Endocrinology and Diabetes Flashcards
1
Q
Define T1DM
A
Metabolic autoimmune disorder from destruction of insulin producing beta cells in the pancreas, resulting in absolute insulin deficiency.
2
Q
Causes of T1DM
A
HLA-DR and HLA-DQ provide protection from or increase susceptibility to diabetes. Environmental factors and viruses may trigger the destruction of beta cells.
3
Q
T1DM risk factors
A
Western countries, FHx, infectious agents, dietary factors.
4
Q
Key presentations of T1DM
A
Polyuria, polydipsia, blurred vision, fatigue, weight loss
5
Q
Signs that a patient has T1DM and not T2DM.
A
Weight loss, young age, FHx of autoimmune disease
6
Q
1st Line investigation for DM
A
Random glucose tolerance test >11.1mmol/L
7
Q
Gold standard investigation for DM
A
HbA1c testing >6.5%
8
Q
Other tests for DM
A
Fasting plasma glucose, 2-hour plasma glucose, plasma/urinary ketones. Low C peptide levels.
9
Q
Criteria for diagnosing diabetes mellitus using glucose testing.
A
Symptoms plus:
- random glucose >11.1
- fasting glucose >7
- 2hr glucose >11.1 after oral GTT
With NO symptoms need 2 confirmatory tests
Ranges are lower when testing for gestational diabetes
10
Q
Differential diagnosis for T1DM
A
T2DM, other types of diabetes
11
Q
Management of T1DM
A
Basal-bolus insulin
Pre-meal insulin correction dose
Amylin analogue
2nd line is fixed insulin dose
12
Q
Microvascular complications of DM
A
Retinopathy, nephropathy, neuropathy
13
Q
Macrovascular complications of DM
A
CAD, cerebrovascular disease, peripheral artery disease
14
Q
Complications of untreated DM
A
Hyperosmolar hyperglycaemic state, DKA, blindness, renal failure, foot amputations, MI
15
Q
Complication of overtreating DM
A
Hypoglycaemia
16
Q
Pathogenesis of T1DM
A
- Autoimmune pancreatic beta-cell destruction
- Up to 90% have autoantibodies to glutamic acid decarboxylase, insulin or islet auto-antigen 2
- Cell destruction proceeds sub-clinically for a long time as insulitis before developing hyperglycaemia after 80-90% cell loss.
- Pts cannot use glucose in peripheral muscles stimulating glucagon secretion
17
Q
Define T2DM
A
Insulin resistance (and less severe insulin deficiency) due to prolonged nutrient excess.
18
Q
Potential causes of T2DM
A
Genetic factors affecting beta-cell development
Beta-cell function with age
Not really any concrete reasons people develop T2DM
19
Q
Risk factors of T2DM
A
Males, certain ethnicities, elderly, central obesity, lack of exercise, high calorie intake
20
Q
Key presentations for T2DM
A
Polyuria, polydipsia, fatigue, blurred vision, genital thrush, hunger
21
Q
Pathophysiology of T2DM
A
- Impaired ability of insulin which increases plasma glucose
- As insulin resistance develops the body shows hypersecretion of insulin before it lowers
- Glucagon and other counterregulatory hormones are secreted more
22
Q
Why is the insulin response to oral glucose different to that of IV glucose?
A
GLP-1 and GIP are incretins released in the GI tract after eating, increasing insulin response. Both of these have short half lives and are broken down by DPP4.
23
Q
What effects does T2DM have on the nephron (not complications)?
A
Upregulates reabsorption of glucose via SGLT2 channels.
24
Q
Management of T2DM (in order)
A
Lifestyle Modification METFORMIN - 1st line 2nd line - Metformin with: - DPP4 inhibitor OR - Pioglitazone OR - Sulphonylurea OR - SGLT2 inhibitor
Then insulin therapy
25
Define hypoglycaemia
A low blood glucose level. <3.0mmol/L represents severe hypoglycaemia and below 4 is an 'alert level'
26
Hypoglycaemia causes
Inappropriate doses of diabetes medication
Excessive alcohol
Skipping/Delaying meals
Intense exercise
27
Hypoglycaemia risk factors
Elderly, males, people outside the home, longer duration of diabetes, patients only using SU.
