Disease Profiles 2 Flashcards

1
Q

Goitre

A

Enlarged palpable thyroid gland that moves on swallowing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Goitre: Pathophysiology

A

Reduced T3 and T4 production causes a rise in TSH that stimulates gland enlargement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Goitre: Aetiologies - Physiological

A

Puberty
Pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Goitre: Aetiologies - Autoimmune Disease (2)

A

Hashimoto’s Thyroiditis
Graves Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Goitre: Aetiologies - Endemic (2)

A

Iodine deficiency
Ingestion of Goitrogens - chemicals that exaggerate the effects of iodine deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Goitre: Aetiologies - Inflammatory disease

A

Acute De Quervain’s Thyroiditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Goitre: Pathophysiology - What develops if compensation fails?

A

Goitrous hypothyroidism state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Goitre: Pathophysiology - Histological findings (4)

A

Rupture of follicles
Haemorrhage
Scarring
Calcification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Diffuse Goitre: Clinical Presentation

A

Entire thyroid gland swells and is smooth to touch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Diffuse Goitre: Clinical Presentation - Mass effects (2)

A

Compression of the trachea - exertional dyspnoea, stridor and wheezing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Diffuse Goitre: Clinical Presentation - In children

A

Cretinism due to dyshormonogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Diffuse Goitre: Investigations - Thyroid Function Tests

A

Normal T3 and T4
High TSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Diffuse Goitre: Management -

A

Treat underlying cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Multi-nodular Goitre: Pathophysiology

A

Recurrent hyperplasia and involution in response to external stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Multi-nodular Goitre: Associated mutations

A

Mutations of the TSH signalling pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Multi-nodular Goitre: Clinical presentation

A

Irregular enlarged thyroid due to nodule formation that is bumpy on palpation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Multi-nodular Goitre: Investigations

A

TFT
US scan - demonstrates whether cystic or solid
FNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Multi-nodular Goitre: Management - If toxic

A

Anti-thyroid drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Multi-nodular Goitre: Management - If significant thyroid problems

A

Radioactive Iodine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Multi-nodular Goitre: Management - If structural problem or significant retrosternal extension

A

Surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Hyperparathyroidism

A

Overactivity of the parathyroid glands with high levels of parathyroid hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Hyperparathyroidism: Primary Hyperparathyroidism

A

Uncontrolled parathyroid hormone produced directly from the tumour of the parathyroid glands

CAUSE - TUMOUR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Hyperparathyroidism: Management

A

Thyroidectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Hyperparathyroidism: Impact on calcium

A

Increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Hyperparathyroidism: Secondary Hyperparathyroidism Pathophysiology

A

Insufficient vitamin D or chronic renal failure leading to low absorption of calcium from the intestines, kidneys and bones

CAUSE - LOW VITAMIN D OR CKD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Hyperparathyroidism: Impact on calcium

A

Hypocalcaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Hyperparathyroidism: Tertiary Hyperparathyroidism

A

Secondary hyperparathyroidism continues for a long time leading to hyperplasia of glands

CAUSE - HYPERPLASIA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Hyperparathyroidism: TFT for Primary Hyperparathyroidism

A

High PTH
High Calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Hyperparathyroidism: TFT for Secondary Hyperthyroidism

A

High PTH
Low or Normal Calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Hyperparathyroidism: TFT for Tertiary Hyperparathyroidism

A

High PTH
High Calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Hyperparathyroidism: Clinical presentation of primary hyperparathyroidism

A

Fatigue
Depression
Bone pain
Myalgia
Nausea
Thirst
Polyuria
Renal stones
Osteoporosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Hyperparathyroidism: Pathophysiology - Function of PTH on Osteoclasts

A

Activates them to increase bone reabsorption and releases calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Hyperparathyroidism: Pathophysiology - Function of PTH on Renal tubules

A

Increased reabsorption of calcium by renal tubules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Hyperparathyroidism: Pathophysiology - Function of PTH on Phosphate

A

Increased urinary excretion of Phosphate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Hyperparathyroidism: Pathophysiology - Function of PTH on Vitamin D

A

Increased synthesis of active forms of Vitamin D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Hyperparathyroidism: Pathophysiology - How PTH regulated?

A

Increased serum calcium inhibits PTH secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Hyperparathyroidism: Pathophysiology - Fibrosa Cystica

A

Unchecked hyperparathyroidism results in the overproduction of PTH with continued osteoclasis - results in osteoporosis, brown tumours and osteitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Hyperparathyroidism: Pathophysiology - Osteoclasis and Clinical Presentation (3)

A

Decreased bone mass - causes fractures, deformity and degenerative joint disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Hyperparathyroidism: Pathophysiology - Osteoporosis location (3)

A

Phalanges
Vertebrae
Femur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Hyperparathyroidism: Pathophysiology - Osteoporosis where are the changes evident?

A

Cortical bone and medullary cancellous bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Hyperparathyroidism: Pathophysiology - Osteoporosis what is present in the marrow spaces?

A

Fibrovascular tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Hyperparathyroidism: Pathophysiology - What are Brown Tumours?

A

Mass of reactive tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Hyperparathyroidism: Pathophysiology - Brown Tumours have what cells present?

A

Giant cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Hyperparathyroidism: Pathophysiology - Brown Tumours have associated what?

A

Haemorrhages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Hyperparathyroidism: Pathophysiology - Brown Tumours Haemorrhages elicit what response? (20

A

Macrophage reactions
Processes of organisation and repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Hyperparathyroidism: Pathophysiology - Brown Tumours present as what on X-ray?

A

Lytic lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Hyperparathyroidism: Primary Hyperparathyroidism Management

A

Surgical removal of the tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Hyperparathyroidism: Secondary Hyperparathyroidism Management

A

Correct Vitamin D deficiency or perform a renal transplant to treat renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Hyperparathyroidism: Tertiary Hyperparathyroidism Management

A

Surgical removal of part of the parathyroid tissue to return PTH to normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Hypercalcaemia

A

High levels of calcium within the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Hypercalcaemia: Aetiologies (6)

A

Excessive PTH secretion
Malignant disease
Genetic syndromes
Drugs
Granulomatous disease
High turnover states

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Hypercalcaemia: Aetiologies - Causes of excessive PTH secretion (2)

A

Primary hyperparathyroidism - due to a single adenoma or diffuse hyperplasia of the parathyroid glands
Tertiary hyperparathyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Hypercalcaemia: Aetiologies - Malignant Disease (3)

A

Metastatic bone destruction
PTH from solid tumours
Osteoclast activating-factors produced by tumours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Hypercalcaemia: Aetiologies - Genetic Syndromes (3)

A

MEN1 and 2
Familial isolated hyperparathyroidism
Familial Hypocalciuric Hypercalcaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Hypercalcaemia: Aetiologies - MEN1 and 2 presentation

A

Most will develop a parathyroid adenoma with hypercalcaemia at a young age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Hypercalcaemia: Aetiologies - Familial hypocalciuric hypercalcaemia Pathophysiology

A

Autosomal dominant deactivating mutation in the calcium sensing receptor resulting in decreased sensitivity of the receptor to the calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Hypercalcaemia: Aetiologies - Drug Examples (2)

A

Vitamin D
Thiazides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Hypercalcaemia: Aetiologies - Granulomatous disease (2)

A

Sarcoidosis
Tuberculosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Hypercalcaemia: Clinical Presentation - Main 4 Symptoms (4)

A

Gallstones
Bone pain
Abdominal pain
Psychiatric Disturbances

STONE BONES GROANS AND PSYCHIC MOANS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Hypercalcaemia: Clinical Presentation - Acute (4)

A

Thirst
Dehydration
Confusion
Polyuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Hypercalcaemia: Chronic Clinical Presentation - Musculoskeletal Symptoms (3)

A

Myopathy
Fractures
Osteopenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Hypercalcaemia: Chronic Clinical Presentation - Cardiovascular

A

Hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Hypercalcaemia: Chronic Clinical Presentation - Gastrointestinal (3)

A

Pancreatitis
Duodenal ulcers
Renal calculi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Hypercalcaemia: Diagnosis - Biochemistry (3)

A

Raised calcium
Serum PTH - elevated PTH
Serum Alkaline Phosphatase - raised with hypercalcaemia in malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Hypercalcaemia: Diagnosis - Imaging required for malignancy (3)

A

X-ray
MRI
Isotope Bone Scan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Hypercalcaemia: Diagnosis - Familial Hypocalciuric Hypercalcaemia (2)

A

Bloods - increased calcium + Urine calcium excretion + PTH elevated
Genetic screening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Hypercalcaemia: Management of Acute Severe Hypercalcaemia - Fluids

A

Rehydrate with 0.9% saline 4-6 L in 24 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Hypercalcaemia: Management of Acute Severe Hypercalcaemia - Consider what medication once rehydrated?

A

Loop diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Hypercalcaemia: Management of Acute Severe Hypercalcaemia - Avoid what medications?

A

Thiazides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Hypercalcaemia: Management of Acute Severe Hypercalcaemia - What drug is given to reduce Calcium?

