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Year 2 > Disease of the pituitary glands > Flashcards

Disease of the pituitary glands Flashcards

1
Q

What is benign pituitary adenoma

A

Adenoma - a benign tumour from glandular structures in the epithelium

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2
Q

Symptoms of benign pituitary adenoma

A
  1. Hormone hyper secretion
  2. Visual problems
  3. Hypopituitarism
  4. Erectile dysfunction
  5. Headache
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3
Q

What is craniopharyngioma

A

Tumour of the pituitary gland embryonic tissue

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4
Q

Symptom of craniopharyngioma

A

Bitemporal hemaniopsia (missing outer parts of vision)
Hydrocephalus
CSF leak

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5
Q

What is Sheehans

A

Pituitary infarctions after labour

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6
Q

What is hypopituitarism

A

Reduced secretion by the pituitary glands

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7
Q

Symptoms of hypopituitarism in males

A
  1. Pale, no body hair and central obesity
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8
Q

Symptoms of hypopituitarism in females

A

Loose body hair

Sallow complexion

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9
Q

What is a sallow complexion

A

losing natural complexion

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10
Q

What is prolactinoma

A

Increased Prolactin

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11
Q

Symptoms of prolactinoma

A

Increased milk production in breast

Galactorrhea

Reduced fertility

Amenorrhoea

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12
Q

Define amenorrhoea

A

Menstruation stops

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13
Q

Define galactorrhea

A

Seeping out of milk

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14
Q

How is Prolactinoma treated

A

Using a dopamine agonist which inhibits prolactin release (CABERGOLINE)

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15
Q

What is Acromegaly

A

Increased GH

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16
Q

Symptoms of acromegaly

A

Thick, greasy and sweaty skin

Enlarged Organs

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17
Q

Why is acromegaly dangerous

A

Increased heart size can result in heart disease

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18
Q

What is Cushing’s syndrome

A

Increased CTH production

TOO MUCH CORTISOL

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19
Q

Symptoms of Cushing’s syndrome

A

Central Obesity

Brushing, think skin, osteoporosis, ulcers and stretch marks (purple)

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20
Q

Definition of Diabetes Mellitus

A
  1. Syndrome of chronic hyperglycaemia due to relative insulin deficiency, resistance or both
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21
Q

What can hyperglycaemia result in

A

Serious microvascular or microvascular problems

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22
Q

What is the normal blood glucose levels

A

Between 3.5-8.0mmol/L under all conditions

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23
Q

What characterises Cushing’s disease

A
  1. INCREASED ACTH

OR

  1. INCREASED CH
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24
Q

What causes Cushing’s disease

A
  1. PITUITARY ADENOMA (pituitary basophilism)
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25
Q

Clinical presentation of Cushing’s Disease

A
  1. Weight Gain
  2. High BP
  3. Poor short term memory
  4. Irritability
  5. Excess hair growth
  6. Impaired immunity
  7. Red-ruddy face
  8. Extra fat around neck
  9. Moon Face
  10. Red stretch marks
  11. Poor concentration
  12. Irregular menstruation

CAUSES DIABETES MELLIITUS

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26
Q

The triad of characteristics seen in male patients with Cushing’s disease

A
  1. Purple striae
  2. Muscle atrophy
  3. Osteoporosis
  4. Kidney Stones
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27
Q

How is Cushing’s disease

A
  1. ACTH blood test (if positive the CT)
  2. dexamethasone suppression test
  3. synACTHen test
  4. CT or MRI of the pituitary for tumour
  5. Inferior petrosal sinus sampling to differentiate between ectopic and adrenal Cushing’s syndrome
  6. Urinary free cortisol test (measures excess cortisol excreted by the kidneys)
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28
Q

How is Cushing’s disease treated

A
  1. Trans-sphenoidal surgery
  2. Pituitary radiation therapy
  3. Bilateral adrenalectomy
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29
Q

What is Cushing’s syndrome

A
  1. INCREASED CRH

2. INCREASED ACTH

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30
Q

Where is CRH produced

A

Hypothalamus (paraventricular neurone)

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31
Q

What causes pseudo-coshing’s syndrome

A
  1. Oestrogen + progesterone tablets
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32
Q

What is Graves’ disease

A
  1. Autoimmune disease that enlarges the thyroid
  2. HYPERTHYROIDISM

Causes EYE DISEASE

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33
Q

What causes the orange peel skin in Graves’