28
Key presentations of hypoglycaemia
Blurred vision, seizures, collapsing, confusion, unusual behaviour, fatigue, feeling hungry
Waking after sleep with headaches, tiredness or night sweats
29
Hypoglycaemia management
Glucose (oral or IV)
| Glucagon and adrenaline
30
DKA management
Fluids and insulin
31
DKA features
acidaemia, hyperglycaemia, ketonemia/ketonuria
32
Difference between DKA and HHS
HHS shows no features of ketogenesis
33
HHS treatment
Fluids and anticoagulants
34
Define hyperthyroidism
Elevated levels of T4/T3 in the blood
35
Causes of hyperthyroidism
75-80% of all cases are caused by Graves' disease
Toxic multinodular goitre
Toxic adenoma
Other rare causes
36
Hyperthyroidism risk factors
Female, elderly, recent pregnancy, autoimmune disease (or FHx), thyroid problems or surgery.
37
Pathophysiology of hyperthyroidism
Overproduction of thyroid hormones OR;
Leakage of preformed thyroid hormones OR;
Ingestion of excess thyroid hormones
38
Key presentations of hyperthyroidism
Heat intolerance, tachycardia, weight loss, oligomenorrhoea, goitre, HTN, proximal muscle wasting, thirst, sweating
39
1st line investigations for hyperthyroidism
TFTs (TSH and T3/4 levels)
Thyroid antibody tests (for Graves' disease)
- TPO
- Thyroglobulin antibodies
40
The gold standard test for hyperthyroidism
TFTs
41
Other testing for hyperthyroidism
Radioactive iodine isotope uptake scan (if antibody negative)
42
Differential diagnosis of hyperthyroidism
Thyroid ultrasound differentiates Graves' from toxic adenoma
| - TSHRAb testing
43
Hyperthyroidism management
```
Anti-thyroid drugs (carbimazole)
- Titration or block and dose regimen
Radioiodine 131 Iodine
Surgery if other options don't work or previously rendered euthyroid
Beta blockers (against HTN)
```
44
Complications of Hyperthyroidism
Heart issues, eye problems, skin issues, osteoporosis
| THYROID STORM
45
What happens in a thyroid storm?
Untreated hyperthyroidism causes very high BP, HR and temperature
46
Define hypothyroidism
Abnormally low levels of T3/4 in the blood
47
Gender differences in hypothyroidism
Much more common in women than men
48
Hypothyroidism causes
Primary
- Primary atrophic hypothyroidism
- Hashimoto's thyroiditis
- Postpartum thyroiditis, iodine deficiency, hyperthyroidism therapy
Secondary and tertiary
- Pituitary/Hypothalamic dysfunction
```
Certain drugs (lithium, amiodarone, interferon-a)
T3 resistance
Isolated TSH deficiency
```
49
Hypothyroidism risk factors
Female, FHx, elderly, autoimmune disease
50
Key presentations of hypothyroidism
Fatigue, cold intolerance, bradycardia, dry skin and hair, mental slowness, pallor, weight gain (myxoedma), goitre
51
1st line tests for hypothyroidism
TFTs
52
Gold Standard test for hypothyroidism
TFTs
53
Other tests for hypothyroidism
Anaemia testing
Increased cholesterol and triglyceride levels
Hyponatraemia
54
Differential diagnosis of hypothyroidism
T1DM, Addison's, Coeliac or other autoimmune conditions
Anaemia and multiple myeloma
End organ damage
55
Management of hypothyroidism
```
ORAL LEVOTHYROXINE (lifelong replacement of T4)
Surgery if needed
```
56
Hypothyroidism complications
Myxoedema coma
Myxoedema 'madness'
Hyperthyroidism from over-treatment
57
Myxoedema coma treatment
```
Oral T3
Oxygen
Monitor CO and BP
Gradual rewarming
Hydrocortisone
Glucose infusion to prevent hypoglycaemia
```
58
Define Graves' disease
Autoimmune process that is the most common cause of hyperthyroidism
59
Graves' disease pathophysiology
Serum IgG antibodies bind to TSH receptors in the thyroid, stimulating thyroid hormone production. TSH receptor antibodies are specific for Graves'.