A

Bisphosphonates - reduces Ca2+ over 2-3 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Hypercalcaemia: Management of Acute Severe Hypercalcaemia - What drug is used if sarcoidosis is present?

A

Prednisolone 40-60 mg/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Hypercalcaemia: Management of Primary Hyperparathyroidism - Indications for Surgery (4)

A

End organ damage
Calcium >2.85 mmol/L
Under 50
Reduced eGFR (<60 mL/min)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Hypercalcaemia: Management of Primary Hyperparathyroidism - Medication

A

Cinacalcet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Hypercalcaemia: Management of Primary Hyperparathyroidism - Cinacalcet Mode of Action

A

Calcium mimetic to reduce PTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Hypocalcaemia: (4)

A

Congenital Absence - DiGeorge Syndrome
Destruction - Surgery, Radiotherapy and Malignancy
Autoimmune Disorders
Hypomagnesaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Hypocalcaemia: Clinical Presentation - Musculoskeletal symptoms (2)

A

Muscle weakness
Muscle cramps and tetany

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Hypocalcaemia: Clinical Presentation - Nervous system symptoms

A

Paraesthesia - fingers, toes and perioral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Hypocalcaemia: Clinical Presentation - Respiratory

A

Bronchospasma or Laryngospasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Hypocalcaemia: Signs - ECG

A

QT elongation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Hypocalcaemia: Signs - Chovsteks Sign

A

Tapping over the facial nerve causes twitch of the ipsilateral muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Hypocalcaemia: Signs - Trosseau Sign

A

Inflation of the sphygmomanometer cuff above systolic pressure for 3 minutes induces tetanic spasm of the fingers and wrist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Hypocalcaemia: Acute Management - Emergency

A

Infusion of IV Calcium Gluconate (10ml 10% over 10 minutes) in 50ml of saline or dextrose
Calcium infusion - 10ml 10% in 100ml infusate at 50ml per hour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Hypocalcaemia: Chronic Management (2)

A

Calcium supplement - 1-2g per day
Vitamin D supplement - 1 alpha-calcidol or depot injection of Cholecalciferol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Hypomagnesaemia

A

Low magnesium levels in the blood serum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Hypomagnesaemia: Aetiologies (4)

A

Alcohol
GI illness with diarrhoea
Pancreatitis
Malabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Hypomagnesaemia: Examples of causative drugs (2)

A

Thiazide
Proton Pump Inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Hypomagnesaemia: Symptoms (4)

A

Anorexia
Nausea and vomiting
Muscle weakness
Fits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Hypomagnesaemia: Signs (3)

A

Cardiac Arrhythmias
Chovestek Sign
Trousseau Sign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Hypomagnesaemia: Diagnosis (2)

A

Low serum magnesium
Measure K+ and Ca2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Hypomagnesaemia: Management

A

Magnesium and Calcium supplementation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Hypomagnesaemia: Main Complication

A

Secondary hypocalcaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Hypomagnesaemia: Complications - Pathophysiology of Secondary Hypocalcaemia

A

Calcium is released from cells is dependent - therefore in magnesium deficiency calcium is high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Hypomagnesaemia: Complications - Secondary hypocalcaemia has what impact on PTH?

A

Inhibited

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Pseudohypoparathyroidism

A

Genetic defect associated with resistance to Parathyroid Hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Pseudohypoparathyroidism: Pathophysiology

A

Genetic mutation causing dysfunction of the Gs alpha subunit - GNAS-1 gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Pseudohypoparathyroidism: Pathophysiology

A

End organ resistance to PTH due to mutation of the Gs alpha-protein that is coupled to the PTH receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Pseudohypoparathyroidism: Clinical Presentation (5)

A

McCune Albright - Bone abnormalities
Obesity
Subcutaneous calcification
Learning disability
Brachadactyly - shortened 4th metacarpal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Pseudohypoparathyroidism: Investigations (2)

A

Low Calcium
High PTH - due to resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Pseudohypoparathyroidism: Pseudo-pseudohypothyroidism

A

Phenotypic defects of pseudohypoparathyroidism without any abnormalities in calcium metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Cushing’s Syndrome

A

Excess cortisol secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Cushing’s Disease

A

Benign Pituitary Adenoma that secretes excess ACTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Cushing’s Disease: More common in what sex?

A

Females

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Cushing’s Disease: Age

A

20-40 year olds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Cushing’s Syndrome: Aetiologies (2)

A

Therapeutic administration of synthetic steroids
Cushing’s Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Cushing’s Syndrome: Aetiologies - ACTH dependent (3)

A

Pituitary adenoma
Ectopic ACTH
Ectopic CRH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Cushing’s Syndrome: Aetiologies - ACTH independent (4)

A

Exogenous steroids
Adrenal adenoma or carcinoma
Adrenal cortical nodular hyperplasia
False positive - severe depression and alcoholism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Cushing’s Syndrome: Pathophysiology - ACTH independent

A

Over-production of cortisol by the adrenal gland due to neoplasia or nodular hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Cushing’s Syndrome: Pathophysiology - ACTH-dependent adrenal enlargement is …

A

Diffuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Cushing’s Syndrome: Pathophysiology - Cushing’s Disease

A

Pituitary secretes increased ACTH to increase cortisol production by the adrenal gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Cushing’s Syndrome: Pathophysiology - ACTH-dependent Ectopic ACTH

A

Carcinoma secretes ACTH e.g. SCLC to increase cortisol production by the adrenal gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Cushing’s Syndrome: Pathophysiology - ACTH-dependent Ectopic CRH

A

Carcinoma secretes CRH e.g. Medullary Thyroid Carcinoma to increase ACTH production by pituitary to increase cortisol by the adrenal gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Cushing’s Syndrome: Consequences of Increased Cortisol Levels - Proteins

A

Reduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Cushing’s Syndrome: Consequences of Increased Cortisol Levels - Proteins

A

Reduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Cushing’s Syndrome: Consequences of Increased Cortisol Levels - Carbohydrates and Lipid

A

Metabolism changed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Cushing’s Syndrome: Consequences of Increased Cortisol Levels - Mineralocorticoid

A

Increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Cushing’s Syndrome: Consequences of Increased Cortisol Levels - Androgens

A

Increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Cushing’s Syndrome: Pathophysiology - Protein loss has what impact? (3)

A

Myopathy - muscular wasting
Osteoporosis - causes fractures
Thin skin - causes striae and bruising

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Cushing’s Syndrome: Pathophysiology - Altered Carbohydrate and Lipid Metabolism has what consequence?

A

Diabetes Mellitus and Obesity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Cushing’s Syndrome: Pathophysiology - Excess mineralocorticoids consequence? (2)

A

Hypertension
Oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Cushing’s Syndrome: Pathophysiology - Excess Androgen results in (3)

A

Virulism - females with male characteristics
Hirsuitism - male hair pattern on women
Acne
Oligo- or Amenorrhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Cushing’s Syndrome: Clinical Presentation - Facial features (2)

A

Plethora - redness of the face
Moon face

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Cushing’s Syndrome: Clinical Presentation - Cardiovascular (2)

A

Hypertension
Oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Cushing’s Syndrome: Clinical Presentation - Metabolic (4)

A

Central obesity
Glycosuria
Diabetes mellitus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Cushing’s Syndrome: Clinical Presentation - Back

A

Buffalo hump

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Cushing’s Syndrome: Clinical Presentation - Skin (6)

A

Bruising
Striae - purple or red
Pigmentation
Thin skin
Hirsutism
Acne

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Cushing’s Syndrome: Clinical Presentation - Musculoskeletal (2)

A

Proximal myopathy - wasting
Osteoporosis - fractures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Cushing’s Syndrome: Clinical Presentation - Reproductive

A

Oligo- or Amenorrhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Cushing’s Syndrome: Clinical Presentation - How is Cushing’s distinguished from Obesity? (5)

A

Thin Skin
Proximal myopathy
Frontal balding in women
Conjunctival oedema
Osteoporosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Cushing’s Syndrome: Diagnosis - Main test

A

Dexamethasone suppression test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Cushing’s Syndrome: Diagnosis - Dexamethaone Suppression Test Description

A

1mg overnight dexamethasone - if the administration fails to suppress the cortisol Cushing’s Syndrome is present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

Cushing’s Syndrome: Diagnosis - Dexamethasone Suppression Test Normal Result

A

Cortisol <50 nmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Cushing’s Syndrome: Diagnosis - Dexamethasone Suppression Test Abnormal Result

A

Cortisol >130 nmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

Cushing’s Syndrome: Diagnosis - 24 hour urine cortisol test Normal Results (2)

A

Total Cortisol <250 nmol/L
Cortisol:Creatinine Ration <25 nmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

Cushing’s Syndrome: Diagnosis - Diurinal Cortisol Variation Procedure

A

Serum/Saliva/Urine Collection - if loss of diurnal variation at 8am and Midnight is present suspect Cushing’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

Cushing’s Syndrome: Diagnosis - If ACTH what is the likely origin?

A

Adrenal gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

Cushing’s Syndrome: Diagnosis - If ACTH is raised what is required next?

