Dermatology and Endocrine COPY COPY Flashcards
1
Q
Give an example of a water soluble hormone.
A
Peptides e.g. TRH, LH, FSH.
2
Q
Are water soluble hormones stored in vesicles or synthesised on demand?
A
Water soluble hormones e.g. peptides are stored in vesicles.
3
Q
How do water soluble hormones e.g. peptides get into a cell?
A
They bind to cell surface receptors.
4
Q
Give an example of a fat soluble hormone.
A
Steroids e.g. cortisol.
5
Q
Are fat soluble hormones stored in vesicles or synthesised on demand?
A
Fat soluble hormones e.g. steroids are synthesised on demand.
6
Q
Give an example of an amine hormone.
A
Noradrenaline and adrenaline.
7
Q
Describe the pathway for noradrenaline synthesis.
A
Phenylalanine -> L-tyrosine -> L-dopa -> dopamine -> NAd and Ad.
8
Q
Name 2 enzymes that break down catecholamines.
A
MAO and COMT.
9
Q
What are noradrenaline and adrenaline broken down into?
A
Normetadrenaline and metadrenaline.
10
Q
Where in a cell are peptide cell receptors located?
A
Peptide cell receptors are located on the cell membrane.
11
Q
Where in a cell are steroid cell receptors located?
A
Steroid cell receptors are located in the cytoplasm.
12
Q
Where in a cell are thyroid/vitamin A and D cell receptors located?
A
Thyroid, vitamin A and D and oestrogen act on nuclear receptors.
13
Q
Give 5 ways in which hormone action is controlled.
A
- Hormone metabolism.
- Hormone receptor induction.
- Hormone receptor down-regulation.
- Synergism e.g. glucagon and adrenaline.
- Antagonism e.g. glucagon and insulin.
14
Q
What layer of the trilaminar disc is the anterior pituitary derived from?
A
Ectoderm (Rathke’s pouch).
15
Q
Name 6 hormones that the anterior pituitary produces.
A
- TSH.
- FSH.
- LH.
- ACTH.
- Prolactin.
- GH.
16
Q
What is the posterior pituitary derived form?
A
The floor of the ventricles.
17
Q
Where are posterior pituitary hormones synthesised?
A
They are synthesised in the para-ventricular and supra-optic nuclei.
18
Q
Name 2 hormones secreted from the posterior pituitary.
A
Oxytocin and ADH.
19
Q
What is the function of ADH?
A
It acts on the collecting ducts of the nephron and increases insertion of aquaporin 2 channels -> there is H2O retention.
20
Q
Give 2 functions of oxytocin.
A
- Milk secretion.
2. Uterine contraction.
21
Q
Which has a longer half life, triiodothyronine or thyroxine?
A
Thyroxine has a half life of 5-7 days whereas triiodothyronine has a half life of only 1 day.
22
Q
Describe the thyroid axis.
A
Hypothalamus -> TRH -> AP -> TSH -> thyroid -> T3 and T4.
T3/4 have a negative feedback effect on the hypothalamus and the anterior pituitary.
23
Q
What would be the effect on TSH if you had an under-active thyroid?
A
TSH would be raised as you have less T3/4 being produced and so no negative feedback.
24
Q
What would a low TSH tell you about the action of the thyroid?
A
A low TSH indicates an over-active thyroid.
Lots of T4 and T3 is being produced and so there is more negative feedback on the pituitary and less TSH.
25
Describe the mechanism of ACTH.
Hypothalamus -> CRH -> AP -> ACTH -> adrenal cortex (zona fasciculata) -> glucocorticoid synthesis e.g. cortisol.
Cortisol has a negative feedback effect on the hypothalamus and the anterior pituitary.
26
Give 3 functions of thyroid hormones (T3/4).
1. Food metabolism.
2. Protein synthesis.
3. Increased sympathetic action e.g. CO and HR.
4. Heat production.
5. Needed for growth and development.
27
Give 3 functions of cortisol in response to stress.
1. Mobilises energy sources -> lipolysis, gluconeogenesis and protein break down.
2. Vasoconstriction.
3. Suppresses inflammatory and immune repsonses.
4. Inhibits non-essential functions e.g. growth and reproduction.
28
Briefly describe the mechanism of LH and FSH.
Hypothalamus -> GnRH -> AP -> FSH/LH -> ovaries/testes.
FSH acts on granulosa cells to produce oestrogen and sertoli cells to stimulate spermatogenesis.
LH acts on theca cells to produce androgens or leydig cells to produce testosterone.
29
What cells does FSH act on?
- In the ovaries: granulosa cells.
| - In the testes: sertoli cells.
30
What cells does LH act on?
- In the ovaries: theca cells.
| - In the testes: leydig cells.
31
What is the function of theca cells?
Theca cells are stimulated by LH to produce androgens that diffuse into granulosa cells to be converted into oestrogen.
32
What is the function of granulosa cells?
Granulosa cells are stimulated by FSH to convert androgens into oestrogen using aromatase.
33
What is the function of sertoli cells?
Sertoli cells produce MIF (mullerian inhibiting factor) and inhibin and activin which acts on the pituitary gland to regulate FSH.
34
What is the function of leydig cells?
Leydig cells are stimulated by LH to produce testosterone.
35
Describe the GH/IGF-1 axis.
what inhibits?
Hypothalamus -> GHRH (+) or SMS (-) -> AP -> GH -> Liver -> IGF-1.
36
What is the function of IGF-1?
- induced protein synthesis, lipolysis, glucose metabolism
| - cell division, cartilage and skeletal growth
37
Briefly describe the mechanism of prolactin.
Hypothalamus -> dopamine (-) -> AP -> prolactin.
Prolactin acts on the mammary glands to produce milk.
38
What would happen to serum prolactin levels if something was to impact on the pituitary stalk and block dopamine release?
Prolactin levels would increase.
39
Give 3 potential consequences of a pituitary tumour.
1. Pressure on local structures e.g. optic chiasm.
2. Hypo-pituitary.
3. Functioning tumour e.g. Cushing's, gigantism, prolactinoma.
40
Give 2 causes of prolactinoma.
1. Pituitary adenoma.
| 2. Anti-dopaminergic drugs (dopamine antagonists)
41
Give 5 symptoms of prolactinoma.
1. Infertility.
2. Golactorrhoea.
3. Amenorrhoea.
4. Loss of libido.
5. Visual field defects and headaches due to local effect of tumour.
42
What investigation and imaging would you do on someone presenting with difficulty getting pregnant, golactorrhoea, amenorrhoea, loss of libido and headaches?
You would measure serum prolactin.
MRI and computerised visual field examination
These are symptoms of prolactinoma.
43
Describe the treatment for prolactinoma.
