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Phase 2A > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Diabetes Mellitus Type 1

A

Autoimmune destruction of pancreatic beta cells leading to complete insulin deficiency

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2
Q

Diabetes Mellitus Type 2

A

Combination of peripheral insulin resistance and less severe insulin deficiency

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3
Q

Diabetic Ketoacidosis

A

A state of uncontrolled catabolism associated with insulin deficiency

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4
Q

Hyperosmolar Hyperglycaemic State

A

A combination of diabetes mellitus with high blood sugar levels to high osmolarity without significant ketoacidosis

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5
Q

Hyperthyroidism

A

Overactivity of the thyroid gland leading to excess thyroid hormones

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6
Q

Hypothyroidism

A

Underactivity of thyroid gland leading to deficiency of thyroid hormones

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7
Q

Grave’s Disease

A

Autoimmune disorder characterised by autoantibodies to TSH- receptor and is the leading cause of hyperthyroidism

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8
Q

Hashimoto’s Thyroiditis

A

Chronic autoimmune thyroiditis which is the leading cause of hypothyroidism

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9
Q

Thyroid Cancer

A

Malignant neoplasm of the thyroid gland

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10
Q

Cushing’s Syndrome

A

Chronic excess of cortisol hormone released by adrenal glands leading to symptoms due to prolonged exposure

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11
Q

Acromegaly

A

Excessive production of growth hormone occurring in adults after fusion of the epiphyseal plates

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12
Q

Conn’s Syndrome

A

Excess aldosterone due to autonomous overproduction that is independent of the renin-angiotensin 2 system = PRIMARY HYPERALDOSTERONISM

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13
Q

Pituitary Adenoma

A

Benign tumours that often arise sporadically in the anterior pituitary gland

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14
Q

Addison’s Disease

A

Primary adrenal insufficiency due to inability of adrenal glands to produce enough steroid hormones

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15
Q

Secondary Adrenal Insufficiency

A

Inadequate stimulation of adrenal cortex by the pituitary or hypothalamus

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16
Q

SIADH

A

Syndrome of inappropriate ADH secretion is caused by increased ADH secretion from the pituitary gland despite a normal plasma volume, causing the body to retain too much water.

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17
Q

Hyperkalaemia

A

High serum potassium over 5.5mmol/L

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18
Q

Hypokalaemia

A

Low serum potassium under 3.5mmol/L

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19
Q

Diabetes Insipidus

A

Passage of large volumes of dilute urine causing rapid dehydration

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20
Q

Hypercalcaemia

A

High calcium levels over 10.5mg/dL in blood serum

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21
Q

Hypocalcaemia

A

Low calcium levels under 8.5mg/dL in blood serum

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22
Q

Thyroid Storm

A

An acute, life threatening, hyper metabolic state induced by excessive release of thyroid hormones - Acute exacerbation of hyperthyroidism

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23
Q

Hyperparathyroidism

A

Abnormally high PTH levels in the blood due to overactivity of the parathyroid glands

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24
Q

Hypoparathyroidism

A

RARE disorder of low PTH levels due to under activity of the parathyroid glands

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25
Q

Neuroendocrine Tumour

A

Carcinoid tumours are the most common

Small, slow growing tumours synthesising a variety of hormones (especially serotonin)

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26
Q

Pheochromocytoma

A

Adrenal medullary tumour that secretes catecholamine

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27
Q

Prolactinoma

A

An adenoma of the anterior pituitary gland causing increased production of prolactin

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28
Q

DM Type 1 signs & symptoms

A
  • polydipsia
  • polyuria
  • weight loss
    USUALLY SHORT HISTORY OF SEVERE SYMPTOMS
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29
Q

DM Type 1 diagnosis

A
  • young
  • BMI < 25
  • signs and symptoms
  • personal or FHx of autoimmune disease
  • random plasma glucose > 11mmol/L
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30
Q

DM Type 1 pathophysiology

A
  • Autoimmune destruction of beta cells in Islets of Langerhans by autoantibodies
  • insulin deficiency and continued breakdown of liver glycogen
  • Muscles/tissues think they are starving
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31
Q

DM Type 1 treatment

A

INSULIN

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32
Q

DM Type 2 pathophysiology

A
  • Insulin resistance due to B cell dysfunction

- Beta cell hypertrophy and hyperplasia result in more insulin in order to remove glucose from blood

