Endocrinology Flashcards
1
Q
Give 2 examples of water-soluble hormones
A
Peptides and monoamines
2
Q
How do water soluble hormones get into a cell
A
Bind to cell surface receptors
3
Q
Are water soluble hormones stored in vesicles or synthesised on demand
A
Stored in vesicles
4
Q
Give an example of a fat soluble hormones
A
Steroids e.g. cortisol
5
Q
Are fat soluble hormones stored in vesicles or synthesised on demand
A
Synthesised on demand
6
Q
Give examples of an amine hormone
A
Adrenaline and noradrenaline
7
Q
Describe the pathway of 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
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
10
Q
What is the posterior pituitary derived from?
A
The floor of the ventricles.
11
Q
Where are posterior pituitary hormones synthesised?
A
They are synthesised in the para-ventricular and supra-optic nuclei.
12
Q
Name 2 hormones secreted from the posterior pituitary
A
Oxytocin and ADH.
13
Q
Does the posterior pituitary produce hormones
A
NO
It stores and secretes hormones produced in the hypothalamus
14
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.
15
Q
Give 2 functions of oxytocin.
A
- Milk secretion.
- Uterine contraction
16
Q
What are hypophysiotropic hormones
A
hormones that control secretion of anterior pituitary hormones
17
Q
Name the 6 hormones secreted from the anterior pituitary
A
FSH
LH
adrenocorticotropic releasing hormone
TSH
Prolactin
GH
18
Q
What secretes glucagon
A
Alpha cells of the islets of Langerhans
19
Q
What secretes insulin
A
Beta cells of the islets of Langerhans
20
Q
Apart from glucagon, name other counterregulatory hormones of insulin
A
Adrenaline
Cortisol
Growth hormone
21
Q
Diagnostic fasting glucose value for diabetes
A
above 7mmol/L.
22
Q
What would a person’s random plasma glucose be if they were diabetic?
A
more than 11.1mmol/L
23
Q
What might someone’s HbA1c be if they have diabetes?
A
> 48mmol/mol
24
Q
What is type 1 diabetes mellitus
A
Autoimmune destruction of pancreatic beta cells leading to complete insulin deficiency.
25
Explain the pathogenesis of type 1 DM
- No insulin production means cells of the body can't take glucose from the blood
- Level of glucose in the blood keeps rising as cells think the body has no glucose supply
= hyperglycaemia
26
At what age does T1DM usually present?
Often people with Type 1 diabetes will present in childhood (age 5 to 15)
27
Describe the pathophysiological consequence of impaired insulin secretion
* Glycogenolysis, gluconeogenesis and lipolysis are not suppressed and there's reduced peripheral glucose uptake
* perceived stress leads to increased Ad and cortisol
* progressive catabolic state and increase levels of ketones
28
Give 3 signs of T1DM
* Polydipsia - extreme thirstiness
* Polyuria - excessive urination
* Unexplained weight loss
29
Investigation of T1DM
* Random plasma glucose of >11.1mmol/L
* Fasting plasma glucose >7mmol/L
* Oral glucose tolerance test: results as above
30
What is type 2 DM
Combination of peripheral insulin resistance and impaired insulin secretion
31
Is ketoacidosis associated with T1 or T2 DM
T1 due to absence of insulin
32
Treatment of T2DM
* Lifestyle modification
* Metformin
* Sulfonylurea E.g gliclazide
* SGLT2 inhibitor - e.g. canagliflozin, empagliflozin
* Insulin
33
Function of SGLT2 inhibitors in T2DM
Give 2 SE
Inhibits reabsorption of glucose in the kidney i.e. glucose excreted in urine
E.g. canagliflozin
* SE: UTI, weight loss
34
How does sulfonylurea work in treating T2DM?
Stimulates insulin secretion by binding to beta cell receptors
35
Give 2 side effects of Sulfonylurea (e.g. gliclazide) for the treatment of T2DM.
