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Endocrine Flashcards

1
Q

What is the function of insulin?

A
  1. Suppress hepatic glucose output
  2. Increase glucose uptake into insulin sensitive tissues
  3. Suppress lipolysis and breakdown of muscle
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2
Q

What is the function of glucagon?

A
  1. Increase hepatic glucose output
  2. Reduce peripheral glucose uptake
  3. Stimulate peripheral release of gluconeogenic precursors
  4. Gluconeogenic precursors = glycerol and AA’s which cause lipolysis and muscle glyconeolysis and breakdown
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3
Q

Define Type I DM

A

Autoimmune destruction of pancreatic beta cells leading to complete insulin deficiency

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4
Q

Epidemiology of Type I DM

A
  1. Presents age 5-15
  2. Accounts for 10% of all diabetes
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5
Q

Risk factors of Type I DM

A
  1. HLA DR3-DQ2 or HLA DR4-DQ8
  2. Northern European
  3. Autoimmune disease - 90%
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6
Q

Pathophysiology of Type I DM

A
  1. Autoantibodies attack Beta cells in Islets of Langerhans
  2. Creates insulin deficiency
  3. Leads to hyperglycaemia
  4. Continuous breakdown of glycogen from liver (gluconeogenesis)
  5. Leads to glycosuria
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7
Q

Signs and symptoms of Type I DM

A
  1. Classic triad = polydipsia, polyuria, weight loss (BMI<25)
  2. Possible ketosis
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8
Q

Diagnosis of Type I DM

A

Random plasma glucose > 11mmol/L
Fasting plasma glucose > 7 mmol/L

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9
Q

Treatment of Type I DM

A
  1. Insulin
  2. Short acting insulin (4-6h)
  3. Longer acting insulin (12-24h)
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10
Q

Aetiology of Type II DM

A
  1. gradual insulin resistance/pancreatic beta cells fail to secrete enough insulin OR BOTH
  2. Cushing’s
  3. Chronic pancreatitis
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11
Q

Risk factors of Type II DM

A
  1. Lifestyle - obesity, exercise, excess calorie/alcohol
  2. Asian men
  3. > 40 yrs
  4. Hypertension
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12
Q

Signs and symptoms of Type II DM

A
  1. Polydipsia
  2. Polyuria
  3. Glycosuria
  4. Central obesity
  5. Slow onset
  6. Blurred vision
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13
Q

Diagnosis of Type II DM

A
  1. Fasting plasma glucose > 7 mmol/L
  2. Random plasma glucose > 11 mmol/L
  3. HbA1c > 48 mmol/L
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14
Q

Treatment of type II DM

A

1st line = lifestyle changes
2nd line = Medications
-Metformin
- If HbA1c remains high; dual therapy of Metformin AND:
-DPP4 inhibitor
-Sulphonylurea
-Pioglitiazone
-If still high triple therapy = above + insulin

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15
Q

Define Diabetic Ketoacidosis (DKA)

A

Complete lack of insulin -> high ketone production

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16
Q

Aetiology of DKA

A
  1. Untreated/undiagnosed T1DM
  2. Infection/illness
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17
Q

Pathophysiology of DKA

A
  1. Absence of insulin -> uncontrolled catabolism -> unrestrained gluconeogenesis and decreased peripheral glucose uptake -> hyperglycaemia
  2. Hyperglycaemia -> osmotic diuresis -> dehydration
  3. Peripheral lipolysis for energy -> FFAs in circulation increase -> FFAs turned to Acetyl CoA -> ketone bodies -> acidosis
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18
Q

Signs of DKA

A
  1. Kussmaul’s breathing
  2. Pear drop breath
  3. Hypotension
  4. Tachycardia
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19
Q

Symptoms of DKA

A
  1. N&V
  2. Weight loss
  3. Reduced mental state
  4. Lethargy
  5. Abdominal pain
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20
Q

Diagnosis of DKA

A
  1. Random plasma glucose > 11 mmol/L
  2. Plasma ketones > 3 mmol/L
  3. Blood pH < 7.35 / bicarb < 15 mmol/L
  4. Urine dipstick: glycosuria & ketonuria
  5. Serum U&E: Raised urea and creatinine
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21
Q

