  • Diuretics
  • Surgery
  • CVD
  • Alcohol excess or illicit drugs
  • Pancreatitis
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56
Q

DKA investigations

A

Bedside:
- Cap BM
- Blood or urinary ketones
- Urine dip to look for UTI
- ECG

Bloods:
- ABG
- U&Es

Imaging:
- Consider CXR for septic screen

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57
Q

Diabetic ketoacidosis management

A
  • A-E
  • IV fluid replacement = IL over 1hour, then 2L over 2 hours, then 2L over 4 hours, the 1L over 6 hours (potassium should be added after the 1st bag depending on levels)
  • Then start a fixed rate insulin infusion at a rate of 0.1units/kg/hour
  • Continue long-actin insulin, but stop short acting
  • Once blood glucose < 14, add a 10% glucose infusion alongside the saline and insulin

Continue fixed rate insulin until:
- Ketones < 0.6
- pH > 7.3

At this point start short-acting insulin if they can eat, stop the infusion 30 min after subcut insulin is given

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58
Q

Diabetic neuropathy features

A

Depends on the type:

Distal symmetrical sensory neuropathy:
- Most common
- Loss of touch, vibration and proprioception in glove and stocking distribution

Small-fibre predominant neuropathy:
- Due to loss of small sensory fibres
- Loss of pain and temp sensation in glove and stocking distribution
- Often has episodes of burning pain

Diabetic amyopathy:
- Inflammation of the lumbosacral or cervical plexus
- Severe pain around the thighs and hips, along w/ proximal muscle weakness

Mononeuritis multiplex:
- Painful neuropathy of 2 distinct peripheral nerves

Autonomic neuropathy:
- Postural hypotension
- Gastroparesis
- Constipation
- Urinary retention
- Arrhythmias
- Erectile dysfunction

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59
Q

Define Charcot Arthropathy

A

A chronic, progressive arthropathy that occurs in pt w/ peripheral neuropathy

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60
Q

Charcot Arthropathy features

A

6 D’s:

  • Destruction of bone and joints
  • Deformity
  • Degeneration
  • Dense bones
  • Debris of bone fragments
  • Dislocation

Typically affects the tarsometatarsal joints

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61
Q

Charcot Arthropathy management

A
  • Prolonged offloading
  • Bisphosphonates
  • Gabapentin/pregabalin
  • Resection of bony prominences
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62
Q

Define Galactorrhoea

A

Inappropriate and spontaneous milk secretion from the breasts unrelated to childbirth or lactation

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63
Q

What are the causes of Galactorrhoea?

A
  • Idiopathic
  • Prolactinoma
  • Drugs = antipsychotics, SSRIs, cimetidine, beta blockers
  • Metabolic conditions = hypothyroidism, liver disease, CKD
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64
Q

Galactorrhoea investigations

A
  • Serum prolactin
  • TFTs
  • U&Es and LFTs
  • MRI pituitary
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65
Q

Galactorrhoea management

A
  • Manage underlying condition
  • Stop offending drug
  • Cabergoline to increase dopamine and thus decrease prolactin
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66
Q

Define Gestational diabetes

A

Glucose intolerance in pegnancy defined as:

  • Fast blood glucose levels of 5.6 or above
  • 2 hour post OGGT levels of 7.8 or above

(5678)

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67
Q

What are the risk factors for Gestational diabetes?

A
  • Previous Hx of GDM
  • Prior delivery of macrosomic baby
  • Maternal obesity
  • Diabetes in a 1st degree relative
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68
Q

What are the foetal complications of Gestational diabetes?

A
  • Macrosomia (BW > 4kg)
  • Pre-term delivery
  • Neonatal hypoglycaemia
  • Increased risk of baby developing T2DM in later life
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69
Q

What are the maternal complications of Gestational diabetes?

A
  • Increased risk of HTN and pre-eclampsia
  • Risk of having it in subsequent pregnancies
  • Increased risk of T2DM
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70
Q

Gestational diabetes management

A
  • Lifestyle modifications if fasting glucose < 7 - if not below 5.6 after 2 weeks then start metformin
  • If blood glucose levels > 7 on presentation - start insulin
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71
Q

Define Goitre

A

An abnormal enlargement of the thyroid gland

2 types:
- Smooth = no distinct nodules
- Nodular = presence of 1 or more distinct nodule which may be hot (functioning) or cold (non-functioning)

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72
Q

What are the causes of smooth Goitres?

A
  • Graves disease
  • Hashimoto’s disease
  • Drugs = lithium, amiodernone
  • Iodine deficiency/excess
  • De Quervain’s thyroiditis
  • Infiltrative diseases = sarcoid, hemochromatosis
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73
Q

What are the causes of nodular Goitres?

A
  • Toxic solitary adenoma
  • Non-functioning adenoma
  • Multinodular goitre
  • Thyroid cyst
  • Thyroid cancer
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74
Q

Goitre features

A
  • Visible and palpable swelling in the neck which moves up on swallowing but not on tongue protrusion
  • Hoarseness
  • Dysphagia (in large goitres)
  • Symptoms of hypo/hyperthyroidism depending on the underlying cause
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75
Q

Goitre investigations

A
  • TFTs
  • US = evaluate size, number and characteristics of nodules
  • FNA = in nodular goitres to assess malignancy
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76
Q

Define Gynaecomastia

A

Enlargement of male breast tissue

Results from a benign increase in glandular breast tissue rather than adipose tissue

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77
Q

What are the causes of Gynaecomastia?