Dopamine agonist e.g. cabergoline
Trans-sphenoidal surgical removal of pituitary tumour
44
Describe growth hormone secretion from the anterior pituitary. not axis, when during day.
It is secreted in a pulsatile fashion and increases during deep sleep.
45
What can cause acromegaly?
A benign pituitary adenoma producing excess GH.
or secondary to cancer (lung) that secretes ectopic GHRH or GH
46
Give 5 symptoms of acromegaly.
1. Change in appearance.
2. Increase in size of hands and feet.
3. Excessive sweating.
4. Headache.
5. Tiredness.
6. Weight gain.
7. Amenorrhoea.
8. Deep voice.
9. Goitre.
47
Give 3 signs of acromegaly. (investigations)
GH: raised
IGF-1: raised
oral glucose tolerance test: raised GH, (raised glucose fails to suppress GH)
48
What co-morbidities are associated with acromegaly?
1. Arthritis.
2. Hypertrophic heart
3. Hypertension
4. Colorectal cancer
5. Type 2 diabetes
49
What investigations might you do on someone who you suspect has acromegaly?
1. Plasma GH levels can exclude acromegaly - not diagnostic!
2. Serum IGF-1 levels raised.
3. Oral glucose tolerance test - diagnostic!
4. MRI of pituitary.
50
What test is diagnostic for acromegaly?
Oral glucose tolerance test - failure of glucose to suppress serum GH.
51
Describe the treatment for acromegaly.
1. Trans-sphenoidal surgical resection.
2. Radiotherapy.
3. Medical therapy: somatostatin analogues (octreotide), dopamine agonists e.g. cabergoline.
52
Give 3 potential complications of trans-sphenoidal surgical resection for the treatment of acromegaly.
1. Hypopituitarism.
2. Diabetes insipidus.
3. Haemorrhage.
4. CNS injury.
5. Meningitis.
53
Give 3 advantages of using dopamine agonists in the treatment of acromegaly.
1. No hypopituitarism.
2. Oral administration.
3. Rapid onset.
54
Give 2 disadvantages of using dopamine agonists in the treatment of acromegaly.
1. Can be ineffective.
| 2. Risk of side effects (confusion, compulsive behaviour)
55
Name a dopamine agonist that can be used in the treatment of acromegaly.
Cabergoline.
56
Give 5 causes of hypothyroidism.
1. Autoimmune thyroiditis e.g. Hashimoto's and atrophic thyroiditis.
2. Post-partum thyroiditis.
3. Iatrogenic - thyroidectomy.
4. Drug induced e.g. carbimazole, amiodarone, lithium.
5. Iodine deficiency.
57
Hypothyroidism: name 3 anti-bodies that may be present in the serum in someone with autoimmune thyroiditis.
1. TPO (thyroid peroxidase).
2. Thyroglobulin.
3. TSH receptor.
58
Give an example of a transient cause of hypothyroidism.
Post-partum thyroiditis
59
Give 2 examples of iatrogenic causes of hypothyroidism.
1. Thyroidectomy.
| 2. Radioiodine therapy.
60
Name 3 drugs that can cause hypothyroidism.
1. Carbimazole (used to treat hyperthyroidism).
2. Amiodarone.
3. Lithium.
61
Why can amiodarone cause hypo/hyperthyroidism?
Because it is iodine rich.
62
Give 5 symptoms of hypothyroidism.
1. Menorrhagia – heavy bleeding.
2. Obesity/weight gain.
3. Malar flush.
4. Constipation
5. Intolerance to cold.
6. Energy levels fall/eyebrow loss.
7. Depression/dry skin and hair.
8. GOITRE!
63
Give 5 signs of hypothyroidism.
1. Mental slowness.
2. Dry thin hair.
3. Bradycardia.
4. Anaemia.
5. Hypertension.
6. Loss of eyebrows.
7. Cold peripheries.
8. Carpal tunnel syndrome.
64
What investigations might you do in someone who you suspect has hypothyroidism?
- TFT's - serum TSH will be raised and T3/T4 will be low.
| - Thyroid antibodies.
65
Describe the management for hypothyroidism.
Levothyroxine.
66
Give 5 causes of thyrotoxicosis.
Thyrotoxicosis - excess thyroid hormone due to any cause:
1. Increased production e.g. Grave's, toxic adenoma.
2. Leakage of T3/4 due to follicular damage.
3. Ingestion.
4. Thyroiditis.
5. Drug induced.
67
Give 2 causes of hyperthyroidism.
1. Grave's disease.
| 2. Toxic adenoma.
68
Briefly describe the pathophysiology of Grave's disease.
Autoimmune disease. TSH receptor antibodies stimulate thyroid hormone production -> hyperthyroidism.
69
Give 5 symptoms of Grave's disease
1. Weight loss.
2. Increased appetite.
3. Irritable.
4. exophthalmos
5. Palpitations.
6. Goitre.
7. Diarrhoea.
8. Heat intolerance.
9. pretibial myxoedema
10. acropathy
70
Give 5 signs of Grave's disease
1. Tachycardia.
2. Arrhythmias e.g. AF.
3. Warm peripheries/ heat intolerance
4. weight loss
5. Pre-tibial myxoedema (raised lesions over the shins)
6. Thyroid acropachy (clubbing and swollen fingers).
7. exophthalmos
71
With what disease would you associated pre-tibial myxoedema and thyroid acropachy?
Grave's disease.
72
Give 5 Grave's opthlmopathy signs.
1. Exophthalmos (bulging eyes).
2. Lid lag stare.
3. Redness.
4. Conjuctivitis.
5. Pre-orbital oedema.
6. Bilateral.
7. Extra-ocular muscle swelling.
73
What investigations might you do in someone who you suspect has hypothyroidism?
TFT's - serum TSH is elevated and T3/4 are depressed
74
What would you see histologically in someone with Grave's disease?
Lymphocyte infiltration and thyroid follicle destruction.
75
Describe the treatment for Grave's disease.
1. Anti-thyroid drugs e.g. carbimazole.
2. Radioiodine drugs.
3. Surgery - partial thyroidectomy.
76
How does carbimazole work in treating Grave's disease?
It targets thyroid peroxidase and so prevents the formation of T3/4.
77
Give a potential serious side effect of taking carbimazole to treat Grave's disease.
Agranulocytosis.
Patient's are advised to seek medical attention if they develop an unexplained sore throat or fever.
78
How do radioiodine drugs work in treating Grave's disease?
Radioiodine drugs emit beta particles that destroy thyroid follicles and so thyroid hormone production is decreased.
79
Give 3 potential complications of a partial thyroidectomy.
1. Bleeding.
2. Hypocalcaemia.
3. Hypothyroidism.
4. Recurrent laryngeal nerve palsy.
80
What disease would you treat with Carbimazole?
Grave's disease.