A

Distinguish Cushing’s Disease and Ectopic ACTH - CRF test with elevated ACTH and Cortisol indicates pituitary source

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Cushing’s Syndrome: Management - Pituitary Source Options (2)

A

Hypopysectomy - transphenoidal route with external radiotherapy
Bilateral Adrenalectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

Cushing’s Syndrome: Management - Adrenal source

A

Adrenalectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

Cushing’s Syndrome: Management - Pharmacological Options (3)

A

Metyrapone
Ketoconazole
Pasiretoide LAR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

Cushing’s Syndrome: Management - Side effect of Ketoconazole

A

Hepatotoxic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

Cushing’s Syndrome: Management - Pasireotide LAR dose

A

10-20 mg monthly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

Adrenal Adenoma

A

Benign neoplasma emerging from the cells of the adrenal cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

Adrenal Adenoma: Appearance

A

Well-circumscribed encapsulated lesions that are small with bright yellow lipids buried within the gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

Adrenal Adenoma: Histological presence

A

Well-differentiated with small nuclei and made of cells resembling adrenocortical cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

Adrenal Adenoma: Clinical presentation if hyperfunctioning gland

A

Manifestations of Cushing’s or Conns Syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

Adrenal Adenoma: When is surgical excision required?

A

Functioning lesion
Large lesion - >3-5 cm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

Adrenocortical Carcinoma

A

Malignancy of the adrenal cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

Adrenocortical Carcinoma: In young patients this is associated with what?

A

Li-Fraumeni Syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

Adrenocortical Carcinoma: Histology - Size

A

Large - often >20cm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

Adrenocortical Carcinoma: Histology - Mitosis

A

Frequent atypical mitoses present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

Adrenocortical Carcinoma: Histology - There is a lack of what?

A

Clear cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

Adrenocortical Carcinoma: Histology - What are the two types of invasion?

A

Capsular or Vascular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

Adrenocortical Carcinoma: Histology - What features may be present? (2)

A

Haemorrhage
Necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

Adrenocortical Carcinoma: Spread - Local invasion of what? (2)

A

Retroperitoneum
Kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

Adrenocortical Carcinoma: Spread - Metastasis is often by what to where?

A

Haemogenous - Liver, Lung and Bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

Adrenocortical Carcinoma: Spread - Involves what? (2)

A

Peritoneum
Pleura

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

Adrenocortical Carcinoma: Clinical Presentation -(2)

A

Abdominal mass effects
Necrosis can cause a fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

Adrenocortical Carcinoma: Management

A

Resection with adjuvant therapy if no metastasis present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

Primary Hyperaldostronism

A

Autonomous production of aldosterone independent of its regulators - Angiotensin II and Potassium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

Primary Hyperaldostronism: Aetiologies (4)

A

Conn’s Syndrome
Bilateral Adrenal Hyperplasia
Genetic mutations
Unilateral hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

Conn’s Syndrome

A

Adrenal Adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

Primary Hyperaldostronism: Conn’s Syndrome - Genetic Pathophysiology

A

KCNJ5 channel mutation - leads to loss of ion selectivity for Na+ causing depolarisation ad therefore increased aldosterone production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

Primary Hyperaldostronism: Main aetiology

A

Bilateral Adrenal Hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

Primary Hyperaldostronism: Examples of Genetic Mutations (5)

A

CLC-2
GIRK4
ATPase
Beta Catenin
Cav3.2/1.3 Channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

Primary Hyperaldostronism: Pathophysiology - Aldosterone impact on cardiac collagen

A

Increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

Primary Hyperaldostronism: Pathophysiology - Aldosterone impact on Sodium

A

Increases retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

Primary Hyperaldostronism: Pathophysiology - Aldosterone impact on Sympathetic Outflow

A

Increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

Primary Hyperaldostronism: Pathophysiology - Aldosterone increases the synthesis of what? (2)

A

Cytokines
ROS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

Primary Hyperaldostronism: Pathophysiology - Aldosterone impact on endothelial function

A

Increased pressor response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

Primary Hyperaldostronism: Clinical Presentation (3)

A

Hypertension
Hypokalaemia
Alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

Primary Hyperaldostronism: Diagnosis - Initially required to confirm what?

A

Aldosterone excess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

Primary Hyperaldostronism: Diagnosis - How is aldosterone excess confirmed?

A

Measure plasma aldosterone and renin - determine ratio

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

Primary Hyperaldostronism: Diagnosis - Raises Aldosterone:Renin ration requires further investigation with what?

A

Saline suppression test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

Primary Hyperaldosteronism: Diagnosis - If saline suppression test fails to suppress ratio by >50% with 2 litres of saline shows what?

A

Confirms Primary Aldosteronism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

Primary Hyperaldostronism: Diagnosis - How to confirm subtype?

A

Adrenal CT for adenoma
Or vein sampling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

Primary Hyperaldostronism: Management - Adrenal Adenoma confirmed source with vein sampling

A

Unilateral Laparoscopic Adrenalectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

Primary Hyperaldostronism: Management - Unilateral laparoscopic Adrenalectomy cures what? (2)

A

Hypokalaemia
Hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

Primary Hyperaldostronism: Management - Bilateral Adrenal Hyperplasia

A

MR Antagonists - Spironolactone or Eplerenone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

Secondary Hyperaldosteronism

A

Increased adrenal production of aldosterone in response to extra adrenal stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

Secondary Hyperaldosteronism: Basic pathophysiology

A

Reduced renal flow leads to excess renin and hence angiotensin II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

Secondary Hyperaldosteronism: Causes of reduced renal blood flow? (3)

A

Obstructive renal artery disease e.g. atheroma or stenosis
Renal vasoconstriction
Oedematous disorders e.g. heart failure or cirrhosis with ascites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

Secondary Hyperaldosteronism: Most common aetiology

A

Renal artery stenosis - due to atheroma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

Secondary Hyperaldosteronism: Can be caused by what in females?

A

Fibromuscular dysplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
184
Q

Secondary Hyperaldosteronism: Clinical presentation

A

Hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
185
Q

Secondary Hyperaldosteronism: Diagnosis - Aldosterone:Renin Ratio

A

High aldosterone
High renin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
186
Q

Secondary Hyperaldosteronism: Diagnosis - How to detect Renal Artery Stenosis?

A

Doppler US
CT Angiogram
MRA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
187
Q

Secondary Hyperaldosteronism: Management

A

Aldosterone Antagonists e.g. Spironolactone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
188
Q

Secondary Hyperaldosteronism: Management of Renal Artery Stenosis

A

Percutaneous Renal Artery Angioplasty via the femoral artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
189
Q

Addisons Disease

A

Primary adrenal insufficiency with decreased production of adrenocortical hormones - glucocorticoids, mineralocorticoids and adrenal androgens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
190
Q

Adrenocortical Insufficiency: Acute Aetiologies - Associated with drugs

A

Rapid withdrawal of steroid treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
191
Q

Adrenocortical Insufficiency: Acute Aetiologies - Crisis in what patients?

A

Patients with chronic adrenocortical insufficiency e.g. stress or infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
192
Q

Adrenocortical Insufficiency: Acute Aetiologies - Involving the adrenal glands (4)

A

Adrenal haemorrhage
Adrenal tuberculosis
Adrenal malignancy
Congenital Adrenal Hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
193
Q

Adrenocortical Insufficiency: Acute Aetiologies - Causes of massive adrenal haemorrhage (4)

A

Newborns
Anti-coagulant treatment
DIC - Disseminated Intravascular Coagulation
Septicaemic infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
194
Q

Adrenocortical Insufficiency: Most common cause of Primary Adrenal Insufficiency?

A

Autoimmune adrenalitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
195
Q

Adrenocortical Insufficiency: Acute Aetiologies - Septicaemic Infection may occur in what syndrome?

A

Waterhouse-Friderichsen Syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
196
Q

Adrenocortical Insufficiency: Chronic Aetiologies - When does Addison’s Disease manifest?

A

Once >90% of the gland is destroyed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
197
Q

Adrenocortical Insufficiency: Addisons Disease - Aetiologies (3)

A

Autoimmune adrenalitis
Infections - TB, Histoplasma or HIV
Metastatic Malignancy - from lung or breast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
198
Q

Adrenocortical Insufficiency: Addisons Disease - Decreases Mineralocorticosteroids have what impacts? (4)

A

Hyperkalaemia
Hyponatraemia
Volume depletion
Hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
199
Q

Adrenocortical Insufficiency: Addisons Disease - Decreased glucocorticoids have what impact?

A

Hypoglycaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
200
Q

Adrenocortical Insufficiency: Addisons Disease - In a crisis what is the presentation? (4)

A

Vomiting
Hypotension
Shock
Abdominal pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
201
Q

Adrenocortical Insufficiency: Addisons Disease - Why is there excess pigmentation?

A

Excess ACTH due to low adrenocorticoids gets degraded to release MSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
202
Q

Adrenocortical Insufficiency: Where do black spots present?

