Endocrinology and Diabetes Flashcards

1
Q

How will someone with hypoglycaemia present?

A

1) Sympathetic Symptoms: tremor, sweating, palpitations tachycardia, hunger
2) Neuroglycopenic Symptoms: Irritable, confused, drowsy, dizziness
3) LOC or Fits

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2
Q

How do you manage hypoglycaemia?

A

If alert and can swallow:
Fruit juice or glucose tablets

If confused but can swallow:
Glucose gels

If unconscious/Nil by mouth:
IV glucose 20%
IM glucagon if no IV access

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3
Q

How could you treat hypoglycaemia in the community?

A

Fruit Juice ideally
Sweets
Full fat coke

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4
Q

After immediate treatment for hypoglycaemia what further steps should be undertaken?

A

1) Need long acting carbohydrate (cereal, biscuits)
2) Then restart IV insulin

Constantly monitor BM

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5
Q

Why can somebody with DM get recurrent hypoglycaemia?

A

Injecting insulin despite not eating
Change of eating habits but haven’t changed insulin dose
Poor glucose monitoring
Drinking alcohol in excess (especially without food)

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6
Q

What does a basal bolus 1:10 quick acting (QA) to carb ratio mean?

A

Bolus:
You need to use 1 unit of QA insulin to every 10g of carbs you eat.

e.g. 30 g is 3 units

Basal is one injection of long-acting insulin all day

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7
Q

A patient is on NovoMix 30. What does this mean and when should the patient take there injection?

A

It is a mix of fast-acting insulin and intermediate insulin.
(aspart)

Should be administered just before meal time.

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8
Q

What are the colours of a NovoMix pen and a NOVORAPID FlexPen?

A

NovoMix 30: Blue
NOVORAPID: Orange + Black

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9
Q

What questions should you ask at an annual diabetic review?

A

Any insulin side effects? (lipodystrophy)
Any hypo events?
Check feet
BP, BM, HbA1c, Cholesterol
Screen for other diseases associated w/ DM

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10
Q

Why does a patient with DKA have a raised respiratory rate?

A

Become acidotic
Respiratory Compensation (hyperventilate to reduce CO2 levels and try and raise pH)

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11
Q

What are the clinical features supportive of DKA?

A

Previous Dgx of DM
Abdo Pain + Vomiting
Tachypnoea
Tachycardia
Polyuria
Polydipsia
Fruity Breath
Hypotensive (dehydrated)

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12
Q

What are the biochemical features of DKA?

A

Glucose: > 11.1 mmol/L
Ketones: > 3 mmol/L
ABG: Acidosis (pH < 7.3)
HCO3-: < 15 mmol/L

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13
Q

What is your immediate management for DKA and why?

A

1) IV Fluids (0.9% NaCl) to prevent hypotension + shock
2) IV Fixed rate insulin (Actrapid)
3) Correct electrolytes (Add K to IV fluids?)

Constant monitoring of fluid balance, ketones, pH, glucose, Bicarb

Treat underlying cause (infection?)

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14
Q

What further investigations do you perform after DKA?

A

Capillary/Lab Glucose
VBG
U+Es, FBC
Blood Cultures
ECG (K+)
CXR
MSU (Mid Stream Urine)
BP monitoring
RR monitoring

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15
Q

When do you need to admit somebody with DKA to HDU?

A

pH less than 7.1
Hypokalaemia
Low GCS
Low Sats
Systolic BP less than 90mmHg
Tachycardia or bradycardia
High Anion Gap

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16
Q

When after DKA should a patient be put back on their regular SC insulin and how should you do it?

A

Ketones < 0.6 mmol/L
pH > 7.3

DO NOT DISCONTINUE IV INSULIN UNTIL 30 MINS AFTER SC INSULIN GIVEN

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17
Q

What is the most likely cause of DKA?

A

1) Infection
2) Not taking enough insulin

Unknown dgx of diabetes

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18
Q

What steps should be taken to prevent future DKA in patients?

A

Education on insulin and ensure the correct dose
Insulin Pump or other continuous monitoring methods

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19
Q

Why are diabetics prone to foot ulcers?

A

Peripheral Neuropathy, so usually get an injury to the foot but carry on weight bearing causing further injury and ulceration.

