ENDOCRINOLOGY Flashcards
(212 cards)
1
Q
What are the 4 cells to make up the islets of langerhans?
A
- Beta cells (70%).
- Alpha cells (20%).
- Delta cells (8%).
- Polypeptide secreting cells.
2
Q
What do a) beta cells b) alpha cells c) delta cells produce?
A
a) insulin
b) glucagon
c) somatostatin
3
Q
What is the importance of the alpha and beta cells being located next to each other in the islets of langerhans?
A
This enables them to ‘cross talk’ - insulin and glucagon show reciprocal action.
4
Q
Describe the physiological processes that occur in the fasting state in response to low blood glucose.
A
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.
5
Q
Describe the effect on insulin and glucagon secretion in the fasting state.
A
Fasting state = low blood glucose.
Raised glucagon and low insulin.
6
Q
Describe the physiological processes that occur after feeding in response to high blood glucose.
A
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.
7
Q
Describe the effect on insulin and glucagon secretion after feeding.
A
Insulin is high and glucagon is low.
8
Q
A diagnosis of diabetes can be made by measuring plasma glucose levels. What would a persons fasting plasma glucose be if they were diabetic?
A
Fasting plasma glucose >7mmol/L.
9
Q
A diagnosis of diabetes can be made by measuring plasma glucose levels. What would a persons random plasma glucose be if they were diabetic?
A
Random plasma glucose >11mmol/L.
10
Q
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?
A
Fasting plasma glucose >7mmol/L and 2-hour value >11mmol/L.
11
Q
What might someone’s HbA1c be if they have diabetes?
A
> 48mmol/mol.
12
Q
What is the affect of cortisol on insulin and glucagon?
A
Cortisol inhibits insulin and activates glucagon.
13
Q
Describe the aetiology of type 1 diabetes mellitus.
A
Beta cells express HLA antigens. Autoimmune destruction -> beta cell loss -> impaired insulin secretion.
14
Q
Is type 1 diabetes characterised by a problem with insulin secretion, insulin resistance or both?
A
Type 1 diabetes is characterised by impaired insulin secretion - there is severe insulin deficiency.
15
Q
At what age do people with T1DM present?
A
Often people with Type 1 diabetes will present in childhood.
16
Q
Give 2 potential consequences of T1DM.
A
- Hyperglycaemia.
2. Raised plasma ketones -> ketoacidosis.
17
Q
Describe the natural history of T1DM.
A
Genetic predisposition + trigger -> insulitis, beta cell injury -> pre-diabetes -> diabetes.
18
Q
T1DM is characterised by impaired insulin secretion. Describe the pathophysiological consequence of this.
A
- Severe insulin deficiency -> glycogenolysis /gluconeogensis /lipolysis all not suppressed
- Addition of reduced peripheral glucose uptake -> hyperglycaemia and glycosuria.
- Perceived stress -> cortisol and Ad secretion -> catabolic state -> increased plasma ketones.
19
Q
Give 3 symptoms of T1DM.
A
- Weight loss.
- Thirst (fluid and electrolyte losses).
- Polyuria (due to osmotic diuresis).
20
Q
Would you associate ketoacidosis with T1 or T2 DM?
A
TYPE 1.
Occurs due to the absence of insulin.
21
Q
Describe the pathophysiology of diabetic ketoacidosis.
A
- INSUFFICIENT insulin -> less glucose available
- Increased KETOGENESIS
- Ketoacidosis
22
Q
Name 3 ketone bodies.
A
- acetoacetate.
- acetone.
- beta hydroxybutyrate.
23
Q
Where does ketogenesis occur?
A
In the liver.
24
Q
Give 4 signs of diabetic ketoacidosis.
A
- Vomiting/ Abdo pain
- KUSSMAUL breathing
- Breath smells of ketones. (fruity)
- Dehydration. (tachycardia/hypotension)
25
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.
26
How is insulin administered in someone with T1DM?
Injected into SC fat/insulin pump
27
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.
28
What is T2DM?
