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Phase 2A revision > Endocrine to work on > Flashcards

Endocrine to work on Flashcards

1
Q

Give 2 causes of primary hyperparathyroidism

A
  • Parathyroid adenoma
  • Hyperplasia
  • Parathyroid cancer
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2
Q

what are the clinical features of hypoparathyroidism?

A 
SYMPTOMS:
CATs go numb
1. convulsions / seizures
2. arrhythmias / anxious
3. tetany / muscle spasms
4. numbness

SIGNS:

  • CHVOSTEK’S SIGN - tap over facial nerve and look for spasm of facial nerves
  • TROUSSEAU’S SIGN - inflate BP cuff 20 mmHg above systolic for 5 mins = hand spasm - hypocalcaemia
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3
Q

what are the signs of hypoparathyroidism?

A
  • CHVOSTEK’S SIGN - tap over facial nerve and look for spasm of facial nerves
  • TROUSSEAU’S SIGN - inflate BP cuff 20 mmHg above systolic for 5 mins = hand spasm - hypocalcaemia
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4
Q

what is chvostek’s sign?

A

sign of hypoparathyroidism

tap over facial nerve and look for spasm of facial nerves

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5
Q

what is trousseau’s sign?

A

sign of hypoparathyroidism

inflate BP cuff 20 mmHg above systolic for 5 mins = hand spasm

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6
Q

what are the causes of hypoparathyroidism?

A
  • secondary to increased serum phosphate
  • severe vitamin D deficiency
  • reduced PTH function
  • drugs - calcitonin, bisphosphonates
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7
Q

Give 2 ECG changes that you might see in someone with hypercalcaemia

A
  1. Tall T waves

2. Shortened QT interval

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8
Q

Name 3 causes of hypocalcaemia

A 
Hypoparathyroidism
Vitamin D deficiency
Hyperventilation
Drugs
Malignancy
Toxic shock
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9
Q

Give 2 ECG changes that you might see in hypocalcaemia?

A
  1. Small T waves

2. Long QT interval

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10
Q

what are the clinical features of diabetic ketoacidosis?

A

SIGNS

  • Breath smells of pear drops (ketones)
  • Kussmaul’s breathing - deep, rapid breathing
  • Tachycardia
  • Hypotension
  • Reduced tissue turgor

SYMPTOMS

  • Nausea and vomiting
  • Dehydration
  • exacerbated by vomiting
  • Weight loss
  • Drowsy/confused
  • Abdominal pain
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11
Q

Give 3 endocrine diseases that can cause diabetes

A
  1. Cushing’s
  2. Acromegaly
  3. Phaeochromocytoma
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12
Q

Describe the treatment pathway for T2DM

A
  1. Lifestyle changes - lose weight, exercise, healthy diet and control of contributing conditions
  2. Metformin
  3. dual therapy of Metformin + one of the following:
    i) DPP4 inhibitor
    ii) sulphonylureas (gliclazide)
    iii) pioglitazone
  4. triple therapy
  5. insulin
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13
Q

How does metformin work in treating T2DM?

A

Increase insulin sensitivity and inhibits glucose production

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14
Q

How does sulfonylurea work in treating T2DM?

A

Stimulates insulin release

block ATP dependent K+ channels in beta cells -> causes depolarisations and opening of voltage gated Ca2+ channels -> stimulates insulin secretion

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15
Q

what are the side effects of Sulfonylurea?

A

Hypoglycaemia
weight gain
hyponatraemia

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16
Q

Name 5 possible diseases of the pituitary

A
  1. Benign pituitary adenoma
  2. Craniopharygioma
  3. Trauma
  4. Apoplexy/Sheehans
  5. Sarcoid/TB
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17
Q

What complications are associated with acromegaly?

A

type 2 diabetes
sleep aponea
heart disease
arthritis

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18
Q

What are the investigations for acromegaly?

A

1st line = IGF-1
2nd line = oral glucose tolerance test
3rd line = pituitary function tests
4th line = MRI

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19
Q

what are the causes of Addison’s disease?

A
  • autoimmune destruction (21-hydroxylase present in 60-90%) - most common in developed countries
  • TB - most common in developing countries
  • adrenal metastases- long term steroid use
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20
Q

What are the investigations for Addison’s disease?