Can cause hypoglycaemia and weight gain
36
Describe the mechanism of action of Biguanide (metformin)
Decreased gluconeogenesis in the liver and increased cell sensitivity to insulin
37
What are potential side effects of taking metformin for T2DM
GI disturbances - anorexia, nausea and diarrhoea
38
Give 4 risk factors of T2DM
Obesity
Hypertension
Above 40 years old
Ethnicity: Afro-Carrib, SA
39
How does T2DM present
* Polydipsia - thirstiness
* Polyuria - excessive urination
* Polyphagia - excessive hunger
* Glucosuria - excessive glucose in urine
40
Explain the pathophysiology of T2DM
* Repeated exposure to high levels of glucose and insulin makes the cells in the body become resistant to the effects of insulin
* Over time, the pancreas (beta cells) becomes fatigued and damaged by producing so much insulin and they start to produce less
* Continued high levels of glucose on the body in light of insulin resistance and pancreatic fatigue leads to chronic hyperglycaemia
41
Investigation of T2DM
* GS: HbA1c test - tells average BG for last 3m
- HbAc1 > 48mmol/mol = diabetes
* Blood tests: random and fasting plasma glucose
* Oral glucose tolerance test
42
Describe the lifestyle modifications suggested for T2DM
Dietary advice - high complex carbs, low fat
Weight loss
Decrease alcohol intake
43
What is diabetic ketoacidosis
When complete lack of insulin results in high ketone production
44
What is the triad for DKA diagnosis
Hyperglycaemia
Ketosis ( blood ketones over 3)
Acidosis (pH less than 7.3)
45
Causes of DKA
Untreated T1DM
Infection/ illness
Myocardial infarction
46
State some ways DKA presents
Acetone-smelling breath (Pear drops)
Nausea and vomiting
Drowsy/confused
Hyperventilation
47
Explain the pathophysiology of DKA
Unrestrained production of glucose and decreased peripheral glucose uptake = hyperglycaemia ----> osmotic diuresis = dehydration
Peripheral lipolysis ---> ^FFA ----> oxidised to acetyl CoA ----> ketones = acidosis
48
Give 3 microvascular complications of DM
Peripheral neuropathy
Retinopathy
Nephropathy
49
Give 4 macrovascular complications of DM
Coronary artery disease
Peripheral artery disease
Hypertension
Stroke
50
How is hypocalcaemia investigated
Ca levels - <8.5mg/dL
ECG - prolonged QT interval
Parathyroid function
51
Give 3 complications of hypocalcaemia
Seizures
Muscle spasm
Cardiac arrest
52
State the 2 signs that commonly present in both hypocalcaemia and hypoparathyroidism
Chvostek's sign and Trousseau's sign
53
Describe Chvostek's sign
tapping over the facial nerve induces spasm of facial muscles
54
Describe Trousseau's sign
Inflating bp cuff to 22mmHg above systolic pressure for 5 mins causes wrist to flex and fingers to draw together
55
Give 3 causes of hypocalcaemia
Hypoparathyroidism
Vit D deficiency
Malignancy
56
Give some symptoms of hypocalcaemia and hypoparathyroidism
CATS go Numb:
Convulsions
Arrhythmias
Tetany - involuntary contraction
Spasm
Numbness
57
Treatment for hypocalcemia
IV calcium gluconate, 10ml of 10% solution over 10 mins (slow)
Vit D supplements
58
What are the causes of primary hypoparathyroidism
Parathyroid gland failure:
* Congenital diseases (DiGeorge)
* Autoimmune destruction
59
What are the causes of secondary hypoparathyroidism
Damage to the parathyroid glands during surgery or receiving radiotherapy
Mg deficiency ( required for PTH secretion)
60
What is the typical bone profile of someone with hypoparathyroidism
Low calcium
Normal/ high phosphate
Low PTH
61
What is pseudohypoparathyroidism
This is when the body is resistant to parathyroid hormone
62
What is hypoparathyroidism
Reduced PTH production
63
Give some causes of hypercalcaemia
Primary hyperparathyroidism
Malignancy
Sarcoidosis
Thiazides
Thyrotoxicosis
Dehydration
Addisons
Acromegaly
64
