PLABABLE

VERSION 1.1

ENDOCRINE
 Hypercalcaemia

Mnemonic Symptoms

Bones Painful bones especially seen in

primary hyperthyroidism
Stones Renal stones

Groans ● Constipation
● Pancreatitis
● Vomiting
● Nausea
Psychiatric ● Lethargy
moans ● Easy fatigue
● Depression

Causes
● Primary hyperparathyroidism
● Malignancy - Multiple myeloma
● Sarcoidosis
● Hyperthyroidism
● Prolonged immobilization
● Thiazides

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 Hypercalcaemia

High

2° Hyperparathyroidism
1° Hyperparathyroidism
● Vit D deficiency
P ● Hyperplasia
● ↓ Calcium intake
T ● Adenoma
● Chronic renal failure
H ● Carcinoma
● Vit D resistant rickets
L
E 1° Hypoparathyroidism PTH independent
V ● Surgical resection of hypercalcaemia
E parathyroid gland ● ↑ intake of calcium
L ● Autoimmune and Vit D
condition ● Malignancy

Low CALCIUM LEVEL High

Treatment
● Immediate: 0.9% NS to increase urinary excretion
of calcium
● Loop diuretic: Furosemide to increase calcium
excretion
● Bisphosphonates: Zoledronic acid to reduce
bone resorption
● Denosumab to reduce bone resorption

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 Hypocalcaemia

Symptoms “CATs go numb”

● Convulsions
● Arrhythmia
● Tetany and carpopedal spasm
● Paraesthesia (perioral, fingers and toes)

Causes
● Low PTH:
○ Parathyroid destruction by surgery,
metastases or amyloidosis
○ Autoimmune
● High PTH:
○ Vit D deficiency
○ PTH resistance - Pseudohypoparathyroidism
● Hyperventilation
● Acute pancreatitis

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 Hypocalcaemia

Signs
● Chvostek’s sign - Tapping of facial nerve
● Trousseau’s sign - Carpopedal spasm following
BP cuff inflation
● Prolonged QT interval

Treatment
● Symptomatic: IV calcium gluconate 10%
● Long term: Oral calcium supplements with vit D

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 Hyperparathyroidism

Cause Labs Others

Primary Parathyroid ↑ Calcium Associated

adenoma with MEN 1
↓ Phosphate and MEN 2a
Hyperplasia
↑ PTH Treatment is
Carcinoma surgery

Secondary CKD causes Low-normal Treatment

parathyroid calcium with calcium
hyperplasia and Vit D
due to long ↑ PTH
standing
hypocalcemia ↑Phosphate
in CKD

Tertiary Autonomous ↑ Calcium Surgery is

production of definite
PTH following ↑ PTH treatment
long standing
chronic ↑ Phosphate Cinacalcet
kidney
disease

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 Diabetes

Type 1 Type 2
(insulin deficiency) (insulin resistance)

Cause Associated with Risk factors:

HLA DR3, DR4 Obesity, Family
and islet cell history, metabolic
autoantibodies syndrome, PCOS,
H/O gestational
Prone for diabetes, and
ketoacidosis physical inactivity

Diagnosis Symptomatic patients:

Random glucose ≥11.1 mmol/L or
fasting ≥7 mmol/L

Asymptomatic patients:
Abnormal random plasma glucose or
two fasting glucose samples ≥7 mmol/L
+ HbA1c of 48 mmol/L (6.5%) or more

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 Diabetes

Type 1 Type 2
(insulin deficiency) (insulin resistance)

Treatment Insulin therapy Metformin

(first line)

Dual-therapy and
Triple-therapy (if
HbA1c >6.5%) of
metformin and
(DPP-4 inhibitor /
sulfonylurea /
pioglitazone)

If HbA1c is still
more than 6.5 - Add
Insulin

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 Diabetes Complications (Acute)

● Common in type 1 DM
● Metabolic acidosis and +ve
urine ketones
DIABETIC
● Treatment: IV 0.9% NS,
KETOACIDOSIS
Insulin infusion with
dextrose and electrolyte
monitoring