Chronic hyperglycemia due to inappropriately low insulin secretion AND peripheral insulin resistance
29
Describe the aetiology for T2DM
Genetics (polygenic) and environment (Associated with obesity, lack of exercise, calorie and alcohol excess)
30
Why is insulin secretion impaired in T2DM?
Impaired insulin secretion is thought to be due to lipid deposition in the pancreatic islets.
31
Describe the pathophysiology of T2DM.
Impaired insulin secretion and resistance -> Impaired Glucose Tolerance -> T2DM -> hyperglycaemia and high FFA's.
32
Is insulin secretion or insulin resistance the driving force of hyperglycaemia in T2DM?
Hepatic insulin resistance is the driving force of hyperglycaemia.
33
Give 3 risk factors for insulin resistance in T2DM.
1. Obesity (mostly central).
2. Physical inactivity.
3. Family history.
34
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.
35
Describe the treatment pathway for T2DM.
1. Lifestyle changes: lose weight, exercise, healthy diet.
2. Metformin. (gradual to avoid GI SE)
3. + LINAGLIPTIN (DPP-4 inhibitor)
4. + GLICAZIDE (sulfonylurea)
5. Try insulin
36
How does metformin work in treating T2DM?
Metformin increases insulin sensitivity and inhibits glucose production.
37
How does sulfonylurea work in treating T2DM?
Sulfonylurea stimulates insulin release.
38
Give a potential consequence of taking Sulfonylurea for the treatment of T2DM.
Hypoglycaemia.
(Sulfonylurea stimulates insulin release).
39
Give 3 microvascular complications of diabetes mellitus.
1. Diabetic retinopathy.
2. Diabetic nephropathy.
3. Diabetic peripheral neuropathy.
40
Give a macrovascular complication of diabetes mellitus.
CV disease and stroke.
41
What is the main risk factor for diabetic complications?
Poor glycaemic control!
42
Give a potential consequence of acute hyperglycaemia?
Diabetic ketoacidosis and hyperosmolar coma.
43
Give a potential consequence of chronic hyperglycaemia?
Micro/macrovascular tissue complications e.g. diabetic reinopathy, nephropathy, neuropathy, CV disease etc.
44
What is the commonest form of diabetic neuropathy?
Distal symmetrical polyneuropathy. (gloves and socks)
45
Give 3 major clinical consequences of diabetic neuropathy.
1. Pain.
2. Autonomic neuropathy.
3. Insensitivity.
46
What is the effect of insulin on peripheral cells?
Insulin binds to receptor which results in activation of tyrosine kinase and initiation of cascade response.
One consequence of this is the migration of GLUT-4 transporters to the cell surface and increased transport of glucose into cell.
47
Name 4 causes of secondary diabetes.
Diabetes is usually primary but may be secondary to:
1. total pancreatectomy
2. acromegaly
3. cushing’s
4. maturity onset diabetes of youth (single gene is affected which alters B-cells function).
48
Give 3 causes of DKA.
1. Unknown.
2. Infections.
3. Treatment errors - not administering enough insulin.
4. Having undiagnosed T1DM.
49
Describe the triad of DKA.
1. Acidaemia – blood pH < 7.3
2. Hyperglycaemia – blood glucose > 11mmol/L.
3. Ketonaemia.
50
Give 4 potential complications of untreated DKA.
1. Oedema.
2. Adult respiratory distress syndrome.
3. Aspiration pneumonia.
4. Thromboembolism.
5. Death.
51
Give 5 symptoms of hypoglycaemia.
1. Seizures
2. Sweating (fight/flight response)
3. Tachycardia (fight/flight response)
4. Anxious/ aggressive
5. Shaking.
52
What class of drugs can cause diabetes?
1. Steroids.
2. Thiazides.
3. Anti-psychotics.
53
In what class of drugs does metformin belong?
Biguanide.
54
Give an example of a sulfonylurea.
Tolazamide and gliclazide.
55
Describe the pain associated with diabetic neuropathy.
- Burning.
- Paraesthesia.
- Nocturnal exacerbation.
56
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.
57
Diabetic neuropathy: give 5 signs of autonomic neuropathy.