60
Clinical manifestations of Graves' disease
Hyperthyroidism presentations
Graves' ophthalmology (bulging eyes, increased tears, photophobia, diplopia, extraocular muscle swelling)
Graves' dermopathy (pretibial myxoedema)
Thyroid acropathy (clubbing and swollen fingers)
61
1st line and gold standard investigation for Grave's disease
TSHR-Ab levels raised (TSH testing already done to establish hyperthyroidism)
62
Management of Grave's disease
Hyperthyroidism management
Corticosteroids for ophthalmopathy
63
Grave's disease complications
Pregnancy issues, heart disorders, thyroid storm, osteoporosis
64
Define Hashimoto's thyroiditis
Autoimmune disease causing thyroid gland damage and primary hypothyroidism
65
Triggers of Hashimoto's thyroiditis
Iodine, infection, smoking
66
Hashimoto's thyroiditis pathophysiology
Cytotoxic (CD8+) cell-mediated thyroid destruction. Patients are hypothyroid but go through an initial toxic phase (Hashi-toxicity)
67
Investigations for Hashimoto's thyroiditis
TFTs, TPO-Ab testing to confirm Hashimoto's
68
Management for Hashimoto's
Levothyroxine therapy
69
Complications of Hashimoto's
Heart problems
Myxoedema coma
Mental health issues
Hypothyroid complications
70
Define Cushing's syndrome
Increased plasma glucocorticoids (cortisol)
71
Causes of Cushing's syndrome
Increased ACTH from pituitary tumour (CUSHING'S DISEASE)
Ectopic ACTH-producing tumours
Increased cortisol due to adrenal adenoma or carcinoma
Exogenous steroids
72
Key presentations of Cushing's syndrome
Central obesity, thin skin, acne, proximal muscle wastage.
| Moon face, buffalo hump, striae, mental changes.
73
1st line tests for Cushing's syndrome
48hr low-dose dexamethasone test (Cushing's fail to suppress cortisol)
24hr urinary free cortisol
Loss of cortisol circadian rhythm
74
Gold standard test for Cushing's syndrome
Inferior petrosal sinus sampling
75
2nd line tests for Cushing's syndrome
ACTH plasma levels, adrenal MRI/CT, pituitary MRI, CXR
76
Cushing's syndrome management
Cortisol hypersecretion should be controlled prior to surgery (metyrapone)
Trans-sphenoidal removal of tumour (Cushing's disease)
Other causes often also require surgically
77
Prognosis of Cushing's syndrome
Very poor if untreated, adrenal carcinomas also have poor prognosis.
78
Define Acromegaly
Excessive GH after fusion of the epiphyseal plates
79
Define Gigantism
Excessive GH before fusion of the epiphyseal plates
80
Acromegaly causes
GH-secreting pituitary tumour (most common), ectopic GHRH excess
81
What does increased GH cause?
Increased IGF-1 levels leading to the changes seen in acromegaly
82
Key presentations of acromegaly.
Thicker skin, increased hand and foot size, facial changes, visual disturbances, fatigue
83
1st line test for acromegaly
GH levels (to rule out acromegaly as detectable levels aren't diagnostic)
84
Gold standard test for acromegaly
Glucose tolerance test (diagnostic if there is no suppression of GH)
85
Other tests for acromegaly
Visual field exam, MRI scan, pituitary function test, prolactin level (for co-secreting tumours)
86
1st line management for acromegaly
Trans-sphenoidal surgery
87
Drug management for acromegaly
Pituitary radiotherapy
SMS agonists - Octreotide
DA agonists
GH antagonists - Pegvisomant
88
Complications of acromegaly
HTN, enlargement of heart, osteoarthritis, T2DM, goitre, vision loss etc.
89
Causes of primary hyperaldosteronism
Adrenal adenoma secreting aldosterone (CONN'S SYNDROME)
Bilateral adrenocortical hyperplasia
90
Risk factors for primary hyperaldosteronism
Hypertension
91
Pathophysiology of primary hyperaldosteronism
Aldosterone causes increased exchange of Na+ and K+ in the DCT as well as increased water retention.
This causes hypokalaemia and increased BP.