● Seen in type 2 DM
● High plasma glucose level,
HYPEROSMOLAR high serum osmolarity
HYPERGLYCAEMIC without significant
STATE ketoacidosis
● Treatment: 0.9% NSl and
electrolyte correction

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Diabetes Complications (Chronic)

● Proteinuria
DIABETIC ● Microalbuminuria
NEPHROPATHY ● Treatment to control HbA1c
● ACEi to prevent progression

● Reduce risk by proper

INCREASED
glycemic and BP control
RISK OF CVD
● Statins

Microvascular changes:
Aneurysms, hard exudates,
haemorrhages, cotton wool
spots, and neovascularisation
DIABETIC
RETINOPATHY
Treatment:
● Early: Glycaemic control
● Late: Panretinal
photocoagulation, intravitreal
steroids and anti- VEGF

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Diabetes Complications (Chronic)

● Glove and stocking

neuropathy
DIABETIC ● Burning, numbness and
NEUROPATHY tingling sensation in the
extremities
● Tight glycemic control and
prevention of foot trauma

● Glycemic and BP control,

Smoking cessation
DIABETIC ● Wound management
FOOT ULCER ● Foot interventions to prevent
ulcer formation such as
well-fitting footwear

PLABABLE
 Diabetes Ketoacidosis

Presentation
● Polyuria
● Polydipsia
● Dehydration
● Sweet smelling breath
● Altered mental status or even coma
● Most common in type 1 diabetes

Signs
● Dry mucous membranes
● Hypotension
● Tachycardia

Precipitating causes: Infection, stoppage of insulin,

drugs such as steroids and thiazides

Investigations
● ↑ Blood sugar level (BSL)
● Positive urine ketones
● ABG shows metabolic acidosis (low bicarb and
low pH)

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 Diabetes Ketoacidosis

Treatment
● 0.9% normal saline
● IV insulin infusion → 5% dextrose when
glucose falls below 12 mmol/L
● Hypokalemia → KCl infusion

Complications
● Cerebral oedema
● Pulmonary oedema
● Cardiac arrhythmia due to electrolyte imbalance

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 MODY

Brain trainer:

A 25 year old non-diabetic presents with mild

hyperglycemia. His father and grandmother had
some form of diabetes. What is the most likely
diagnosis?

➔ Maturity onset diabetes of the young

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 Latent autoimmune diabetes of
adulthood (LADA)

Latent autoimmune diabetes of the adult (LADA) is a

variant of type 1 diabetes which develops much slower
than type 1 diabetes.

It develops slowly and often mistaken for type 2

diabetes mellitus since it develops in adulthood.

Test to request for LADA:

GAD antibody testing

This test will help distinguish LADA from type 2

diabetes

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 Glycosuria

Brain trainer:

A non-diabetic patient after surgery has

glycosuria. What is the most likely diagnosis?

➔ Stress hyperglycemia

Infection or stress→cortisol→hyperglycaemia

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 Pre-Diabetes

Brain trainer:

What laboratory values are found with impaired

glucose intolerance?

➔ Fasting → 5.5 to 6.9 mmol/l

➔ 2 hr post-prandial → 7.8 to 11.0 mmol/l

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 Hyperprolactinaemia

Causes
● Prolactinoma
● Hypothyroidism
● Drugs: antipsychotics (risperidone & haloperidol)
and domperidone
● Brain injury

Presentation
● Females: Inhibits FSH and LH causing menstrual
irregularity (amenorrhea) and galactorrhoea
● Males:
○ Secondary hypogonadism
○ Reduced libido
○ Gynecomastia
○ Erectile dysfunction
● Visual symptoms: Bilateral hemianopia
● Headache

Bitemporal Hemianopia
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 Hyperprolactinaemia

Investigations
● ↑ serum prolactin level
● Pituitary MRI
● Visual field testing

Dopamine agonist
(cabergoline or
bromocriptine)