Treatment of DKA

A
  1. ABC management
  2. 0.9% saline IV
  3. IV insulin
  4. Restore electrolytes
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22
Q

Define Hyperosmolar hyperglycaemic state (HHS)

A
  1. Marked hyperglycaemia
  2. Hyperosmolality
  3. Mild/no ketosis
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23
Q

Aetiology of HHS

A
  1. Untreated/undiagnosed T2DM
  2. Infection/illness
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24
Q

Pathophysiology of HHS

A
  1. Low insulin -> increased gluconeogenesis -> hyperglycaemia but enough insulin to inhibit ketogenesis
  2. Hyperglycaemia -> osmotic diuresis -> dehydration
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25
Q

Signs and symptoms of HHS

A
  1. Reduced mental state
  2. Lethargy
  3. Severe dehydration
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26
Q

Diagnosis of HHS

A
  1. Random BLOOD glucose > 30 mmol/L
  2. Urine dipstick: glucosuria
  3. Plasma osmolality: high
  4. U+E: low total body K+, high serum K+
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27
Q

Treatment of HHS

A
  1. 0.9% saline IV
  2. Insulin at low rate of infusion
  3. Restore electrolytes
  4. Low Molecular Weight Heparin (LMWH)
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28
Q

Define hyperthyroidism

A
  1. Clinical effect of excess thyroid hormone
  2. Primary - abnormally high thyroid function
  3. Secondary - abnormally high Thyroid Stimulating Hormone (TSH) production
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29
Q

Aetiology of hyperthyroidism

A
  1. Graves Disease - 65-75%, autoimmune, F>M 9:1
  2. Toxic multinodular goitre
  3. Toxic adenoma
  4. Metastatic follicular thyroid cancer
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30
Q

Epidemiology of hyperthyroidism

A
  1. Young women 20-40 yrs
  2. Grave’s disease 0.5%
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31
Q

Risk factors of hyperthyroidism

A
  1. Smoking
  2. Stress
  3. HLA-DR3
  4. Other autoimmune disease
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32
Q

Pathophysiology of hyperthyroidism

A

Increase in T3 hormone leads to:
-> increased metabolic rate
-> cardiac output
-> bone resorption
-> activates sympathetic nervous system

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33
Q

Signs and symptoms of hyperthyroidism

A
  1. Hot & sweaty
  2. Diarrhoea
  3. Hyperphagia (excessive eating)
  4. Weight loss
  5. Palpitations
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34
Q

Diagnosis of hyperthyroidism

A
  1. Thyroid function test (TFT) - elevated T4/T3
  2. Primary hyperthyroidism = decreased TSH
  3. Secondary hyperthyroidism = increased TSH
  4. Thyroid autoantibodies (anti-TSHR)
  5. Ultrasound + CT head
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35
Q

Treatment of hyperthyroidism

A
  1. Drug management
    a. Beta-blockers - rapid symptom relief
    b. 1st line Carbimazole - blocks synthesis of T4
    c. 2nd line Propylthiouracil - prevents T4->T3
    conversion
  2. Radioiodine
  3. Thyroidectomy
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36
Q

Pathophysiology of Grave’s Disease

A
  1. IgG autoantibodies bind to TSH receptors
  2. Increase T4/T3 production
  3. React with orbital autoantigens
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37
Q

What are some additional symptoms of Grave’s (except hyperthyroidism onoes)

A
  1. Thyroid eye disease
    • Eyelid retraction
    • Periorbital swelling
    • Proptosis (bulging eyes)
  2. Pretibial myxoedema
  3. Thyroid acropachy (nail clubbing,digit swelling)
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38
Q

Epidemiology of hypothyroidism

A
  1. 4/1000 per year
  2. > 40yrs
  3. F>M 6:1
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39
Q

Pathophysiology of hypothyroidism

A

Inadequate T3 to increase metabolic rate for normal body functions

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40
Q

Aetiology of hypothyroidism

A
  1. Autoimmune causes
    • Hashimotos (inflammation -> goitre)
    • primary atrophic hypothyroidism
  2. Iodine deficiency
  3. Hypopituitarism
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41
Q