A
  • SynACTHen test = giving synthetic ACTH does not increase cortisol levels
  • Serum electrolytes = low Sodium, high Potassium
  • FBC: Anaemia and eosinophilia
  • Morning serum cortisol = Reduced
  • Adrenal CT or MRI
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21
Q

what are the features of addisonian crisis?

A 
Vomiting
abdominal pain
profound weakness
hypoglycaemia 
hypovolemic shock
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22
Q

What is the management of adrenal crisis?

A

Immediate IV Hydrocortisone

Fluid resuscitation - saline (IV)

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23
Q

what is the clinical presentation of grave’s dermopathy?

A

Pretibial myxoedema – raised, purple red symmetrical skin lesions over anterolateral aspects of shin

Thyroid acropachy – clubbing, swollen fingers and periosteal bone formation

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24
Q

what is pretibial myxoedema?

A

raised, purple red symmetrical skin lesions over anterolateral aspects of shin

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25
Q

what is thyroid achropachy?

A

clubbing, swollen fingers and periosteal bone formation

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26
Q

Name 5 risk factors for Graves disease

A
  1. Female
  2. Genetic association
  3. E.coli
  4. Smoking
  5. Stress
  6. High iodine intake
  7. Autoimmune diseases
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27
Q

Name 5 autoimmune diseases associated with thyroid autoimmunity

A
  1. T1DM
  2. Addison’s disease
  3. Pernicious anaemia
  4. Vitiligo
  5. Alopecia areata
  6. Rheumatoid arthritis
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28
Q

Name 4 types of sporadic non toxic goitre

A
  1. Diffuse –> physiological –> Graves
  2. Multi nodular
  3. Solitary nodule
  4. Dominant nodule
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29
Q

what are the causes of hyperthyroidism?

A
  • Grave’s disease
  • Toxic multinodular goitre
  • Solitary toxic nodule/adenoma - benign
  • De Quervarians thyroiditis
  • Postpartum thyroiditis
  • Drug induced
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30
Q

Name 4 drugs which can induce hyperthyroidism

A
  1. Iodine
  2. Amiodarone
  3. Lithium
  4. Radioconstrast agents
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31
Q

What are the 4 main treatments for hyperthyroidism?

A
  1. Beta blockers - PROPRANOLOL
  2. Anti-thyroid drugs - CARBIMAZOLE
  3. Radioiodine
  4. Surgery - partial/total thyroidectomy
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32
Q

Give 5 side effects of anti-thyroid drugs

A
  1. Rash
  2. Arthralgia
  3. Hepatitis
  4. Neuritis
  5. Vasculitis
  6. Agranulocytosis - very serious
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33
Q

Briefly explain thyroid crisis/storm

A

Rapid deterioration of thyrotoxicosis

Hyperpyrexia, tachycardia and extreme restlessness Delirium –> coma –> death

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34
Q

What is the treatment for a thyroid crisis?

A

Large doses of oral carbimazole, oral propranolol, oral potassium iodide and IV hydrocortisone

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35
Q

Name 4 causes of primary hypothyroidism

A
  1. autoimmune thyroiditis
  2. postpartum thyroiditis
  3. iatrogenic
  4. drug induced
  5. iodine deficiency
  6. congenital
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36
Q

Give 2 examples of iatrogenic causes of hypothyroidism

A
  1. Thyroidectomy

2. Radioiodine therapy

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37
Q

Name 4 drugs that can cause hypothyroidism

A
  1. Carbimazole (used to treat hyperthyroidism)
  2. Amiodarone
  3. Lithium
  4. Iodine
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38
Q

Name 3 triggers of Hashimoto’s thyroiditis

A
  1. Iodine
  2. Infections
  3. Smoking
  4. Stress
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39
Q

what are the complications of Hashimoto’s thyroiditis?

A

hyperlipidaemia

Hashimoto’s encephalopathy

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40
Q

what are the clinical features of DI?

A

SYMPTOM

  • Polyuria
  • Polydipsia
  • No glycosuria

SIGNS

  • Dry mucosa
  • Sunken eyes
  • Changes in skin turgidity
  • Can lead to dehydration
  • Hypernatremia
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41
Q

what are the causes of cranial DI?

A 
Idiopathic 
Congenital defects in ADH gene 
Disease of hypothalamus 
Tumour – metastases, posterior pituitary 
Trauma – neurosurgery
Infiltrative disease
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42
Q

what are the causes of nephrogenic DI?