Treatment

Radiotherapy or Surgery
drug withdrawal

PLABABLE
 Thyroid Disorders

Hypothyroidism Hyperthyroidism
Decreased appetite but Increased appetite and
weight gain weight loss

Cold intolerance Heat intolerance

Constipation Diarrhoea

Bradycardia Palpitations and

tachycardia

Menstrual irregularities - Menstrual irregularities -

Menorrhagia Oligomenorrhea

Tiredness and lethargy Irritability and weakness

● Deep hoarse voice ● Tremor

● Reduced libido ● Increased sweating
● Brisk reflex
● Lid lag
● Palmar erythema

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 Thyroid Disorders

Hypothyroidism Hyperthyroidism
Causes Primary: Graves disease
(low T4 and high Antimicrosomal
TSH) antibodies against
Autoimmune - thyroid peroxidase
Hashimoto’s and
thyroiditis Antithyroglobulin
antibodies
Iodine deficiency
Toxic nodular
Drugs - Amiodarone goitre
and antithyroid
medications De Quervain’s
thyroiditis
Congenital
hypothyroidism Exogenous thyroid
ingestion
Secondary:
(Low TSH and T4)
● Hypopituitarism
● Isolated TSH
deficiency

PLABABLE
 Thyroid Disorders

Hypothyroidism Hyperthyroidism
Treatment Thyroxine (T4) Anti-thyroid drugs
supplementation ● Carbimazole
Bone marrow
If due to iodine suppression and
deficiency then cutis aplasia
replacement of (pregnancy)
iodine ● Propylthiouracil
Liver failure

Radio-iodine therapy

Thyroidectomy

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 Hyperthyroidism (pregnancy)

Pre-pregnancy and first trimester:

● Propylthiouracil

2nd, 3rd trimester + post-pregnancy

● Carbimazole
● Partial thyroidectomy (in 2nd trimester if
carbimazole is not effective)

Notes:
● Carbimazole has risk of aplasia cutis and
omphalocele in the fetus.
● Propylthiouracil: risk for hepatotoxicity in the mother
● Lowest possible dose should be prescribed
● Radioiodine therapy contraindicated

PLABABLE
 Thyroid Crisis

Brain trainer:

What is the management for thyroid storm?

➔ Propylthiouracil
➔ Palpitations → beta-blocker
➔ If infective etiology → broad-spectrum IV
antibiotics

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 Postpartum Thyroiditis

Brain trainer:

What medication is indicated to control the

symptoms of postpartum thyroiditis?

➔ Beta-blocker (palpitations + sweating)

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 ADH Disorders

Diabetes insipidus SIADH

(decreased ADH) (excess ADH)
Symptom Polyuria (>3L of urine/day)
s
Polydipsia and thirst

Causes Cranial: Small cell lung

Decreased secretion cancer
of ADH
Meningitis and
● Craniopharyngiom encephalitis
a
● Head injury Drugs:
● Sarcoidosis and Chlorpropamide
tuberculosis Oxytocin
● Infections: Amitriptyline
Meningitis and
encephalitis
● Post-radiotherapy

Nephrogenic:
ADH resistance

● Lithium
● Renal tubular
acidosis
● CKD
● Idiopathic
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 ADH Disorders

Urine Cranial Nephro- Psychogenic

Osmolality DI genic DI polydipsia
Normal <300 <300 <300
Water <300 <300 >800
deprivation
Desmopressi >800 <300 >800
n injection

Treatment

Diabetes Insipidus SIADH

Central: Desmopressin ● Fluid restriction

(mild cases)
Nephrogenic: High ● Demeclocycline
dose desmopressin with ● Conivaptan and
or without thiazide and tolvaptan
NSAIDs

PLABABLE
 Cushing’s Syndrome

Prolonged exposure to either endogenous or

exogenous cortisol

ACTH dependent ACTH independent

Cushing’s disease Adrenal adenoma

(ACTH from pituitary)