81
What disease would you treat with levothyroxine?
Hypothyroidism.
82
Give 5 metabolic changes that occur in pregnancy.
1. Increased EPO, cortisol and NAd.
2. High CO.
3. High cholesterol and triglycerides.
4. Pro thrombotic and inflammatory state.
5. Insulin resistance.
83
Give 5 gestational syndromes.
1. Pre-eclampsia.
2. Gestational diabetes.
3. Obstetric cholestasis.
4. Gestational thyrotoxicosis.
5. Postnatal depression.
6. Post partum thyroiditis.
84
At what week are foetal thyroid follicles and T4 synthesised?
Week 10.
85
Why can hCG activate TSH receptors and cause hyperthyroidism?
HCG and TSH are glycoprotein hormones with very similar structures. HCG can therefore activate TSH receptors.
86
Is hypothyroidism or thyrotoxicosis more common in pregnancy?
Hypothyroidism is more common in pregnancy.
87
How can you differentiate between Grave's disease and gestational thyrotoxicosis?
- Grave's: symptoms predate pregnancy; symptoms are severe during pregnancy; goitre and TSH-R antibodies present.
- Gestational thyrotoxicosis: symptoms do not predate pregnancy; lots of N/V - hyperemesis gravidarum associated. No goitre or TSH-R antibodies.
88
Give 3 potential consequences of untreated hypothyroidism in pregnancy.
1. Gestational hypertension.
2. Placental abruption.
3. Post partum haemorrhage,
4. Low birth weight.
5. Neonatal goitre.
89
Give 3 potential consequences of untreated hyperthyroidism in pregnancy.
1. Intra-uterine growth restriction.
2. Low birth weight.
3. Pre-eclampsia.
4. Risk of still birth/miscarriage.
90
What disease is described as being a 'disorder of carbohydrate metabolism characterised by hyperglycaemia'?
Diabetes mellitus.
91
What are the 4 cells to make up the islets of langerhans?
1. Beta cells (70%).
2. Alpha cells (20%).
3. Delta cells (8%).
4. Polypeptide secreting cells.
92
What do beta cells produce?
Insulin.
93
What do alpha cells produce?
Glucagon.
94
What do delta cells produce?
Somatostatin.
95
What is the importance of the alpha and beta cells being located next to each other in the islets of langerhans?
This enables them to 'cross talk' - insulin and glucagon show reciprocal action.
96
Describe the mechanism of insulin secretion from beta cells.
Glucose binds to beta cells -> glucose phosphorylated to make ATP -> K+ channels close -> membrane depolarisation -> Ca2+ channels open, influx -> insulin release.
97
Describe the physiological processes that occur in the fasting state in response to low blood glucose.
Low blood glucose = high glucagon and low insulin.
- Glycogenolysis and gluconeogenesis.
- Reduced peripheral glucose uptake.
- Stimulates the release of gluconeogenic precursors.
- Lipolysis and muscle breakdown.
98
Describe the effect on insulin and glucagon secretion in the fasting state.
Fasting state = low blood glucose.
| Raised glucagon and low insulin.
99
How many carbon precursors are needed for gluconeogenesis?
3.
100
Describe the physiological processes that occur after feeding in response to high blood glucose.
High blood glucose = high insulin and low glucagon.
- Glycogenolysis and gluconeogenesis are suppressed.
- Glucose is taken up by peripheral muscle and fat cells.
- Lipolysis and muscle breakdown suppressed.
101
Describe the effect on insulin and glucagon secretion after feeding.
Insulin is high and glucagon is low.
102
A diagnosis of diabetes can be made by measuring plasma glucose levels. What would a persons fasting plasma glucose be if they were diabetic?
Fasting plasma glucose >7mmol/L.
103
A diagnosis of diabetes can be made by measuring plasma glucose levels. What would a persons random plasma glucose be if they were diabetic?
Random plasma glucose >11mmol/L.
104
A diagnosis of diabetes can be made by measuring plasma glucose levels. What would the results of the oral glucose tolerance test be if someone was diabetic?
Fasting plasma glucose >7mmol/L and 2-hour value >11mmol/L.
105
What might someone's HbA1c be if they have diabetes?
>48mmol/mol.
106
What is the affect of cortisol on insulin and glucagon?
Cortisol inhibits insulin and activates glucagon.
107
Describe the aetiology of type 1 diabetes mellitus.
Beta cells express HLA antigens. Autoimmune destruction -> beta cell loss -> impaired insulin secretion.
108
Is type 1 diabetes characterised by a problem with insulin secretion, insulin resistance or both?
Type 1 diabetes is characterised by impaired insulin secretion - there is severe insulin deficiency.
109
At what age do people with T1DM present?
Often people with Type 1 diabetes will present in childhood.
110
Give 2 potential consequences of T1DM.
1. Hyperglycaemia.
| 2. Raised plasma ketones -> ketoacidosis.
111
Describe the natural history of T1DM.
Genetic predisposition + trigger -> insulitis, beta cell injury -> pre-diabetes -> diabetes.
112
T1DM is characterised by impaired insulin secretion. Describe the pathophysiological consequence of this.
Severe insulin deficiency -> glycogenolysis/gluconeogensis/lipolysis all not suppressed AND reduced peripheral glucose uptake -> hyperglycaemia and glycosuria.
Perceived stress -> cortisol and Ad secretion -> catabolic state -> increased plasma ketones.
113
Give 3 symptoms of T1DM.
1. Weight loss.
2. Thirst (fluid and electrolyte losses).
3. Polyuria (due to osmotic diuresis).
114
Would you associate ketoacidosis with T1 or T2 DM?
TYPE 1.
Occurs due to the absence of insulin.
115
Describe the pathophysiology of diabetic ketoacidosis.
No insulin -> lipolysis -> FFA's -> oxidised in liver -> ketone bodies -> ketoacidosis.
116
Name 3 ketone bodies.
- acetoacetate.
- acetone.
- beta hydroxybutyrate.
117
Where does ketogenesis occur?
In the liver.
118
Give 4 signs of diabetic ketoacidosis.
1. Hypotension.
2. Tachycardia.
3. Kussmaul’s respiration.
4. Breath smells of ketones.
5. Dehydration.
119
Describe the treatment for T1DM.
1. EDUCATION - make sure the patient understands the benefits of good glycaemic control.
2. Healthy diet - low in sugar, high in carbohydrates.
3. Regular activity, healthy BMI.
4. BP and hyperlipidaemia control.
5. Insulin.
120
How is insulin administered in someone with T1DM?
Injected into SC fat.
121
Other than SC injections, how else can insulin be administered?
Insulin pump.
122
Give 4 potential complications of insulin therapy.