A
  1. Infiltration of autoantibodies under the skin = inflammation and fibrous plaques
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34
Q

Wha autoantibodies are found in Graves’ disease

A
  1. Thyroid stimulating immunoglobulins (long-term stimulation of TSH)
  2. Thyroid growth immunoglobulins (Bind to TSH receptor causing overgrowth of thyroid follicles)
  3. Thyrotrophin binding-inhibiting immunoglobulins (inhibits union of TSH and its receptor)
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35
Q

Complications of graves’ disease

A

OSTEOPOROSIS due to increased excretion of calcium and phosphorous in urine and stool

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36
Q

Clinical Presentation of Graves’ disease

A
  1. Tachycardia
  2. Diffuse palpable loiter with audible bruit
  3. Exophthalmos (pushed out eyes)
  4. Fatigue
  5. Weight loss with increased appetite
  6. Heat intolerance
  7. Tremulousness
  8. Palpitations

DIAGNOSTIC OF GRAVES’ DISEASE:

  1. Exophthalmos
  2. Pretibial myxoedema
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37
Q

What is pretibial myxoedema

A

Waxy, red discolouration of the skin (orange peel skin)

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38
Q

What is Goiter

A
  1. Is an enlarged thyroid gland
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39
Q

Diagnostics of graves’ disease

A
  1. CT or ULTRASOUND to see loiter
  2. FBC (Overproduction of thyroid hormones T3 + T4 - TSH is undetectable + thyroid levels normal, elevated iodine)
    Autoantibodies
  3. Biopsy
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40
Q

Differential diagnosis of Graves’

A
  1. Thyroid adenoma

2. Toxic multi nodular goitre

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41
Q

How is Graves’ managed

A
  1. Antithyroid drugs (Carbimazole)
  2. Radioiodine
  3. Thyroidectomy
  4. PROPRANOLOL for tachycardia and nausea
  5. Difficulty closing eyes treated with lubricant gel and orbital decompression for bulging eyes
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42
Q

What is Hashimoto’s thyroiditis

A
  1. Autoimmune disease in which the thyroid gland is destroyed
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43
Q

In what gender is Hashimoto’s disease common in

44
Q

Clinical presentation of Hashimoto’s thyroiditis

A
  1. Fatigue
  2. Weight Gain
  3. Puffy face
  4. Arthralgia
  5. Myalgia
  6. Constipation
  7. Bradycardia
  8. Problems having a pregnancy
45
Q

Appearance of thyroids in Hashimoto’s thyroiditis

A

FIRM, LARGE and LOBULATED

46
Q

What causes enlargement of the thyroid in Hashimoto’s thyroiditis

A
  1. Lymphocytic infiltration and fibrosis

2. Thyroid peroxidase and thyroglobulin cause destruction

47
Q

Risk factor of hashimoto’s thyroiditis

A
  1. CTLA-4 gene mutation

2. Down Syndrome

48
Q

Diagnostic of Hashimoto’s thyroiditis

A
  1. Hard non-painful loiter
  2. Periorbital myedema
  3. Test for TSH, free T3,T4 and anti-thyroglobulin antibodies

Anti-thyroid peroxidase antibodies

49
Q

Differential diagnosis of Hashimoto’s thyroiditis

A
  1. Depression
  2. Fibromyalgia
  3. Erectile dysfunction
50
Q

How is Hashimoto’s thyroiditis treated

A

LEVOTHYROXINE

Avoid eating large amounts of iodine

51
Q

What is Conn’s Syndrome

A
  1. Primary hyperaldosteronism (excess production of aldosterone from adrenal glands)
52
Q

What causes conn’s syndrome

A

1.Potassium deficiency and high BP

53
Q

Clinical presentation of Conn’s Syndrome

A
  1. Muscle spasms
  2. Muscle weakness
  3. Tingling
  4. Excessive urination
  5. High BP
  6. Muscle cramps
  7. Headaches

SCEREAST CO as renin levels are raised

54
Q

What causes Conn’s syndrome

A
  1. Bilateral idiopathic adrenal hyperplasia

2. ADRENAL ADENOMA

55
Q

Pathophysiology of Conn’s Syndrome

A
  1. Aldosterone increases activity of basolateral membrane sodium-potassium ATPase and ENac channels
  2. These actions caused increased EC Na and fluid volume, reduced extracellular potassium
  3. Aldosterone acts on intercalated cells to stimulate proton ATPase - proton secretion that acidifies urine and alkalinises extracellular fluid