Usaully have peripheral vascular disease too so have poor blood flow so unable to heal quickly

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20
Q

What features in a diabetic’s toes would make you suspect osteomyelitis?

A

Deep Ulcer (if probe ulcer and probe touches bone)
Swelling toes
Bruised toes
Pain in toes
Red toes

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21
Q

What investigations do you request if you suspect osteomyelitis?

A

X-ray
ESR/CRP/FBC
Blood Cultures + Swab Ulcer

Bone biopsy?

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22
Q

What does osteomyelitis look like on X-ray?

A

Osteopenia (bony erosion visible)
Periosteal Reaction (formation of new bone in response to injury)

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23
Q

What common organisms are involved in an infected diabetic foot ulcer and what antibiotics are commonly used?

A

Staph aureus - Flucloxacillin (doxycycline if allergic)
E coli
Klebsiella

Severe: add metronidazole

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24
Q

Describe the multidisciplinary care of diabetes related foot disease. What are the key steps in involved in ulcer healing?

A

Regular ulcer cleaning + wound dressing

Feet Screening from podiatrist
General diabetes monitoring from doctors/CNS

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25
Q

Why would a glucose monitor say error?

A
  • Blood test sample smeared or not large enough
  • Test strip incorrectly inserted
  • Wrong test strip used
  • Temperature of the strip is too warm or cold
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26
Q

What is the glucose conc if the reader says “Hi”?

A

Above 30 mmol/L

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27
Q

If a test confirms hyperglycaemia, what other test will you do?

A

Ketones

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28
Q

What is Hyperosmolar Hyperglycaemic state (HHS) and how does it present?

A

Hypovolaemia
Hyperglycaemia (30mmol/L+)
NO KETONURIA OR ACIDOSIS
Osmolality 320mosm/kg+

Confused, low GCS, dehydrated

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29
Q

What is the initial management of HHS?

A

1) IV NaCl (1L over 1hr) [caution in elderly]
2) Constant monitoring of glucose, ketones, BP, fluid status
If ketonuria or hyperglycaemia then insulin infusion
3) Correct electrolyte disturbances (K)
5) Prophylactic LMWH

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30
Q

What are the complications of HHS?

A

Mortality
Cerebral Oedema
Blood clots
Lactic Acidosis

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31
Q

What’s the target for HbA1c in DMII?

A

Below 6.5%
But can be relaxed on an individualistic basis (elderly or reduced life span, or at risk of hypo or drive or operate heavy machinery e.g.)

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32
Q

What’s a diabetes education course?

A

Helps you to lose weight (food choices)
Helps with dosing of insulin and monitoring of glucose

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33
Q

What’s the management for DMII?

A

1) Lifestyle Change
2) Metformin (Metformin MR if can’t tolerate) - Inhibits hepatic gluceogenesis
3) Empagliflozin (SGL2i) - increases Urinary excretion of Glucose
4) Sulfonylurea - Stimulates B cell insulin production
5) Pioglitazone - Reduces hepatic glucose output

Incretins:
Exenatide (stimulate gut-controlled insulin release) GLP-1
Sitagliptin (DDP-4i - Increase GLP-1 levels)

Insulin in late stages of disease

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34
Q

If a patient has a patient has CKD/microalbuminuria as well as diabetes what does this mean?

A

Higher QRisk score
Increases chance of CVD Death

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35
Q

What effect does DMI have on Potassium?

A

Insulin drives K into cells
Serum Potassium raised
Total body Potassium is low
Insulin can cause hypokalaemia so always have to observe K levels

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36
Q

How do we diagnose diabetes?

A

HbA1c levels in blood test
Fasting Plasma Glucose

Anti-insulin Ab (not routinely tested but will show in DMI)
Serum C-peptide will be low in type 1 (later on)

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37
Q

What are some causes of secondary diabetes?

A

Viral (CMV)
HIV Drugs, Steroids
Endocrine Disorders (Cushing’s)
Pancreatitis/Pancreatic Cancer
CF
Haemochromatosis
PCOS
PheochromocytomaW

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38
Q

What are the ADRs and contraindications to Metformin?

A

B12 Deficiency
GI Upset

Low eGFR
Hold metformin if having iodine contrast

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39
Q

Where do you have to be careful when prescribing Gliclazide?