1. Hypoglycaemia.
2. Lipohypertrophy at ejection site.
3. Insulin resistance.
4. Weight gain.
5. Interference with life style.
123
Is type 2 diabetes characterised by a problem with insulin secretion, insulin resistance or both?
Type 2 DM is characterised by impaired insulin secretion AND insulin resistance.
124
Describe the aetiology of T2DM.
Genetic predisposition and environmental factors e.g. obesity and lack of exercise.
125
Why is insulin secretion impaired in T2DM?
Impaired insulin secretion is thought to be due to lipid deposition in the pancreatic islets.
126
Describe the pathophysiology of T2DM.
Impaired insulin secretion and resistance -> impaired glucose tolerance -> T2DM -> hyperglycaemia and high FFA's.
127
Is insulin secretion or insulin resistance the driving force of hyperglycaemia in T2DM?
Hepatic insulin resistance is the driving force of hyperglycaemia.
128
Give 3 risk factors for insulin resistance in T2DM.
1. Obesity.
2. Physical inactivity.
3. Family history.
129
What happens to insulin resistance, insulin secretion and glucose levels in T2DM?
- Insulin resistance increases.
- Insulin secretion decreases.
- Fasting and post-prandial glucose increase.
130
Why do you rarely see diabetic ketoacidosis in T2DM?
Insulin secretion is impaired but there are still low levels of plasma insulin. Even low levels of insulin can prevent muscle catabolism and ketogenesis.
131
Describe the treatment pathway for T2DM.
1. Lifestyle changes: lose weight, exercise, healthy diet.
2. Metformin.
3. Metformin + sulfonylurea.
4. Metformin + sulfonylurea + insulin.
5. Increase insulin dose as required.
132
How does metformin work in treating T2DM?
metformin decreases the amount of glucose released by liver, and makes body more sensitive to insulin
133
How does sulfonylurea work in treating T2DM?
Sulfonylurea stimulates insulin release.
134
Give a potential consequence of taking Sulfonylurea for the treatment of T2DM.
Hypoglycaemia.
(Sulfonylurea stimulates insulin release).
135
Give 3 microvascular complications of diabetes mellitus.
1. Diabetic retinopathy.
2. Diabetic nephropathy.
3. Diabetic peripheral neuropathy.
136
Give a macrovascular complication of diabetes mellitus.
CV disease and stroke.
137
What is the main risk factor for diabetic complications?
Poor glycaemic control!
138
Give a potential consequence of acute hyperglycaemia?
Diabetic ketoacidosis and hyperosmolar coma.
139
Give a potential consequence of chronic hyperglycaemia?
Micro/macrovascular tissue complications e.g. diabetic reinopathy, nephropathy, neuropathy, CV disease etc.
140
What is the commonest form of diabetic neuropathy?
Distal symmetrical polyneuropathy.
141
Give 3 major clinical consequences of diabetic neuropathy.
1. Pain.
2. Autonomic neuropathy.
3. Insensitivity.
142
Describe the pain associated with diabetic neuropathy.
- Burning.
- Paraesthesia.
- Nocturnal exacerbation.
143
Diabetic neuropathy clinical consequences: what is autonomic neuropathy?
Autonomic neuropathy - damage to the nerves that supply body structures that regulate functions such as BP, HR, bowel/bladder emptying.
144
Diabetic neuropathy: give 5 signs of autonomic neuropathy.
1. Hypotension.
2. HR affected.
3. Diarrhoea/constipation.
4. Incontinence.
5. Erectile dysfunction.
6. Dry skin.
145
What are the consequences of insensitivity as a result of diabetic neuropathy?
Insensitivity -> foot ulceration -> infection -> amputation.
146
Describe the distribution of insensitivity as a result of diabetic neuropathy?
Insensitivity starts in the toes and moves proximally. Glove and stocking distribution.
147
Give 5 risk factors for diabetic neuropathy.
1. POOR GLYCAEMIC CONTROL.
2. Hypertension.
3. Smoking.
4. HbA1c.
5. Overweight.
6. Long duration of DM.
148
Describe the treatments for diabetic neuropathy.
1. Improve glycaemic control.
2. Antidepressants.
3. Pain relief.
149
PVD is a potential complication of Diabetes. Give 6 signs of acute ischaemia.
1. Pain
2. Pallor
3. Pulseless
4. Paralysis
5. Paraesthesia
6. Perishing cold
150
Give 5 ways in which amputation can be prevented in someone with diabetic neuropathy.
1. Screening for insensitivity.
2. Education.
3. MDT foot clinics.
4. Pressure relieving footwear.
5. Podiatry.
6. Revascularisation and abx.
151
Would there be increased or decreased pulses in a diabetic neuropathic foot?
There would be increased foot pulses.
152
Give 5 risk factors for diabetic retinopathy.
1. Long duration DM.
2. Poor glycaemic control.
3. Hypertension.
4. Insulin treatment.
5. Pregnancy.
6. High HbA1c.
153
Describe the pathophysiology of diabetic retinopathy.
Micro-aneurysms -> pericyte loss and protein leakage -> occlusion -> ischaemia.
154
How can diabetic retinopathy be sub-divided?
Diabetic retinopathy is divided into:
- Proliferative - evidence of neovascularisation in retina.
- Non-proliferative.
155
What is the treatment for diabetic retinopathy?
People with diabetes are offered regular screening to assess visual acuity.
- Laser therapy treats neovascularisation.
156
What is the hallmark of diabetic nephropathy?
Development of proteinuria and progressive decline in renal function.
157
What happens to the glomerular basement membrane in someone with diabetic nephropathy?
On microscopy there is thickening of the glomerular basement membrane.
158
Give one way in which the presentation of diabetic nephropathy differs between T1 and T2DM.
T1 DM: microalbuminuria develops 5-10 years after diagnosis.
T2 DM: microalbuminuria is often present at diagnosis.
159
Describe the treatment for diabetic nephropathy.
1. Glycaemic and BP control.
2. ARB (losartan) /ACEi (captopril)
3. Proteinuria and cholesterol control.
160
Name the suprasellar neoplasm that can result from benign cysts and calcification of Rathke's pouch?
Craniopharyngioma.
161
Give 4 signs of Craniopharyngioma.
1. Raised ICP.
2. Vision affected.
3. Growth failure.
4. Puberty affected.
162
Give 4 local effects of pituitary adenoma.
1. Headaches.
2. Visual field defects - bitemporal hemianopia.
3. prevent pituitary function
4. function pituitary tumour
163
What is the affect of hypothyroidism on TSH and T4 levels?
- TSH will be high.
| - T4 will be low.
164
What is the affect of hyperthyroidism on TSH and T4 levels?
- TSH will be low.
| - T4 will be high.
165
What is the affect of hypopituitarism on TSH and T4 levels?
- TSH will be low.
| - T4 will be low.