1. Hypotension.
2. HR affected.
3. Diarrhoea/constipation.
4. Incontinence.
5. Erectile dysfunction.
6. Dry skin.
58
What are the consequences of insensitivity as a result of diabetic neuropathy?
Insensitivity -> foot ulceration -> infection -> amputation.
59
Give 5 risk factors for diabetic neuropathy.
1. POOR GLYCAEMIC CONTROL.
2. Hypertension.
3. Smoking.
4. HbA1c.
5. Overweight.
6. Long duration of DM.
60
PVD is a potential complication of Diabetes. Give 6 signs of acute ischaemia.
1. Pulseless.
2. Pale.
3. Perishing cold.
4. Pain.
5. Paralysis.
6. Paraesthesia.
61
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.
62
Would there be increased or decreased pulses in a diabetic neuropathic foot?
There would be increased foot pulses.
63
What is the hallmark of diabetic nephropathy?
Development of proteinuria and progressive decline in renal function.
64
What happens to the glomerular basement membrane in someone with diabetic nephropathy?
On microscopy there is thickening of the glomerular basement membrane.
65
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.
66
Describe the treatment for diabetic nephropathy.
1. Glycaemic and BP control.
2. ARB/ACEi.
3. Proteinuria and cholesterol control.
67
What is the metabolic emergency characteristic of T2DM?
hyperosmolar hyperglycaemic state
68
What are the risk factors for hyperosmolar hyperglycaemic state?
1. Insufficient oral hypoglycaemic agents!
2. Infection (most common) e.g. pneumonia
3. Consumption of glucose rich foods
4. Concurrent meds e.g. thiazide diuretics or steroids
69
Describe the pathophysiology of hyperosmolar hyperglycaemic state
Endogenous insulin levels are reduced but are still sufficient to inhibit hepatic ketogenesis but insufficient to inhibit hepatic glucose production.
(no ketogenesis just hyperglycaemia)
70
What would be the clinical presentation of someone with hyperosmolar hyperglycaemic state?
Severe DEHYDRATION (2ndary to osmotic diuresis)
Decreased level of consciousness
Hyperosmolality
Stupor
Bicarbonate is not lowered
71
How do you diagnose hyperosmolar hyperglycaemic state?
- Hyperglycaemia > 11 mmol/L
- Urine stick test shows heavy glycosuria
- Plasma osmolality is v. high
72
What is the treatment for hyperosmolar hyperglycaemic state?
1. Lower rate infusion of insulin
2. Fluid replacement with 0.9% saline
3. LMWH!!! (SC Enoxaparin)
4. Restore electrolyte loss (K+)
73
How often are diabetics reviewed?
Every 12 months
74
What is checked for in a review of a diabetic patient?
1. HbA1C
2. BP
3. cholesterol
4. eye screening
5. foot and leg check
6. kidney function test
7. diet advice/ BMI
8. sexual advice/support
9. injection sites review
10. emotional/psychological help
75
What is the grading system for diagnosing with HbA1C result?
1. 6% (below 42 mmol/mol) is considered non-diabetic
2. 6-6.4% (42 to 47 mmol/mol) indicates impaired fasting glucose regulation and is considered prediabetes
3. 6.5% or more (48 mmol/mol and above) indicates the presence of type 2 diabetes
76
How is diabetes diagnosed?
1. Symptoms + 1 abnormal blood result
3. No symptoms + 2 separate abnormal blood results
4. HbA1c of 48mmol/mol (6.5%)
77
What blood glucose would someone with Impaired Fasting Glucose (prediabetes) have?
6.1 - 6.9 mmol/l
78
What blood glucose results would you expect 2hr post prandial?
7.8 - 11 = Impaired Glucose Tolerance
| >11 = Diabetes
79
What do results of IGT/ IFG suggest?
Insulin resistance but NOT diabetes (prediabetes)
80
How would you manage a patient who is prediabetic?
1. Lifestyle advice
| 2. Annual review
81
What is the criteria for diagnosing a patient with DM2?
1. Symptomatic + 1 abnormal blood result
2. Asymptomatic + 2 separate abnormal glucose result
3. Abnormal HbA1C
82
Give 4 potential symptoms of DM2
MOSTLY ASYMPTOMATIC but can have
1. Polyuria
2. Polydipsia
3. Unexplained weight loss
4. Visual blurring
5. Genital thrush
83
How would you diagnose and manage diabetic ketoacidosis?