Symptoms of hypercalcaemia
Bones - pain
Stones - kidney
Groans - nausea
Moans - depression
65
Give an ECG change seen in hypercalcaemia
short QT
66
Investigation of hypercalcaemia
* Fasting serum Ca and phosphate - confirm mild hypercalcaemia
* Serum PTH and Ca - raised
* Ultrasound
* 24h urinary Ca
67
Treatment for hypercalcaemia
* rehydration with normal saline
* bisphosphonates
* Loop diuretics such as furosemide
68
Symptoms of hyperparathyroidism
Hypercalcaemia:
Bones - painful
Kidney stones
Abdominal - constipation and nausea
Depression and lethargy
69
Give 3 complications of untreated DKA
Coma
Cerebral oedema
Thromboembolism
70
How is DKA managed
1. ABC management
2. Replace fluid with IV 0.9% NaCl
3. IV insulin and glucose (prevent hypoglycaemia)
4. Restore electrolytes e.g K+
71
How can insulin treatment for DKA cause hypokalaemia
Insulin decreases K+ levels in the blood by redistributing it into cells via increased Na/K pump activity causing low serum K+ levels = Hypokalaemia
72
What are 2 differences in the presentation of T2DM compared to T1DM
T2DM can often display Central obesity and slower onset
73
What is a serious complication of uncontrolled T2DM
Hyperosmolar hyperglycaemic state
74
Describe the diagnosis and characteristics of HHS
Severe hyperglycaemia (>30mmol/L)
Hyperosmolality (>320 mmol/kg)
Mild/ no ketosis
Urine dipstick: Glucosuria
75
Describe the pathophysiology of HHS
Decreased insulin levels are:
• insufficient to inhibit gluconeogenesis (hyperglycaemia -> osmotic diuresis)
but
• sufficient enough to inhibit ketogenesis
Severe volume depletion -> raised serum osmolarity -> hyper viscosity of blood
76
Give 3 signs and symptoms of HHS
Confusion and reduced mental state
Severe dehydration
Lethargy
77
Treatments of HHS
1st line: Fluid replacement - 0.9% saline IV
Restore electrolyte loss (K+)
Low molecular weight heparin (LMWH) to decrease risk of thromboembolism
Give insulin
78
What is a functioning tumour
When a tumour derived from endocrine tissue produces hormones of the original tissue
79
What is a common structure affected by a pituitary tumour
optic chiasm
80
A pituitary tumour is pressing upwards on the optic chiasm; this compresses the nasal fibres. What visual field defect will be seen
Bitemporal hemianopia
81
If a pituitary tumour applies pressure on the cavernous sinus what could happen
cranial nerve palsies
82
How does a 3rd nerve palsy present
Depression and abduction of eye
Drooped eyelid
83
What can cause a raised prolactin level
Stress
Antidopaminergic drugs (anti-psychotics)
Lactotroph adenoma
84
Signs and symptoms of prolactinomas
Amenorrhea - absence of periods
Galactorrhoea - Milky nipple discharge
Low libido
Infertility
Visual field defect
85
Treatment for prolactinoma
1st line: Dopamine agonists e.g. cabergoline
2nd line: combined oral contraceptive
Trans-sphenoidal surgery for men and post-menopausal women
86
What is prolactinoma
Lactotroph cell tumour of the pituitary producing excess prolactin which initiates lactation and breast development
87
What investigations are done to diagnose prolactinoma
prolactin levels
Pituitary MRI
88
What is cushing syndrome
Refers to the signs and symptoms that develop after Long term exposure to excessive cortisol
89
Signs and symptoms of cushings syndrome
Stretch marks
Thin skin (bruising)
Central obesity
Round moon face
Depression
90
What is cushings syndrome and cushings disease
Disease: caused by a pituitary adenoma secreting excess ACTH
Syndrome: high cortisol of any cause
91
4 causes of Cushing’s syndrome
Iatrogenic - steroid use (most common)
Adrenal adenoma secreting cortisol
Cushing’s disease
Ectopic ACTH
92
What is ectopic ACTH
ACTH secreting tumour outside of the pituitary and adrenal glands e.g. small cell lung cancer
93