A

Occurs due to an imbalance in the actions of oestrogen (stimulates breast growth) and androgens (inhibit growth)

  • Obesity = increases peripheral conversion of androgens to oestrogens
  • Chronic liver disease = reduces livers capacity to metabolise oestrogen
  • Anabolic steroid use
  • Tumours = Sertoli cell, Leydig cell, germ cell tumours all can produce oestrogen
  • Chronic illness = testosterone is supressed more than oestrogen during periods of malnourishment
  • Hyperthyroidism = increases conversion of androgens to oestrogen
  • Hypogonadotrophic hypogonadism = lower testosterone
  • Hyperprolactinaemia
  • testicular failure
  • Drugs = spironolactone (anti-androgen effects), ketoconazole, GnRH agonists, chemo
  • Cannabis
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78
Q

Gynaecomastia features

A

Symmetrical (in relation to the nipple), rubbery enlargement of the breasts in men

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79
Q

Gynaecomastia investigations

A
  • Bloods = LFTs, U&Es, TFTs, testosterone levels, oestradiol levels, LH/FSH levels, prolactin levels
  • Imagine = breast USS, testicular USS (to assess for tumours)
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80
Q

Gynaecomastia management

A
  • Observation and reassurance = most cases resolve over time
  • Treat underlying cause
  • Medication = selective oestrogen receptor modulators (tamoxifen) and androgens (danazol)
  • Breast reduction surgery in long standing cases where medical management has not been successful
  • Psychological help
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81
Q

Define Hirsutism

A

A clinical condition where females have excess hair growth in a male pattern distribution including the face, back, chest and abdomen

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82
Q

What are the causes of Hirsutism?

A
  • PCOS (most common in women of reproductive age)
  • Androgen-secreting tumours
  • Congenital adrenal hyperplasia
  • Cushing’s
  • Acromegaly
  • Severe insulin resistance
  • Idiopathic
  • Drugs = steroids, phenytoin, ciclosporin
  • Anorexia nervosa
  • Hypothyroidism
  • Familal traits
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83
Q

Hirsutism investigations

A
  • Serum testosterone
  • Other hormone levels = DHEAS, 17-hydroxyprogesterone, prolactin, TSH as indicated
  • Pelvic USS = to identify polycystic or tumours
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84
Q

Hirsutism management

A
  • Treat underlying cause
  • Cosmetic = shaving, waxing, laser hair removal
  • Medical = anti-androgens (spironolactone, flutamide), OCC, insulin-sensitising drugs
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85
Q

What are the causes of Hyperaldosteronism?

A

Primary (increased aldosterone secretion):
- Conn’s syndrome (adrenal adenoma or bilateral adrenal hyperplasia)
- Familial
- Adrenal carcinoma

Secondary (increased activation of RAAS):
- Renal artery stenosis
- HF
- Liver cirrhosis
- Reninoma
- CKD
- Acute glomerulonephritis

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86
Q

Hyperaldosteronism features

A
  • HTN
  • Hypokalaemia
  • Muscle weakness/fatigue
  • Assythmias
  • Metabolic alkalosis
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87
Q

Describe the Renin-angiotensin-aldosterone system

A

1) Renin is released from the kidneys in response to low BP, low sodium or sympathetic NS activation
2) Renin converts angiotensinogen to angiotensin 1
3) Angiotensin 1 is converted to angiotensin 2 by ACE
4) Angiotensin 2 increases BP by: vasoconstriction, stimulating aldosterone release, stimulating ADH release, promoting thirst
5) Aldosterone acts on the DCT and collecting ducts where it causes the reabsorption of sodium and the excretion of potassium

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88
Q

Hyperaldosteronism investigations

A

1st line = Aldosterone:Renin ration - high ratio suggests hyperaldosteronism

2nd line:
- HRCT or MRI to locate adrenal lesions
- Selective venous sampling (Gold standard for locating source)

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89
Q

Hyperaldosteronism management

A

Medical:
- In cases of bilateral adrenal hyperplasia = K-sparing diuretics (spironolactone, amiloride, eplerenone)

Surgical:
- If due to adrenal adenoma = resection of tumour or affected adrenal gland

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90
Q

Define Hyperosmolar hyperglycaemic state (HHS)

A

A life-threatening condition associated w/ T2DM - it results from severe hyperglycaemia, profound dehydration and altered mental state (due to insulin deficiency and osmotic diuresis)

Suspect in pts w/:
- Marked hyperglycaemia (>30) w/out significant ketosis (<3) or acidosis (pH > 7.3, bicarb > 15))
AND
- Osmolality > 320

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91
Q

What are the risk factors associated w/ Hyperosmolar hyperglycaemic state?

A
  • T2DM
  • Advanced age
  • Infections or illness
  • Medications that affect glucose metabolism
92
Q

Hyperosmolar hyperglycaemic state features

A
  • Profound dehydration w/ dry mucous membranes
  • Polydipsia and polyuria
  • Altered mental state - confusion to coma
  • Neuro = seizure or focal deficits
  • Hypotension
  • Tachycardia
93
Q

Hyperosmolar hyperglycaemic state investigations

A
  • BM
  • Serum osmolality
  • U&Es
  • Urinalysis for ketones
  • Evaluation of underlying cause
94
Q

Hyperosmolar hyperglycaemic state management

A
  • Fluid resuscitation is mainstay - w/ saline
  • Glucose levels should not fall by >5mmol per hour
  • Insulin (0.05 units/kg/hr) can be commenced if sugars stop falling by fluids alone, or if there is ketosis
95
Q

What are the different types of Hyperparathyroidism?