A

Can cause hypoglycaemia
Warn drivers, elderly, machinery workers

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40
Q

When shouldn’t you prescribe glitazones? (Pioglitazone)

A

Cause Fluid retention and increase fracture risk

No in HF, Osteoporosis, Bladder cancer

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41
Q

What’s the main issue with flozins?

A

Thrush
UTI
Low BP

Hold if ill or fasting

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42
Q

Give an example of a fast acting, short action, intermediate and long action insulin?

A

FA: NovoRapid
SA: Actrapid
IA: Humulin I
LA: Glargine

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43
Q

What can we do if somebody is struggling with their BM with insulin injections?

A

Insulin Pump (constantly measures and pumps when needed)
Still need to inject before food

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44
Q

What are the short term complications of diabetes?

A

Hypoglycaemia
DKA
HHS
UTIs

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45
Q

What are the long term complications of Diabetes?

A

macrovascular:
Diabetic Foot Ulcers
Stroke
HTN
Coronary Artery Disease

microvascular:
Peripheral Neuropathy
Retinopathy
CKD

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46
Q

What are the risk factors for DMII?

A

Older Age
Black African or South Asian
FH
Obesity
High Carb Diet

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47
Q

How does DMII present?

A

Tiredness
Polyuria/Polydipsia
Glucosuria
Acanthosis Nigerians (thickening/darkening of skin)

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48
Q

What drug is first line for HTN in DMII?

A

ACEi

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49
Q

What clinical features will be present with an adrenal crisis?

A

Post infection/surgery/trauma
On long term steroids (steroid withdrawal)

Fatigue
N+V
Hypotensive
Tachycardia
Reduced consciousness/confusion

Hyponatraemia/Hyperkalaemia
^Urea
Hypoglycaemia

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50
Q

What is the immediate management for an adrenal/addisonian crisis?

A

1) ABCDE
2) IV Hydrocortisone
3) IV Fluids
4) IV glucose if hypoglycaemic

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51
Q

What advice can you give to long term steroid users/patients with Addison’s to prevent crisis?

A

Always have a steroid emergency card/medical alert jewellery with you
Double your steroid dose in times of illness
If severe D+V/surgery may beed glucocorticoids IV/IM

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52
Q

How does a patient present with hyponatraemia?

A

Confusion/Drowsiness
Nausea
Fatigue
Irritability

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53
Q

What medications can cause low Na?

A

Citalopram (SSRIs) (older age)
NSAIDs
Thiazide/Thiazide-Like Diuretcis
Loop Diuretics
Antipsychotics
Carbamazepine

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54
Q

What clinical assessments can help guide the management of hyponatraemia?

A

Can be caused water excess or sodium depletion

Urine Sodium:
>20mmol/L:
Addison’s
Diuretics
Renal Failure

<20mmol/L:
D+V
Burns
CF
HF
Liver disease

Urine Osmolality:
High:
SIADH

Low:
Hypothyroidism

TFT needed to rule out!
Serum Osmolality can be helpful

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55
Q

What’s the relevance of fluid status in hyponatraemia?

A

High:
Nephrotic Syndrome
CF
Liver Disease

Low:
D+V?

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56
Q

How do we tailor management of hyponatraemia in different scenarios?

A

Asymptomatic:
FLUID RESTRICTION

Hypovolemic:
Saline Fluids

Euvolemic:
Fluid Restriction

Hypervolemic:
Furosemide

SIADH:
Fluid/Salt Restriction + Loop Diuretic
Demeclocycline
Vaptans (emergency)

57
Q

What should you check if hyponatraemia isn’t improving?

A

Mg + Ca levels

58
Q

How quickly should you aim to correct the serum sodium in hyponatraemia?

A

4 to 6 mmol/l in a 24-hour period

59
Q

What complication can occur if sodium is corrected too rapidly? What symptoms are seen?

A

Osmotic Demyelination Syndrome (Central Pontine Myelinolysis)

Astrocyte apoptysis

Stroke like (irreversible):
Dysarthria
Dysphagia
Paralysis
Seizures
Confusion/Comas
Locked-in Syndrome

60
Q

What abnormality is picked up by an optician with a pituitary adenoma?