Dx =
- Acideamia (blood pH)
- Hyperglycaemia
- Ketonaemia/ketoniuria
Mx = Fluid/Insulin
84
Give 4 hypoglycaemic agents and their mechanism of action
1. Metformin - reduces gluconeogensis in liver + increases insulin sensitivity)
2. Gliclazide (sulfonylurea) - stimulates beta cells to secrete insulin
3. Sitagliptin (DPP4 inhibitor) - stimulates insulin secretion
4. Pioglitazone (enhance uptake of FFA and glucose)
85
Which hypoglycaemic agents may cause weight gain?
Gain = Gliclazide + PioGlitazone
86
Describe the thyroid axis.
Hypothalamus -> TRH -> AP -> TSH -> thyroid -> T3 and T4.
T3/4 have a negative feedback effect on the hypothalamus and the anterior pituitary.
87
What would be the effect on TSH if you had an under-active thyroid?
TSH would be raised as you have less T3/4 being produced and so no negative feedback.
88
What would a low TSH tell you about the action of the thyroid?
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.
89
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.
90
Give 4 causes of thyrotoxicosis.
Thyrotoxicosis - excess thyroid hormone due to any cause:
1. Increased production e.g. Grave's, toxic adenoma.
2. Leakage of preformed T3/4 due to follicular damage.
3. Ingestion of excess thyroid hormone
4. Drug induced e.g. iodine/lithium
91
Give 2 causes of hyperthyroidism.
1. Grave's disease
| 2. Toxic adenoma
92
What is the epidemiology of hyperthyroidism?
1. Female
| 2. 20-40 y/o
93
What are the symptoms of hyperthyroidism?
1. Diarrhoea
2. Weight loss
3. Sweats
4. Heat intolerance
5. Palpitations
6. Tremor/ anxiety
7. Hyperphagia
8. Menstrual disturbance
94
Give 8 signs of hyperthyroidism
1. Tachycardia.
2. Arrhythmias e.g. AF.
3. Warm peripheries.
4. Muscle spasm.
5. Eye lid lag = Onycholysis
6. Eye lid retraction = Exophthalmos
95
How would you diagnose hyperthyroidism?
1. Thyroid function tests:
- Primary = low TSH, high T3/T4
- Secondary = high TSH, high T3/T4
2. Thyroid autoantibodies (Thyroid peroxidase, thyroglobulin, TSH receptor antibody)
3. Radioactive iodine isotope uptake scan
96
What is the treatment for hyperthyroidism?
1. Beta blockers - rapid symptom control in attacks
2. CARBIMAZOLE = anti-thyroid drug
3. Radioiodine therapy
4. Thyroidectomy
97
Briefly describe the pathophysiology of Grave's disease.
1. Autoimmune disease.
2. TSH receptor antibodies stimulate thyroid hormone production (TRAb)
3. Excess TH secretion from thyroid
98
With what disease would you associated pre-tibial myxoedema and thyroid acropachy?
Grave's disease (+ diffuse goitre)
99
Give 4 signs of Grave's ophthalmology
1. EXTRAOCULAR MUSCLE SWELLING
2. Eye discomfort
3. Lacrimation
4. Diplopia
5. EXOPTHALMOS
100
What antibody would you find high levels of in Grave's disease?
1. TSH Receptor STIMULATING Antibody (TRAb)
2. Thyroglobulin/ Thyroperoxidase (TPO) antibodies
- also found in autoimmune hypothyroidism
101
What would you see histologically in someone with Grave's disease?
1. Lymphocyte infiltration
| 2. Thyroid follicle destruction.
102
What antibody is responsible for the pathology of autoimmune hypothyroidism?
1. TSH Receptor BLOCKING Antibody
| 2. Thyroglobulin/ Thyroperoxidase (TPO) antibodies
103
What are risk factors for thyroid autoimmunity?