A
  • Primary = caused by parathyroid adenoma, hyperplasia of all 4 glands or parathyroid carcinoma
  • Secondary = due to Vit D deficiency, abnormal PTH activity or inadequate Ca intake
  • Tertiary = occurs after prolonged secondary hyperparathyroidism due to CKD, gland becomes hyperplastic
96
Q

Hypercalcaemia features

A
  • Bones= bone pain
  • Stones = renal stones
  • Groans = GI issues - N&V, constipation, indigestion
  • Psychiatric moans = lethargy, fatigue, memory loss, psychosis, depression
97
Q

Hyperparathyroidism investigations

A
  • Ca levels
  • Phophate levels
  • PTH levels
  • ALP levels

Primary HPT = high Ca, low Phos, high/normal PTH, high ALP

Secondary = low/normal Ca, low/high Phos, high PTH, high ALP

Tertiary = normal/high Ca, low/normal Phos, high PTH, high ALP

Vit D deficiency = normal/low Ca, low Phos, high PTH, high ALP

98
Q

Hyperparathyroidism management

A
  • Primary = parathyroidectomy
  • Secondary = address underlying cause, Vit D replacement and phosphate binders
  • Tertiary = total/subtotal parathyroidectomy, Cinacalcet (mimics Ca action on tissues)
99
Q

What does PTH do?

A
  • Stimulates osteoclasts
  • Increases Ca reabsorption in the DCT
  • Increases phosphate excretion
  • Stimulates alpha-hydroxylate to activate vit D in the kidneys
100
Q

What does Vitamin D do?

A

Stimulates osteoclast activity and Ca absorption in the gut

101
Q

Define Thyrotoxicosis

A

A syndrome resulting from the presence of excessive thyroid hormones, not always due to thyroid overactivity

102
Q

What are the causes of Hyperthyroidism?

A

Primary:
- Grave’s
- Toxic adenoma
- Toxic multinodular goitre
- Thyroiditis

Secondary:
- Amiodarone
- Lithium
- TSH producing adenoma
- Choriocarcinoma (bHCG can activate TSH receptors)
- Gestational hyperthyroidism
- Pituitary resistance to thyroxine (-ve feedback failure)
- Struma ovarii (ectopic thyroid tissue in ovarian tumours)

103
Q

Hyperthyroidism features

A
  • Increased basal metabolic rate
  • Heat intolerance
  • Tachycardia and arrhythmias
  • WL
  • Diarrhoea
  • Sweaty skin
  • Insomnia and sleep disturbances
  • Restlessness and tremor
  • Goitre
  • Mood disturbances
  • Menstrual disturbances

Grave’s specific:
- Exophthalmos, proptosis and lid lag
- Thyroid acropachy = soft tissue welling in extremities (nail clubbing and periosteal new bone growth)
- Pretibial myxoedema = mucopolysaccharide deposition in the dermis leading to oedema and skin thickening, mostly in the shins

104
Q

Hyperthyroidism investigations

A
  • TFTs = high T4, low TSH
  • Antibody tests
  • Thyroid US
  • Radioiodine uptake test = diffuse uptake in Grave’s, focal uptake in a toxic nodule
105
Q

Hyperthyroidism management

A

Medical:
- Antithyroid drugs (1st line) = Carbimazole or propylthiouracil
- Propranolol for symptomatic relief
- Radioiodine = for definitive treatment, kills the thyroid tissue and then you replace w/ levothyroxine

Surgery:
- Thyroidectomy + replacement = for pts w/ large goitres causing compression, suspicion of malignancy or when other treatment is contraindicated or refused

106
Q

Define Thyroid storm

A

A life-threatening emergency due to thyrotoxicosis

It is often triggered by stressors e.g. surgery, trauma or infection

107
Q

Thyroid storm features

A
  • Restlessness and agitation
  • High-output heart failure
  • Profound tachycardia
  • Fever
  • Delirium and altered mental state
108
Q

Thyroid storm management

A
  • Counteract peripheral action of thyroxine = propranolol and digoxin to control HR and manage cardiac symptoms
  • Inhibit thyroid synthesis = propylthiouracil through a NG tube and Lugol’s iodine
  • Inhibit peripheral conversion of T4 to more active T3 = prednisolone or hydrocortisone
  • Supportive care = fluids, cooling measures, address precipitating factors
109
Q

Define Hypocalcaemia

A

Serum Ca levels < 2.1

110
Q

What are the causes of Hypocalcaemia?

A

W/ low PTH:
- Hypoparathyroidism
- Impaired PTH excretion = low magnesium, calcimimetics (cinacalet), Ca receptor mutations

W/ high PTH:
- Vit D deficiency
- Pseudohypoparathyroidism
- Bisphosphonate use

Due to compartmental shift:
- Alkalosis (increases Ca affinity for binding to albumin)
- Massive blood transfusion
- Artefact
- Osteoblastic mets
- Hungry bone syndrome (after parathyroidectomy)
- Acute pancreatitis
- Severe hyperphosphataemia which leads to complex formation w/ Ca e.g. secondary to tumour lysis syndrome, rhabdomyolysis, paraentral feeding

111
Q

Hypocalcaemia features

A

SPASMODIC:

  • Spasms (trousseau’s sign)
  • Perioral paraesthesia
  • Anxiety/irritability
  • Seizures
  • Muscle tone increase (colic, dysphagia)
  • Orientation impairment (confusion)
  • Dermatitis
  • Impetigo herpetiformis
  • Chvostek’s sign
  • ECG shows prolonged QTc
112
Q

Hypocalcaemia management

A
  • Address underlying cause
  • Mild = oral supplements
  • Severe (ECG changes/clinical features) = IV calcium gluconate
113
Q

Define Hypoglycaemia

A

Blood glucose < 3.5

114
Q

What are the causes of Hypoglycaemia?