Describe the diagnosis process for cushing's syndrome
First exclude oral steroids
1st line: Random plasma cortisol: if high do further tests
Gold standard: Overnight dexamethasone suppression test: cortisol should be low in a healthy patient
Other: Positive urinary cortisol (24h) - doesn’t show underlying cause
MRI brain
abdomen and chest CT
94
What is the treatment for cushing's caused by a pituitary adenoma
Transsphenoidal surgery
95
What is the treatment for cushing's caused by an adrenal adenoma
adrenalectomy
96
What is the treatment for cushing's that has an latrogenic cause
Stop medication if possible
97
Give 4 complications associated with cushing's
CV disease
Hypertension
DM
Osteoporosis
98
Give 3 complications of prolactinoma
Infertility
Sight loss
Raised intracranial pressure
99
What is acromegaly
Release of excess growth hormone causing overgrowth of all systems
100
Causes of acromegaly
Pituitary adenoma (most common)
Ecoptic GH production from small cell lung cancer
101
Describe the pathophysiology of acromegaly
GH acts directly on tissues such as liver, muscle, bone or fat, as well as indirectly through induction of insulin like growth factor (ILGF-1)
102
Give 3 complications of acromegaly
Sleep apnea - overgrowth of pharynx
T2DM
Heart disease
103
State 5 presenting features of acromegaly
Large hands, nose, tongue and feet
Prominent forehead and brow
Profuse sweating
Increased jaw size
Visual field defects
104
What is the 1st line investigation for acromegaly
Insulin like growth factor 1 test. Raised with acromegaly
105
Why is testing random serum GH not a reliable way to diagnose acromegaly
Levels of GH vary throughout the day for normal people and increases when stressed, pregnant and during puberty
106
Describe the gold standard method for acromegaly diagnosis
Oral glucose tolerance test
In a healthy subject: glucose is given and this suppresses GH
In a patient with acromegaly, GH is not suppressed
107
What is the 1st line treatment for acromegaly
Transsphenoidal resection surgery (if cause is adenoma)
108
What 3 different drugs are used to treat acromegaly
Somatostatin analogue - octreotide (longer half-life)
GH receptor antagonists - pegvisomant
Dopamine agonist - cabergoline
109
What are common symptoms of hypoglycaemia
Shaking
Sweating
Palpitations
Poor concentration
Nausea
110
What plasma glucose level is classed as hypoglycaemia
Less than 3.9 mmol/l (70mg/dl)
111
Symptoms of severe hypoglycaemia
Reduced consciousness
Coma
Death
112
What causes hypoglycaemia
Long duration of diabetes
increasing age
Addison’s
Drugs - SE sulfonylureas or excess insulin
113
How is hypoglycaemia treated
Fast acting glucose (lucozade) and slow acting carb (biscuits)
Unconscious: IV dextrose and IM glucagon
114
Give 3 characteristics of pseuodohypoparathyroidism
Mild learning difficulties
Short 4th metacarpals
Obesity
115
Causes of primary hyperparathyroidism
Single benign adenoma (80%)
Hyperplasia of all glands
116
What is primary hyperparathyroidism
Tumour/ hyperplasia of parathyroid gland produces excess PTH
117
What is secondary hyperparathyroidism
Increased secretion of PTH to compensate hypocalcaemia
High PTH, low CA
118
What causes secondary hyperparathyroidism
Chronic kidney failure or Low Vit D leads to low absorption of Ca = hypocalcaemia
119
What is tertiary hyperparathyroidism
Autonomous secretion of PTH even after correction of calcium deficiency due to CKD
120
Causes of tertiary hyperparathyroidism
Develops from prolonged secondary hyperparathyroidism
Parathyroid glands become hyperplastic to further increase excess PTH secretion
121
How does PTH increase Ca
PTH increases Calcium through bone resorption, gut absorption, renal reabsorption and activating Vit D
122