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33
Q

DM Type 2 signs and symptoms

A
  • ASYMPTOMATIC
  • develop signs of hyperglycaemia if severe (polyuria and polydipsia)
  • glycosuria
  • central obesity
  • slow onset
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34
Q

DM Type 2 diagnosis

A
  • HbA1C test
  • blood glucose test
  • random higher than 11.1 mol/L
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35
Q

DM Type 2 treatment

A
  • lifestyle modification
  • 1st line therapy = metformin
  • 2nd line = dual therapy
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36
Q

DKA pathophysiology

A
  • complete absence of insulin leads to unrestrained increased hepatic gluconeogenesis
  • hyperglycaemia caused
  • osmotic diuresis in kidneys causing dehydration
  • peripheral lipolysis increases FFA and these are oxidised to ketones in liver
  • LEADS TO METABOLIC ACIDOSIS
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37
Q

DKA characterised triad

A
  • hyperglycaemia
  • raised plasma ketones
  • metabolic acidosis
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38
Q

DKA signs

A
  • reduced tissue turgor
  • Kussmaul’s breathing - deep and rapid
  • fruity breath
  • hypotension
  • tachycardia
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39
Q

DKA symptoms

A
  • diabetes symptoms
  • nausea and vomiting
  • weight loss
  • drowsy/confused
  • abdominal pain
  • sunken eyes/dry tongue
  • dehydration
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40
Q

DKA diagnosis

A
  • random plasma glucose > 11.1mmol/L
  • plasma ketones > 3mmol/L
  • pH < 7.35
  • bicarbonate < 15mmol/L
  • urine dipstick shows glycosuria and ketouria
  • U&E often raised when dehydrated
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41
Q

DKA treatment

A
  • ABC
  • fluid replacement
  • IV insulin
  • restore electrolytes
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42
Q

DKA complications

A
  • coma
  • cerebral oedema
  • thromboembolism
  • aspiration pneumonia
  • death
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43
Q

Hyperosmolar hyperglycaemic state pathophysiology

A

Decreased insulin levels insufficient to inhibit hepatic glucose production but sufficient to inhibit hepatic ketogenesis

44
Q

HHS signs and symptoms

A
  • decreased levels of conciousness
  • severe dehydration
  • hyperglycaemia
  • hyperosmolality
  • no ketones in blood/urine
45
Q

HHS diagnosis

A
  • random plasma glucose > 11mmol/L
  • urine dipstick = glycosuria
  • high plasma osmolality
46
Q

HHS treatment

A
  • same as DKA
  • fluid replacement
  • LMWH - reduce thromboembolism risk
  • restore electrolytes
  • insulin if severe
47
Q

Hyperthyroidism pathophysiology

A 
PRIMARY = excess T3/4 production from thyroid leads to compensatory decrease of TSH secretion
SECONDARY = excess TSH secretion from pituitary leads to excess T3/4 production from thyroid (RARE)
48
Q

Hyperthyroidism signs and symptoms

A
  • weight loss despite increased appetite
  • palpitations
  • tachycardia
  • tremor
  • diarrhoea
  • anxiety/agitation
  • sweaty skin
  • heat intolerance
  • proximal muscle weakness
  • oligomenorrhoea
49
Q

Hyperthyroidism diagnosis

A
  • identify cause
  • check thyroid antibodies (Graves)
  • look for goitre/nodules
  • radioactive iodine uptake test (RAIU) - greater uptake in Graves
  • thyroid function tests
    PRIMARY = low TSH, high T3/4
    SECONDARY = high TSH, high T3/4
50
Q

Hyperthyroidism treatment

A
  • B blockers decrease somatic nervous system action
  • Carbimazole = antithyroid drug
  • Radioiodine therapy - destruction of thyroid tissue
  • Thyroidectomy
51
Q

Hypothyroidism pathophysiology

A
  • PRIMARY = insufficient thyroid hormone production from the thyroid gland
  • SECONDARY = insufficient TSH production from pituitary gland (RARE)
52
Q

Most common causes of hypothyroidism in developed and developing countries

A 
Developed = Hashimoto's thyroiditis
Developing = iodine deficiency
53
Q

Hypothyroidism signs

A
  • bradycardia
  • slow reflexes
  • ataxia
  • cold peripheries
  • ascites
  • round, puffy face
54
Q

Hypothyroidism symptoms

A
  • hoarse voice
  • goitre
  • weight gain
  • constipation
  • cold intolerance
  • menorrhagia
  • tiredness
  • lethargy
55
Q