A
  • Drugs = insulin, Sulphonylureas, GLP-1 analogues, DDP-4 inhibitors, Beta-blockers
  • Alcohol
  • Acute liver failure
  • Sepsis
  • Adrenal insufficiency
  • Insulinoma
  • Glycogen storage disease
115
Q

Hypoglycaemia features

A

Adrenergic symptoms (<3.3):
- Trembling
- Sweating
- Palpitations
- Hunger
- Headache

Neuroglycopenic symptoms (<2.8):
- Double vision
- Difficulty concentrating
- Slurred speech
- Confusion
- Coma

116
Q

Hypoglycaemia management

A

Mild (pt is conscious):
- ABCDE
- 15-20g of fast acting carbohydrate (glucose tablet/gel, non-diet soda, sweets, frit juice)
- Follow up w/ slower carbohydrates (e.g. toast)

Severe (pt unconsciousness/seizing):
- ABCDE
- 200ml 10% dextrose IV (or 20% via large vein)
- If no IV access = 1mg IM glucagon (doesn’t work if alcohol ingestion as alcohol blocks gluconeogenesis)

117
Q

What are the causes of Hypogonadism?

A

Primary:
- Klinefelter’s (XXY)
- Orchitis
- Testicular trauma
- Chemo
- Radiation

Secondary:
- Kallmann’s (failure of GNRH neurons to migrate resulting in anosmia and hypogonadotropic hypogonadism)
- Pituitary adenomas
- Hyperprolactinaemia
- Anorexia nervosa
- Opioid use
- Glucocorticoid use
- HIV
- Hemochromatosis

118
Q

Hypogonadism features

A
  • Lethargy
  • Weakness
  • Weight gain
  • Loss of libido
  • Erectile dysfunction
  • Gynecomastia
  • Depression
  • Infertility
  • Osteoporosis
119
Q

Hypogonadism investigations

A
  • FBC, U&E, LFTs
  • Bone profile
  • Fasting glucose and lipids
  • PSA
  • Oestrogen, testosterone, sex hormone binding globulin (SHBG)
  • LH/FSH
  • Prolactin
  • TSH/thyroxine
  • Cortisol
  • Pituitary MRI
  • CXR
  • Karotyping
120
Q

Hypogonadism management

A

HRT = either topical, buccal, oral or IM testosterone

121
Q

What are the causes of Hypoparathyroidism?

A
  • Neck surgery or radiation therapy
  • AI polyendocrine syndrome
  • Familial forms
122
Q

Hypoparathyroidism features

A
  • Hypocalcaemia
  • Neuropsychiatry = anxiety, depression, cognitive impairment
  • Ocular symptoms = cataracts, impaired night vision
  • Dental abnormalities = dental enamel hypoplasia, tooth discolouration
123
Q

Hypoparathyroidism investigations

A
  • Serum Ca (low) and phosphate (high)
  • PTH levels (low/inappropriately normal)
  • Vit D levels
  • Low urinary Ca
  • Prolonged QTc
124
Q

Hypoparathyroidism management

A

Ca and Vit D supplementation

Close monitoring

125
Q

What are the causes of Hypothyroidism?

A
  • AI = Hashimoto’s, atrophic thyroiditis, polyendocrine syndromes
  • Iatrogenic = surgical removal, radioablations, radiation therapy
  • Congenital = Thyroid aplasia, Pendred syndrome (defect in thyroxine synthesis)
  • Iodine deficiency/excess
  • Infiltrative disorders = sarcoid, haemochromatosis
126
Q

Hypothyroidism features

A
  • Peripheral = dry/thick skin, brittle hair, scanty secondary sexual hair
  • Queen Anne’s sign = loss of other 1/3 of eyebrows
  • Cold intolerance
  • Head and neck = macroglossia, puffy face, goitre
  • Cardiac = bradycardia, cardiomegaly
  • Neuro = carpal tunnel, slow relaxing reflexes, cerebellar ataxia, peripheral neuropathy, loss of concentration
  • Joint pain
  • Menorrhagia
127
Q

Hypothyroidism investigations

A
  • TFTs (1st line)
  • Antibody testing = anti-TPO, anti-thyroglobulin, Anti-TSH receptor
  • Imaging and biopsy
  • Iodine levels
128
Q

Hypothyroidism management

A
  • Levothyroxine
  • Recheck TFTs every 3 moths after initiation, and adjust dose accordingly
  • Once the TSH level is stable (2 similar measurements w/in reference range 3 months apart) then check TFTs annually
  • During pregnancy, LT4 is usually increased by 25-50mg
129
Q

Define Infertility

A

The failure to conceive over a 2-year period despite regular (3-4x a week) unprotected sexual intercourse

130
Q

What are the causes of Infertility?

A

Natrual:
- Increasing age
- Smoking and obesity
- Tight fitting underwear (males)
- Excessive alcohol
- Anabolic steroid use
- Illicit drugs

Genetic:
- Turner’s
- Klinefelter’s

Ovulation/endocrine:
- PCOS
- Pituitary tumours
- Sheehan’s
- Hyperprolactinaemia
- Cushing’s
- POI

Tubal abnormalities:
- Congenital
- Adhesions secondary to PID

Uterine abormalities:
- Bicornate
- Fibroids
- Asherman’s syndrome
- Endometriosis

Cervical abnormalities:
- After biopsy or LLETZ

Testicular:
- Cryptorchidism
- Varicocele
- Cancer
- Congenital defects

Ejaculation:
- Obstruction
- Retrograde ejaculation
- Premature ejaculation

131
Q

Infertility (female) investigations

A

Bedside:
- Thorough Hx
- Speculum and bimanual exam to assess for obvious abnormalities
- STI screen

Bloods:
- Serum progesterone testing (performed 7 days before period) - a rise in progesterone indicates a corpus luteum has formed
- Prolactin
- LH/FSH
- Anti-Mullerian hormone = measure ovarian reserves
- TFTs