What is the typical PTH/bone profile of someone with primary hyperparathyroidism
high PTH, high calcium low phosphates
123
how is hyperparathyroidism investigated
•PTH, Ca, Phosphate levels
• DEXA scan - bone density
• Xray - pepperpot skull
• Ultrasound for renal stones
124
How is hyperparathyroidism treated
primary - parathyroidectomy
Ca correction - treat Vit D deficiency (ergocalciferol) or kidney transplant for CKD
125
What are the treatments for hypoparathyroidism
IV Calcium gluconate
oral Calcitriol
Synthetic PTH
126
What is goitre
Swelling or nodules that develop on the thyroid gland
127
What is hyperthyroidism
Excess thyroid hormone:
Primary - abnormal increased thyroid function
Secondary - abnormal increased TSH production
128
Causes of hyperthyroidism
Graves disease (75-80%)
Toxic multinodular goitre
De Quervain's thyroditis
Iodine excess
129
Signs and symptoms of hyperthyroidism
Hot and sweaty
Diarrhoea
Tachycardia
Weight loss
130
Risk factors of hyperthyroidism
Smoking
Young/ middle aged women (20-40)
Stress
131
Describe the pathophysiology of hyperthyroidism
Increased T3 increases metabolic rate, CO, bone resorption and activates SNS
132
Investigations of hyperthyroidism
* Thyroid function tests: high T4
Primary (thyroid pathology) = low TSH
Secondary (overstimulation by TSH) = inappropriately high TSH
133
Describe the drug management for hyperthyroidism
1st line: Carbimazole - blocks synthesis of T4 (SE= sore throat)
2nd line: Propylthiouracil - alternative in first trimester of pregnancy
Propranolol - control thyrotoxic symptoms
134
Excluding drugs, what are the treatments for hyperthyroidism
Radioiodine - beta particles cause ionisation of thyroid cells
Thyroidectomy
135
What is thyrotoxicosis
* clinical syndrome that results when tissues are exposed to high levels of circulating thyroid hormone
* Thyroid storm is the severe end of the spectrum
136
Symptoms of thyroid storm
* Fever
* CV dysfunction
* Profuse sweating
* Nausea and vomiting
137
Explain the pathophysiology of graves disease
IgG autoantibodies bind to and activate TSH receptors causing the autonomous production of T4/T3
They also react with orbital autoantigens
138
Give symptoms of graves disease
Thyroid eye disease: eyelid retraction and periorbital swelling (exophthalmos)
Pretibial myxoedema - orange peel texture on legs
Thyroid acropachy
139
3 features of thyroid acropachy
Digital Clubbing
swelling of hands and feet
New Bone growth
140
What is a supporting investigation done to confirm whether a patient has graves
Positive TSH receptor antibodies
141
Why is PTU used instead of carbimazole to treat hyperthyroidism in young women hoping to get pregnant
Carbimazole is teratogenic - causes fetal abnormalities
142
Define hypothyroidism
Lack of thyroid hormone
1- abnormal decreased thyroid function
2 - abnormal decreased TSH production
143
Causes of primary hypothyroidism
Hashimotos thyroiditis - most common
De Quervain's thyroiditis
Drug therapy
Iodine deficiency
144
Give 2 drugs that can cause hypothyroidism
Lithium toxicity
Amiodarone - high iodine content
145
Causes of secondary hypothyroidism
Pituitary failure - not enough TSH - Hypopituitarism
146
5 Clinical features of hypothyroidism
Weight gain
Fatigue
Constipation
Dry, coarse scalp
Cold intolerance
147
Investigations for hypothyroidism
TFT: low T3/4
High TSH in primary, Low TSH in secondary
148
What Ab are found in almost all patients with autoimmune hypothyroidism
Thyroid peroxidase and thyroglobulin antibodies
149
Treatment for hypothyroidism
Levothyroxine (synthetic T4)
150
Complications of hypothyroidism
Heart disease
Pregnancy problems
Myxoedema coma
151
Give 3 autoimmune diseases associated with thyroid autoimmunity
T1DM
Addison's disease
Vitiligo
152
What is hashimoto's thyroiditis
autoimmune disease