92
1st line investigations for primary hyperaldosteronism
```
Discontinue drugs that can affect renin activity
Plasma aldosterone : renin ratio (ARR)
Serum hypokalaemia (not always present)
Bilateral adrenal vein sampling
```
93
Other investigations for primary hyperaldosteronism
High urinary K+, ECG, CT/MRI adrenals
94
Differential diagnosis of primary aldosteronism
Secondary hyperaldosteronism (from high renin and angiotensin II levels)
Different hyperplasia from Conn's disease with adrenal CT/MRI
95
Management of primary hyperaldosteronism
Laparoscopic surgery. Aldosterone antagonists - Spironolactone
96
Complications of primary hyperaldosteronism
Heart attacks, heart failure, kidney failure, early death
97
Causes of pituitary mass lesions
Non-functioning pituitary adenomas, craniopharyngioma, Rathke's cysts, meningioma, lymphocytic hypophysitis
98
Local effects of pituitary mass lesions
Bilateral hemianopia, headache, hypopituitarism, cranial nerve palsy
99
Gold standard test for pituitary mass lesion
MRI pituitary
100
Other tests in pituitary mass lesions
Hormone tests, visual defect test
101
Treatment of choice for pituitary mass lesions
Trans-sphenoidal surgery.
Then radiotherapy with SMS and DA agonists. Treatment for any hormone imbalances.
102
Define Addison's disease (primary adrenal insufficiency)
Destruction of the entire adrenal cortex. This results in aldosterone, cortisol and androgen deficiency.
103
Causes of Addison's disease
Autoimmune adrenalitis
TB
Surgical removal of adrenal cortex
Schilder's disease
104
Key presentation of Addison's disease
Postural hypertension, bronze pigmentation of skin, weight loss and wasting, confusion, GI disturbance, polydipsia
105
1st line investigations for Addison's disease
Synacthen test (short ACTH stimulation test)
Adrenal antibodies
Bloods - cortisol, raised calcium and potassium, low sodium
Hypoglycaemia
106
Gold standard test Addison's disease
Synacthen test
| means syn. ACTH en test!
107
Other investigations used in Addison's disease diagnosis
CXR, AXR
108
Differential diagnosis
Secondary adrenal insufficiency - no bronze pigmentation, stop causative drugs
109
Addison's disease management
Hydrocortisone
Fludrocortisone (replaces aldosterone)
Mineralocorticoids to correct postural hypotension
110
Complication of Addison's disease
ADRENAL CRISIS
111
Describe an adrenal crisis
Hypotension and CV collapse - SHOCK
Hyponatraemia, hyperkalaemia
Treatment: Fluids and IV hydrocortisone ASAP
112
Define hyperkalaemia
Inappropriately high blood potassium level >5.0mmol/L
113
Causes of hyperkalaemia
```
Vigorous exercise (self-limiting)
Low levels of aldosterone
Kidney disease
Excessive consumption (IV fluids)
Increased cellular release in acidosis
Drugs (beta blockers)
```
114
Risk factors for hyperkalaemia
CKD
| Diabetes (DKA)
115
Pathophysiology of hyperkalaemia
Insulin deficiency = not enough K+ follows insulin into cells
Acidosis = H+ exchanged into cells with K+
Beta blockers inhibit K+ pumping into cell
Cell lysis causes intracellular K+ to be released
116
Key presentations of hyperkalaemia
Cramping, weakness/flaccid paralysis, arrhythmias and arrest
Kussmaul respiration (if metabolic acidosis)
117
1st line tests for hyperkalaemia
U+Es, urinary K+
118
Other tests for hyperkalaemia
ECG, creatinine, GFR evaluation
119
Urgent management of hyperkalaemia
Insulin
| Calcium gluconate
120
Non-urgent management of hyperkalaemia
Potassium binders (decrease uptake in gut)
121
ECG for hyperkalaemia
Tall, tented T waves, small P waves and wide QRS complexes
122
Define hypokalaemia
Inappropriately low blood potassium (<3.5mmol/L)
123
Causes of hypokalaemia
```
DIURETIC TREATMENT
Hyperaldosteronism
Beta-2 agonists
Renal disease (Gitelman's, Liddle's Bartter's)
Vomiting/Diarrhoea
Too much insulin
Alkalosis
```
124
Pathophysiology of hypokalaemia
K+ uptake into cells is stimulated by insulin, beta-adrenergic stimulation and theophyllines.
Potassium levels are also heavily controlled by the kidneys (90% of filtered K+ is reabsorbed in PCT) and potassium is also secreted from the principal cells of the collecting ducts.