Hypothyroidism diagnosis

A
  • TFT
    PRIMARY = high TSH, low T3/4
    SECONDARY = low TSH, low T3/4
  • thyroid antibodies - TPO in Hashimoto’s
56
Q

Hypothyroidism treatment

A
  • lifelong oral levothyroxine (T4)
57
Q

Grave’s disease pathophysiology

A
  • Beta cells produce IgG antibodies against TSH receptor
  • stimulating antibodies cause stimulation of thyroid gland to release T3/4
  • leads to increased thyroid function and thyroid hyperplasia (goiter)
58
Q

Graves triad

A
  • hyperthyroidism
  • pretibial myxedema
  • opthalmopathy
59
Q

Grave’s signs and symptoms

A
  • diffuse, smooth goiter

- hyperthyroidism symptoms

60
Q

Grave’s diagnosis

A
  • usually apparent on clinical examination
  • detecting TSH receptor antibodies
  • TFTs = low TSH, high T3/4
61
Q

Grave’s treatment

A
  • beta blockers to control symptoms
  • Carbimazole or propylthiouracil (PTU)
  • radioactive iodine therapy
62
Q

Hashimoto’s pathophysiology

A
  • B lymphocytes produce antibodies against TPO and thyroglobulin
  • autoimmune destruction causes inflammation and therefore eventual destruction of gland
63
Q

Hashimoto’s signs and symptoms

A
  • hypothyroidism symptoms

NON TENDER, PAINLESS RUBBERY GOITER WITH SYMMETRICAL ENLARGEMENT

64
Q

Hashimoto’s diagnosis

A
  • TFTs = high TSH, low T3/4
  • antibody screen
    anti-TPO antibody = positive
    anti- Tg antibody = positive
65
Q

Hashimoto’s treatment

A
  • levothyroxine for moderate/severe (synthetic T4)

- monitor if mild

66
Q

Thyroid cancer types

A
  • Papillary carcinoma
  • follicular carcinoma
  • anaplastic carcinoma
  • medullary carcinoma
67
Q

Well differentiated thyroid cancers

A
  • papillary

- follicular

68
Q

Poorly differentiated thyroid cancers

A
  • medullary

- anaplastic

69
Q

Thyroid cancers affecting thyrocytes

A
  • follicular
  • anaplastic
  • papillary
70
Q

Thyroid cancer affecting parafollicular cells

A
  • medullary
71
Q

Thyroid cancer signs and symptoms

A
  • asymptomatic nodule
  • firm and painless nodule
  • neck lymph nodes may be swollen
  • tracheal deviation potentially present
  • late stage = dysphagia, hoarseness
72
Q

Thyroid cancer diagnosis

A
  • normal TSH level
  • Ultrasound shows nodular with irregular margins
  • Tumour markers
    thyroglobulin or calcitonin (in medullary)
73
Q

Thyroid cancer treatment

A
  • surgery
  • followed by radioactive iodine ablation
  • TSH suppression with levothyroxine
74
Q

Thyroid cancer prognosis

A
  • almost 100% 5y survival rate for thyrocyte cancers that are well differentiated
  • very poor prognosis (30% 5ySR) for localised anaplastic
75
Q

Cushing’s pathophysiology

A

ACTH dependent - excessive ACTH secretion by pituitary gland

ACTH independent - adrenal adenomas causing excess cortisol production

76
Q

Cushing’s signs and symptoms

A
  • central obesity
  • plethoric complexion
  • moon face
  • stretchmarks
  • osteoporosis
  • diabetes/insulin resistance
  • thin skin
  • easy bruising
77
Q

Cushing’s diagnosis

A
  • drug history (mainly caused by oral steroids)
  • random plasma cortisol screening
  • 24hr urinary free cortisol levels
  • overnight dexamethasone suppression test
  • test plasma ACTH
78
Q

Cushing’s treatment

A
  • dependent on cause
  • pituitary adenoma = transsphenoidal surgical resection
  • adrenal adenoma = adrenalectomy
79
Q

Acromegaly pathophysiology

A
  • too much GH excreted due to pituitary adenoma
  • GH travels to tissues such as liver causing increase in IGF-1
  • stimulates skeletal muscle and soft tissue growth
80
Q

Acromegaly signs

A
  • acral enlargement
  • big tongue
  • prominent supraorbital ridge
  • puffy lips, eyes, skin
  • obstructive sleep apnoea
  • hypertension
  • insulin resistance
81
Q