A

Buccal mucosa
Dark palmar creases
Dark finger spaces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
203
Q

Adrenocortical Insufficiency: Diagnosis - Biochemistry Results (3)

A

Hyponatraemia
Hyperkalaemia
Hypoglycaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
204
Q

Adrenocortical Insufficiency: Diagnosis - Hormone markers

A

Increased renin
Decreased aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
205
Q

Adrenocortical Insufficiency: Diagnosis - What test should be conducted?

A

Short Synacthen Test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
206
Q

Adrenocortical Insufficiency: Diagnosis - Short Synacthen Test process and results

A

Measure plasma cortisol before and 30 minutes after injection of synthetic ACTH -
Normal Baseline - >250 nmol/L
Normal Post-ACTH - >550 nmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
207
Q

Adrenocortical Insufficiency: Management - First line treatment

A

Hydrocortisone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
208
Q

Adrenocortical Insufficiency: Management - Dose of Hydrocortisone

A

15-30 mg daily in divided doses to mimic diurnal rhythm

209
Q

Adrenocortical Insufficiency: Management - If in an Addison Crisis what is done?

A

Give IV Hydrocortisone

210
Q

Adrenocortical Insufficiency: Management - Second line

A

Fludrocortisone - aldosterone replacement

211
Q

Adrenocortical Insufficiency: Management - Must monitor what on Fludrocortisone?

A

Blood Pressure
Potassium

212
Q

Adrenocortical Insufficiency: Management of Adrenal Crisis - First stage

A

100mg IV Hydrocortisone then 200mg over 24 hours by continuous IV infusion in glucose or 50mg 6 hourly

213
Q

Adrenocortical Insufficiency: Management of Adrenal Crisis - Second stage for rehydration

A

NaCl 0.9% - 3-4 L over 24 hours

214
Q

Adrenocortical Insufficiency: Management of Adrenal Crisis - Second stage for resuscitation

A

500ml fluid bolus of NaCl 0.9% over 15 minutes then replace electrolyte deficits

215
Q

Adrenocortical Insufficiency: Management - Sick Day Rules for moderate illness or surgery under local anaesthetic

A

Double the glucocorticoid use

216
Q

Adrenocortical Insufficiency: Management - Sick Day Rules for Severe Illness, Colonoscopy or Acute trauma

A

Hydrocortisone 100mg IV at onset followed by continuous infusion of hydrocortisone 200mg over 24 hours OR Intramuscular 100mg of Hydrocortisone followed by 50mg every 6 hours

217
Q

Adrenocortical Insufficiency: Secondary Adrenal Insufficiency

A

Lack of production of ACTH by the pituitary gland

218
Q

Adrenocortical Insufficiency: Tertiary Adrenal Insufficiency

A

Lack of CRH secretion by the hypothalamus

219
Q

Adrenocortical Insufficiency: Difference in clinical presentation for Secondary or Tertiary insufficiency (2)

A

Skin is pale as no increased ACTH
No hypertension - as aldosterone production is intact

220
Q

Neuroblastoma

A

Malignant neuroendocrine tumour of the sympathetic nervous system that originates from neural crest cells

221
Q

Neuroblastoma: Usually diagnosed when?

A

18 months of age - 40% in infancy

222
Q

Neuroblastoma: 40% of cases arise where?

A

Adrenal medulla

223
Q

Neuroblastoma: 60% of cases arise where?

A

Sympathetic chain

224
Q

Neuroblastoma: Composed of what?

A

Primitive appearing cells - may show maturation and differentiation towards ganglion cells

225
Q

Neuroblastoma: What predicts prognosis?

A

Amplification of N-myc and expression of telomerase

226
Q

Neuroblastoma: Presents (early/late)

A

Late - due to mass effects of tumour or metastasis being main cause of symptoms

227
Q

Neuroblastoma: Clinical presentation (5)

A

Loss of appetite
Vomiting
Weight loss
Fatigue
Bone pain

228
Q

Neuroblastoma: Management for high risk patients

A

Multi-agent chemotherapy, Surgery and Radiotherapy

229
Q

Phaeochromocytoma

A

Catecholeamine-secreting tumour that is typically derived from chromaffin cells of the adrenal medulla

230
Q

Phaeochromocytoma: Where are paragangliomas located?

A

Extra-adrenal

231
Q

Phaeochromocytoma: Extra-adrenal paragangliomas are located where? (5)

A

Head
Neck
Thorax
Pelvis
Bladder

232
Q

Phaeochromocytoma: Rule of 10s

A

10% extra-adrenal
10% bilateral
10% are cases. ofmetastasis
10% are NOT associated with hypertension

233
Q

Phaeochromocytoma: Associated genetic mutations (5)

A

Neurofibrooma Type I
MEN2 - associated with RET
VHL
Succinate Dehydrogenase enzymes
Tuberous Sclerosis

234
Q

Phaeochromocytoma: More often malignant if associated with what?

A

Germline mutation of. theBeta unit of Succinade Dehydroxynate

235
Q

Phaeochromocytoma: Secrete what?

A

Catecholeamines

236
Q

Phaeochromocytoma: Rare cause of what?

A

Secondary hypertension

237
Q

Phaeochromocytoma: Commonly metastatises to where? (4)

A

Skeleton - most common
Regional lymph nodes
Liver
Lung

238
Q

Phaeochromocytoma: Onset is normally what?

A

Gradual

239
Q

Phaeochromocytoma: Histology - Tumour cells form a what?

A

Zellballen

240
Q

Phaeochromocytoma: Histology - Colour progression

A
  1. Yellow
  2. Red or Brown
  3. Haemorrhagic or Necrotic
241
Q

Phaeochromocytoma: Histology - K2Cr2O7 has what impact on the tumour?

A

Turns tumour dark brown due to oxidation of catecholeamines

242
Q

Phaeochromocytoma: Hypertension occurs when?

A

On stress, exercise or palpation of the tumour

243
Q

Phaeochromocytoma: Clinical Presentation - Classic Triad

A

Hypertension
Headache
Sweating

244
Q

Phaeochromocytoma: Clinical Presentation - Paraganglioma of the bladder is associated with what?

A

Micturition

245
Q

Phaeochromocytoma: Clinical Presentation - Signs of Complications (5)

A

Left Ventricular Failure
Myocardial necrosis
Stroke
Shock
Paralytic ileus of the bowel

246
Q

Phaeochromocytoma: Clinical Presentation - Cardiovascular symptoms

A

Tachycardia or Paradoxysmal Bradycardia

247
Q

Phaeochromocytoma: Diagnosis - Main test

A

2 x 24 hour catecholamine or metanephrite tests - take these at time of symptoms

248
Q

Phaeochromocytoma: Diagnosis - Glucose

A

Elevates

249
Q

Phaeochromocytoma: Diagnosis - Potassium

A

Hyperkalaemia - potential

250
Q

Phaeochromocytoma: Diagnosis - Haematocrit and Hb

A

Elevated

251
Q

Phaeochromocytoma: Diagnosis - Calcium

A

Mild Hypercalcaemia

252
Q

Phaeochromocytoma: Management - Pre-operative management

A

Full alpha blockade (phenocybenzamine) followed by beta blockade (propanolol) when stable

253
Q

Phaeochromocytoma: Management - Definitive option

A

Laparoscopic Surgery with Chemotherapy if malignant

254
Q

Congenital Adrenal Hyperplasia

A

Inherited group of disorders characterised by a deficiency in the enzymes necessary for cortisol synthesis

255
Q

Congenital Adrenal Hyperplasia: Pathophysiology - Main aetiology

A

Autosomal Recessive 21-alpha Hydroxylase Deficiency

256
Q

Congenital Adrenal Hyperplasia: Pathophysiology - Deficiency of 21-alpha Hydroxylase Deficiency prevents what?

A

Formation of Deoxycorticosterone and Deoxycortisol to increase levels of precursors

257
Q

Congenital Adrenal Hyperplasia: Pathophysiology - Deficiency of P-450 11 Beta Enzyme prevents formation of what?

A

Cortisol

258
Q

Congenital Adrenal Hyperplasia: Pathophysiology - Deficiency of P-450 C-17 prevents formation of what? (3)

A

Cortisol
DHEA
Androstenedione

259
Q

Congenital Adrenal Hyperplasia: Pathophysiology - Classic type is diagnosed when?

A

In infancy

260
Q

Congenital Adrenal Hyperplasia: Pathophysiology - Classic type typically diagnosed by what?

A

Virilisation and salt wasting

261
Q

Congenital Adrenal Hyperplasia: Pathophysiology - Non-Classic type typically presents when?

A

In adolescence or adult hood

262
Q

Congenital Adrenal Hyperplasia: Pathophysiology - Non-Classic type typically presents how? (3)

A

Hirsutism
Menstrual disturbance
Infertility - due to anovulation

263
Q

Congenital Adrenal Hyperplasia: Pathophysiology - Classic Type has the biochemical pattern of what?

A

Addisons Disease

264
Q

Congenital Adrenal Hyperplasia: Pathophysiology - Increased volume of precursors causes what to occur?