A
  • Hypokalaemia
  • Hypercalcaemia
  • Drugs
    - lithium chloride
    - Demeclocycline
    - glibenclamide
  • Renal tubular acidosis
  • Sickle cell disease
  • Prolonged polyuria of any cause
  • Familial (mutation in ADH receptor)
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43
Q

Give 3 possible differential diagnosis’s of DI

A
  1. DM
  2. Hypokalaemia
  3. Hypercalcaemia
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44
Q

What is the treatment for nephrogenic DI?

A
  • treat cause
  • thiazide diuretics - (BENDROFLUMETHIAZIDE) - Produces hypovolaemia which will encourage the kidneys to take up more Na+ and water in proximal tubule
  • NSAIDs - IBUPROFEN - Lower urine volume and plasma Na+ by inhibiting prostaglandin synthase. Prostaglandins locally inhibit the action of ADH
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45
Q

What is the treatment for cranial DI?

A
  • Treat underlying condition
  • Thiazide diuretics (BENDROFLUMETHIAZIDE) - sensitise renal tubules to endogenous vasopressin
  • DESMOPRESSIN - high activity at V2 receptor
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46
Q

Give 4 causes of polyuria

A
  1. Hypokalaemia
  2. Hypercalcaemia
  3. Hyperglycaemia
  4. Diabetes insipidus
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47
Q

what are the clinical features of SIADH?

A 
SYMPTOMS:
Nausea and vomiting
Headache
Lethargy
Cramps
Weakness
Confusion / irritability

SIGNS
raised JVP
oedema
ascites

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48
Q

what are the causes of SIADH?

A 
brain injury
infection
hypothyroidism
cancers
lung diseases
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49
Q

what are the investigations for SIADH?

A
  • ADH levels
  • U and Es (low sodium normal potassium),
  • fluid status

distinguish SIADH from salt & water depletion - test with 1-2L of
0.9% saline:
• Sodium depletion will respond
• SIADH will NOT RESPOND

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50
Q

Describe the treatment for SIADH

A
  1. Restrict fluid - <1L/day
  2. Give salt
  3. Loop diuretics - furosemide
  4. Demeoclocycline - inhibitor of ADH
  5. ADH-R antagonists - vaptans - primate water excretion with no loss of electrolytes
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51
Q

Give 4 local effects a pituitary adenoma

A
  1. Headaches
  2. Visual field defects - bitemporal hemianopia
  3. Cranial nerve palsy and temporal lobe epilepsy
  4. CSF rhinorrhoea
52
Q

Describe the triad of signs for DKA

A
  1. Hyperglycaemia - blood glucose >11 mmol/L
  2. Acidaemia - blood pH <7.3 or plasma bicarbonate <15 mmol/L
  3. Raised plasma ketones - urine ketones >2+
53
Q

Give 4 causes of DKA

A
  1. Unknown
  2. Infection
  3. Treatment error - not administering enough insulin
  4. Having undiagnosed T1DM
54
Q

Give 4 potential complications of untreated DKA

A
  1. Cerebral oedema
  2. Adult respiratory distress syndrome
  3. Aspiration pneumonia
  4. Thromboembolism
  5. Death
55
Q

Name 3 other types of diabetes other than T1DM, T2DM and DI

A
  1. Maturity onset diabetes of the young (MODY)
  2. Permanent neonatal diabetes
  3. Maternal inherited diabetes and deafness
56
Q

Name 3 exocrine causes of Diabetes

A
  1. Inflammatory - actue/chronic pancreatitis
  2. Hereditary haemochromatosis
  3. Pancreatic neoplasia
  4. Cystic fibrosis
57
Q

what are the clinical features of pheochromocytoma?

A 
SYMPTOMS
Headache
Profuse Sweating
Palpitations
Tremor 
SIGNS
Hypertension
Postural hypotension
Tremor
hypertensive retinopathy
Pallor
58
Q

what are the different types of pheochromocytoma?

A
  1. Familial type - more NAd

2. Sporadic - more Ad

59
Q

What are the investigations for pheochromocytoma?

A
  • Plasma metanephrines and normetanephrines = GOLD STANDARD
  • 24 hour urinary total catecholamines
  • CT – look for tumour
60
Q

What is the treatment for pheochromocytoma?