1. Genes - HLA-D3
2. Environment - stress/ smoking
3. Endogenous - pregnancy/ birthweight
104
What autoimmune diseases are associated with thyroid autoimmunity?
1. DM1
2. Addisons
3. Pernicious anaemia
4. Vitiligo
105
What is a goitre?
1. Palpable and visible thyroid enlargement
| 2. Endemic in iodine deficient areas
106
How does carbimazole work in treating Grave's disease?
It targets thyroid peroxidase and so prevents the formation of T3/4.
107
How do radioiodine drugs work in treating Grave's disease?
1. Emit beta particles
2. Destroy follicular cells
3. Inhibit production of T4/T3
108
Is hypothyroidism or thyrotoxicosis more common in pregnancy?
Hypothyroidism is more common in pregnancy
109
Give 7 symptoms of hypothyroidism
1. Fatigue / tiredness / lethargy
2. Cold intolerance
3. Weight gain
4. Myalgia
5. Constipation
6. Oedema
7. Menorrhagia
110
What are the signs of hypothyroidism?
```
B radycardia
R flexes relax slowly
A taxia
D ry/ thin hair/skin
Y awning
```
```
C old hands
A ascites
R ound/ puffy face
D defeated demeanour
I mmobile
C ongestive HF
```
111
Which drugs can be responsible for hyperthyroidism?
1. AMIODARONE
2. Iodine
3. Lithium
112
What is amiodarone normally used to treat?
Cardiac arrhythmias but has high iodine content so can cause thyrotoxicosis!
113
What are the common causes of hypothyroidism?
1. Hashimoto’s thyroiditis
2. Iodine deficiency
3. Previous radioiodine therapy
4. Over-treatment of hyperthyroidism
114
What is the mechanism of Hashimoto's thryoiditis?
Autoimmune disease causing hypothyroidism!
| - associated with presence of anti-TPO antibodies
115
What electrolyte disturbance is often seen in hypothyroidism?
Hypo Natraemia!
116
What is Cushing's syndrome?
1. A set of signs/symptoms resulting from chronic glucocorticoid excess
2. with a loss of normal feedback mechanisms.
117
What is Cushing's disease?
Bilateral adrenal hyperplasia due to ACTH hypersecretion by pituitary adenoma.
118
What is an ACTH independent cause of Cushing's syndrome?
1. ORAL STEROIDS (iatrogenic)
| 2. Adrenal adenomas
119
What are 2 ACTH dependent causes of Cushing's syndrome?
1. Cushing's disease
| 2. Ectopic Cushing's syndrome
120
What is ectopic Cushing's syndrome?
Due to paraneoplastic syndrome e.g. small cell lung cancer producing ACTH
121
Describe the cortisol axis
Hypothalamus -> CRH -> AP -> ACTH -> Adrenal cortex -> Glucocorticoids (cortisol)
122
What is ACTH?
Adrenocorticotropic hormone
123
What are the signs and symptoms of Cushing's?
```
C Cataracts / Central obesity
U Ulcers
S Striae
H HTN / Hyperglycaemia / Hirsutism
I Infections increase
N Necrosis
G Glucosuria / Growth retardation
O Osteoporosis
I mmunosuppression
D iabetes
```
124
How would you investigate for the presence of Cushing's disease?
1. Overnight dexamethasone suppression test
- failure to suppress cortisol.
2. Late night salivary cortisol
- loss of circadian rhythm.
3. Urinary free cortisol is raised.
4. Loss of circadian rhythm.
125
What is the treatment for Cushing's?
1. If iatrogenic: Stop steroids
2. Cushing’s Disease: Transphenoidal removal of pituitary adenoma
3. Adrenal adenoma: Adrenalectomy*, radiotherapy
4. Ectopic ACTH: Surgery to remove tumour if location known
126
Why may someone who has had an adrenalectomy develop brown pigmentation of the skin?
NELSON'S DISEASE
| - no negative feedback on ACTH levels which can cause ACTH to build up in the body tissues
127
Which electrolyte disturbance is Cushing's associated with?
HypoKalaemia
| - metabolic alkalosis
128
Give an example of primary adrenal insufficiency
Addison's disease
129
What is the most common cause of primary adrenal insufficiency world wide?