A

Bitemporal Hemianopia

61
Q

What condition is treated by Desmopressin?

A

Diabetes Insipidus

62
Q

What are some causes of hypernatraemia?

A

D+V
Burns
Diabetes Insipidus
Conn’s Syndrome
Iatrogenic (excessive saline)

63
Q

What is the immediate management for hypernatraemia?

A

5% Dextrose/ 0.9% (Half strength) Saline [HYPOTONIC RESUS]

Oral water if can tolerate

Apixiban (^Na is pro-thrombotic)

64
Q

What are the potential complications of acute severe hypernatraemia?

A

Cerebral Oedema
Subarachnoid/Subdural Haemorrhage

65
Q

What are some causes of hypocalcaemia? How would we investigate each one?

A

Post-thyoidectomy Hypocalcaemia (Hx)
Hypoparathyroidism (PTH levels)
CKD (U+Es, renal function)
Vit D deficiency (bloods)
Hypomagnasaemia (GI losses) (U+Es)

66
Q

What is the immediate management (investigations/treatment for acute hypocalcaemia?

A

ECG (prolonged QT)

Bloods:
Serum adjusted calcium and phosphate
PTH
U+Es
Magnesium
Vitamin D

Acute Management:
IV Calcium Gluconate
5% IV dextrose
Cholecalciferol (if Vit D deficient)

67
Q

What’s the long term treatment for hypocalcaemia?

A

Hypoparathyroidism:
Alfacalcidol (Vit D) + Oral Ca supplements

Mg deficiency:
Stop precipitating drugs
Give IG Mg replacement

68
Q

What are the most severe potential complications of acute hypocalcaemia

A

Torsade de Pointes
Seizures
Arrhythmias

69
Q

What are the 2 likely causes of hypercalcaemia? How do you differentiate between them?

A

Primary/Tertiary Hyperparathyroidism
Malignancy (Bone mets, multiple myeloma, PTHrP)

PTH levels:
High - primary hyperparathyroidism
Low - Malignancy

70
Q

What is the acute management of hypercalcaemia?

A

IV Fluids (saline)
IV bisphosphonates (move Ca to bone)
Treat underlying cause

71
Q

What medications help lower Ca levels and how long does it take?

A

Zoledronic Acid (bisphosphonate - moves Ca to bone)

Takes days - 1 week to work

72
Q

List some less common causes of hypercalcaemia?

A

Sarcoidosis
Thiazides
Dehydration
Addison’s
Thyrotoxicosis
Familial Hypocalciuric Hypercalcaemia

73
Q

What are the symptoms of hyperthyroidism?

A

Irritability
Hair thinning
Brittle Nails
Weight loss
Palpitations
Tremor
Increased appetite
Sweats

74
Q

What are the common physical signs o/e of hyperthyroidism?

A

Finger Clubbing
Lid retraction/Proptosis (Grave’s)
Tachycardia (Sinus or AF)
Resting Tremor
Lid-lag
Goitre
Palmar erythema

75
Q

What will TFTs show in hyperthyroidism?

A

High Thyroxine (T3/T4)
Low TSH (undetectable)

76
Q

What are the treatment options for hyperthyroidism?

A

1) Carbimazole
Propanolol (to control until thyroid function normal)
2) Radioactive iodine or thyroidectomy if severe (cause hypothyroidism)

77
Q

What are some issues regarding hyperthyroidism drugs?

A

Carbimazole + PTU (Propylthiouracil) both cause neutropenia (FBC if get sore throat/ulcers). Both in breastmilk too

Carbimazole harmful in first 2 trimesters (PTU instead)

RLN palsy in thyroidectomy
Iodine causes patient to emit radiation so avoid contact with children/pregnancy

78
Q

What are the common symptoms of hypothyroidism?

A

Tiredness
Weight gain
Constipation
Intolerance to cold
Low mood
Hoarse Voice

79
Q

What are the common signs seen in hypothyroidism?

A

Cold hands
Dry/thin hair
Non-pitting oedema
Bradycardia
Myxodema (puffy eyes)
Pallor

80
Q

What do TFTs show with hypothyroidism

A

Low T3/T4 (Thyroxine)
High TSH

81
Q

What are the treatment options for hypothyroidism?