thyroid gland is attacked via cell and antibody-mediated immune processes causing inflammation and dysfunction
153
Explain the pathophysiology of hashimoto's thyroiditis
formation of antithyroid antibodies that attack the thyroid tissue, causing progressive fibrosis
154
What is De Quervain's thyroiditis
Self-limited inflammation of thyroid gland
155
Cause of DQ's thyroiditis
Often occurs following a viral infection
156
Explain the pathophysiology of DQ's thyroiditis
4 phases:
Phase 1- lasts 3-6 weeks: hyperthyroidism, painful goitre, Raised ESR
Phase 2- Lasts 1-3 weeks: Euthyroid (normal function)
Phase 3- weeks to months: Hypothyroidism
Phase 4- Thyroid structure and function goes back to normal
157
State the 4 main types of thyroid cancer
Papillary
Follicular
Medullary
Anaplastic
158
What is the treatment for T1DM
Patient education - monitoring carb intake and blood sugar levels
Subcutaneous insulin:
* basal: detemir (2x)
* bolus: lispro injected 30mins before meals
159
What is basal insulin
Long acting insulin
Used to maintain stable insulin level throughout the day
160
What is bolus insulin
Faster acting insulin
Taken 30 mins pre-meal to give insulin spike
161
What is MODY
Maturity onset diabetes of youth
Rare auto dom diagnosed < 25y
162
Treatment for MODY
sulfonylurea
163
Complications of a total thyroidectomy
Increased risk of recurrent laryngeal nerve damage or hypoparathyroidism
164
What is Conn’s syndrome
Primary hyperaldosteronism due to an aldosterone producing adrenal adenoma
165
What is primary hyperaldosteronism
Adrenal dysfunction causing raised aldosterone levels
- serum renin will be low as it is suppressed by high bp
166
What is secondary hyperaldosteronism
Inappropriate activation of the RAAS = raised renin which = raised aldosterone
167
Explain the pathophysiology of Conn’s syndrome
Excess production of aldosterone independent of RAAS results in:
- high Na and water retention
- increased K+ excretion from kidneys
- low renin release
168
Presentation of Conn’s syndrome
Often asymptomatic
Possible:
Hypertension
Headaches
Hypokalaemia
Weakness
169
What investigation are used in the diagnosis of Conn’s
- Aldosterone-renin ratio: high (>70%)
- Low plasma K+
- CT/MRI to locate adrenal lesions
- selective adrenal venous sampling ( gold standard )
170
What is the first line treatment for Conn’s
Aldosterone antagonists - control BP and K+ levels (Spironolactone)
171
What is the gold standard treatment for Conn's
Surgical removal of adenoma
172
Define cranial diabetes insipidus
ADH deficiency: Hypothalamus doesn't produce ADH for the post pituitary to secrete
173
Define nephrogenic diabetes insipidus
ADH resistance/insensitivity: collecting ducts of kidney don't respond to ADH
174
Define SIADH
syndrome of inappropriate secretion of ADH
175
Presentation of DI
Polyuria
Polydipsia
Dehydration
(NO GLUCOSURIA)
176
State 3 causes of cranial DI
Brain tumours - craniopharyngioma
head trauma
Infections - TB, meningitis
177
Give 4 causes of nephrogenic DI
Inherited - mutation in ADH receptor
Drugs - lithium
Systemic disease - chronic kidney disease
Electrolyte disturbance - hypokalaemia, hypercalcaemia
178
Describe the diagnosis and investigations for DI
• GS: water deprivation test
• Urine osmolality - low (<200)
• Serum osmolality - high (>300)
• Serum Na - norm/high
• Serum glucose - exclude DM if glucosuria not seen
179
What is the gold standard test for DI and why
Water deprivation test
Can distinguish between cranial and nephrogenic
180
Describe the water deprivation test
1) Used to confirm DI
Deprived of fluid for 8 hours
Urine osmolality is measured hourly.
* Urine still dilute indicates DI (dehydration = normal response)
2) distinguish between cranial and nephrogenic DI
Desmopressin is administered IM.