A

Diversion to androgen pathway to increase testosterone and dihydrotestosterone

265
Q

Congenital Adrenal Hyperplasia: Diagnostic Test

A

Basal or Stimulated 17-OH Progesterone

266
Q

Congenital Adrenal Hyperplasia: Management - Children

A

Replacement of glucocorticoids and mineralocorticoids
Surgical correction

267
Q

Congenital Adrenal Hyperplasia: Management - Adults

A

Glucocorticoid replacement
Control androgen excess
Restore fertility

268
Q

Congenital Adrenal Hyperplasia: Management - In adults must avoid what?

A

Steroid over-replacement

269
Q

Pituitary Adenoma

A

Benign tumour derived from the cells of the anterior pituitary

270
Q

Pituitary Adenoma: Can be associated with what disease?

A

MEN1 Werner Syndrome

271
Q

Pituitary Adenoma: These are derived from what?

A

Cells of the anterior pituitary gland

272
Q

Pituitary Adenoma: What is classification dependent on?

A

Hormone produced

273
Q

Pituitary Adenoma: What is the most common functional tumour?

A

Prolactinoma

274
Q

Pituitary Adenoma: Prolactinoma Clinical Presentation

A

Infertility
Lack of Libido
Amenorrhoea

275
Q

Pituitary Adenoma: Second most common functional tumour

A

Growth Hormone Secreting Adenoma

276
Q

Pituitary Adenoma: Growth Hormone Secreting Adenoma Pathophysiological present

A

Increase in Insulin-like Growth Factors stimulates the growth of bone, cartilage and connective tissue

277
Q

Pituitary Adenoma: Growth Hormone Secreting Adenoma results in what? (2)

A

Gigantism
Acromegaly

278
Q

Pituitary Adenoma: ACTH-secreting Adenoma - Usually present. aswhat?

A

Micro-adenomas

279
Q

Pituitary Adenoma: ACTH-secreting Adenoma - Clinical presentation

A

Cushing’s Disease - causes bilateral adrenocortical hyperplasia

280
Q

Pituitary Adenoma: Histology - Size of micro-adenomas

A

<1cm

281
Q

Pituitary Adenoma: Histology - Size of macro-adenomas

A

> 1cm

282
Q

Pituitary Adenoma: Histology - Large adenomas have what impact?

A

Impact the visual field

283
Q

Pituitary Adenoma: Histology - Infarction caused by large adenomas can lead to what?

A

Panhypopituitarism

284
Q

Pituitary Adenoma: Histology - Which subsets behave aggressivley?

A

Those with mitotic figures and p53 mutations

285
Q

Pituitary Adenoma: Clinical Presentation - Enlargement of the Pituitary has what impact on the cranial nerves?

A

Compresses the optic chaisma on cranial nerves 3, 4 and 6

286
Q

Pituitary Adenoma: Histology - Compression of the optic chiasma has what impact?

A

Bi-temporal Hemianopia

287
Q

Pituitary Adenoma: Histology - Compression on the residual pituitary gland can result in what? (5)

A

Hypoadrenalism
Hypothyroidism
Hypogonadism
Diabetes Insipidus
GH deficiency

288
Q

Pituitary Adenoma: Management Options (2)

A

Transphenoidal Surgery
Replace the hormones

289
Q

Craniopharyngioma

A

Benign tumour arising in the sellar or suprasella region

290
Q

Craniopharyngioma: Derived from what?

A

Rathke’s Pouch

291
Q

Craniopharyngioma: Bimodal incidence pattern

A

5-15 years old
60-70 years old

292
Q

Craniopharyngioma: Majority are located where?

A

Suprasellar region

293
Q

Craniopharyngioma: Pattern of growth

A

Slow growth - may be cystic or calcified

294
Q

Craniopharyngioma: Clinical Presentation (2)

A

Headaches
Visual disturbances

295
Q

Craniopharyngioma: May cause what in children?

A

Growth retardation

296
Q

Craniopharyngioma: Investigation

A

CT or MRI of the head

297
Q

Craniopharyngioma: Prognosis

A

Good - especially if <5cm

298
Q

Craniopharyngioma: Management

A

Radiotherapy

299
Q

Craniopharyngioma: Complication of radiotherapy

A

Small Cell Carcinoma

300
Q

Hypopituitarism

A

Inadequate production of one or more pituitary hormone as a result of damage to the pituitary gland and/or hypothalamus

301
Q

Hypopituitarism: Aetiologies - Potential causative tumours (3)

A

Pituitary Tumours
Local Brain Tumours - Astrocytoma, Meningioma, Glioma or Clival Chordoma
Secondary Metastatic Lesions - from the lung and breast

302
Q

Hypopituitarism: Aetiologies - Granulomatous Disease (3)

A

Tuberculosis
Histocytosis
Sarcoidosis

303
Q

Hypopituitarism: Aetiologies - Vascular Disease

A

Polyarteritis

304
Q

Hypopituitarism: Aetiologies - Trauma (2)

A

RTA
Skull fractures

305
Q

Hypopituitarism: Aetiologies - Hypothalamic Disease (2)

A

Syphilis
Meningitis

306
Q

Hypopituitarism: Aetiologies - Autoimmune disease

A

Sheenan Syndrome Post-pregnancy

307
Q

Hypopituitarism: Aetiologies - Infection

A

Meningitis

308
Q

Hypopituitarism: Pathophysiology - Becomes symptomatic when?

A

More than 80% of pituitary cells are damaged

309
Q

Hypopituitarism: Pathophysiology - Consequences on Anterior Pituitary Gland (4)

A

Growth Hormone - Causes growth failure
TSH - Causes hypothyroidism
LH or FSH - Causes hypogonadism
ACTH - Causes hypoadrenal symptoms

310
Q

Hypopituitarism: Pathophysiology - Consequences on Posterior Pituitary Gland

A

Diabetes Insipidus

311
Q

Hypopituitarism: Pathophysiology - Panhypopituitarism

A

Deficiency in all anterior pituitary hormones

312
Q

Hypopituitarism: Aetiologies of Panhypopituitarism (3)

A

Pituitary tumours
Surgery
Radiotherapy

313
Q

Hypopituitarism: Anterior Hypopituitarism - Clinical Presentation of Secondary Hypothyroidism, Hypoadrenalism and Hypogonadism (2)

A

Tiredness
General malaise

314
Q

Hypopituitarism: Anterior Hypopituitarism - Clinical Presentation of Hypothyroidism (7)

A

Weight gain
Slow thought and action
Dry skin
Cold tolerance
Constipation
Bradycardia
Hyperthermia

315
Q

Hypopituitarism: Anterior Hypopituitarism - Clinical Presentation of Hypoadrenalism (3)

A

Mild hypotension
Hyponatraemia
Cardiovascular collapse

316
Q

Hypopituitarism: Anterior Hypopituitarism - Clinical Presentation of Hypogonadism (5)

A

Loss of libido
Loss of secondary sexual hair
Amenorrhoea
Erectile dysfunction
Osteoporosis

317
Q

Hypopituitarism: Anterior Hypopituitarism - Clinical Presentation of Hypoprolactinaemia (3)

A

Galactorrhoea
Hypogonadism
Amenorrhoea

318
Q

Hypopituitarism: Anterior Hypopituitarism - Clinical Presentation of long-standing panhypopituitarism

A

Pallor with hairlessness

319
Q

Hypopituitarism: Clinical Presentation of Posterior Hypopituitarism (2)

A

Diabetes Insipidus - Polyuria or Polydipsia

320
Q

Hypopituitarism: Diagnosis - What tests are best for the steroid axis? (2)

A

Synacthen Test
Insulin Tolerance Test

321
Q

Hypopituitarism: Diagnosis - What should results be in a post-menopausal woman?

A

High LH and FSH

322
Q

Hypopituitarism: Diagnosis - When is testosterone sampled?

A

9am fasting sample

323
Q

Hypopituitarism: Diagnosis - Steroid Test for Pituitary

A

9am ACTH

324
Q

Hypopituitarism: Diagnosis - Steroid Test for Periphery

A

9am Cortisol

325
Q

Hypopituitarism: Diagnosis - Pituitary test for Thyroid

A

TSH

326
Q

Hypopituitarism: Diagnosis - Peripheral test for Thyroid

A

Thyroxine (fT4)

327
Q

Hypopituitarism: Diagnosis - Pituitary test for Sex Hormones

A

LH and FSH

328
Q

Hypopituitarism: Diagnosis - Peripheral Test for Sex Hormones

A

Testosterone or Oestradiol

329
Q

Hypopituitarism: Diagnosis - Pituitary Test for Growth Hormone

A

GH

330
Q

Hypopituitarism: Diagnosis - Peripheral Test for Growth Hormone

A

Insulin Growth Factor 1

331
Q

Hypopituitarism: Diagnosis - Pituitary Test for Prolactin

A

Prolactin

332
Q

Hypopituitarism: Diagnosis - Test for Posterior Pituitary Gland

A

Plasma or Urine Osmolarity

333
Q

Hypopituitarism: Management

A

Replacement Therapy

334
Q

Hypopituitarism: Management - TSH deficiency with dose

A

Thyroxine - 100-150 mcg/day

335
Q

Hypopituitarism: Management - ACTH deficiency and dose

A

Hydrocortisone - 10-25 mg/day split 2-3 times per day

336
Q

Hypopituitarism: Management - Diabetes insipidus

A

Desmospray Nasal Spray or Desmopressin tablets

337
Q

Hypopituitarism: Management - Growth Hormone Deficiency

A

Daily Subcutaneous Injection of Growth Hormone

338
Q

Hypopituitarism: Management - Testosterone options and doses (4)