Aldosterone stimulates K+ and H+ secretion in exchange for Na+ in the principal cells – decreased K+ stimulates aldosterone.
125
Key presentations of hypokalaemia
Usually asymptomatic
Arrhythmias and palpitations
Cramps, muscle weakness, constipation
126
1st line test for hypokalaemia
U+Es, urinary K+
127
Other tests for hypokalaemia
ABG to test alkalosis
Digoxin tests
TSH tests
ECG
128
Management of hypokalaemia
Mild - oral K+
Severe - IV K+
Aldosterone receptor antagonists if hyperaldosteronism
129
Complications of hypokalaemia
Bradycardia with CV collapse, arrhythmias and acute respiratory failure from muscle paralysis.
130
ECG changes in hypokalaemia
U wave present, no t wave/t wave inversion, long PR and long QT
131
Define SIADH
Inappropriately high secretion of ADH which leads to increased water retention and hyponatraemia.
Characterised by euvolaemia.
132
Causes of SIADH
Ectopic ADH production (lung cancer or infections)
CNS causes
Drugs (CARDISH)
- Chemotherapy
- Antidepressants
- Recreational drugs
- Diuretics
- Inhibitors (ACEi or SSRIs)
- Sulphonylureas
- Hormones
133
Pathophysiology of SIADH
Increased ADH = increased water reabsorption. This increases blood volume and decreases plasma osmolality, therefore causing dilutional hyponatraemia.
Increased blood volume causes the heart to release ANP and BNP which decreases blood volume back to normal and even further decreases plasma osmolality.
Causes euvolaemia, hyponatraemia and high urinary sodium.
134
Key symptoms of SIADH
Headache, nausea, mental slowing, confusion, unstable gait.
Acute symptoms include coma, convulsion and respiratory arrest.
135
1st line investigations for SIADH
Plasma (<275) and urine osmolality (>100). Spot urine sodium (>40)
136
Other investigations for SIADH
TSH, cortisol, assessment of underlying causes (CXR)
137
Management of SIADH
Remove causal factor
Fluid restriction <1L/24hr if asymptomatic. Sometimes you need demeclocycline if fluid restriction if not tolerated.
Severe symptomatic cases require hypertonic saline.
138
Definition of DI
Insufficient amount of ADH
139
Causes of DI
Cranial DI = posterior pituitary producing too little ADH
Nephrogenic DI = kidney does not respond to the ADH in the blood
140
Key presentations of DI
Polyuria, polydipsia and dehydration
141
1st line investigation for DI
Water deprivation test
Hypertonic saline test - measures copeptin levels
142
Management of DI
Cranial DI = desmopressin
Nephrogenic DI = Bendroflumethiazide, NSAIDs - more difficult to treat
Excision of tumour if indicated
143
Complications of DI
Chronic dehydration, hypotension, kidney damage, tachycardia, weight loss
144
Define hypercalcaemia
An excess of calcium in the blood >2.6mmol/L
145
Causes of hypercalcaemia
Hypercalcaemia of malignancy
Primary hyperparathyroidism
Drugs - thiazides, vitamin D analogues, vitamin A, lithium
Excessive calcium intake (milk-alkali syndrome)
146
Risk factors for hypercalcaemia
Immobility, FHx, severe dehydration, drug use
147
Pathophysiology of hypercalcaemia
PTH increases calcium reabsorption, vitamin D activation in the kidney and increases bone resorption
In primary hyperparathyroidism is when there is an inappropriate rise in PTH despite a rise in calcium.
148
Key presentations of hypercalcaemia
```
Bones - pain, osteoporosis
Stones - kidney stones
Moans - abdominal pain, constipation
Groans - confusion, anxiety
Seizure - short QT interval
```
149
1st line investigations for hypercalcaemia
Raised serum calcium
24hr urinary calcium
PTH levels
150
Other investigations for hypercalcaemia
Renal function baseline
Malignancy investigation
Serum TSH and ACTH
151
Differential diagnosis of hypercalcaemia
Albumin levels
152
Management of hypercalcaemia
Aggressive rehydration - IV 0.9% saline
Bisphosphonates (IV pamidronate)
Oral prednisolone
Long-term you control the underlying malignancy (chemo or radio)
Parathyroid surgery if primary hyperparathyroidism
153
Define hypocalcaemia
Low levels of calcium in the blood (<2.1mmol/L)
154
Causes of hypocalcaemia
Vitamin D deficiency
Hypoparathyroidism
Pseudo-hypoparathyroidism (PTH resistance)
Increased phosphate levels due to CKD or phosphate therapy
155
Pathophysiology of hypocalcaemia
Low levels of PTH or a resistance to PTH causes decreased calcium reabsorption and decreased bone resorption
Low vitamin D levels decreases gut absorption of calcium
156
Key presentations of hypocalcaemia
```
Chvostek's sign
Trousseau's sign
Numbness, cramps, anxiety, neuromuscular issues
Cataracts, prolonged QT on ECG.