Signs and symptoms of hypothyroidism

A
  1. Fatigue + lethargy
  2. Weight gain + loss of appetite
  3. Cold
  4. Constipation
  5. Goitre
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42
Q

Diagnosis of hypothyroidism

A
  1. TFTs - decreased T4 and T3
  2. Primary hypo = increased TSH
  3. Secondary hypo = decreased TSH
  4. Autoantibodies
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43
Q

Treatment of hypothyroidism

A

Levothyroxine (T4)

44
Q

Define Cushing’s syndrome

A
  1. Long term exposure
  2. Excessive cortisol hormone
  3. Released by adrenal glands
45
Q

Pathophysiology of Cushing’s

A
  1. Adrenocorticotropic hormone (ACTH) dependent
    • ACTH secreting from pituitary adenoma
    • Ectopic ACTH production from small cell lung
      cancer
  2. ACTH independent
    • Steroid use
      -Adrenal adenoma
46
Q

Signs and symptoms of Cushing’s

A
  1. Moon face
  2. Central obesity
  3. Buffalo hump
  4. Acne
  5. Striae
47
Q

Diagnosis of Cushing’s

A
  1. Random plasma cortisol - raised
  2. Overnight dexamethasone suppression test - cortisol won’t be suppressed in Cushing’s
  3. Urinary free cortisol
  4. Plasms ACTH
48
Q

Treatment of Cushing’s

A
  1. If due to steroid - stop use
  2. Removal of pituitary adenoma
  3. Adrenalectomy
  4. Cortisol synthesis inhibition
    • Metryapone
    • Ketoconazole
49
Q

Define Acromegaly

A

Excess GH -> overgrowth of all systems

50
Q

Aetiology of Acromegaly

A
  1. Pituitary adenoma = most common
  2. Secondary product of a malignancy that secretes ectopic GH (e.g. Lung cancer)
51
Q

Pathophysiology of acromegaly

A

GH acts directly on tissue

52
Q

Signs and symptoms acromegaly

A
  1. Prominent forehead and brow
  2. Increased jaw size
  3. Large facial features and extremities
  4. Bitemporal hemianopia
  5. Profuse sweating
53
Q

Diagnosis of acromegaly

A

1st line - insulin like growth factor 1 test = raised
Gold standard - oral glucose tolerance test

54
Q

Treatment of acromegaly

A
  1. Transsphenoidal resection surgery
  2. Somatostain analogue
  3. GH receptor antagonist
  4. Dopamine agonist
55
Q

Define prolactinoma

A

Benign adenoma of pituitary gland producing excess Prolactin

56
Q

Pathophysiology of prolactinoma

A
  1. 2 types of prolactinoma
    • Micro: tumour < 10mm diameter on MRI
    • Macro: tumour > 10mm on MRI
  2. Increased release of prolactin -> galactorrhoea
    • milk production stimulated
    • inhibit FSH anf LH
57
Q

Signs and symptoms prolactinoma

A
  1. Visual field defect
  2. Headache
  3. Oligomenorrhoea
  4. Infertility
  5. Galactorrhoea
58
Q

Diagnosis of prolactinoma

A
  1. Serum prolactin levels
  2. MRI head
59
Q

Treatment of prolactinoma

A
  1. 1st line - dopamine agonists: Bromocriptine
  2. Gold standard - transsphenoidal resection surgery of pituitary gland
60
Q

Define Conn’s syndrome

A

Primary hyperaldosteronism due to aldosterone producing adenoma

61
Q

Pathophysiology of Conn’s

A

Excess production of aldosterone; independent of renin-angiotensin system
-> High Na+ and water retention
-> Increased K+ excretion in kidneys
-> Low renin release

62
Q

Signs and symptoms of Conn’s

A

1.Hypertension
2. Hypokalaemia
3. Nocturia
4. Polyuria
5. Mood disturbance

63
Q

Diagnosis of Conn’s

A
  1. Aldosterone:Renin ratio blood test = increased
  2. Plasma potassium = reduced
  3. U+E
64
Q

Treatment of Conn’s

A
  1. 1st line - Spironolactone if hyperplasia
  2. Gold standard - Laparoscopic adrenalectomy if adenoma

MAIN AIM
- lower BP
- decrease aldosterone levels
- resolve electrolyte imbalance