Imaging:
-TVUS
- Hysterosalpingography
- Laparoscopy

132
Q

Infertility (male) investigations

A

Bedside:
- Thorough Hx
- Testicular exam
- Semen analysis

Bloods:
- Serum testosterone
- LH/FSH
- TFTs

133
Q

Infertility management

A

Treat underlying cause

Conservative:
- WL
- Smoking cessation
- Stress and alcohol reduction

Medical:
- Clomiphene (increases ovulation)
- FSH/LH injections
- GnRH or DA agonists

Surgical:
- IVF
- Intracytoplasmic sperm injection

134
Q

MEN-1 features

A

3 Ps

  • Parathyroid hyperplasia/adenoma
  • Pancreas = gastrinomas or insulinomas
  • Pituitary = prolactinomas
135
Q

MEN-2a features

A

2 Ps, 1 M

  • Pheochromocytomas
  • Parathyroid hyperplasia/adenoma
  • Medullary thyroid cancer
136
Q

MEN-2b features

A

1 P, 2 Ms

  • Pheochromocytomas
  • Medullary thyroid cancer
  • Mucosal Neuromas = on lips, tongues and eyes

(+ Marfanoid habitus = tall stature, arachnodactyly)

137
Q

MEN investigations

A
  • Genetic testing for mutations in MEN1 or RET genes
  • Hormonal assays
  • CT/MRI to look for tumours
138
Q

What are the BMI classifications of Obesity?

A
  • Overweight = 25 - 29.9
  • Class 1 = 30 - 34.9
  • Class 2 = 35 - 39.9
  • Class 3 (severe) = > 40
139
Q

Obesity management

A

Conservative:
- Dietary
- Exercise
- CBT and motivation counselling

Medical:
- Orlistat (lipase inhibitor)
- GLP-1 receptor agonists (e.g. liraglutide) - these should be discontinued after 12 wks if pt has not lost at least 5% of their initial body weight

Surgical - for BMI > 40, or > 35 with significant symptoms:
- Gastric bypass
- Sleeve gastrectomy
- Adjustable gastric banding
- Biliopancreatic diversion

140
Q

Define Osteomalacia

A

Metabolic bone disease due to Vit D deficiency that occurs after the epiphyses close

Characterised by osteopenia and disordered bone calcification (excess osteoid and unmineralised collagenous tissue)

141
Q

Osteomalacia features

A
  • Pain in lower back, hips and pelvis
  • Pseudofractures or Looser’s zones = incomplete stress fractures
  • Bone tenderness
  • Muscle weakness
142
Q

Osteomalacia investgiations

A
  • Vit D levels, Ca and phosphate
  • Bone biopsy (gold standard)
  • XR
143
Q

Osteomalacia management

A
  • Replenish Vit D and Ca
144
Q

Define Osteoporosis

A

Skeletal disease characterised by reduced bone mass and altered microarchitecture of the bone tissue

This results in increased bone fragility and increased fracture risk

Defined as DEXA scan T-score of -2.5 or lower

145
Q

What are the risk factors for Osteoporosis?

A

SHATTERED FAMILY

  • Steroid use
  • Hyperthyroidism/parathyroidism
  • Alcohol and smoking
  • Thin (BMI < 22)
  • Testosterone deficiency
  • Early menopause
  • Renal/liver failure
  • Erosive/inflammatory bone disease
  • Diabetes
  • Family Hx
146
Q

Osteoporosis features

A
  • Back pain due to fractured/collapsed vertebra
  • Loss of height over time
  • Stooped posture
  • Fractures from low-impact trauma
147
Q

Osteoporosis investigations

A
  • DEXA = -2.5 or lower
  • X ray
  • PTH, Ca and vit D levels
  • FRAX score = assessment of 10-year risk of major osteoporotic fracture
148
Q

Osteoporosis management

A
  • Bisphosphonates = to all pts w/ T score < -2.5, or T score -1 to -1.5 w/ a high FRAX score, or to all pts > 75 with a low-energy fracture
  • Denosumab
  • Ca supplements
149
Q

Define Pheochromocytoma

A

A catecholamine (adrenaline, noradrenaline and dopamine) secreting tumour that originates in the adrenal medulla

When a similar tumour arises in sympathetic nerve tissue = paraganglioma

150
Q

Pheochromocytoma features

A
  • Episodic HTN (esp when adrenals compressed)
  • Anxiety
  • WL
  • Fatigue
  • Palpitations
  • Excessive sweating
  • Headaches
  • Flushing
  • Fever
  • SOB
  • Abdo pain
  • Tremor
151
Q

Pheochromocytoma investigations

A
  • Plasma metanephrines (breakdown product of catecholamines) followed by urinary metanephrines = will be elevated
  • Adrenal CT
  • Paragangliomas can be identified using iodine-labelled metaiodobenzylguanidine (MIBG) scans or PET scans
152
Q

Pheochromocytoma management

A
  • Initial alpha blockade w/ phenoxybenzamine to prevent intraoperative hypertensive crisis
  • Beta blockers can then be added to manage tachycardia or arrhythmias if neccessary
  • Then, surgical resection
153
Q

What does the anterior pituitary secrete?

A
  • Growth hormone
  • Prolactin
  • LH and FSH
  • Thyroid stimulating hormone
  • Adrenocorticotrophin
154
Q

What does the posterior pituitary secrete?