Muscle spasms and seizures
```
157
1st line test for hypocalcaemia
Serum calcium
PTH levels
Serum and urine creatinine
158
Other tests for hypocalcaemia
25-hydroxyvitamin D level, parathyroid antibodies, magnesium levels, metacarpal x-ray
159
Differential diagnosis of hypocalcaemia
GI tract dysfunction
| Low albumin levels
160
Management of hypocalcaemia
In vitamin D deficiency use cholecalciferol
In other cases, alpha-hydroxylated vitamin D derivatives
Oral calcium supplements
Severe symptoms require calcium gluconate
161
Complications of hypocalcaemia
Acute seizures/tetany, basal ganglia calcification, parkinsonism
162
Causes of hyperparathyroidism
Primary - parathyroid adenoma, hyperplasia, carcinoma, lithium (results in hypercalcaemia)
Secondary - vitamin D resistance (results in hypocalcaemia)
Tertiary - glands become autonomous after many years of secondary hyperparathyroidism (results in hypercalcaemia)
163
Key presentations of hyperparathyroidism
Primary - often asymptomatic
Secondary - kidney disease with skeletal or CV complications
164
1st line testing for hyperparathyroidism
Serum calcium and PTH, raised alkaline phosphatase
165
Gold standard testing for hyperparathyroidism
PTH immunoassay
166
Other tests for hyperparathyroidism
Ultrasound, radioisotope scans, DEXA bone density scan
167
Management of hyperparathyroidism
Treat severe hypercalcaemia first – medical emergency
Primary – surgical removal of adenoma
Secondary and tertiary – calcium correction - calcimimetics
Total or subtotal parathyroidectomy
Bisphosphonates
Chemotherapy in malignancy
168
Hyperparathyroidism complications
Kidney stones, acute pancreatitis, peptic ulceration, calcification of the cornea
169
Causes of hypoparathyroidism
Genetic diseases - Di George syndrome
Acquired - complication of surgery or radiotherapy
Transient - premature neonates
Inherited - pseudohypoparathyroidism, pseudopseudohypoparathyroidism
170
Risk factors for hypoparathyroidism
Recent neck surgery, FHx
171
1st line tests for hypoparathyroidism
PTH level, serum calcium and phosphate, 24hr urine calcium, creatinine
172
Gold standard testing for hypoparathyroidism
Parathyroid immunoassay
173
Other tests used in hypoparathyroidism
Hand x-ray, ECG, ECHO of heart (Di George)
174
Management of hypoparathyroidism
Diet high in calcium and low in phosphates
| Calcium and vitamin D supplements
175
Complications of hypoparathyroidism
Kidney stones, arrhythmias, cataracts, dental and bone disorders
176
Causes of neuroendocrine tumours
MEN1 or MEN2
Neurofibromatosis type 1
VHL syndrome
ALL ARE INHERITED CONDITIONS
177
Key presentations for neuroendocrine tumours
Depends on where in the body it is.
GI - diarrhoea, constipation, abdomen pain
Lung - wheezing and cough
Symptoms caused by increased hormone levels
178
Prognosis of neuroendocrine tumours
Poor prognosis since most tumours are diagnosed after having spread
179
Define pheochromocytoma
Rare tumour of the adrenal medulla that secretes adrenaline and noradrenaline.