A

Levothyroxine on an empty stomach with water
(low dose for elderly/IHD patients)

82
Q

What is subclinical hyperthyroidism? What can be some causes of this?

A

Normal T3/T4
Low TSH
(absent/mild symptoms)

Recent Tx for hyperthyroidism

83
Q

What is subclinical hyporthyroidism? What can be some causes of this?

A

Normal T3/T4
High TSH

Amiodarone
Poor thyroxine compliance

May or may not need Tx

84
Q

What are some causes of hyperthyroidism (thyrotoxicosis)?

A

Grave’s Disease
Toxic Multinodular Goitre
Acute phase of Hashimoto’s
Amiodarone therapy

85
Q

What antibodies will be +ve in grave’s disease?

A

TSR

86
Q

What will you find on clinical examination with Grave’s disease?

A

Exophthalmos/Proptosis
Pretibial Myxoedema (discoloured waxy skin on shins due to glycosaminoglycans deposits under skin)
Goitre
Finger Clubbing

87
Q

What is thyroid storm? How does it present and how do we treat it?

A

Acute Thyrotoxic Crisis
Fever
Tachycardia
Delirium
N+V
HTN
Hyperthyroid classic symptoms

Fluids
Carbimazole/PTU
B Blockers
Dexamethasone

88
Q

What are some specific issues around carbimazole and Propylthiquaracil?

A

Carbimazole - Pancreatitis
PTU - Liver reactions

Both cause bone marrow suppression
If patient presents with sore throat (urgent FBC & aggressive treatment)

89
Q

What are some causes of hypothyroidism?

A

Hashimoto’s Thyroiditis
Iodine Deficiency (developing world)
Excessive hyperthyroidism Tx/Thyroid Surgery
Lithium
Amiordarone
Postpartum thyroiditis
Secondary hypothyroidism (pituitary related)

90
Q

What are the 3 levels of adrenal cortex from outer>inner and what do they secrete

A

Zona Glomerulosa (Salt) - Aldosterone [mineralocorticoids]
Zona Fasciculata (Sugar) - Cortisol [glucocorticoid]
Zona Reticularis (Sex) - Androgens

91
Q

What does the adrenal medulla secrete?

A

Stress Hormones:
Adrenaline
Noradrenaline
Dopamine

92
Q

What time is best to check cortisol levels?

A

9am (highest in morning)

93
Q

What are primary and secondary causes of Addison’s disease?

A

Primary:
1) Autoimune
Infection (HIV)
Vascular
Mets/tumour/sarcoidosis

Secondary:
Pituitary tumour/surgery
ACTH deficiency

94
Q

How does Addison’s present?

A

Hyperpigmentation (palmar creases) - ACTH - ^MSH by melanocytes
Fatigue
Muscle Weakness
Loss of libido/pubic hair
Weight loss
Nausea + abdo pain
Dizziness/syncope

95
Q

What will investigations show with Addison’s disease?

A

Hyponatraemia
Hyperkalaemia
Hypoglycaemia
Hypercalcaemia
High urea
Mild anaemia

9am: Low cortisol w/ HIGH ACTH

Low ACTH - Secondary

Autoantibodies present in autoimmune

96
Q

What is the management for Addison’s?

A

Hyrdocortisone (replace cortisol)
Fludrocortisone (replace aldosterone)

Given Steroid ID card (double dose or IM in illness)

97
Q

How does a Short Synacthen test work? What will show in primary Addison’s disease?

A

GIVEN Synacthen (synthetic ACTH)
Cortisol levels taken before and after dose

If cortisol doesn’t double then primary Addison’s disease

98
Q

How does Hyperaldosteronism/Conn’s syndrome present?

A

Hypertension
Hypokalaemia (muscle weakness)
Metabolic Alkalosis

99
Q

What are some causes of secondary hyperaldosteronism?

A

Excessive Renin:
Renal Artery Stenosis
HF
Liver cirrhosis/ascites

100
Q

What investigation is needed for hyperaldosteronism and how will it look?

A

Aldosterone-to-renin ratio

Primary hyperaldosteronism:
High Aldosterone
Low Renin

Secondary:
High Aldosterone
High Renin

101
Q

What is the management for hyperaldosteronism?