166
What is the treatment for thyroid hypopituitarism?
Levothyroxine.
167
Give a cause of primary hypogonadism.
Klinefelter's syndrome - extra X chromosome.
168
What is the affect of primary hypogonadism on testosterone and FSH/LH levels?
- Testosterone will be low.
| - FSH/LH will be high.
169
What is the affect of hypopituitarism on testosterone and FSH/LH levels?
- Testosterone will be low.
| - FSH/LH will be low.
170
When should serum testosterone be measured?
At 9am due to circadian rhythm.
171
Give 5 consequences of androgen deficiency in a male.
1. Loss of libido.
2. High pitched voice.
3. Loss of facial, axillary, limb and pubic hair.
4. Loss of erections.
5. Poorly developed scrotum and penis.
172
What is the treatment for hypogonadism?
Testosterone gel/injection.
- Can improve BMD, QOL and libido etc.
173
What syndrome is characterised by a congenital deficiency of GnRH?
Kallmann's syndrome.
174
Are the levels of oestradiol and FSH/LH low or high before puberty?
Before puberty there are very low levels of these hormones in the serum.
175
What is the affect of primary ovarian failure on oestradiol and FSH/LH levels?
- FSH/LH is high.
| - Oestradiol is low.
176
What is the affect of hypopituitarism on oestradiol and FSH/LH levels?
- FSH/LH are low.
| - Oestradiol is low.
177
What is the affect of primary adrenal insufficiency on cortisol and ACTH levels?
- Cortisol is low.
| - ACTH is high.
178
What is the affect of hypopituitarism on cortisol and ACTH levels?
- Cortisol is low.
| - ACTH is low.
179
What can lead to elevated levels of prolactin?
1. Stress!
2. Drugs.
3. Pressure on the pituitary stalk.
180
What stimulates the posterior pituitary to release ADH?
Osmoreceptors in the hypothalamus detect raised plasma osmolarity -> posterior pituitary is signalled to release ADH.
181
Give 5 signs of diabetes insipidus.
1. Excessive urine production (>3L/24h).
2. Very dilute urine - <300 mOsmol/Kg.
3. Severe thirst.
4. Hypernatraemia (serum).
5. Dehydration.
182
What investigations might you do to determine whether someone has diabetes insipidus?
1. Measure 24-hour urine volume - >3L/24h = suggests DI.
2. Plasma biochemisty - hypernatraemia.
3. urine osmolality (low), serum osmolality (high)
3. Water deprivation test (desmopressin (synthetic ADH)) - urine will not concentrate when asked not to drink.
183
What is the treatment for cranial diabetes insipidus?
Desmopression.
184
Give 4 causes of polyuria.
1. Hypokalaemia.
2. Hypercalcaemia.
3. Hyperglycaemia.
4. Diabetes insipidus.
185
Would TSH and T4 be high or low in someone with sub-clinical hypothyroidism?
TSH would be high but T4 would be normal. These patients are often asymptomatic and well.
(Hypothyroidism: high TSH and low T4).
186
What is Cushing's syndrome?
A set of signs/symptoms resulting from chronic glucocorticoid excess with a loss of normal feedback mechanisms.
187
What can cause Cushing's syndrome?
1. Adrenal Tumour (adenoma or carcinoma).
2. Pituitary tumour (Cushing's disease).
3. Exogenous steroids.
4. Ectopic ACTH syndrome.
188
What is Cushing's disease?
Pituitary adenoma that secretes excessive ACTH => (cushings syndrome) hypercorticolism
ACTH dependent.
189
Give 7 signs/symptoms of Cushing's disease.
1. Central obesity.
2. Moon face.
3. Hypertension.
4. buffalo hump
5. Abdominal striae.
6. Mood change.
7. Osteoporosis.
8. Muscle thinning.
9. Weight gain.
10. Menstrual abnormalities
190
What investigations might you do in someone with Cushing's syndrome?
1. Overnight dexamethasone suppression test - failure to suppress cortisol.
2. Late night salivary cortisol - loss of circadian rhythm.
3. Loss of circadian rhythm.
191
What is the treatment for Cushing's syndrome?
1. Trans sphenoidal removal of pituitary adenoma
2. surgical removal of adrenal or paraneoplastic (ectopic) tumour
PLUS: permanent post surgical corticosteroid replacement therapy
192
What is SIADH?
Syndrome of inappropriate ADH secretion.
Too much ADH = very concentrated urine and hyponatreamia (serum Na)
193
Give 3 symptoms of SIADH.
Relate to hyponatraemia
1. Fatigue
2. Nausea.
3. Malaise.
4. Headache.
5. Confusion.
6. muscle aches + cramps
194
Give 3 causes of SIADH.
1. Post operative
2. Infection (lung pneumonia)
3. Head injury
4. Drugs (amiodarone, thiazide like dietetics, NSAIDs)
5. Malignancy
6. Meningitis
195
Describe the treatment for SIADH.
Treat underlying cause (stop causative med), correct Na slowly to prevent central pontine myelinolysis
1. IV hypertonic saline
2. Fluid restriction
3. ADH receptor blockers (Tolvaptan)
196
What is Conn's syndrome?
Primary hyperaldosteronism - high aldosterone levels independent of RAAS activation -> H2O and sodium retention and potassium and H+ excretion.
197
What are the 3 main signs of Conn's syndrome?
1. Hypertension.
2. Hypokalaemia.
3. Alkalosis
Aldosterone => increase Na reabsorption, decreased K reabsorption, increased H+ secretion in collecting ducts
198
Give 3 symptoms of Conn's syndrome. A deficiency in which electrolyte causes these symptoms?
1. Muscle weakness.
2. Tiredness.
3. Polyuria.
Due to potassium deficiency - hypokalaemia.
199
What can cause Conn's syndrome?
Adrenal adenoma.
200
What hormone is raised in Conn's syndrome and what hormone is reduced? Where are these hormones synthesised?
1. Aldosterone is raised - synthesised in the zona glomerulosa.
2. Renin is reduced - synthesised by the juxta-glomerular cells.
201
What investigations might you do in someone to confirm a diagnosis of Conn's syndrome?
1. Bloods - U+E, renin (low) and aldosterone (high).
| 2. MRI to look for adrenal tumour
202
Give 4 ECG changes that you might see in someone with Conn's syndrome.
Hypokalaemia
1. Increased amplitude and width of P waves.
2. Flat T waves.
3. ST depression.
4. Prolonged QT interval.
5. U waves.
203
What is the treatment for Conn's syndrome?
1. Laparoscopic adrenalectomy.
| 2. Spironolactone (aldosterone antagonist).
204
What does the parathyroid control?
Serum calcium levels.
A low serum calcium triggers the release of PTH and a high serum calcium triggers c-cells to release calcitonin.