A
  • Oxytocin
  • Vasopressin (ADH)
155
Q

Pituitary adenoma features

A
  • Specific hormone imbalance (if functional)
  • Headache (localised to front of head, persistent)
  • Bitemporal hemianopia
156
Q

Pituitary adenoma management

A
  • Tran-sphenoidal surgery
  • Radiotherapy in cases where complete tumour removal is not possible or reoccurs
  • Medication to target overproduction of functioning hormones
157
Q

Prolactinoma features

A

Women:
- Oligomenorrhea or amenorrhea
- Galactorrhoea
- Infertility
- Vaginal dryness

Men:
- Erectile dysfunction
- reduced facial hair growth

Both:
- Headaches
- Visual field defects

158
Q

What’s the difference between a micro and macroprolactinoma?

A
  • Micro < 10mm, macro > 10mm
  • Micro prolactin levels < 200, macro > 200 (usually above 1000)
  • Micro = hyperprolactinaemia, macro = hyperprolactinaemia + mass effects
159
Q

Prolactinoma management

A

Medical:
- Dopamine agonists (cabergoline) to increase dopamine inhibition

Surgery:
- Trans-sphenoidal resection +/- radiotherapy

160
Q

Define Hypopituitarism

A

Inadequate production of 1 or more pituitary hormones

Deficiencies in GH, FSH, LH, TSH, ACTH and ADH

161
Q

Hypopituitarism features

A

Depends on the missing hormone

GH:
- Central obesity
- Dry skin
- Reduced muscle strength
0 Decreased exercise tolerance

FSH/LH = Hypogonadotropism

TSH = hypothyroidism

ACTH = adrenal deficiency:
- Fatigue
- Anorexia
- Sarcopenia
- Myalgia
- GI upset

ADH = vasopressin deficiency

162
Q

Define Impaired fasting glucose

A

Fasting blood glucose levels between 6.1 - 6.9

163
Q

Define Impaired glucose tolerance

A

2-hour oral glucose tolerance test values between 7.8 - 11.1

164
Q

Define Pseudohypoparathyroidism

A

A genetic condition where the target organs (bones, kidneys and gut) fail to respond to normal levels of PTH

165
Q

Pseudohypoparathyroidism features

A
  • Short stature and shortened fingers
  • Hypocalcaemia
  • Bone pain and fractures
166
Q

Pseudohypoparathyroidism investigations

A
  • Hypocalcaemia on serum Ca
  • Normal or elevated PTH levels
167
Q

Pseudohypoparathyroidism management

A
  • Calcium supplements
  • Vit D supplements
168
Q

Define Secondary diabetes

A

A form of diabetes where there is a clear causative factor other than the typical insulin resistance or beta cell failure associated w/ T2DM

169
Q

What are the causes of secondary diabetes?

A

Pancreatic:
- Cystic fibrosis
- Chronic pancreatitis
- Haemochromatosis
- Cancer

Endocrine:
- Cushing’s = elevated cortisol leads to insulin resistance
- Acromegaly = elevated GH leads to insulin resistance
- Pheochromocytoma = chronic catecholamine-induced glucose intolerance
- Thyrotoxicosis = thyroid hormone excess can enhance hepatic gluconeogenesis and glycogenolysis and impair insulin secretion

Drugs:
- Steroids
- Atypical neuroleptics
- Thiazides
- Beta blockers = can inhibit insulin secretion

Glycogen storage disease (types 1 and 2)

170
Q

What does Cortisol do?

A

Metabolic:
- Increases blood sugar = glucose and glycogen synthesis in liver, breakdown of glycogen in muscles, decreases glucose uptake in muscles and adipose,
- Decreases protein synthesis
- Lipolysis

Immune:
- Prevents release of cytokines
- Inhibits T cell proliferation

Electrolytes:
- Increases Na absorption in gut
- Increases K (cellular shift due to increased Na)

171
Q

What are the side effects of metformin?

A

Lactic acidosis (avoid if renal impairment) and GI disturbances (switch to modified release)

172
Q

What are the side effects of Sulfonylureas (e.g. Gliclazide)?

A

Hypoglycaemia and weight gain

173
Q

What are the side effects of Pioglitazone?

A

Fluid retention (worsens HF) and weight gain

174
Q

What are the side effects of SGLT2 inhibitors?

A

DKA when used w/ insulin

Increased risk of UTIs

175
Q

What are the side effects of DPP-4 inhibitors (e.g. sitagliptin)?

A

Hypoglycaemia, GI upsets

176
Q

What are the side effects of GLP1 analogues?

A

Hypoglycaemia, GI upsets and may increase risk of pancreatitis when used w/ DPP-4 inhibitors

177
Q

Define Subclinical hyperthyroidism

A

A condition where TSH levels are below the reference range, but T3 and T4 levels are w/in normal range

Pts are usually asymptomatic, but may show moderate signs of hyperthyroidism

178
Q

What are the causes of Subclinical hyperthyroidism?

A
  • Early Grave’s disease
  • Autonomic nodular disease
  • Exogenous intake of thyroid hormones or iodine
  • Transient thyroiditis
179
Q

Subclinical hyperthyroidism investigations

A
  • 2 TFT results showing supressed TSH but normal T3/4, 3-6 months apart
  • Rule out transient causes
180
Q

Define Subclinical hypothyroidism

A

A condition where TSH levels are slightly raised (<10) but T3 and T4 levels are normal

Pts are usually asymptomatic, but may show moderate signs of hypothyroidism

181
Q

What are the causes of Subclinical hypothyroidism?

A
  • Early thyroid failure
  • Hashimoto’s
  • Lithium/amiodarone/radioiodine treatment
182
Q

Subclinical hypothyroidism investigations

A
  • 2 TFT results showing elevated TSH but normal T3/4, 3-6 months apart
  • Rule out transient causes
183
Q

Subclinical hypothyroidism management

A

Most pts require no treatment other than regular monitoring

If TSH > 10 or pt is symptomatic, consider replacing thyroxine

184
Q

What are the causes of SIADH?