A tumour of the sympathetic NS
180
Risk factors of pheochromocytoma
FHx of pheochromocytoma, MEN 2, VHL syndrome
181
Key presentations of pheochromocytoma
Episodic headache, sweating, tachycardia, HTN, anxiety, GI disturbance, fever, Raynaud's phenomenon
182
1st line treatment for pheochromocytoma
Urinary and plasma metanephrines
| Genetic testing
183
Differential diagnosis of pheochromocytoma
Alcohol withdrawal, labile essential hypertension, hyperventilation
184
Management of pheochromocytoma
Surgery if possible
Complete alpha and beta blockade (alpha MUST precede beta)
Iv hydration
Clinical and biochemical review
185
Complications of pheochromocytoma
Cardiomyopathy, myocarditis, cerebral haemorrhage, PE
186
Hyperprolactinaemia causes
Physiological
- pregnancy
- stress
- sleep
- exercise
- sex
Pathological
- PROLACTINOMAS
- co-secretion in tumours causing acromegaly
- stalk compression
- primary hypothyroidism
Drugs
- oestrogens
- DA agonists
- antidepressants
- antiemetics
187
Pathophysiology of Hyperprolactinaemia
Increased prolactin causes increased lactation and blocks action of GnRH and LH
188
Key presentations of hyperprolactinaemia
```
Galactorrhoea
Amenorrhoea or Oligomenorrhoea
Delayed or arrested puberty
Decreased libido
Visual defects and headache
```
189
1st line tests for hyperprolactinaemia
Prolactin levels in blood (0900h to 1600h)
Pregnancy testing
190
Other investigations for hyperprolactinaemia
Visual field defects
Anterior pituitary function tests
TFTs
Pituitary MRI
191
Management of hyperprolactinaemia
DOPAMINE AGONISTS - Cabergoline
Trans-sphenoidal surgery rarely used if DA agonists don't work
192
Define delayed puberty
Absence of secondary sexual characteristics by 14 (girls) or 16 (boys). MUCH MORE COMMON IN BOYS - so with girls likely to be more serious
193
Causes of delayed puberty
Idiopathic
Hypogonadotropic hypogonadism
- sexual infantilism related to gonadotropin deficiency
Hypergonadotropic hypogonadism
- primary gonadal issues
Constitutional delay of growth and puberty (CDGP) - just naturally late bloomers
Genetic conditions
- Kallman
- Klinefelter
- Turner
194
Key presentations of delayed puberty
Lack of secondary sex characteristics by appropriate age (Thelarche, adrenarche, pubarche, voice changes)
195
1st line investigations of delayed puberty
Assessment of LH, FSH, oestradiol and testosterone
196
Other investigations of delayed puberty
TFTs, bone age x-rays, assessment for pelvic abnormalities
197
Management of delayed puberty
Sometimes non needed.
Short-term, low-dose sex hormone therapy used to induce puberty if delay is great or child's mental health is suffering
In hypogonadism, pubertal induction is required (oestrogen then progesterone or testosterone)
198
Complications of delayed puberty
Infertility
| Mental health issues
199
Define precocious puberty
Onset of secondary sexual characteristics before 8 (girls) or 9 (boys)
MUCH MORE COMMON IN GIRLS - with boys more likely to be serious
200
Causes of precocious puberty
```
Idiopathic
Cerebral - tumour or brain damage
CAH, McCune-Albright syndrome
Testicular or ovarian syndromes
HCG-, androgen- or oestrogen-secreting tumours (peripheral)
```
201
Key presentations of precocious puberty
Early breast growth and menarche
Axial, pubic and/or facial hair.
Rapid growth, acne and body odour
202
Investigations for precocious puberty
LH, FSH, oestrogen and progesterone or testosterone. X-ray for bone age.
203
Management of precocious puberty
Long-acting GnRH analogues (if gonadotropin-dependent)
Inhibitors of steroidogenesis, antiandrogens and aromatase inhibitors (if gonadotropin-independent)
204
Define hypopituitarism
Deficiency of any hormone produced in the pituitary. Panhypopituitarism = deficiency is all hormones excreted by the anterior pituitary.
205
Causes of hypopituitarism
PROP1 and POU1F1 mutations affecting anterior development
Trauma from surgery
Pituitary or hypothalamic tumours
206
Tests for hypopituitarism
Testing each pituitary axis
MRI pituitary
insulin tolerance test (ACTH and GH deficiency)
207
Management of hypopituitarism
Hydrocortisone and levothyroxine ASAP
Sex hormone replacement
GH replacement
Surgery for tumours?