205
What hormone does the parathyroid secrete and what is its function?
PTH - secreted in response to low serum calcium.
- Bones: increased bone resorption
- Kidney: Increased Ca reabsorption (decreased phosphate reabsorbtion)
- Gut: Increased active vet D formation => increased intestinal Ca absorption
206
What is released by c-cells in the parathyroid in response ot high serum calcium?
Calcitonin.
207
What is the affect of hyperparathyroidism on serum calcium levels?
Hyperparathyroidism -> hypercalcaemia.
208
Give 5 symptoms of hyperparathryoidism.
Hyperparathyroidism -> hypercalcaemia:
1. Renal/biliary stones.
2. Bone pain.
3. Abdominal pain.
4. Polyuria.
5. Depression, anxiety, malaise.
Stones,bones, groans, thrones, moans.
209
Give 3 causes of hyperparathyroidism.
1. Primary: parathyroid adenoma - ↑PTH ↑Calcium ↓Phosphate.
2. Secondary: insufficient Vit D
3. Prolonged uncorrected secondary => parathyroid hyperplasia => increased baseline PTH
210
Describe the treatment for hyperparathyroidism.
1. High fluid intake, low calcium diet, vitamin D
2. Excision of adenoma.
3. Correct underlying cause.
4. Parathyroidectomy.
211
What is the affect of hypoparathyroidism on serum calcium levels?
Hypoparathyroidism -> hypocalcaemia.
212
Give 5 symptoms of hypoparathryoidism.
Hypoparathyroidism -> hypocalcaemia:
1. Spasm.
2. Paraesthesia around mouth and lips.
3. Anxious/irritable.
4. Seizures.
5. Increased muscle tone.
6. Confusion.
7. Dermatitis.
8. Impetigo herpetiformis.
9. QT prolongation.
213
What is the treatment for hypoparathyroidism?
Calcium supplements.
214
Give 5 causes of hypocalcaemia.
1. Dietary insufficiency
2. Hypoparathyroidism
3. Vit D deficiency
4. CKD
5. Drugs (carbimazole, amiodarone, lithium)
6. Osteomalacia
215
Give 2 ECG changes that you might see in someone with hyperparathyroidism.
Hyperparathyroidism -> hypercalcaemia and so:
1. Tall T waves.
2. Shorted QT interval.
216
Give 2 ECG changes that you might see in someone with hyoparathyroidism.
Hyoparathyroidism -> hypocalcaemia and so:
1. Small T waves.
2. Long QT interval.
217
What is phaeochromocytoma?
a tumour of the chromatin cells (adrenal medulla) that secretes unregulated and excessive Ad
218
Give 5 symptoms of phaeochromocytoma.
Classic triad of:
1. Headache.
2. Sweating.
3. Tachycardia.
Also:
4. Hypertension.
5. Palpitations.
6. Tremor.
7. Arrhythmia.
8. Confusion.
219
What investigations might you do in order to diagnose someone with having a phaeochromocytoma?
Bloods - raised WCC
| Plasma free metanephrines (gold standard): increased plasma metadrenaline and normetadrenaline.
220
What is the treatment for phaeochromocytoma?
1. Alpha blocker (phenoxybenzamine)
2. Beta blockers (propanolol)
3. Surgical resection of tumour.
221
What is the major concern in someone with phaeochromocytoma?
Phaeochromocytomare are a dangerous but treatable cause of hypertension.
222
Describe the different types of subcutaneous insulins that can be given to people with T1DM.
1. Ultra-fast acting e.g. Humalog - taken before eating in conjunction with a long-acting insulin at night.
2. Long-acting insulin e.g. insulin glargine - taken before going to bed.
3. Pre-mixed insulin e.g. NovoMix - taken twice daily.
223
What is adrenal insufficiency?
Adrenocortical insufficiency resulting in a reduction of mineralocorticoids, glucocorticoids and androgens.
224
Give 6 symptoms of adrenal insufficiency.
1. Tanned - pigmentation.
2. Tired.
3. Tearful.
4. Thin - weight loss.
5. Headaches.
6. Abdominal cramps.
7. Myalgia.
8. Throwing up.
9. Weakness.
225
Give 5 primary causes of adrenal insufficiency?
1. Addison's disease (autoimmune destruction of the adrenal cortex).
2. Congenital adrenal hyperplasia (CAH).
3. TB.
4. Adrenal metastases.
5. Drugs.
6. Haemorrhage.
7. Infection.
226
What investigations might you do in someone who you suspect has adrenal insufficiency?
1. Bloods - FBC, U+E (↓Na+ and ↑K+ - due to ↓ aldosterone - ↑Ca2+, ↑Urea).
2. ↓ Glucose.
3. ACTH stimulation test - Addison's will not respond.
227
What is the treatment for adrenal insufficiency?
Hormone replacement - any steroids e.g. hydrocortisone.
In addison's disease replace aldosterone with fludrocortisone.
228
Give 3 causes of hypokalaemia.
1. Diuretics.
2. D+V.
3. Conn's syndrome.
4. Insulin.
229
Give 5 symptoms of hypokalaemia.
1. Muscle weakness.
2. Hypotonia.
3. Hyporeflexia.
4. Palpitations.
5. Arrhythmia.
6. Nausea and vomiting.
7. Cramps.
230
What ECG changes might you see in someone with hypokalaemia?
1. Increased amplitude and width of P waves.
2. ST depression.
3. Flat T waves.
4. U waves.
5. QT prolongation.
231
Give 3 causes of hyperkalaemia.
1. AKI.
2. NSAIDs.
3. Metabolic acidosis.
4. K+ sparing diuretics.
232
Give 3 symptoms of hyperkalaemia.
1. Weakness.
2. Palpitations.
3. Tachycardia.
4. Chest pain.
233
What ECG changes might you see in someone with hyperkalaemia?
1. Tall tented T waves.
2. Wide QRS.
3. Small P waves.
234
Give 3 causes of hypercalcaemia.
1. Hyperparathyroidism.
2. Hypercalcaemia of malignancy.
3. Vitamin D toxicity.
4. Myeloma.
235
What biochemical test might you want to do to establish the cause of hypercalcaemia?
PTH measurement.
236
How can hypercalcaemia be treated?
1. IV normal saline.
2. IV furosemide.
3. IV calcitonin.
237
A man presents with a history of weight loss, polyuria and nocturia. He is very unwell. The GP performs a capillary blood glucose which is found to be 17.2mmol/l. What is the most likely diagnosis of this mans symptoms?
Type 1 Diabetes Mellitus.
238
What is the treatment for someone presenting with ketoacidosis?