Ectopic ACTH producing Adrenal carcinoma

tumours

Excess ACTH Exogenous glucocorticoid

administration administration

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Cushing’s Syndrome

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 Cushing’s Syndrome

Investigation
To confirm cushing’s syndrome:
● 24-hour urinary free cortisol
● Low-dose dexamethasone suppression test
To identify the cause:
● Plasma ACTH: High - ACTH dependent
● Plasma ACTH: Low - ACTH independent
If ACTH is high to differentiate between pituitary
and ectopic cause:
● High-dose dexamethasone test
● MRI pituitary
If ACTH is low:
CT or MRI scan of abdomen to look for adrenal
tumour

Treatment
● Medications to inhibit cortisol synthesis
○ Metyrapone
○ Ketoconazole
○ Mitotane
● Surgery - Pituitary tumour
● Removal of exogenous corticosteroid
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 Pheochromocytoma

High levels of catecholamine production

Symptoms and signs
● Palpitations
● Profuse sweating
● Anxiety
● Sense of doom
● Headache
● Tremor
● Hypertension

Investigation
● 24-hour urinary metanephrines and VMA
● CT abdomen to locate the tumour

Associated with
● Multiple endocrine neoplasia (MEN 2A and 2B)
● Neurofibromatosis
● Von Hippel-Lindau syndrome

Treatment
Surgery after preoperative alpha-blocked with
phenoxybenzamine

PLABABLE
 Adrenal Insufficiency

Primary adrenal insufficiency/Addison’s disease

● Autoimmune cause
● Infections and haemorrhage
● Congenital adrenal hyperplasia
● Drugs: ketoconazole
Secondary adrenal insufficiency
● Hypothalamic and pituitary failure
● Long term steroid medication

Clinical features
Acute: Hypotension, shock, abdominal pain and
vomiting
Chronic: Fatigue, weakness, weight loss, salt
cravings, syncope, vomiting, and hyperpigmentation
in buccal mucosa and lips (primary)
Labs
● Low sodium and high potassium
● Early morning cortisol - Low
● ACTH: high in primary and low in secondary
● ACTH stimulation test: Cortisol does not rise

Treatment
● Hydrocortisone (Glucocorticoid)
● Fludrocortisone (Mineralocorticoid)
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 Addisonian Crisis

Causes
● Withdrawal of chronic steroid therapy
● Infection or stress

Clinical features
● Shock (confusion, postural hypotension,
tachycardia and oliguria)
● Abdominal pain (may be severe enough to mimic
an acute abdomen)
● Hypoglycaemia

Labs
● Cortisol and ACTH level
● FBC, U&Es, blood glucose
● Cultures (blood/urine/sputum)

Treatment
● IV fluids if shocked
● IV hydrocortisone 100mg
● Hypoglycaemia → IV glucose infusion
● If the condition improves in 72 hours → Switch to
oral steroids
● If an adrenal pathology is identified →
Fludrocortisone may be indicated

PLABABLE
 Hyperaldosteronism

Primary hyperaldosteronism or Conn’s

syndrome:
● Adrenal adenoma
● Adrenal hyperplasia
● Adrenal carcinoma

Secondary hyperaldosteronism
● Renin producing tumour
● Renal artery stenosis
Clinical features
● Hypertension
● Hypokalemia
● Metabolic alkalosis

Investigations
● Renin and aldosterone levels
● CT/MRI
● Adrenal venous sampling (gold standard for
primary)

Treatment
● Aldosterone antagonist - spironolactone
● Surgery: adrenalectomy

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 Sheehan Syndrome

Postpartum hypopituitarism due to pituitary necrosis

as a result of intra-partum or post-partum
haemorrhage causing hypotension

Symptoms
● Absence of lactation
● Amenorrhea or oligomenorrhea
● Hypothyroidism
● Adrenal insufficiency