A

Adrenal Adenoma: laparoscopic adrenalectomy
Bilateral adrenocortical hyperplasia: spironolactone (aldosterone antagonist)

102
Q

How can pituitary tumours present? What imaging do we use?

A

Functional (secrete excess hormones):
Acromegaly
Cushing’s
Prolactinoma

Non-functioning:
Hypopituitarism
Compression of optic chasm (bi-temporal hemianopia)

Pituitary MRI

103
Q

How does a prolactinoma present?

A

In women:
Amenorrhoea
Infertility
Galactorrhoea
Osteoporosis

In men:
Impotence
Loss of libido
Galactorrhoea

Bi-temporal hemianopia

104
Q

What are some causes of high prolactin?

A

Prolactinoma
Pregnancy/breast feeding
Anti-psychotics/metoclopramide/haloperidol
PCOS

105
Q

What is the management of a prolactinoma?

A

Dopamine Agonist (Cabergoline or bromocriptine)

Trans-spheonidal surgery if no response but usually is

106
Q

What causes acromegaly?

A

Growth Hormone excess
Usually - pituitary adenoma
(RARE paraneoplastic - lung/pancreatic cancer)

107
Q

How does acromegaly present?

A

Large hands and feet
Frontal bossing of forehead
Large ears
Protruding of jaw
Carpel tunnel
Large ears/nose/tongue
Headaches
Menstrual irregularities

Hypertrophic heart
HTN
Diabetes

108
Q

What investigations are needed for acromegaly?

A

Pituitary MRI - pituitary adenoma

Oral glucose tolerance test:
Growth hormone level before and after glucose (glucose normally surpresses GH)

IGF-1 can be raised in bloods

Colonoscopy Screen - ^incidence of colorectal cancer

109
Q

What is the management for acromegaly?

A

Trans-sphenoidal surgery to remove adenoma

If can’t tolerate surgery:
Bromocriptine
Somatostatin analogues
Radiotherapy

Colonic Screening!!

110
Q

What hormones (medications) are given in hypopituitarism?

A

Deficient in…
ACTH - Hydrocortisone
TSH - Levothyroxine
Gonadotropin - Testosterone/oestrogen/progesterone
GH - GH

111
Q

What are the causes of Cushing’s syndrome?

A

Cushing’s disease (pituitary adenoma secreting ACTH)
Adreanal adenoma (secreting ACTH)
Paraneoplastic syndrome (lung cancer)
Exogenous steroids

112
Q

What is pseudo-cushing’s?

A

Mimics Cushing’s
Usually alcohol excess/depression

113
Q

How does Cushing’s syndrome present?

A

Round face
Central obesity
Purple Striae
Buffalo hump
Proximal limb wasting
Hirsutism
Erythematous face
Osteoporosis

Diabetes
Bruise early

114
Q

What investigations are needed if you suspect Cushing’s?

A

24 urine free cortisol collection
Overnight dexamethasone suppression test
FBC
U&Es (adrenal adenoma secreting aldosterone - HYPOKALAEMIA)
HbA1C
MRI brain (pituitary adenoma)
CT chest (lung cancer)
CT Abdo (adrenal tumour)

115
Q

How does the dexamethasone suppression test and what does it show for each cause of Cushing’s?

A

Given a dose of dexamethasone before bed and cortisol/ACTH levels tested in the morning
Can be high or low dose

Ectopic ACTH (lung)
High ACTH + Cortisol

Adrenal adenoms:
Low ACTH + High cortisol

Pituitary adenoma (Cushing’s disease):
High ACTH + Supressed cortisol with high dose test (not low dose)

116
Q

What’s the management of Cushing’s disease?

A

Pituitary adenoma: Trans-sphenoidal surgery
Adrenal tumour: Laparoscopic adrenalectomy
Lung cancer: treat if can

117
Q

How does Diabetes insipidus present?

A

Polyuria
Polydipsia
Dehydration
Postural hypotension

118
Q

How does cranial vs nephropgenic diabetes inspidus differ? How can we figure out which one is the cause?

A

Cranial:
Hypothalamus doesn’t produce ADH
Brain trauma
Genetic mutation

Nephrogenic:
CD of kidney doesn’t respond to ADH
Genetic
Kidney disease (PCKD)
Electrolyte disturbances (High Ca/Low K)

Water deprivation test

119
Q

What investigations are needed for diabetes insipidus?