A

Without HTN crisis:
1st Line: Alpha blockers: PHENOXYBENZAMINE
Most patients will eventually get the tumour removed and then managed medically.

With HTN crisis:
1st Line: Antihypertensive agents: PHENTOLAMINE

61
Q

What is the management of a phaeochromocytoma crisis?

A

Non-competitive alpha-blocker e.g. phenoxybenzamine
Excision of paraganglioma
Biochemistry: measure plasma and serum metanephrines

62
Q

Give 5 risk factors for diabetic retinopathy

A
  1. Long duration DM
  2. Poor glycaemic control
  3. Hypertensive
  4. On insulin treatment
  5. Pregnancy
  6. High HbA1c
63
Q

Describe the treatment for diabetic nephropathy

A
  1. Glycaemic and BP control
  2. Angiotensin receptor blockers/ACE inhibitors - RAMIPRIL or CANDESARTAN
  3. Proteinuria and cholesterol control
64
Q

Give 5 risk factors for diabetic neuropathy

A
  1. Poor glycaemic control
  2. Hypertension
  3. Smoking
  4. High HbA1c
  5. Overweight
  6. Long duration DM
65
Q

Why do isolated mononeuropathies result from in diabetic neuropathy?

A

Occlusion of vasa nervorum - small arteries that provide blood supply to peripheral nerves

66
Q

Describe the pain associated with diabetic neuropathy

A

Burning
Paraethesia
Allodynia - triggering of pain from stimuli that doesn’t usually cause pain

67
Q

Describe the treatments for diabetic neuropathy

A
  1. Improve glycaemic control
  2. tricyclic antidepressants - AMITRIPTYLINE
  3. Pain relief - PARACETAMOL and TRAMADOL
68
Q

what infections can poorly controlled diabetes lead to?

A
  1. UTIs
  2. Staphylococcal infection of skin
  3. Mucocutaneous candidiasis
  4. Pyelonephritis
  5. TB
  6. Pneumonia
  7. rectal abscess
69
Q

How do incretin based agents treat diabetes?

A

Influence glucose homeostasis via:

  • glucose dependent insulin secretion
  • postprandial glucagon suppression
  • slowing gastric emptying
70
Q

How do Thiazolidinediones treat diabetes?

A

Effective glucose lowering agents

71
Q

What diseases are associated with polycystic ovary syndrome?

A
  1. Insulin resistance - T2DM
  2. Hypertension
  3. Hyperlipidaemia
  4. CV disease
72
Q

Give 5 symptoms of polycystic ovary syndrome

A
  1. Amenorrhoea
  2. Oligomenorrhoea
  3. Hirsutism
  4. Acne
  5. Overweight
  6. Infertility
73
Q

What criteria can be used to make a diagnosis of polycystic ovary syndrome?

A

Rotterdam diagnostic criteria

  1. Menstrual irregularity
  2. Clinical or biochemical evidence of hyperandrogenism
  3. Polycystic ovaries on USS
74
Q

Describe the treatment for polycystic ovary syndrome

A
  1. Hirsutism therapy - shaving/waxing excess hair OR oestrogen (e.g. OCP)
  2. Menstrual disturbance therapy - cyclic oestrogen/progesterone
  3. Metformin can improve hyperinsulinaemia and regulates menstrual cycle
75
Q

A 27-year- old woman comes to see you because she is having infrequent periods (oligomenorrhoea). You note, on examination, that she has facial acne and is overweight. What is the most likely diagnosis? Give 3 other signs you might see in this patient

A 
Polycystic ovary syndrome
Other signs: 
1. Hirsutism
2. Amenorrhoea
3. Infertility
76
Q

What investigations might you do in someone to confirm a diagnosis of Conn’s syndrome?

A
  • first line = aldosterone renin ratio - high
  • increased plasma aldosterone levels that aren’t suppressed with 0.9% saline infusion or fludrocortisone administration - DIAGNOSTIC
  • Bloods - plasma potassium = low
    4. ECG - flat T waves, ST depression and long QT
77
Q

Give 4 ECG changes you might see in someone with Conn’s syndrome

A
  1. Increased amplitude and width of P waves
  2. Flat T waves
  3. ST depression
  4. Prolonged QT interval
  5. U waves
78
Q

What is adrenal hyperplasia?

A

Defective enzymes mediating the production of adrenal cortex products - low levels of cortisol and high levels of male hormones

79
Q

How does adrenal hyperplasia present?