TB!
| UK = Adisson's
130
What is adrenal insufficiency?
Adrenocortical insufficiency resulting in a reduction of mineralocorticoids, glucocorticoids and androgens.
131
Give 6 symptoms of adrenal insufficiency.
1. Tall
2. Tanned
3. Thin
4. Tired
5. Tearful
6. Toned (lean)
7. Throwing up (GI symptoms)
132
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.
4. Test for 21-hydroxylase adrenal autoabs (+ve in 80% of Addison’s)
133
What is the treatment for adrenal insufficiency?
1. Hydrocortisone (replaces glucocorticoids)
| 2. Fludrocortisone ( replaces mineralocorticoids)
134
What symptoms are an Addisonian crisis characterised by?
SHOCK
| - severe hypotension and loss of a lot of fluid through vomiting / reduced reabsorption of Na+
135
How would you treat someone in Adrenal crisis?
- fluids
| - hydrocortisone
136
What type of metabolic abnormality does Addison's disease most commonly cause?
Normal anion gap metabolic acidosis
137
What are the causes of secondary adrenal insufficiency?
1. iatrogenic
| 2. vomiting and abdo pain due to electrolyte imbalance
138
What is the blood supply of the anterior pituitary?
1. The anterior pituitary has no arterial blood supply
| 2. Receives blood through a portal venous circulation from the hypothalamus
139
Give 4 common diseases of the pituitary
1. Benign pituitary adenoma
2. Trauma
3. Sarcoid / TB
4. Craniopharygioma
140
What hormones does the anterior pituitary secrete?
1. ACTH
2. LH/ FSH
3. GRH
4. Somatostatin
141
What hormones does the posterior pituitary secrete?
1. Oxytocin
| 2. Anti-Diuretic Hormone
142
What are the 3 clinical outcomes of having a Craniopharygioma?
1. Pressure on local structure e.g. optic nerves – Bitemporal hemianopia
2. Pressure on normal pituitary – hypopituitarism
3. Functioning tumour
143
Give 3 examples of functional tumours
– Prolactinoma
– Acromegaly
– Cushing’s disease
144
How would you treat a prolactinoma?
Dopamine agonist eg Cabergoline/ bromocriptine.
145
Where is the pituitary gland?
1. Lies just inferior to the optic chiasm
| 2. Connected to the hypothalamus via pituitary stalk (infundibulum)
146
Where are oxytocin/ vasopressin formed?
In the hypothalamus!!!
They are only stored in posterior pituitary
147
Describe the GH/IGF-1 axis.
Hypothalamus -> GHRH (+) or SMS (-) -> AP -> GH -> Liver -> IGF-1.
148
What is the function of IGF-1?
It induces cell division, cartilage and skeletal growth and protein synthesis.
149
Briefly describe the mechanism of prolactin.
Hypothalamus -> dopamine (NEGATIVE) -> AP -> prolactin.
Prolactin acts on the mammary glands to produce milk.
150
What would happen to serum prolactin levels if something was to impact on the pituitary stalk and block dopamine release?
Prolactin levels would increase.
151
Give 2 causes of prolactinoma.
1. Pituitary adenoma.
| 2. Anti-dopaminergic drugs.
152
Give 5 signs of prolactinoma.
1. Infertility.
2. Golactorrhoea. (milky nipple discharge)
3. Amenorrhoea.
4. Loss of libido.
5. Visual field defects and headaches due to local effect of tumour.
153
Describe growth hormone secretion from the anterior pituitary.
1. Pulsatile
| 2. Increases during deep sleep
154
What is acromegaly?
1. Increased production of growth hormone occurring in adults
2. After fusion of the epiphyseal plates
155
What can cause acromegaly?
A benign pituitary adenoma
156
Give 6 typical presenting features of acromegaly
1. Acral enlargement
2. Arthralgia
3. Maxillofacial changes
4. Excessive sweating
5. Headache
6. Hypogonadal symptoms (low libido)
157
What maxillofacial changes would you expect to see in a patient with acromegaly?
1. Prognathism - jaw protrusion.
2. Interdental separation.
3. Large tongue.
158
How would you diagnose a patient with 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.