HYPERNATRAEMIA
HYPOKALAEMIA
METABOLIC ALKALOSIS

56
Q

How is Conn’s Syndrome diagnosed

A
  1. Renin to aldosterone ration is high
  2. Saline suppression test
  3. Fludrocortisone suppression test
  4. CT scanning
57
Q

How is Conn’s syndrome treated

A
  1. Adrenalectomy for unilateral tumour

2. Spironolactone for both glands

58
Q

How is postpartum thyroiditis treated

A
  1. Thyroidectomy

2. Radioactive iodine treatment or external neck irradiation for head and neck cancer

59
Q

What drugs can induce hashimoto’s thyroiditis

A
  1. Carbimaxole
  2. Lithium
  3. Amiodarone (high iodine content and stops conversion of T4 - T3)
60
Q

Why doe iodine deficiency result in loiter

A
  1. TSH stimulation and thyroid enlargement because thyroxine needs iodine to be produced
61
Q

Risk factors for thyroid carcinoma

62
Q

Types of thyroid carcinoma

A
  1. PAPILLARY in young people
  2. FOLLICULAR
  3. ANAPLASTIC
  4. Lymphoma
  5. Calcitonin C cell (medullary cell carncioma)
63
Q

Where do papillary carcinomas arise from

A
  1. Thyroid epithelium
64
Q

Where do follicular arise form

A

Thyroid epithelium

65
Q

Where do follicular thyroid cancer spread to

A

Lung and bone

66
Q

What do thyroid tumours secrete

A

Thyroglobulin *tumour marker)

67
Q

Clinical presentation of thyroid tumours

A
  1. Cervical lymphadenopathy
  2. Lung cerebral ,hepatic and bone metastases
  3. Thyroid is hard and irregular
  4. Dysphagia nd horseless of voice due to tumour compression
68
Q

Differential diagnosis fo thyroid cancers

69
Q

Diagnostics of thyroid cancer

A
  1. Fine needle aspiration cytology biopsy
  2. Blood tests for TSH, T4 and T3
  3. Ultrasound of thyroid
70
Q

Treatment of thyroid cancer

A
  1. Radioactive iodine which will destroy cancer
  2. LEVOTHYROXINE to reduce TSH
  3. Chemotherapy
71
Q

How are papillary and follicular carcinomas treated

A

Total thyroidectomy

Ablative radioactive iodine

72
Q

What thyroid carcinoma doe snot respond to iodine

A

Anapaestic carcniomas

Treated with radiotherapy

73
Q

How is medullary carcinoma treated

A

Thyroidectomy

Lymph node removal

74
Q

What limit is hyperkalaemia

A

Serum > 5.5 mmol/L

75
Q

What is the medical emergency reading for hyperkalaemia

A

> 6.5 mol/L

76
Q

What is the most common cause of hyperkalaemia

A
  1. Renal impairment (AKI or oliguric renal failure)
  2. VIGOROUS EXCERCISE
  3. Drug interference (ACEI, potassium sparing diuretics and NSAIDs - ramipril, spironollacone and ibuprofen)
77
Q

What conditions can cause yperkalaemia

A
  1. Diabetic ketoacidosis
  2. Metabolic acidosis
  3. Tissue necrosis
  4. Rhabdomyolysis (release of K+ from necrosing skeletal muscles)
  5. Tumour lysis syndrome
78
Q

What substance increases potassium load

A

Potassium chloride

2. Transfusion of stored blood

79
Q

Pathophysiology of hyperkalaemia

A
  1. K+ rise causes decreased difference between outside of the cell and cardiac myocytes - AP threshold is decreased so abnormal heart rhythms)

Ventricular fibrillation and cardiac arrest

80
Q

Clinical presentation of hyperkalaemia

A
  1. Asymptomatic
  2. Fast irregular pulse, chest pains, weakness and light headedness
  3. Muscle weakness
  4. Fatigue
  5. Associated with metabolic acidosis
  6. KUSSMAUL’s repsiration
81
Q

Differential diagnosis of hyperkalaemia

A
  1. Haemolysis

2. Thrombocythaemia (increased platelets) as K+ leaks out of platelets after clotting

82
Q

Diagnostics of hyperkalaeia

A
  1. Serum K+ over 5.5

2. ECG: Tall tented T waves, small P waves and wide QRS complex

83
Q

How is hyperkalaemia treated

A
  1. Treat underlying cause
  2. POLYSTYRENE SULFONATE RESIN which bind stop K+ in gut
  3. K+ restriction in diet
  4. Take of ACEI, NSAID or spironolactone
84
Q