A
  • Pituitary tumour
  • Tumours = SCLC, thymoma, lymphoma
  • Pulmonary disease = infections, pneumothorax, asthma, CF
  • CNS = infections, head injury (SAH)
  • Drugs = chemo, psychiatric drugs
  • Idiopathic
185
Q

What does ADH do?

A

Binds to aquaporin 2 channels in the collecting duct to increase water reabsorption

Vasoconstricts to increase BP

186
Q

SIADH features

A

Symptoms largely due to resulting dilutional hyponatraemia:
- Muscle cramps
- N&V
- Confusion, coma
- Seizures

187
Q

SIADH investigations

A
  • U&E = hyponatraemia
  • Plasma osmolality = low (<270)
  • Urine sodium = high (>20)
  • Urine osmolality = high (>100)
188
Q

SIADH management

A
  • Fluid restriction
  • Treat underlying cause
  • Monitor and correct sodium levels
  • Demeclocycline = reduces collecting ducts sensitivity to ADH
189
Q

What are the different types of Thyroid cancer?

A
  • Papillary = most common, occurs at 30-40 yrs, can met to bone a lung, excellent prognosis
  • Follicular = more common in women and places w/ low iodine, occurs at 30-60 yrs, mets to bone and lung
  • Medullary = originates from calcitonin-producing C cells, presents w/ hypocalcaemia and diarrhoea due to increased calcitonin, associated w/ MEN 2, mets to lymph nodes, worse prognosis
  • Anaplastic = rarest, occurs 60-70 yrs, rapidly growing mass w/ median survival of 8 months
  • Thyroid lymphoma = NHL, occurs 50-80 yrs, strongly associated w/ Hashimoto’s
190
Q

Thyroid cancer investigations

A
  • Thyroid USS for imaging
  • FNA for cytology
  • TSH and calcitonin levels
191
Q

Thyroid cancer features

A

Depend on the type, common ones include:

  • Lump/swelling in the neck
  • Voice changes
  • Dysphagia
  • Pain in neck or throat
  • Persistent cough
192
Q

Thyroid cancer management

A
  • Thyroidectomy or lobectomy followed by radioactive iodine treatment
  • then lifelong replacement
  • Chemo + radiation for anaplastic
193
Q

Define Waterhouse-Friderichsen syndrome

A

Bilateral adrenal haemorrhage and failure due to DIC caused by a significant bacterial infection

Most commonly due to Neisseria meningitides

194
Q

Waterhouse-Friderichsen syndrome features

A
  • Systemic illness due to infection
  • Septic shock due to adrenal insufficiency = marked hypotension, altered mental status
  • Multi-organ dysfunction
195
Q

Waterhouse-Friderichsen syndrome management

A
  • Aggressive fluid therapy
  • Vasopressor support
  • Broad-spectrum abx
  • Corticosteroid replacement therapy
196
Q

Define Congenital Adrenal Hyperplasia

A

A group of aurtosomalresessive disorders chaarcterised by impaired steroid hormone synthesis w/in the adrenal cortex due to enzyme defects

The most common type = 21-hydroxylase deficiency (an enzyme critical for the production of gluco/mineralocorticoids, cortisol and aldosterone) - it leads to elevated 17-hydroxyprogesterone levels

197
Q

Congenital Adrenal Hyperplasia features

A

Depends on the enzyme defects, typically features include:
- Ambiguous genitalia (esp in females) due to in-utero exposure to excessive androgens
- Salt wasting crisis at birth = diarrhoea and vomiting, hyponatraemia, hyperkalaemia, circulatory shock and metabolic acidosis
- Virilisation = development of masculine secondary sexual characteristics in females
- Precocious puberty in men

198
Q

Congenital Adrenal Hyperplasia investigations

A
  • 17-hydroxyprogesterone and ACTH are elevated in CAH
  • Cortisol is low
  • Corticotropin stimulation test is the gold standard for diagnosis
  • Genetic testing = Can confirm the diagnosis and identify the specific enzyme defect
  • Ultrasound can help in the assessment of internal sex organs in patients with ambiguous genitalia
199
Q

Congenital Adrenal Hyperplasia management

A
  • Addisonian crisis = fluids, NaCl replacement
  • Hydrocortisone and fludrocortisone
  • Sick day rules
  • Surgery to fix virilisation
200
Q

Congenital Adrenal Hyperplasia complications

A
  • Growth suppression
  • metabolic syndrome
  • Infertility
201
Q

Define Addisonian crisis

A

Acute, life-threatening deficiency in cortisol leading to hyponatraemia, hyperkalaemia and hypoglycaemia

202
Q

Addisonian crisis features

A

Symptoms:
- Fatigue/malaise
- Abdo pain
- N&V
- Myalgia
- Headache

Signs:
- Dehydration
- Hypotension
- Hypovolaemic shock
- Low-grade fever
- Confusion or coma
- Seizures

203
Q

Addisonian crisis management

A
  • ABCDE
  • Fluid resuscitation
  • IV or IM hydrocortisone 100mg as soon as suspected
  • Then regular hydrocortisone
  • IV glucose to correct hypoglycaemia
204
Q

Define Pituitary apoplexy

A

Infarction or haemorrhage of the pituitary gland

205
Q

Pituitary apoplexy features

A
  • Sudden and severe headache
  • Confusion
  • Fatigue
  • Fever
  • N&V
  • Addisonian crisis due to hypopituitarism and no ACTH
206
Q

Define Sheehan’s syndrome

A

Hypopituitarism due to large blood loss during child birth

This leads to ischaemia of the pituitary gland

207
Q

Define De Quervain’s thyroiditis

A

A self-limiting inflammatory illness of the thyroid gland usually due to a viral infection

208
Q

De Quervain’s thyroiditis features

A

Has 4 phases:
1) Thyroid swelling and discomfort w/ thyrotoxicosis (+fever like illness)
2) Brief euthyroid phase
3) Hypothyroid phase
4) Recovery euthyroid phase

Usually resolves w/in 3-6 months

209
Q

Define Hypokalaemia

A

Potassium levels < 3.5

210
Q

What are the causes of Hypokalaemia?