A

IM Injection of Sustanon - every 3-4 weeks
Testogel or Tostran skin gel
Prolonged IM injection of Nebido - 10-14 weeks
Oral Restandol tablets

339
Q

Hypopituitarism: Management - Female sex steroid deficiency

A

HRT/Oestrogen/Progesterone Pill

340
Q

Hypopituitarism: Risk of Testosterone Replacement (3)

A

Polycythaemia - increases risk of stroke and MI
Prostate enlargement - monitor via PR and PSA
Hepatitis for oral tablets

341
Q

Diabetes Insipidus: Familial Aetiology

A

DIDMOAD Wolfram Syndrome

342
Q

Diabetes Insipidus: DIDMOAD Wolfram Syndrome presentation

A

Diabetes Inspidus + Diabetes Mellitus + Optic Atrophy + Deafness

343
Q

Diabetes Insipidus: Acquired Aetiologies (5)

A

Autoimmune
Tumours
Trauma
Infiltration
Infections

344
Q

Diabetes Insipidus: Aetiologies - Tumours (3)

A

Cranipharyngioma
Hypothalmic tumour
Pituitary tumour

345
Q

Diabetes Insipidus: Aetiologies - Trauma (3)

A

Road accidents
Skull fracture
External irradiation

346
Q

Diabetes Insipidus: Aetiologies - Infiltration

A

Sarcoidosis

347
Q

Diabetes Insipidus: Aetiologies - Infections (3)

A

Tuberculosis
Meningitis
Inflammatory disorders of the hypothalamus and pituitary

348
Q

Diabetes Insipidus: Pathophysiology - Nephrogenic cause

A

Renal resistance to ADH

349
Q

Diabetes Insipidus: Aetiologies of Nephrogenic DI (2)

A

Familial - AVPR2 Receptor Mutations
Renal Disease

350
Q

Diabetes Insipidus: Clinical presentation

A

Polydipsia
Polyuria with dilute urine

351
Q

Diabetes Insipidus: Diagnosis - Main test

A

Water Deprivation Test

352
Q

Diabetes Insipidus: Diagnosis - Water Deprivation Test Process

A

Patients stop drinking for 2-3 hours before the first measurement
Check serum and urine osmolarities hourly for 8 hours then 4 hours after giving Desmopressin

353
Q

Diabetes Insipidus: Diagnosis - Water Deprivation Test Normal Urine:Serum Osmolarity

A

> 1.8-2

354
Q

Diabetes Insipidus: Diagnosis - Water Deprivation Test how to determine if cranial or nephrogenic?

A

If ratio is low but improves after Desmopressin that is cranial

355
Q

Diabetes Insipidus: Management - Options (3)

A

Desmospray - nasal spray of 10-60 mcg/day
Desmopressin oral tablets - 100-1000 mcg/day
Desmopressin injection - 1-2 mcg IM per day

356
Q

Diabetes Insipidus: Management - When is treatment given?

A

At night

357
Q

Acromegaly

A

Growth Hormone stimulates skeletal and soft tissue growth

358
Q

Acromegaly: Name in children

A

Gigantism - if acquired before epiphyseal fusion

359
Q

Acromegaly: Main aetiology

A

GH-secreting Pituitary Adenoma

360
Q

Acromegaly: Clinical presentation - Impact on soft tissue (4)

A

Thickened skin
Large jaw
Sweaty
Large hands

361
Q

Acromegaly: Clinical presentation - Impact on nasopharynx

A

Thickened - to cause snoring and sleep apnoea

362
Q

Acromegaly: Clinical presentation - Impact on cardiovascular system (2)

A

Hypertension
Cardiac failure

363
Q

Acromegaly: Clinical presentation - Impact on metabolism

A

Diabetes Mellitus

364
Q

Acromegaly: Clinical presentation - Impact on colon

A

Colonic polyps - increased risk of colon cancer

365
Q

Acromegaly: Diagnosis - Gold Standard

A

Glucose Tolerance Test

366
Q

Acromegaly: Diagnosis - Glucose Tolerance Test Process

A

75g oral glucose - then GH is checked at 0, 30, 60, 90 and 120 minutes

367
Q

Acromegaly: Diagnosis - Glucose Tolerance Test Suppression normal GH result

A

Normally suppressed to <0.4 ug/L after glucose

368
Q

Acromegaly: Diagnosis - When is acromegaly indicated in the GTT suppression test?

A

GH unchanged or a paradoxical rise is present

369
Q

Acromegaly: Management - First Line

A

Surgery via transphenoidal approach

370
Q

Acromegaly: Management - Pharmacological Options (3)

A

Sandostatin LAR
Lanreotide
Octreotide

371
Q

Acromegaly: Management - Sandostatin LAR dose

A

IM 10-30mg per 28 days

372
Q

Acromegaly: Management - Lanreotide Autogel dose

A

SC 60-120 mg per 28 days

373
Q

Acromegaly: Management - Sandostatin/Lanreotide short-term side effects (3)

A

Flatulence
Diarrhoea
Abdominal Pain

374
Q

Acromegaly: Management - Sandostatin LAR/Lanreotide long term side effects (2)

A

Gall stones within 6 months
Biliary colic - due to inhibited contraction of gall bladder

375
Q

Acromegaly: Management - Dopamine agonist example

A

Cabergoline

376
Q

Acromegaly: Management - Cabergoline dose

A

Up to 3g weekly

377
Q

Acromegaly: Management - Growth Hormone Antagonist example

A

Pegvisomant

378
Q

Acromegaly: Management - Pegvisomant Dose

A

Subcutaneous 10-30 mg per day

379
Q

Acromegaly: Management - Pegvisomant Mechanism of Action

A

Binds to the growth Hormone receptor to block GH activity to decrease IGF-1 and increase GH

380
Q

Acromegaly: Complications - GH excess can result in what? (3)

A

Formation of colon polyps and cancer
Hypertension
Cardiac failure

381
Q

Hyperprolactinaemia

A

Abnormally high levels of prolactin within the blood

382
Q

Hyperprolactinaemia: Aetiologies - Physiological causes (3)

A

Breast feeding
Pregnancy
Stress

383
Q

Hyperprolactinaemia: Aetiologies - Pharmaceutical causes (3)

A

Any drug that reduces dopamine:
- Dopamine antagonists e.g. Metoclopramide
- Anti-psychotics e.g. Phenothiazines
- Anti-depressants - TCA, Cocaine, Oestrogens

384
Q

Hyperprolactinaemia: Aetiologies - Pathological causes (4)

A

Hypothyroidism
Stalk compression - due to pituitary adenomas and masses
Damage to the stalk
Prolactinoma

385
Q

Hyperprolactinaemia: Clinical Presentation - Females present when?

A

Early

386
Q

Hyperprolactinaemia: Clinical Presentation - Females (5)

A

Galactorrhoea
Menstrual irregularity
Decreased libido
Ammenorrhoea
Infertility

387
Q

Hyperprolactinaemia: Clinical Presentation - Males present when?

A

Late

388
Q

Hyperprolactinaemia: Clinical Presentation - Male presentation (4)

A

Impotence
Visual field abnormalities
Headaches
Anterior pituitary malfunction

389
Q

Hyperprolactinaemia: Diagnosis

A

Raised serum prolactin

390
Q

Hyperprolactinaemia: Management

A

Dopamine Agonists - Cabergoline

391
Q

Hyperprolactinaemia: Management - Second Line Management

A

Transphenoidal surgery or radiotherapy

392
Q

Infertility

A

Failure to achieve a clinical pregnancy after 12 months or more of regular unprotected sexual intercours in a couple who have never had a child

393
Q

Infertility: Female Infertility - Anovulatory Infertility

A

Infertility due to lack of ovulation

394
Q

Infertility: Female Infertility - Physiological causes (4)

A

Before puberty
During pregnancy
Lactation
Menopause

395
Q

Infertility: Female Infertility - Hypothalmic Gynaecological Aetiologies (4)

A

Anorexia
Excessive exercise
Stress
Kallman’s Syndrome

396
Q

Infertility: Female Infertility - Pituitary Gynaecological Aetiologies (3)

A

Hyperprolactinaemia
Tumours
Sheehan Syndrome

397
Q

Infertility: Female Infertility - Ovarian Gynaecological Aetiologies (2)

A

PCOS
Premature ovarian failure

398
Q

Infertility: Female Infertility - Pharmaceutical Aetiologies (3)

A

Depo-provera
Explanon
OCP

399
Q

Infertility: Female Infertility - Common causes of secondary infertility (5)

A

Tubal disease
Fibroids
Endometriosis or Adenomyosis
Obesity
Over 30 years old

400
Q

Infertility: Male Infertility - Endocrine causes (4)

A

Hypogonadotrophic hypogonadism
Hypothyroidism
Hyperprolactinaemia
Diabetes

401
Q

Infertility: Male Infertility - Non-obstructive aetiologies (4)

A

47 XXY
Chemotherapy
Radiotherapy
Undescended testes

402
Q

Infertility: Male Infertility - Clinical features of non-obstructive infertility (3)

A

Low testicular volume
Reduced secondary sexual characteristics
Vas deferens present

403
Q

Infertility: Male Infertility - Endocrine features of non-obstructive infertility (3)

A

High LH
High FSH
Low testosterone

404
Q

Infertility: Male Infertility - Obstructive Aetiologies (3)

A

Congenital absence
Infection
Vasectomy

405
Q

Infertility: Male Infertility - Clinical features of Obstructive Infertility (3)

A

Normal testicular volume
Normal secondary sexual characteristics
Vas deferens may be absent

406
Q

Infertility: Male Infertility - Endocrine features of Obstructive infertility? (3)

A

Normal LH
Normal FSH
Normal Testosterone

407
Q

Infertility: Diagnosis - How. totest for infection?