65
Q

Define Addison’s

A

Primary adrenal insufficiency

66
Q

Aetiology of Addison’s

A
  1. Autoimmune destruction
  2. TB
  3. Adrenal metastases
67
Q

Pathophysiology of Addison’s

A

Destruction of adrenal cortex
-> decreased production of glucocorticoid (cortisol) and mineralocorticoid (aldosterone)

68
Q

Signs and symptoms of Addison’s

A
  1. Tanned
  2. Lean
  3. Fatigue
  4. Pigmented palmar creases
  5. Postural hypotension
69
Q

Diagnosis of Addison’s

A
  1. 1st line - U+E = hyponatraemia, hyperkalaemia, hypoglycaemia
  2. Gold standard - Short SynACTHen test
    • Presents with low cortisol, high ACTH
    • Plasma renin and aldosterone: high renin,
      low aldosterone
70
Q

Treatment of Addison’s

A
  1. Hydrocortisone - replaces cortisol
  2. Fludrocortisone - replaces aldosterone
71
Q

Define SIADH

A
  1. Syndrome of Inappropriate ADH
  2. Excess ADH secretion causing water reabsorption in collecting ducts
72
Q

Aetiology of SIADH

A
  1. Post-op major surgery
  2. Infection
  3. Head injury
  4. Medication (thiazide diuretics)
73
Q

Signs and symptoms of SIADH

A
  1. Headache
  2. Nausea
  3. Fatigue
  4. Muscle cramps
  5. Confusion
74
Q

Diagnosis of SIADH

A

U+E = hyponatraemia
Urine Na+ = high
Urine osmolality = high
NEED to exclude hyponatraemia
- -ve short SynACTHen Test - exclude adrenal
insufficiency
- No D+V
- No history of diuretic use
- No AKI/CKD

75
Q

Treatment of SIADH

A
  1. Stop causative medication
  2. Fluid restriction
  3. Tolvaptan (ADH receptor blocker)
76
Q

Define hyperkalaemia

A

> 5.5 mmol/L

77
Q

Aetiology of hyperkalaemia

A
  1. Impaired excretion
    • AKI/CKD
    • Drug affect (ACEi, NSAIDS, beta blockers)
    • Renal tubular acidosis
    • Addison’s
  2. Increased intake
    • IV K+ therapy
    • Increased dietary intake
  3. Shift to extracellular
    • Metabolic acidosis
    • Decreased insulin
78
Q

Symptoms of hyperkalaemia

A
  1. Fatigue
  2. Weakness
  3. Chest pain
  4. Palpitations
79
Q

Signs of hyperkalaemia

A
  1. Arrhythmia
  2. Reduced power + reflexes
  3. Flaccid paralysis
80
Q

Diagnosis of hyperkalaemia

A
  1. ECG
    • small/absent P wave
    • Prolonged PR interval (>200ms)
    • Wide QRS interval (>120ms)
  2. Bloods - FBC U+E
  3. Urine osmolality and electrolytes
81
Q

Treatment of hyperkalaemia

A
  1. ABC
  2. Cardiac monitoring
  3. Calcium gluconate - protect myocardium
  4. Insulin+dextrose or nebulised salbutamol - drive K+ intracellularly
82
Q

Define hypokalaemia

A

<3.5 mmol/L

83
Q

Aetiology of hypokalaemia

A
  1. Increased excretion
    • Renal disease
    • Drug effect
    • GI loss (D+V)
    • Conn’s syndrome
  2. Decreased intake
    • Dietary deficiency or fasting
  3. Shift to intracellular
    • Metabolic alkalosis
    • Drug effect
    • Agonists - SABAs and LABAs
84
Q

Signs of hypokalaemia

A
  1. Arrhythmia
  2. Hypotonia
  3. Hyporeflexia
  4. Muscle paralysis
  5. Rhabdomyolysis
85
Q

Symptoms of hypokalaemia

A
  1. Fatigue
  2. Weakness
  3. Cramps
  4. Palpitations
  5. Constipation
86
Q

Diagnosis of hypokalaemia

A
  1. ECG
    • Prolonged PR interval
    • ST depression
    • Flat T waves
    • Prominent U waves
  2. Bloods - FBC, U+E
  3. Urine osmolality and electrolytes
87
Q