A

Renal (urine K > 20):
- Diuretics (furosemide, thiazides)
- Renal tubular acidosis
- Endocrine = Conn’s, Cushing’s
- Hypomagnesaemia

Extra-renal:
- Inadequate intake
- Gut loss = dialarhoea, vomiting, ileostomy, VIPoma, Zollinger-Ellison syndrome
- Redistribution into cells = beta agonists, insulin, theophylline, alkalosis (swaps for H+)

211
Q

Hypokalaemia features

A
  • Muscle weakness/cramps
  • Paraesthesia
  • Polyuria/polydipsia
  • Constipation
  • ECG = flattened T waves, prominent U waves, ST depression
212
Q

Hypokalaemia management

A
  • K between 3-3.5 = SandoK
  • K < 3 = cardiac monitoring, correct magnesium (low mag causes renal K wasting) and IV replacement (no more than 10mmol/hr in a peripheral vein)
213
Q

Define Hyperkalaemia

A

Potassium > 5.5

214
Q

Hyperkalaemia features

A
  • Paraesthesia
  • Muscle weakness
  • Oliguria
  • Arrhythmias (esp VF)
  • ECG = Tall tented T waves, flattened P waves, widened QRS complexes
215
Q

What are the causes of Hyperkalaemia?

A

Impaired excretion:
- AKI
- CKD
- ACEi
- Potassium sparing diuretics
- NSAIDs
- Heparins
- Ciclosporin
- Trimethoprim
- Renal tubular acidosis type 4
- Addison’s

Increased release from cells:
- Lactic acidosis
- Insulin deficicency
- Rhabdomyolysis
- Tumour lysis syndrome
- Massive haemolysis
- Digoxin toxicity
- Beta-blockers

216
Q

Hyperkalaemia management

A
  • Mild = 5.5-5.9 = repeat
  • Moderate = 6-6.4 = give potassium binders if can tolerate PO, give Calcium gluconate if ECG changes, give Insulin-glucose IV infusion, then give salbutamol if not coming down
  • Severe = >6.5 = give potassium binders if can tolerate PO, give Calcium gluconate, give Insulin-glucose IV infusion, then give salbutamol if not coming down
217
Q

What are the causes of Hypomagnesaemia

A

Decreased gut absorption:
- PPIs
- Insufficient intake
- Alcoholism
- Dialarhoea
- Malabsorption
- SB bypass
- Vomiting
- Short bowel syndrome

Redistribution to intracellular space;
- Refeeding syndrome
- Insulin
- Acute pancreatitis
- Alcohol withdrawal

Increased renal excretion:
- Loop and thiazide diuretics
- Digoxin
- Gentamicin
- Chemo
- Renal tubular acidosis
- Dialysis
- Genetic

218
Q

Hypomagnesaemia features

A
  • Weakness
  • Paraesthesia
  • Seizures
  • Confusion/Coma
  • Hypocalcaemia = low mag stops PTH release
  • Hypokalaemia = stimulates renal K loss
  • Ventricular arrhythmias
  • Chondrocalcinosis
219
Q

Hypomagnesaemia management

A
  • Mild (0.5-0.7) = oral replacement if symptomatic
  • Moderate (0.4-0.5) = magnesium salts (can cause diarrhoea) if asymptomatic, IV if symptomatic
  • Severe (<0.4) = IV replacement
220
Q

What are the causes of Hyponatraemia in a hypovolaemic patient?

A

Urinary Na > 20 (renal loss):
- Addison’s
- Renal failure
- Diuretics
- Osmotic diuresis

Urinary Na < 20 (loss elsewhere):
- Diarrhoea & vomiting
- Fistulae
- Burns
- Small bowel obstruction
- Excessive sweating

221
Q

What are the causes of Hyponatraemia in a euvolemic patient?

A

High urine osmolality = SIADH

Normal urine osmolality:
- Water intoxication
- Severe hypothyroidism
- Glucocorticoid insufficiency

222
Q

What are the causes of Hyponatraemia in a hypervolaemic patient?

A

Failures = cardiac, liver, renal

Nephrotic syndrome

223
Q

What are the causes of Hypernatraemia in a hypovolaemic patient?

A

Renal:
- Osmotic diuresis
- Loop diuretics

Other:
- D&V
- GI fistulae
- Burns

224
Q

What are the causes of Hyponatraemia in a hypervolaemic patient?

A
  • NaCL infusion
  • Salt water ingestion
  • Cushing’s syndrome
  • Conn’s syndrome
225
Q

What are the causes of Hyponatraemia in a euvolemic patient?

A
  • Vasopressin insufficiency
  • Vasopressin resistance
226
Q

Hypernatraemia symptoms

A
  • Fever and flushed skin
  • Restlessness/irritability
  • Increased BP
  • Oedema
  • Fluid retention
  • Oliguria
227
Q

Hyponatraemia symptoms

A

LOW SODIUM:

  • Levels of consciousness altered
  • Orthostatic hypotension
  • Weakness
  • Seizures
  • Osmolality low (serum)
  • Diarrhoea
  • Increased ICP
  • Urine osmolality high
  • More bowel sounds

Year 6 (12 decks)

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