A

High serum osmolality
Low urine osmolality
High urine collection test
Water deprivation test

120
Q

How does the water deprivation test work and what do the results mean?

A

Patients will avoid fluids for 8 hours:
Primary polydipsia: High urine osmolality
Diabetes insipidus: low urine osmolality

Then given desmopressin:
Cranial: High urine osmolality
Nephrogenic: Low urine osmolality

121
Q

What is the management for diabetes insipidus (x2)?

A

Cranial: Desmopressin (monitor Na as can go low)
Look for Pituitary disease

Nephrogenic:
Ensure plenty of fluids
Low salt/protein diet
Diuretics
NSAIDs

122
Q

How does SIADH present?

A

Low Na:
Headache
Fatigue
Muscle aches/cramps
Confusion

Usually euvolemic

123
Q

How is SIADH diagnosed in terms of electrolyte levels?

A

Euvolaemia
Hyponatraemia
Low serum osmolality
High Urine sodium/osmolality

124
Q

What are some causes of SIADH?

A

Paraneoplastic (lung)
Brain pathology (trauma/infection)
Infections (pneumonia)
Drugs (SSRIs, carbamazepine)

125
Q

How can we manage SIADH?

A

Fluid restriction
Tolvaptan (vasopressin receptor antagonist)
Treat underlying cause

126
Q

What is the pathophysiology behind Osmotic demyelination syndrome?

A

1) When Na levels drop Na moves to brain cells
2) To prevent cerebral oedema the brain reduces solutes so water moves across back to other cells
3) So brain cells have low osmolality
4) If Na in blood rises too quickly, water will leave brain and move to the higher conc of Na in the blood
5) Causing demyelination of neurones

127
Q

How does hypercalcaemia present?

A

STONES (kidney stones)
BONES (painful bones)
ABDO GROANS (constipation+abdo pain)
THRONES (N+V)
MOANS (fatigue, depression)

Polyuria
Polydipsia

128
Q

What part of the bowel absorbs Ca?

A

Ileum (So malabsorption here could cause hypocalcameia)

129
Q

What investigations would you ask for in hypercalcaemia?

A

Serum Ca
CXR (PTHrP)
PTH
Urine Ca
25OH- Vit D
U+Es,TFTs,LFTs,FBC,Cortisol
US KUB

130
Q

How does hypocealcaemia present?

A

Tingling in hands
Hand Spasm
Perioral numbness
Laringospasm
Prolonged QT (ECG)
Seizures

+ve Chvostek’s sign (facial spasm when cheek is tapped)

131
Q

What is the pathophysiology. behind Vit D, PTH, Ca and phosphate?

A

PTH raises serum Ca by:
^absorption from bone
^absorption from kidneys
converts 25-hydroxycholecalciferol to calcitriol

PTH increases excretion of phosphate

1) Vit D3 from the sun
2) In the liver Vit D3 converted to 25-hydroxyvitamin D
3) In the kidney 25-hydroxyvitamin D to calcitriol
5) Calcitriol increases Ca reabsorption in the gut

132
Q

What are the following normal ranges of Na, K, Ca?

A

Na (133-146 mmol/L)
K (3.5-5.3 mmol/L)
Adjusted Ca (2.2-2.6 mmol/L)

133
Q

What are some causes of hyponatraemia?

A

Addison’s
Diuretics
NSAIDs
PPIs
CKD
HF
CLD
SIADH
Hypothyroidism
GI Losses
Nephrotic syndrome

134
Q

What are some causes of hypernatraemia?

A

Dehydration
Osmotic fiuresis
Excessive saline

135
Q

Why does someone with diabetes insipidus cause dehydration?

A

Water loss from polyuria
High serum osmolality
Stimulation of osmoreceptors causing thirst

136
Q

Explain the electrolyte abnormalities of diabetes insipidus?

A

Hypernatreamia due to poor water loss
Pre-renal impairment due to dehydration - high creatinine and urea

137
Q

What 2 immediate interventions for diabetes insipidus?

A

Fluid replacement
Desmopressin

138
Q

What are some complications of hypernatraemia?

A

Stroke
VTE
Seizures
Loss of consciousness

139
Q
A