Treatment of hypokalaemia

A
  1. K+ - PO/IV
  2. Other electrolytes required
88
Q

What are the two types of diabetes insipidus

A
  1. Cranial
  2. Nephrogenic
89
Q

Symptoms of diabetes insipidus

A
  1. Polyuria
  2. Polydipsia
  3. Dehydration
90
Q

Pathophysiology of diabetes insipidus

A
  1. Impaired water resorption from kidneys
    -> large volumes of dilute urine because of
    reduced ADH
    -> Secretion from posterior pituitary (cranial)
    OR
    -> Impaired response of the kidney to ADH
    (nephrogenic)
91
Q

Aetiology of cranial diabetes insipidus

A
  1. Idiopathic
  2. Congenital
  3. Tumour
  4. Trauma
  5. Infection
92
Q

Aetiology of nephrogenic diabetes insipidus

A
  1. Inherited
  2. Metabolic (low K+, high Na+)
  3. Drugs
  4. Chronic renal disease
93
Q

Diagnosis of diabetes insipidus

A
  1. Gold standard - 8h water deprivation test to diagnose
  2. Desmopressin test = establish cranial (urine output decrease) or nephrogenic (little/no change)
  3. Cranial MRI
94
Q

Treatment of diabetes insipidus

A
  1. Rehydration
  2. Cranial - Desmopressin (synthetic ADH)
  3. Nephrogenic - Bendroflumethiazide
95
Q

Define hyperparathyroidism

A
  1. Excessive secretion of parathyroid hormone (PTH)
  2. Primary - parathyroid gland produces excess PTH
  3. Secondary - increased secretion of PTH to compensate hypocalcaemia
  4. Tertiary - Autonomous secretion of PTH even after correction of calcium deficiency due to CKD
96
Q

Aetiology of hyperparathyroidism

A
  1. Primary
    -Adenomas
    -Hyperplasia of all glands
  2. Secondary
    • CKD/low Vit D
  3. Tertiary
    • Develops from prolonged secondary hyperparathyroidism
97
Q

Signs and symptoms of hyperparathyroidism

A

BONES - bone pain
STONES - renal calculi
MOANS - psychic moans
GROANS - abdominal groans
Hypercalcaemia

98
Q

Diagnosis of hyperparathyroidism

A
  1. PTH/bone profile: high PTH, high Ca2+, low phosphates
  2. Primary - raised Ca2+
  3. Secondary - low serum Ca2+, high PTH
  4. Tertiary - Raised Ca2+ + raised PTH
  5. DEXA scan, x ray (Salt and pepper degradation of bone), ultrasound for stones
99
Q

Treatment of hyperparathyroidism

A
  1. Primary
    • surgical removal of adenoma
    • Give bisphosphonates
  2. Secondary
    • Calcium correction
  3. Tertiary
    • Cinacalcet (calcium mimetic)
    • Total/part parathyroidectomy
100
Q

Define hypoparathyroidism

A
  1. Reduced PTH production
  2. Primary = gland failure
    -Autoimmune destruction
    • Congenital - DiGeorge syndrome (22q11 del)
  3. Secondary
    • surgical removal
    • Mg depletion (Mg required for PTH secretion)
101
Q

Pathophysiology of hypothyroidism

A
  1. Hypocalcaemia
  2. Hyperphosphatemia
  3. Neurons become more excitable
102
Q

Signs of hypoparathyroidism

A
  1. Chvostek’s sign - facial nerve tap induces spasm
  2. Trousseau’s sign - BP cuff causes wrist flexion and fingers pull together
103
Q

Symptoms of hypoparathyroidism

A
  1. Convulsion
  2. Arrhythmias
  3. Tetany (involuntary muscle contraction)
  4. Spasm
  5. Numbness
104
Q

Diagnosis of hypoparathyroidism

A
  1. Bloods-bone profile
    • Decreased Ca2+
    • Elevated/normal phosphate
    • Decreased PTH
  2. ECG
    • Prolonged QT + ST segments
105
Q

Treatment of hypoparathyroidism

A
  1. IV calcium
  2. AdCal D3 - Calcitriol
  3. Synthetic PTH

SJ Phase 2a (13 decks)

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