A

Endocervical swab for chlamydia

408
Q

Infertility: Diagnosis - Check for immunity of what and how?

A

Blood Rubella IgG

409
Q

Infertility: Diagnosis - Symptoms of Rubella Syndrome (3)

A

Microcephaly
Patent Ductus Arteriosus
Cateracts

410
Q

Infertility: Diagnosis - What hormones should be tested and when?

A

Midluteal Progesterone Level - Day 21 of 28 day cycle or 7 days prior to expected period in prolonged cycles

411
Q

Infertility: Diagnosis - What progesterone suggests ovulation?

A

> 30 nmol/L

412
Q

Infertility: Diagnosis - How to test for tubal patency?

A

Laproscopy

413
Q

Infertility: Diagnosis - Contraindications for Laproscopy (3)

A

Obesity
Previous pelvic surgery
Crohn’s Disease

414
Q

Infertility: Diagnosis - If laparoscopy is contraindicated what is done?

A

Hysterosalpingiogram

415
Q

Infertility: Diagnosis - If Hirsute test what? (2)

A

Testosterone
Sex Hormone Binding Globulin

416
Q

Infertility: Diagnosis - If Amenorrhoea test what? (2)

A

Chromosome analysis
Endocrine profile - HCG, Prolactin, TSH, Testosterone, SHBG, LH, FSH and Oestradiol

417
Q

Infertility: Male Diagnostic Test

A

Semen analysis - twice over 6 weeks apart

418
Q

Infertility: Male Diagnosis - If abnormal semen analysis (5)

A

LH
FSH
Testosterone
Prolactin
Thyroid function

419
Q

Infertility: Male Diagnosis - If azoospermic or severely abnormal semen (4)

A

Endocrine profile
Chromosome analysis and Y chromosome microdeletion analysis
Screen for CF
Testicular biopsy

420
Q

Infertility: Male Diagnosis - If abnormal on genital examination

A

Scrotal US

421
Q

Infertility: Female Management - Vitamin Supplements (2)

A

Folic Acid - 400 micrograms daily before pregnancy and for the first 12 weeks
Vitamin D - 10 micrograms per day for pregnanct or lactating women

422
Q

Infertility: Female Management - Examples of reproductive surgery (3)

A

Division of pelvic adhesions
Removal of tubal block
Removal of polyps and fibroids

423
Q

Hydrosalpinges

A

Fallopian tube filled with water

424
Q

Infertility: Female Management - Patients with hydrosalpinges

A

Laparoscopic salpingectomy before IVF treatment

425
Q

Infertility: Male Management - Surgical options

A

Surgery for obstructed vas deferens

426
Q

Infertility: Male Management - Oligozoospermia Mild Disease

A

Intrauterine insemitation

427
Q

Infertility: Male Management - Oligozoospermia Options (2)

A

Intracytoplasmic Sperm Injection - sperm into egg
Surgical sperm aspiration - sperm recovery from epididymis or testicle combinded with ICSI

428
Q

Infertility: Complications of Management - Risk of ovulation induction or assisted conception? (3)

A

Ovarian hyperstimulation
Multiple pregnancy
Ovarian cancer

429
Q

Infertility: Complications of Management - Ovarian Hyperstimulation occurs when?

A

If injectable hormone medication

430
Q

Ovulation Disorders: Group I

A

Hypothalmic Failure

431
Q

Ovulation Disorders: Group I - Aetiologies (5)

A

Stress
Excessive exercise
Anorexia
Kallman’s Syndrome
Isolated Gonadotrophin Deficiency

432
Q

Ovulation Disorders: Group I - Endocrine profile (3)

A

Low FSH + LH + Oestrogen
Normal prolactin
Negative progesterone challenge

433
Q

Ovulation Disorders: Group II

A

Hypothalamic-Pituitary Dysfunction

434
Q

Ovulation Disorders: Group II - Endocrine profile (3)

A

Normogonadotrophic
Normoestrogenic
Anovulation - PCOS

435
Q

Ovulation Disorders: Group III

A

Ovarian failure due to follicular depletion

436
Q

Ovulation Disorders: Group III - Endocrine profile (2)

A

High FSH + LH
Low Oestrogen

437
Q

Premature Ovarian Failure

A

Menopause before 40 years of age

438
Q

Aetiologies of Premature Ovarian Failure (4)

A

Turner Syndrome
Autoimmune ovarian failure
Bilateral oophrectomy
Pelvic chemotherapy or radiotherapy

439
Q

Ovulation Disorders: Menstrual bleeding normally lasts how long?

A

<5 days

440
Q

Oligomenorrhoea

A

Menstrual cycles >42 days - having less than 8 periods per year

441
Q

Amenorrhoea

A

Absent menstruation
- Primary - never menstruated
- Secondary - Menstruation started then stops

442
Q

Ovulation Disorders: Diagnosis - How to confirm regular cycles?

A

Mid-luteal D21 serum Progesterone >30 nmol/L in 2 samples

443
Q

Ovulation Disorders: Diagnosis - Progesterone Challenge Test process and results

A

Administration of progesterone to induce a period (provera 5mg BD x 5 days)
Withdrawal bleed usually within 7-10 days of progesterone - this indicates normal oestrogen

444
Q

Ovulation Disorders: Diagnosis - If progesterone challenge test results in no bleeding what may this indicate? (4)

A

Low oestrogen
Uterine or Endometrial abnormalities
Cervical stenosis
Asherman’s Syndrome

445
Q

Ovulation Disorders: Group I Management

A

Pulsatile GNRH (SC/IB pump) OR daily gonadotrophin daily injections

446
Q

Ovulation Disorders: Group I Management - Monitoring

A

Ultrasound monitoring of follicle tracking

447
Q

Anorexia Nervosa

A

An eating disorder characterised by a pathological fear of gaining weight and distorted body image

448
Q

Anorexia Nervosa: Clinical Presentation (5)

A

Low BMI
Loss of Hair
Lanugo - thin soft and unpigmented hair

449
Q

Anorexia Nervosa: Endocrine Profile (3)

A

Low FSH
Low LH
Low Oestradiol

450
Q

Polycystic Ovary Syndrome

A

Disorder characterised by hyperandrogenism, anovulation and/or the presence of polycystic ovaries

451
Q

Polycystic Ovary Syndrome: Affects what % of women of reproductive age?

A

5-15%

452
Q

Polycystic Ovary Syndrome: Exacerbated by what?

A

Weight gain

453
Q

Polycystic Ovary Syndrome: Impact of glucose on this disorder?

A

Glucose acts as a co-gonadotrophin to LH - elevates LH and changes LH:FSH ratio

454
Q

Polycystic Ovary Syndrome: Impact of insulin on this disorder?

A

Lowers SHBG to increase free testosterone

455
Q

Polycystic Ovary Syndrome: Clinical Presentation (4)

A

Obesity
Hirsutism
Acne
Menstrual Cycle Abnormalities

456
Q

Polycystic Ovary Syndrome: Diagnosis - What criteria is used?