1. ABCDE.
2. IV normal saline.
3. IV soluble insulin via syringe driver and sliding scale.
4. Restore potassium levels.
5. Look for underlying cause.
239
pH 7.1; pCO2 1.2 kPa; pO2 11.1 kPa; Bicarbonate 4mmol/l.
| Interpret this blood gas result.
Severe metabolic acidosis.
240
Give 3 causes of severe metabolic acidosis.
1. Diabetic ketoacidosis.
2. Severe sepsis.
3. Uraemia.
4. Lactic acidosis.
241
What is hirsutism?
Excess hair growth in women in a male pattern.
242
What is the cause of hirsutism?
Hirsutism indicates increased androgen production by the ovaries or adrenal glands, most commonly polycystic ovary syndrome.
243
What diseases are associated with polycystic ovary syndrome?
1. Insulin resistance and so T2DM.
2. Hypertension.
3. Hyperlipidaemia.
4. CV disease.
244
Give 5 symptoms of polycystic ovary syndrome.
1. Amenorrhoea.
2. Oligomenorrhoea.
3. Hirsutism.
4. Acne.
5. Overweight.
6. Infertility.
245
What criteria can be used to make a diagnosis of polycystic ovary syndrome?
Rotterdam diagnostic criteria:
1. Menstrual irregularity.
2. Clinical or biochemical evidence of hyperandrogenism.
3. Polycystic ovaries on USS.
246
Describe the treatment for polycystic ovary syndrome?
1. Hirsutism therapy: shaving/waxing excess hair OR oestrogens e.g. OCP.
2. Menstrual disturbance therapy: cyclic oestrogen/progesterone.
3. Metformin can improve hyperinsulinaemia and regulates the menstrual cycle.
247
A 27-year- old woman comes to see you because she is having infrequent periods (oligomenorrhoea). You note, on examination, that she has facial acne and is overweight. What is the most likely diagnosis? Give 3 other signs you might see in this patient.
Polycystic ovary syndrome.
Other signs:
1. Hirsutism.
2. Amenorrhoea.
3. Infertility.
248
Describe insulin action at muscle and fat cells.
Insulin binds to membrane receptors -> intracellular signalling cascade stimulated -> GLUT-4 mobilisation to plasma membrane -> GLUT-4 integrates into plasma membrane -> glucose enters cell via GLUT-4.
249
Which bacteria is responsible for causing impetigo?
Staphylococcus aureus.
250
What is the treatment for impetigo?
Flucloxacillin.
251
Give 5 symptoms of DKA.
1. Polyuria.
2. Polydipsia.
3. Weight loss.
4. Nausea/vomiting.
5. Confusion.
6. Weakness.
252
Give 3 causes of DKA.
1. Unknown.
2. Infections.
3. Treatment errors - not administering enough insulin.
4. Having undiagnosed T1DM.
253
Describe the triad of DKA.
1. Acidaemia – blood pH < 7.3
2. Hyperglycaemia – blood glucose > 11mmol/L.
3. Ketonaemia.
254
Give 4 potential complications of untreated DKA.
1. Oedema.
2. Adult respiratory distress syndrome.
3. Aspiration pneumonia.
4. Thromboembolism.
5. Death.
255
Give 5 symptoms of hypoglycaemia.
1. Hunger.
2. Sweating.
3. Tachycardia.
4. Anxious.
5. Shaking.
256
Give 3 endocrine diseases that can cause diabetes.
1. Cushing's.
2. Acromegaly.
3. Phaeochromocytoma.
257
What class of drugs can cause diabetes?
1. Steroids.
2. Thiazides.
3. Anti-psychotics.
258
Give 3 secondary causes of adrenal insufficiency.
1. Hypopituitarism.
2. Withdrawal from long term steroids.
3. Infection.
4. Radiotherapy.
259
An adrenal crisis is a common presentation of adrenal insufficiency. Give 3 features of an adrenal crisis.
1. Hypotension.
2. Fatigue.
3. Fever.
4. Hypoglycaemia.
5. Hyponatraemia.
6. Hyperkalaemia.
260
How would you treat an adrenal crisis?
IV Hydrocortisone and IV saline.
| restore fluid and electrolytes
261
State whether sodium and potassium levels would be high or low in someone with adrenal insufficiency.
- Hyponatraemia.
- Hyperkalaemia.
Lack of aldosterone and so less sodium is reabsorbed and less potassium is excreted.
262
17 year old man presents with intermittent headaches and anxiety. He is sweating and vomiting. His BP is 223/159 and his pulse is 115. What is the likely cause?
Phaeochromocytoma crisis!
Hypertension and tachycardia = phaeochromocytoma until proved otherwise; especially in younger patients.
263
What are the investigation AND management of a phaeochromocytoma crisis?
investigations: measure plasma free metanephrines (increased)
1) alpha-blocker (phenoxybenzamine)
2) BB (propranolol)
3) adrenalectomy
264
Give 3 causes of hyponatraemia.
1. SIADH.
2. Sodium deficiency.
3. Renal failure.
4. Malignancy.
265
Define hyponatraemia.
Serum sodium <135mmol/L.
266
Give 3 signs of hyponatraemia.
1. Anorexia.
2. Confusion.
3. Headache.
4. Lethargy.
5. Weakness.
267
What is the treatment for acute hyponatraemia?
Give a bolus dose of saline.
268
What are the units for osmolality?
mOsmol/Kg.
269
What is the primary cation in ICF?
K+.
270
What is the primary cation in the ECF?
Na+.
271
what are the primary anions in the ECF?
Cl- and HCO3-.
272
What is the effect of water excess on thirst and ADH secretion?
Decreased thirst and decreased ADH -> reduced intake and increased excretion.
273
What is the effect of water deficit on thirst and ADH secretion?
Increased thirst and increased ADH -> increased water intake and reduced secretion.
274
What GPCR does ADH bind to on renal tubules?
V2.
275
Do you have hypernatraemia or hyponatraemia in diabetes insipidus?
Hypernatraemia.
276
Give 3 causes of cranial diabetes insipidus.
1. Tumours.
2. Trauma.
3. Infections.
4. Idiopathic.
5. Genetic - AR.
277
Give 3 causes of nephrogenic diabetes insipidus.
1. Osmotic diuresis - diabetes mellitus.
2. Drugs (lithium)
3. CKD.
4. electrolyte imbalances (hypercalcaemia and hypokalaemia)
278
In what class of drugs does metformin belong?
Biguanide.
279
Give an example of a sulfonylurea.
Tolazamide and gliclazide.
280
Give a sign of Cushing's syndrome that is due to impairments in carbohydrate metabolism.
Diabetes mellitus.
281
Give a sign of Cushing's syndrome that is due to electrolyte disturbances.
1. Sodium retention.
| 2. Hypertension.
282
People with Cushing's syndrome may have immune dysfunction. Give a consequence of this.
Increased susceptibility to infection.