A

Salt loss
Females - ambiguous genitalia with common urogenital sinus
Males - no signs at brith, subtle hyperpigmentation and possible penile enlargement

80
Q

Briefly describe the pathophysiology of adrenal hyperplasia

A

Defective 21-hydroxylase –> disruption of cortisol biosynthesis
With or without aldosterone deficiency and androgen excess

81
Q

What diagnostic test would be done to confirm adrenal hyperplasia?

A

Serum 17-hydorxyprogesterone (precursor to cortisol) = high

82
Q

What is the treatment for adrenal hyperplasia?

A

Glucocorticoids - hydrocortisone
Mineralocorticoids - control electrolytes
If salt loss - sodium chloride supplement

83
Q

what are the clinical features of hyperkalaemia?

A 
SYMPTOMS
Fatigue
Generalised weakness
Chest pain
Palpitations
SIGNS
Arrhythmias
Reduced power
Reduced reflexes
Signs of underlying cause
84
Q

what are the causes of hyperkalaemia

A

IMPAIRED EXCRETION

  • AKI and CKD
  • drug effect
  • renal tubular acidosis (T4)

INCREASED INTAKE

  • IV therapy
  • increased dietary intake

SHIFT TO EXTRACELLULAR

  • metabolic acidosis
  • rhabdomyolysis
85
Q

What ECG changes might you see in someone with hyperkalaemia?

A

GO - absent P waves
GO LONG - prolonged PR
GO TALL - Tall T waves
GO WIDE - Wide QRS

86
Q

What is a complication for someone with hyperkalaemia?

A

Myocardial infarction –> death

87
Q

what are the clinical features of hypokalaemia?

A 
SYMPTOMS:
Asymptomatic
Fatigue
Generalised weakness
Muscle cramps and pain
Palpitations

SIGNS:
Arrhythmias
Muscle paralysis and rhabdomyolysis

88
Q

Give 3 causes of hypokalaemia

A
  • INCREASED EXCRETION
    • drugs e.g. thiazide, loop
    • renal disease
    • GI loss
    • increased aldosterone

REDUCED INTAKE
- dietary deficiency

SHIFT TO INTRACELLULAR
- drugs e.g. insulin, salbutamol

89
Q

What ECG changes might you see in someone with hypokalaemia?

A
  1. Increased amplitude and width of P waves
  2. ST depression
  3. Flat T waves
  4. U waves
  5. QT prolongation
90
Q

Name 5 types of thyroid cancer

A
  1. Papillary - thyroid epithelium
  2. Follicular - thyroid epithelium
  3. Anaplastic - thyroid epithelium
  4. Lymphoma
  5. Medullary - calcitonin C cells
91
Q

How does a medullary cancer of the thyroid present?

A

Diarrhoea
Flushing episodes
Itching

92
Q

what is the clinical presentation of de quervain’s thyroiditis?

A

Usually accompanied by fever, malaise and pain in the neck

93
Q

what is the treatment for de quervain’s thyroiditis?

A

Treat with aspirin and only give prednisolone for severely symptomatic
cases

94
Q

what are the side effects of metformin?

A

GI upset

lactic acidosis

95
Q

what is the mechanism of action for SGLT-2 inhibitors?

A

inhibits resorption of glucose in the kidney

96
Q

what are the side effects of SGLT-2 inhibitors?

A

UTI

97
Q

what is the mechanism of action for glitazones?

A

Activate PPAR-gamma receptor in adipocytes to promote adipogenesis and fatty acid uptake

98
Q

what are the side effects of glitazones?

A

Weight gain

Fluid retention

99
Q

what is the mechanism of action for levothyroxine?

A

synthetic T4

100
Q

what is the diagnostic criteria for diabetic ketoacidosis?

A

glucose >11mmol/L
pH <7.3
bicarbonate <15mmol/L
ketones >3mmol/l or ketones in urine

101
Q

what are the risk factors for hyperosmolar hyperglycaemic state?

A
  • infection
  • consumption of glucose rich fluids
  • concurrent medication (thiazides or steroids)
102
Q

what is the pathophysiology of hyperosmolar hyperglycaemic state?

A
  • Endogenous insulin levels are reduced but are still sufficient to inhibit hepatic ketogenesis but insufficient to inhibit hepatic glucose production
103
Q

what are the investigations for hyperosmolar hyperglycaemic state?