159
Give 2 treatment options for acromegaly
1. Transphenoidal surgery to remove the adenoma
2. Somatostatin anologues e.g. OCREOTIDE
3. GH antagonist e.g. PEGVISOMANT
160
What co-morbidities are associated with acromegaly?
1. Arthritis.
2. Cerebrovascular events.
3. Hypertension and heart disease.
4. Sleep apnea.
5. T2 DM.
161
Name a dopamine agonist that can be used in the treatment of acromegaly.
Cabergoline
162
Give 3 potential complications of trans-sphenoidal surgical resection for the treatment of acromegaly.
1. Hypopituitarism.
2. Diabetes insipidus.
3. Haemorrhage.
163
Which electrolyte disturbance is characteristically caused by acromegaly?
Hypercalcaemia
164
What is hyperaldosteronism?
Excess production of aldosterone independent of the renin-angiotensin-aldosterone system
165
What is the most common cause of primary hyperaldosteronism?
CONN'S SYNDROME
166
What can cause Conn's syndrome?
Adrenal adenoma
167
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.
168
What are the 2 main signs of Conn's syndrome?
1. HYPOKALAEMIA
| 2. Hypertension
169
What would be the clinical presentation of Conns?
1. HYPOKALAEMIC
- Constipation
- Weakness and cramps
- Paraesthesia
- Polyuria and polydipsia
2. HYPERTENSION (inc blood volume)
170
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. Plasma aldosterone/renin ratio can be used as an initial screening test - raised ratio indicates the need for further tests.
171
Give 4 ECG changes that you might see in someone with Conn's syndrome.
1. Increased amplitude and width of P waves.
2. Flat T waves.
3. ST depression.
4. Prolonged QT interval.
5. U waves.
172
What is the treatment for Conn's syndrome?
1. Laparoscopic adrenalectomy.
| 2. Spironolactone (aldosterone antagonist).
173
What does the parathyroid control?
Serum calcium levels.
A low serum calcium triggers the release of PTH.
174
What does a high serum calcium level trigger the release of?
Calcitonin from C cells
175
What hormone does the parathyroid secrete and what is its function?
PTH
1. Increases bone resorption by osteoclasts
2. Increases calcium reabsorption at the kidney
3. Activates vitamin D which then acts on the intestine to increase calcium absorption.
176
What is the affect of hyperparathyroidism on serum calcium levels?
Hyperparathyroidism -> hypercalcaemia.
177
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.
178
Give 3 causes of hyperparathyroidism.
1. Primary: PARATHYROID ADENOMA
- ↑PTH ↑Calcium DECREASED Phosphate.
2. Secondary: Physiological Hypertrophy
- in an attempt to correct low calcium.
3. Prolonged uncorrected hypertrophy.
179
```
What would the blood results show of patients with
- primary
- secondary
- tertiary
hyperparathyroidism?
```
Primary: ↑PTH, ↑Ca, ↓Phosph
Secondary: ↑PTH, ↓Ca, ↑Phosph
Tertiary: ↑everything (progression of secondary)
180
Other than bloods, what investigations would you carry out on a patient with hyperparathyroidism?
1. Increased 24hr urinary calcium excretion
| 2. DEXA bone scan for osteoporosis
181
How do you treat hyperparathyroidism?
1. High fluid intake, low calcium diet.
2. Excision of adenoma/ correct underlying cause
3. Parathyroidectomy
182
What would you see on an ECG of a patient with hypokalaemia?
U (wave) have No Pot (K+), No T (inverted) but a long PR and QT
183
Give 3 causes of hyperkalaemia.
1. AKI.
2. NSAIDs.
3. Metabolic acidosis.
4. K+ sparing diuretics.
184
Give 3 symptoms of hyperkalaemia.
1. Weakness.
2. Palpitations.
3. Tachycardia.
4. Chest pain.
185
What ECG changes might you see in someone with hyperkalaemia?
1. Tall tented T waves.
2. Wide QRS.
3. Small P waves.
186
What can cause excess secretion of potassium?
High levels of aldosterone ( Conn's)
187
What can cause reduced secretion of potassium?