283
Why is it important to take a drug history when speaking to someone with potential Cushing's?
To exclude exogenous glucocorticoid exposure as a potential cause.
284
Name a drugs that suppress cortisol synthesis and so can be used in the treatment of Cushing's disease.
mifepristone.
285
When might you see signs of hypercortisolism without Cushing’s disease?
1. Pregnancy.
2. Depression.
3. Alcohol dependence.
4. Obesity.
5. exogenous steroids
286
Would you expect a patient with SIADH to be hypovolaemic, euvolaemic or hypervolaemic?
Euvolaemic.
287
Describe 5 features of the essential criteria for SIADH.
1. Hyponatreamia (<135mmol/L).
2. Plasma hypo-osmolality.
3. High urine osmolality.
4. Clinical euvolaemia.
5. Increased urinary sodium excretion with normal salt and water intake.
288
Name 3 diseases that you must exclude in someone who you suspect could have SIADH.
1. Renal disease.
2. Hypothyroidism.
3. Hypocortism.
4. Recent diuretic use.
289
Would you associate SIADH with hyponatraemia or hypernatraemia?
Hyponatraemia <135mmol/L.
290
Would you associate SIADH with plasma hypo-osmolality or hyper-osmolality?
Plasma hypo-osmolality <275mOsm/Kg.
291
Would you associate SIADH with a high or low urine osmolality?
High urine osmolality.
292
Give 2 clinical signs of hypervolaemia.
1. Ascites.
| 2. Oedema.
293
Give 3 clinical signs of hypovolaemia.
1. Hypotension.
2. Tachycardia.
3. Decreased skin turgor.
4. Dry mucus membranes.
294
Define puberty.
Puberty describes the physiological, morphological and behavioural changes as the gonads switch from infantile to adult forms.
295
What is the first sign of puberty in girls?
Menarche.
296
What hormone is responsible for regulating the growth of the breasts and female genitalia?
Ovarian oestrogen.
297
Which hormones are responsible for controlling the growth of pubic and axillary hair in females?
Ovarian and adrenal androgens.
298
What is the first sign of puberty in boys?
First ejaculation, often nocturnal.
299
What are the roles of testicular androgens in male puberty?
1. Development of external genitalia.
2. Growth of pubic and axillary hair.
3. Deepening of voice.
300
What scale is used to describe physical development based on external sex characteristics?
Tanner scale.
301
What is thelarche?
Breast development.
| - Takes about 3 years and is controlled by oestrogen.
302
Describe the 3 stages of thelarche.
1. Ductal proliferation.
2. Adipose deposition.
3. Enlargement of areola and nipple.
303
What is adrenarche?
Maturation of the adrenal gland - the development of the zona reticularis cells.
Peri-pubertal adrenal androgen production -> body odour and mild acne.
304
Give 2 signs of adrenarche.
1. Body odour.
| 2. Mild acne.
305
What is pubarche?
Growth of pubic hair.
306
What term is used to describe the onset of secondary sexual characteristics before 8/9 y/o?
Precocious puberty.
307
What must you rule out as a cause of precocious puberty in boys?
Brain tumour!
308
What is the treatment for precocious puberty?
GnRH super agonist to suppress pulsatility of GnRH secretion.
309
What is delayed puberty?
The absence of secondary sexual characteristics by 14y/o or 16y/o.
310
What is precocious puberty?
The onset of secondary sexual characteristics before 8/9 y/o.
311
What is the most likely cause of delayed puberty in boys?
Constitutional delay - runs in the family; late menarche in mum or delayed growth spurt in father.
312
Give 3 consequences of delayed puberty.
1. Psychological problems.
2. Reproduction defects.
3. Reduced bone mass.
313
What must you rule out in girls with delayed puberty and short stature?
Turner Syndrome (45X)!
They might also have recurrent ear infections.
314
Give 5 functional causes of delayed puberty.
1. Anorexia.
2. Bulimia.
3. Over exercising.
4. CKD.
5. Drugs.
6. Stress.
7. Sickle cell.
315
What investigations might you do in someone with delayed puberty?
1. FBC - red cell count especially.
2. U+E.
3. LH/FSH measurements.
4. TFT's.
5. Karyotyping for Turners.
316
What is hypergonadotropic hypogonadism?
Primary gonadal failure!
| - Testes or ovarian failure.
317
What is the affect of hypergonadotropic hypogonadism on FSH/LH and oestrogen/testosterone?
High FSH/LH low oestrogen/testosterone.
318
Give 2 examples of hypergonadotropic hypogonadism.
1. Turner Syndrome (45X).
| 2. Klinefelter's syndrome (47XXY).
319
What is hypogonadotropic hypogonadism?
Secondary gonadal failure!
| - Hypopituitary or problems with the hypothalamus.
320
What is the affect of hypogonadotropic hypogonadism on FSH/LH and oestrogen/testosterone?
Low FSH/LH and low testosterone/oestrogen.
321
Give an example of hypogonadotropic hypogonadism.
Kallman syndrome.
322
What is Turner syndrome?
In Turner syndrome the patient is missing an X chromosome - 45X. It is an example of primary gonadal failure (hypergonadotropic hypogonadism).
323
Give 3 signs of Turner syndrome.
1. Short stature.
2. Delayed puberty.
3. CV and renal malformations.
4. Recurrent otitis media.
324
What is Klienfelter's syndrome?
In Klinefelter's syndrome the patient has an extra X chromosome - 47XXY. It is an example of primary gonadal failure (hypergonadotropic hypogonadism).
325
Give 2 signs of Klinefelter's syndrome.
1. Azoospermia.
2. Gynaecomastia (enlargement of male breast tissue).
3. Increased risk of breast cancer.
4. Testicular size <5ml.
326
Why might someone with Klinefelter's syndrome have fertility problems?
Azoospermia - semen contains no sperm.
327
Give 4 symptoms of Klinefelter's syndrome.
1. Reduced pubic hair.
2. Tall stature.
3. Reduced IQ.
4. Small testicles (<5ml).
328
What cancer is someone with Klinefelter's at an increased risk of developing?
Breast cancer.
329
What is Kallman syndrome?
Congenital deficiency of GnRH. It is an example of secondary gonadal failure -
hypogonadotropic hypogonadism.
330
What must you test in a person who you suspect has Kallman syndrome?
Smell! 75% are ansomia.
331
How is Kallman syndrome inherited?
X linked recessive or dominant.
332
How do you treat asymptomatic SIADH?
Fluid restriction.
333
How do you treat symptomatic SIADH of acute onset?
Give 3% saline.
334
Name 2 drugs that can be used to treat acromegaly. What class of drugs do they belong to?
1. Cabergoline - dopamine agonist.
| 2. Octreotide - somatostatin analogue.