A

Random plasma glucose >11mmol/L
Urine dipstick: glucosuria
Plasma osmolality - high
U+E - ↓ total body K+, ↑serum K+

104
Q

what is the treatment for hyperosmolar hyperglycaemic state?

A
  • Replace fluid - 0.9% saline IV
  • Insulin - At low rate of infusion!
  • Restore electrolytes - e.g. K+
  • LMWH
105
Q

what conditions is hashimotos thyroiditis associated with?

A
  • other autoimmune conditions - coeliac disease, T1DM, vitiligo
  • MALT lymphoma
106
Q

what are the side effects of levothyroxine?

A
  • usually due to excessive doses

- GI disturbance, cardiac arrhythmias and neurological tremors

107
Q

what is the mechanism of action for carbimazole?

A

prevents thyroid peroxidase from producing T3 and T4

108
Q

what are the side effects of GH receptor antagonists e.g. pegvisomant?

A
  • reactions at injection site
  • GI disturbance
  • hypoglycaemia
  • chest pain
  • hepatitis
109
Q

what is the mechanism of action for vasopressin antagonists e.g. tolvaptan?

A
  • inhibits vasopressin-2 receptor -> increases fluid excretion
  • causes aquaresis (excretion of H2O with no electrolyte loss) -> increased Na+
110
Q

what are the side effect of vasopressin antagonists e.g. tolvaptan?

A
  • GI disturbance
  • headache
  • increased thirst
  • insomnia
111
Q

what is the mechanism of action for vasopressin analogues e.g. desmopressin?

A

binds to V2 receptors -> aquaporin 2 inserted in collecting duct which increases water reabsorption

112
Q

what are the side effects of vasopressin analogies e.g. desmopressin?

A
  • headache
  • facial flushing
  • nausea
  • seizures
113
Q

what is the mechanism of action for metyrapone?

A
  • blocks cortisol synthesis by irreversibly inhibiting steroid 11 beta-hydroxide
114
Q

what are the side effects of metyrapone?

A
  • GI disturbance
  • headache
  • dizziness
  • drowsiness
  • hirsutism
115
Q

how would cortisol levels react to the synacthen test if there was secondary adrenal insufficiency?

A

short ACTH = no change

long ACTH = increase

116
Q

what investigation can be used to differentiate between cushing’s syndrome and cushing’s disease?

A

dexamethasone suppression test
- overnight = cushing’s syndrome (including disease) is confirmed when there is no suppression

  • 48 hours = cushing’s syndrome (not disease) = no suppression
117
Q

what cells do carcinoid tumours originate from?

A

enterochromaffin cells

118
Q

what do carcinoid tumours produce?

A

serotonin mainly

bradykinin
substance P
insulin
glucagon
ACTH
119
Q

what are the most common sites for carcinoid tumours?

A 
appendix (45%)
terminal ileum (30%)
120
Q

are carcinoid tumours malignant?

A
  • all carcinoid tumours are considered malignant
121
Q

what is carcinoid syndrome?

A

when there is hepatic involvement - hepatic metastases

122
Q

what is the clinical presentation of carcinoid tumours?

A
  • bluish-red flushing of face and neck(bradykinin release)
  • appendicitis/GI obstruction
  • RUQ pain (hepatic mets)
  • bronchoconstriction/bronchospasm with cough (bradykinin release)
  • congestive heart failure
  • diarrhoea
123
Q

what are the investigations for carcinoid tumours?

A
  • liver USS - confirms liver mets
  • urinalysis - high conc of 5-hydroxyindolacetic acid
  • CXR chest/pelvis
  • MRI/CT
124
Q

what is the treatment for carcinoid tumours?

A 
octreotide/lanreotide = somatostatin analogues
cure = surgical resection
125
Q

what is carcinoid crisis?

A
  • tumour outgrows blood supply/handled too much in surgery
    LIFE-THREATENING
  • vasodilation, hypotension, tachycardia, bronchoconstriction, hyperglycaemia
126
Q

what is the treatment for carcinoid crisis?

A

high dose OCTREOTIDE

127
Q

what are the clinical features of Conn’s syndrome?

A
  • hypertension
  • nocturia and polyuria
  • mood disturbance
  • difficulty concentrating
  • hypokalaemia

Phase 2A revision (38 decks)

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