Acromegaly symptoms

A
  • headaches
  • bitemporal hemianopia
  • hypopituitarism
  • sweating
  • decreased libido
  • amenorrhoea
  • galactorrhoea
82
Q

Acromegaly diagnosis

A
  • serum IGF-1 levels (raised)
  • oral glucose tolerance test (GH remains high)
  • changes in ring/shoe size
  • MRI of pituitary fossa
83
Q

Acromegaly treatment

A
  • transsphenoidal surgical resection

- Medical therapy (somatostatin analogues or dopamine agonists)

84
Q

Conn’s pathophysiology

A
  • excess aldosterone produced
  • increased Na+ resorption and K+ secretion
  • hypertension and potential hypokalaemia
85
Q

Conn’s signs and symptoms

A
  • hypertension
  • hypokalaemia
  • mood disturbance
  • difficulty concentrating
  • polyuria and polydipsia
86
Q

Conn’s diagnosis

A
  • low plasma potassium
  • high aldosterone/renin ratio
  • CT/MRI of adrenal glands - looking for adenomas/hyperplasia
  • selective adrenal venous sampling (G Standard)
87
Q

Conn’s treatment

A
  • benign tumour = unilateral adrenalectomy

- bilateral hyperplasia = aldosterone antagonists (spironolactone)

88
Q

Pituitary adenoma pathophysiology

A
  • tumour with good margins

- secretory can cause hyperpituitarism

89
Q

Pituitary adenoma signs and symptoms

A
  • hyperpituitarism if microcytic
  • hypopituitarism if macrocytic non secretory
  • headache
  • bitemporal hemianopia
  • diplopia
90
Q

Pituitary adenoma diagnosis

A
  • cranial contrast MRI
  • CT scan
  • hormone assays
91
Q

Pituitary adenoma treatment

A
  • non secretory/asymptomatic = monitor
  • 1st line = transsphenoidal hyposectomy
  • 2nd line = pituitary irradiation
92
Q

Addison’s pathophysiology

A
  • usually damage to the adrenal cortex or metabolic failure in hormone production
93
Q

Addison’s signs and symptoms

A
  • hyperpigmentation
  • postural hypertension
  • hypoglycaemia
  • fatigue
  • weight loss
  • weakness
94
Q

Addison’s diagnosis

A
  • low serum calcium
  • high serum potassium
  • low serum glucose
  • anaemia
  • adrenal CT or MRI
  • morning serum cortisol is reduced
95
Q

Addison’s treatment

A
  • if hypoadrenalism suspected = 100mg of hydrocortisone and saline immediately!
  • glucocorticoids and mineralocorticoids
  • treat underlying cause
96
Q

Addisonian crisis

A
  • severe hypotension and dehydration often after illness or trauma
  • high dose hydrocortisone given
97
Q

Secondary adrenal insufficiency pathophysiology

A
  • hypothalamic pituitary disease leading to decreased ACTH production
  • long term steroid therapy leading to hypothalamic pituitary suppression
98
Q

2nd adrenal insufficiency signs and symptoms

A
  • same as addison’s apart from no hyperpigmentation
  • fatigue
  • weight loss
  • N&V
  • weakness
99
Q

2nd adrenal insufficiency diagnosis

A
  • same as Addison’s but more focused on ACTH level
  • ACTH stimulation test - not a large enough rise in cortisol
  • ACTH level = very low (Addison’s will be high)
100
Q

2nd adrenal insufficiency treatment

A
  • steroid therapies
  • replacement glucocorticoids and mineralocorticoids
  • education on long term steroid use
101
Q

SIADH pathophysiology

A
  • increased ADH secretion leads to receptor-mediated signalling cascade in distal convoluted tubules and collecting duct
  • build up of additional aquaporin 2 in luminal cell membrane
  • water drawn out of urine into tissues
  • release of ADH no longer inhibited by fall in plasma osmolality
102
Q

SIADH signs

A
  • raised JVP
  • oedema
  • ascites
  • cheyne-stokes respiration
  • mild hyponatraemia
  • fits/coma if severe
103
Q

SIADH symptoms

A
  • N&V
  • headache
  • lethargy
  • cramps
  • weakness
  • confusion
104
Q

SIADH diagnosis

A
  • ADH levels elevated
  • U&E’s show low sodium, high or normal potassium
  • decreased serum osmolality
105
Q

SIADH treatment

A
  • fluid restriction
  • increased salt intake
  • increased osmolality
  • treat underlying cause

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