How is K+ > 7.0 treated

A

EMERGENCY:
Stabilise cardiac membrane with IV 10ml 10% CALCIUM GLUCONATE (reduces excitability of myocytes)
2. IV ACTRAPID (brings K+ into cells by increasing uptake of glucose by them) + GLUCOSE to stop hypoglycaemia
3. Nebulised SALBUTAMOL (drives K+ into cells)

85
Q

Definition of HYPOKALAEMIA

A
  1. Serum K+ < 3.5

2. K+ < 2.5 (URGENT TREATMENT)

86
Q

What causes hypokalaemia

A
  1. Increased renal excretion
  2. Mineralocorticoids
  3. Renal disease
  4. Reduced dietary K+ intake
  5. Redistribution to cells (beta agonist)
  6. GI losses (vomiting, diarrhoea)
87
Q

What causes increased renal excretion of K+

A
  1. BENDROFLUMETHIAZIDE (thaizide diuretics)
  2. Loop diuretics (FUROSEMIDE)
  3. Increased aldosterone secretion (Cushing’s - excess cortisol causes excess aldosterone and Conn’s)
88
Q

How does Nephrotic syndrome cause hypokalaemia

A

Leaky kidneys = increased aldosterone secretion and K+ loss

89
Q

What renal diseases cause hypokalaemia

A
  1. Renal tubular acidosis type I and II
90
Q

Clinical presentation of hypokalaemia

A
  1. Muscle weakness
  2. Cramps
  3. Muscle weakness
  4. Hypotonia
  5. Hyporeflexia
  6. Tetany (muscle spasms)
  7. Constipation
  8. Arrythmias
91
Q

How is Hypokalaemia diagnosed

A
  1. FBC

2. ECG: Inverted T waves. prominent U waves and long PR interval and depressed ST segments

92
Q

How is Hypokalaemia diagnosed

A
  1. ORAL SANDO-K supplements
  2. SPIRONOLACTONE

or IV K+ in severe

93
Q

When do we not give IV K+

A

Oliguric or as fast stat bolus dose

94
Q

Define carcinoid tumours

A
  1. Tumours originating from enterchromaffin cells which produce SEROTONIN
95
Q

What do carcinoid tumours produce

A

SEROTONIN (5HT)

96
Q

Serotonin effects:

A
  1. Bowel function
  2. MOOD
  3. Clotting
  4. Nausea
  5. BMD
  6. Vasoconstriction
  7. Increases force of contraction and HR
97
Q

Were are carcinoid tumours commonly found

A

Terminal ileum and appendix (present as acute appendicitis)

98
Q

What is carcinoid syndrome

A
  1. HEPATIC inovolevemnt - metastases
99
Q

Clinical presentation of carcinoid syndrome

A
  1. Secretion of Bradykinin ,tachykinin, substance P, gastrin, glucagon and ACTH (Cushing’s)
  2. Bluish-red flushing on face and neck caused by bradykinin release
  3. GI tumours = appendicitis or obstruction
  4. Hepatic metastases - right quadrant pain
  5. Bronchoconstriction and spasms due to bradykinin
  6. Congestive heart failure - Serotonin induced fibrosis causing tricuspid incontinence and pulmonary stenosis
  7. Diarrhoea
100
Q

What is a carcinoid crisis

A
  1. When tumour outgrows its blood supply or is hailed too much during surgery
101
Q

Why is carcinoid crisis life threatening

A
  1. VASODILATION - bradykinin
  2. HYPOTENSION - ACTH
  3. TACHYCARDIA - serotonin
  4. BRONCHOCONSTRTCION - brady kinin
  5. HYPERGLYCAEMIA - glucagon and ACTH
102
Q

How is carcinoid crisis treated

A

OCTREOTIDE (reduces tumour hormone secretion)

103
Q

Differential diagnosis of carcinoid tumour

A

GI stromal tumour from interstitial canal cells

104
Q

What are interstitial canal cells

A

Pacemakers for gut contraction

105
Q

Diagnosis of carcinoid tumour

A
  1. ULTRASOUND of liver
  2. URINE shows high conc of 5-hydroxyindoleacetic acid (metabolite of 5-HT)
    3/ CXR of chest and pelvis
  3. MRI and CT to find primary tumours

Year 2 (155 decks)

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