1. Addison's (low levels of aldosterone)
2. ACE Inhibitors- block the binding of aldosterone to receptor
3. AKI- decreased filtration rate so more K+ is maintained in blood
188
How would you treat hyperkalaemia?
1. Non-urgent-
Polystyrene sulphonate resin= Binds K+ in the gut decreasing uptake
2. Urgent-
Calcium gluconate= decreases VF risk in the heart
Insulin= drives K+ into the cells
189
What are the causes of hypocalcaemia?
```
H - hypoparathyroidism
A - Acute pancreatits
V - Vit D deficiency
O - osteoMALACIA
C - CKD
```
190
What are the signs and symptoms of hypocalcaemia?
```
S - spasms
P - peripheral paraesthesia
A - anxious
S - seizures
M – muscle tone increase
```
191
Hypocalcaemia: What investigations and treatment?
ECG- Long QT interval
Treatment-
Mild= Adcal – everyone's on it!
Severe= Calcium gluconate
192
Give 3 causes of hypercalcaemia.
1. Hyperparathyroidism.
2. Hypercalcaemia of malignancy.
3. Vitamin D toxicity.
4. Myeloma.
193
What biochemical test might you want to do to establish the cause of hypercalcaemia?
PTH measurement
194
How can hypercalcaemia be treated?
1. IV normal saline.
2. IV furosemide.
3. IV calcitonin.
4. Bisphosphonates
195
What is hypercalcaemia of malignancy?
Malignancy causes unregulated breakdown of bone leading to increased calcium levels in the blood.
196
Which malignancies most commonly cause hypercalcaemia of malignancy?
1. Myeloma!
| 2. Non- Hodgkins Lymphoma
197
What are the 2 underlying causes of diabetes insipidus?
1. Too little ADH from posterior pituitary gland (cranial)
| 2. Kidney not responding to ADH (nephrogenic)
198
Give 3 causes of cranial diabetes insipidus.
1. Tumours.
2. Trauma.
3. Infections.
199
Give 3 causes of nephrogenic diabetes insipidus.
1. Osmotic diuresis - diabetes mellitus.
2. Drugs. (lithium)
3. CKD.
200
Give 3 signs of diabetes insipidus.
1. Polyuria
2. Polydipsia
3. Dehydration
201
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. Water deprivation test - urine will not concentrate when asked not to drink.
202
What is the treatment for diabetes insipidus?
Cranial DI = Desmopressin
| Nephrogenic DI = Bendroflumethizide, NSAIDs
203
How do diuretics work in treating Diabetes insipidus?
1. causes more Na+ excretion
| 2. the increased water lost makes body responds by reducing GFR, so treat DI
204
What is SIADH?
Syndrome of inappropriate ADH secretion.
Too much ADH = very concentrated urine and hyponatreamia.
205
Give 3 symptoms of SIADH.
1. Anorexia.
2. Nausea.
3. Malaise.
4. Headache.
5. Confusion.
206
Give 3 causes of SIADH.
1. Malignancy.
2. CNS disorders e.g. meningitis, brain tumour, cerebral haemorrhage.
3. Drugs.
207
Describe the treatment for SIADH.
1. Restrict fluid!
2. Give salt.
3. Loop diuretics e.g. furosemide.
4. ADH-R antagonists e.g. vaptans - can be used when people find fluid restriction challenging.
208
Give 5 diseases that are associated with obesity.
1. T2DM.
2. Hypertension.
3. CAD.
4. Stroke.
5. Osteoarthritis.
6. OSA.
7. Infertility.
209
Describe the association between obesity and shift work.
Obesity is more prevalent in people who do shift work.
Sleeping out of phase affects the metabolic circadian rhythm.
210
Which brain structure is responsible for appetite regulation?
Hypothalamus.
- Lateral hypothalamus: hunger centre.
- Ventromedial: satiety centre.
211
Define obesity.
Having a very high amount of body fat in relation to lean body mass. BMI >30kg/m2.
212
Give 3 group's of people in whom obesity is common.
1. Lower SE groups.
2. Older people.
3. People with disabilities.