Labs
● Low TSH and T4
● Low ACTH and cortisol
● Low LH and FSH
● Low estrogen

Treatment is with specific hormone replacement

Note: Pituitary apoplexy due to pituitary tumour

presents with acute headache, visual field defect and
symptoms of hormone deficiency

PLABABLE
 Amenorrhoea

Primary: Never had menses till 13 years without

secondary sexual characteristics and 15 years with
secondary sexual characteristics

Causes
● Constitutional delay
● Ovarian failure
● Hypothalamic failure
● Kallmann’s syndrome and Imperforate hymen
● Congenital adrenal hyperplasia

Secondary: Absence of menses for 6 months in

someone who have had menses before

Causes
● Pregnancy and lactation
● Menopause
● Premature ovarian failure and PCOS
● Pituitary and hypothalamic disease, and
hyperprolactinemia

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 Amenorrhoea

Investigation
● Primary ovarian failure: FSH and LH increased
● PCOS: LH:FSH ratio is increased
● Hyperprolactinemia:
○ Pituitary tumour (MRI)
○ ↑ Serum prolactin level
● Hypothyroidism:
○ Low T3
○ Low T4

Treatment
● Hormone replacement therapy - ovarian failure
● Treatment focussed on specific condition

PLABABLE
 Acromegaly

↑ Growth hormone secretion due pituitary tumour

Clinical features
● Enlargement of hands and feet
● Frontal bossing
● Macroglossia
● Prognathism (enlargement of jaw)
● Coarse facial features
● Hypertension, cardiomyopathy and arrhythmias
● Type 2 diabetes mellitus

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 Acromegaly

Labs
● IGF-1 (screening)
● Oral glucose tolerance test to confirm
● MRI scan of pituitary

Treatment
● Trans-sphenoidal surgery is the treatment of
choice
● Somatostatin analogues - octreotide
● GH receptor antagonist - pegvisomant
● Radiotherapy

PLABABLE
 Metabolic Acidosis

Arterial pH <7.35 and plasma bicarbonate <22

mmol/L
H+ excess:
● Ketoacidosis - Starvation and DM
● Lactic acidosis - Heart failure, Drugs
● Methanol, Salicylate and Ethylene glycol
poisoning
● Renal failure and Type 1 RTA

Loss of bicarbonate:
● Diarrhoea
● Type 2 RTA
● Drugs: acetazolamide

Respiratory compensation immediately by

hyperventilation

Renal compensation by increased bicarbonate

absorption or H+ excretion

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 Metabolic Alkalosis

Arterial pH > 7.45

Causes
● Vomiting (loss of H+)
● Hyperaldosteronism
● Hypokalemia (H+ shifts outside and K+ shifts
inside the cell)

● Respiratory compensation occurs immediately

and involves decreased respiratory rate to
increase PCO2
● Renal compensation occurs late and involves
increased excretion of bicarbonate

PLABABLE
Respiratory Acidosis & Alkalosis

Respiratory acidosis Respiratory alkalosis

Hypoventilation Hyperventilation
(PaCO2 > 45 mmHg) (PaCO2 < 35 mmHg)

● Severe asthma or ● Panic attack

COPD
● Aspirin toxicity (mixed
● Suppression of respiratory alkalosis
respiratory center by and metabolic
drugs such as opioids acidosis)

● Obesity
hypoventilation
syndrome

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 Pseudogout

Brain trainer:

A 29 year old woman presents with a swollen,

painful right knee joint.She also complains of
constipation, feeling cold and weight gain. Joint
aspiration of her knee joint will show what
finding?

➔ Positive birefringent crystals

PLABABLE
 Image Attributions

https://commons.wikimedia.org/wiki/File:Visual_field_bitemporal_hemianopia.png
RobertB3009 CC BY-SA 4.0

https://commons.wikimedia.org/wiki/File:Acromegaly_facial_features.JPEG
Philippe Chanson and Sylvie Salenave CC BY 2.0

https://en.wikipedia.org/wiki/File:Gout2010.JPG
James Heilman, MD CC BY-SA 3.0

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