A

Rotterdam

457
Q

Polycystic Ovary Syndrome: Diagnosis - Rotterdam Diagnostic Criteria

A

Must score 2/3:
- Chronic Anovulation
- Polycystic Ovaries on US - 12+ 2-9mm follicles with increased ovarian volume
Hyperandrogenism - clinical or biochemical

458
Q

Polycystic Ovary Syndrome: Diagnosis - Endocrine Features (3)

A

High free androgens - Oestrogen
High LH or normal gonadotrophins
Impaired glucose tolerance

459
Q

Polycystic Ovary Syndrome: Management - First Line

A

Oral Clomifene Citrate - 50-100 mg tablet on days 2-6

460
Q

Polycystic Ovary Syndrome: Management - Second Line

A

Daily Gonadotrophin Therapy - HMG (FSH + LH) + rFSH

461
Q

Polycystic Ovary Syndrome: Management - Third Line

A

Laparoscopic Ovarian Diathermy - disrupts ovarian cortex and stroma

462
Q

Premature Ovarian Failure: Aetiologies (4)

A

Genetic - Fragile X Syndrome, Turner’s Syndrome or XX gonadal agenesis
Autoimmune ovarian failure
Oophrectomy
Chemo- or Radiotherapy

463
Q

Premature Ovarian Failure: Clinical Presentation (5)

A

Hot flushes
Night sweats
Atrophic vaginitis
Amenorrhoea
Infertility

464
Q

Premature Ovarian Failure: Diagnosis - Endocrine Features (3)

A

High FSH
High LH
Low Oestradiol

465
Q

Premature Ovarian Failure: Management

A

HRT

466
Q

Tubal Disease: Aetiologies of Infective Types (3)

A

Pelvic Inflammatory Disease
Transperitoneal spread
Iatrogenic

467
Q

Tubal Disease: Examples of Pelvic Inflammatory Disease (4)

A

Chlamydia
Gonorrhoea
Syphilis
TB

468
Q

Tubal Disease: Aetiologies for transperitoneal spread (2)

A

Appendicitis
Intra-abdominal abscesses

469
Q

Tubal Disease: Iatrogenic causes of infective tubal disease (3)

A

IUCD Insertion
Hysterectomy
Hysterosalpingogram

470
Q

Tubal Disease: Non-infective Aetiologies (5)

A

Endometriosis
Surgical - via sterilisation or ectopic pregnancies
Fibroids
Polyps
Salpingitis isthmica Nodosa

471
Q

Tubal Disease: Pelvic Inflammatory Disorder - Clinical Presentation (8)

A

Abdominal and Pelvic Pain
Febrile
Vaginal discharge
Dyspareunia - recurrent genital pain associated with sexual intercourse
Cervical excitation
Dysmenorrhoea
Infertility
Ectopic pregnancy

472
Q

Endometriosis

A

Presence of endometrial glands outside the uterine cavity

473
Q

Tubal Disease: Endometriosis - Most likely cause

A

Retrograde menstruation

474
Q

Tubal Disease: Endometriosis - Clinical presentation (6)

A

Dysmenorrhoea
Dysparenuria
Menorrhagia
Painful defaecation
Chronic pelvic pain
Infertility

475
Q

Tubal Disease: Endometriosis - Diagnosis

A

US Scan - shows chocolate cysts on ovary

476
Q

Male Hypogonadism

A

Clinical syndrome comprising signs, symptoms and biochemical evidence of testosterone deficiency

477
Q

Male Hypogonadism: Peak of incidence

A

40-79 years old

478
Q

Male Hypogonadism: Primary Hypogonadism - Congenital Causes (3)

A

Klinefelter’s Syndrome
Cryptochidism
Y-chromosome microdeletions

479
Q

Male Hypogonadism: Primary Hypogonadism - Acquired causes (6)

A

Testicular trauma or torsion
Chemotherapy or Radiotherapy
Varicocele
Orchitis - Mumps
Infiltrative diseases - haemochromatosis
Medications e.g. Glucocorticoids and Ketoconzaole

480
Q

Male Hypogonadism: Primary Hypogonadism - Pathophysiology

A

Decreased testosterone causes decreased negative feedback
Anterior pituitary secretes higher amounts of LH or FSH to cause hypergonadotrophic hypogonadism

481
Q

Male Hypogonadism: Primary Hypogonadism - What is the main effect?

A

Spermatogenesis

482
Q

Male Hypogonadism: Secondary Hypogonadism - Pathophysiology

A

Hypothalamus or Pituitary is affected causing low LH or FSH despite low testosterone to cause hypogonadotrophic hypogonadism

483
Q

Male Hypogonadism: Secondary Hypogonadism - Congenital causes (2)

A

Kallmann’s Syndrome
Prader-Willi Syndrome

484
Q

Male Hypogonadism: Secondary Hypogonadism - Acquired causes (6)

A

Pituitary damage
Hyperprolactinaemia
Obesity
Medications - Steroid or Opioids
Eating disorders
Excessive exercise

485
Q

Male Hypogonadism: Secondary Hypogonadism - Causes of pituitary damage (5)

A

Tumours
Infiltrative Disease
Infection
Apoplexy
Head Trauma

486
Q

Male Hypogonadism: Clinical Presentation - Pre-Pubertal Onset Sexual organs

A

Small male sexual organs e.g. small testes volume, penis and prostate

487
Q

Male Hypogonadism: Clinical Presentation - Pre-Pubertal Onset Skin

A

Decreased body hair

488
Q

Male Hypogonadism: Clinical Presentation - Pre-Pubertal Onset Voice

A

High-pitched voice

489
Q

Male Hypogonadism: Clinical Presentation - Pre-Pubertal Onset Sex Drive

A

Low libido

490
Q

Male Hypogonadism: Clinical Presentation - Pre-Pubertal Onset MSK (3)

A

Gynaecomastia
Decreased bone mass
Decreased muscle mass

491
Q

Male Hypogonadism: Clinical Presentation - Pre-Pubertal Onset Limbs

A

Eunuchoidal Habitus - Tall slim with long arms and legs

492
Q

Male Hypogonadism: Clinical Presentation - Pre-Pubertal Onset with Kallmann’s Syndrome

A

Asomnia

493
Q

Male Hypogonadism: Clinical Presentation - Post-Pubertal Onset Sex (2)

A

Decreased libido
Decreased spontaneous erections

494
Q

Male Hypogonadism: Clinical Presentation - Post-Pubertal Onset Hair

A

Decreased pubic and axillary hair and shaving frequency

495
Q

Male Hypogonadism: Clinical Presentation - Post-Pubertal Onset Musculoskeletal system (3)

A

Gynaecomastia
Decreased bone mass
Decreased muscle mass

496
Q

Male Hypogonadism: Diagnosis - Main test

A

Testosterone measurement

497
Q

Male Hypogonadism: Diagnosis - Testosterone measurement

A

Measure total testosterone and SHBG - calculate free testosterone

498
Q

Male Hypogonadism: Diagnosis - Measure Testosterone when?

A

Between 8-11 am as it peaks in the morning

499
Q

Male Hypogonadism: Diagnosis - Factors that increase [SHBG] (6)

A

Ageing
Hyperthyroidism
Hyperoesteogenaemia
Liver disease
HIV
Use of anti-convulsants

500
Q

Male Hypogonadism: Diagnosis - Factors that decrease [SHBG] (8)

A

Obesity
Insulin resistance and diabetes
Hypothyroidism
Growth hormone excess
Glucocorticoids
Androgens
Progestins
Nephrotic syndrome

501
Q

Male Hypogonadism: Management - First Line

A

Testosterone Replacement Therapy

502
Q

Male Hypogonadism: Testosterone Replacement Therapy - Contraindications (4)

A

Confirmed hormone responsive cancer e.g. prostate or breast cancer
Possible prostate cancer - increased PSA
Haematocrit >50%
Severe sleep apnoea or heart failure

503
Q

Male Hypogonadism: Testosterone Replacement Therapy - When is monitoring required?

A

3-6 months then annually

504
Q

Klinefelter’s Syndrome: Pathophysiology

A

Non-disjunction 47 XXY or 46 XY or 47 XXY mosaicism

505
Q

Klinefelter’s Syndrome: Clinical presentation in males

A

Infertile due to tubular damage and have small firm testes

506
Q

Klinefelter’s Syndrome: Increases the risk of what? (2)

A

Breast cancer
Non-Hodgkin Lymphoma

507
Q

Kallmann’s Syndrome

A

Genetic disorder that causes that causes hypogonadotropic hypogonadism and an impaired sense of smell

508
Q

Kallmann’s Syndrome: Higher incidence in what sex?

A

Males

509
Q

Kallmann’s Syndrome: Characterised by what?

A

Isolated GnRH deficiency with hyposmia or anosmia

510
Q

Kallmann’s Syndrome: Clinical presentation (4)

A

Unilateral renal agenesis
Red-green colour blindness
Cleft lip or palate
Bimanual synkinesis

511
Q

Multiple Endocrine Neoplasia Type I

A

Hereditary endocrine cancer syndrome

512
Q

Multiple Endocrine Neoplasia Type I: Characterised primarily by what? (4)

A

Tumours of the:
- Parathyroid Glands
- Endocrine Gastroenteropancreatic tract
- Anterior pituitary

513
Q

Multiple Endocrine Neoplasia Type I: Inheritance pattern

A

Autosomal dominant

514
Q

Von Hippel-Lindau

A

Inherited disorder causing multiple tumours of the CNS and viscera

515
Q

Von Hippel-Lindau: Pathophysiology

A

Autosomal dominant mutation in the VHL gene which leads to an accumulation of HIF proteins and stimulation of cellular proliferation

516
Q

Neurofibromatosis Type I

A

Genetic condition that causes tumours along the nervous system

517
Q

Neurofibromatosis Type I: Pathophysiology

A

Mutation in the NF1 gene

518
Q

Neurofibromatosis Type I: Diagnosis

A

> 2 of the following are diagnostic

> 5 cafe au lait macules
Neurofibromatosis of any type - most common is neurofibroma
Axillary or inguinal freckling
Optic glioma
2 Lisch nodules
Distinctive osseous lesion
First degreee relative with NF 1