8 hours later urine osmolality is measured again
181
Describe the results of a water deprivation test for a patient with cranial DI
Patients with cranial DI respond to desmopressin with a reduction in urine output and an increase in urine osmolality to >750 mmol/kg
182
Describe the results of a water deprivation test for a patient with nephrogenic DI
Don't respond to desmopressin
No or little reduction in urine output and no increase in urine osmolality (as they are insensitive to ADH)
183
Treatment for cranial DI
Desmopressin - high activity at V2 receptor
184
Treatment for nephrogenic DI
Thiazide diuretics (Bendroflumethiazide) - offset water losses
NSAIDs - reduce urine output
185
What is a complication of DI
Hypernatremia
186
Give 2 causes of hyponatraemia
Excess water - most common
Salt loss
187
What would be the serum Na of someone with hyponatraemia
<135 mmol/l
(norm = 135-144)
188
Give 3 symptoms of hyponatraemia
Headache
Nausea
Confusion
189
Treatment for hyponatraemia
Stop hypotonic fluids
Assess underlying causes
190
Give 4 causes of SIADH
Meds - thiazide diuretics, carbamazepine, SSRI
Malignancy - SCLC
TB
Stroke
191
Explain the pathophysiology of SIADH
* Excessive ADH = excessive water reabsorption in collecting ducts
* Water dilutes Na in the blood = hyponatraemia
* Water reabsorption isn't significant enough to cause fluid overload = euvolemic hyponatraemia
* Urine more concentrated - high urine osmolality & high urine Na
192
Symptoms of SIADH
Largely due to hyponatraemia:
Headache
Fatigue
Muscle aches
193
Describe the diagnosis and investigation of SIADH
Usually diagnosed by exclusion
- Euvolaemia
- U+E = hyponatraemia
- low serum osmolality
- high urine and Na osmolality
194
Treatment of SIADH
Establish and treat cause
Fluid restriction (<1L/24h) - correct hyponatraemia
Vasopressin receptor antagonist (Tolvaptan)
195
What is a complication of SIADH
Central pontine myelinolysis - correct Na slowly to avoid this
196
What is adrenal insufficiency
Where the adrenal glands don't produce enough steroid hormones particularly aldosterone and cortisol
197
Define primary adrenal insufficiency (Addison's disease)
When the adrenal glands have been damaged resulting in reduced cortisol and aldosterone
198
Give 2 common causes of Addison's disease
Autoimmune adrenalitis (inflammation) - most common in developed countries
TB - most common worldwide
199
What is secondary adrenal insufficiency
Inadequate adrenocorticotropic hormone stimulating the adrenal glands resulting in low levels of cortisol release
200
Give 2 causes of secondary adrenal insufficiency
Radiotherapy
Pituitary macroadenoma
201
What is tertiary adrenal insufficiency
Result of inadequate CRH release by the hypothalamus
202
Causes of tertiary adrenal insufficiency
Usually the result of patients being on long term oral steroids (>3w) causing suppression of the HPA axis
203
Presentation of Addison's
* Hyperpigmentation especially in the palmar creases - only in primary AI
* lethargy, weight loss,
* Postural hypotension and hypoglycaemia
* vitiligo and loss of pubic hair
204
Give 3 biochemical indicators of adrenal insufficiency
* Low Na, high K (SIADH)
* Eosinophilia
* Borderline elevated TSH
205
Investigations for AI
* Renin/ Aldo: elevated renin and low aldo in Addison's
* Low cortisol
* low Na, high K
* High ACTH in primary, Low/ normal ACTH in secondary
* Short synacthen test
206
State and explain the gold standard test for AI
Short synacthen test: ideally in the morning
* Patient injected with synthetic ACTH (synacthen)
* cortisol measured at baseline, 30 & 60 mins
* failure of cortisol to rise (less than double baseline) indicates addison's
207
What is an adrenal crisis
This is when the level of cortisol drops significantly and symptoms of AI worsen
208
How is an adrenal crisis treated
* Immediate hydrocortisone 100mg IV/IM
* Fluid resuscitations (saline)
* Continued hydrocortisone until recovered 6 hourly
* Wean dose to normal when stable
209
Treatment for AI
Hydrocortisone (15-25mg divided into 2-3 doses) - replace cortisol
Fludrocortisone - replace aldosterone
210
When should the dose of hydrocortisone be doubled
If unwell with fever/flu like illness as cortisol is needed for stress response
211
What is MODY
Maturity onset diabetes of youth
Rare auto dom diagnosed < 25y
212
What is pheochromocytoma
neuroendocrine tumour of the chromaffin cells found in the adrenal medulla
causes excessive release of adrenaline and noradrenaline
213
Causes of pheochromocytomas
Usually inherited
Neurofibromatosis
Multiple endocrine neoplasia syndrome
214
Signs and symptoms of pheochromocytoma
Headache
hypertension
Palpitations
Tremor
Pallor
215
Investigations for pheochromocytoma
* Increased plasma metanephrines and normetanephrines ( longer 1/2 life than Adr & NAd)
* CT - tumour
* 24h Urinary catecholamines
216
Treatment for pheochromocytoma
1st line: alpha blockers (phenoxybenzamine)
* Surgery to remove tumour
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What is a complication of pheochromocytoma and how is this treated
HTN crisis ( 180/120 bp)
Treated with ant hypersensitive agent: phentolamine
218
What is carcinoid syndrome
Occurs due to release of serotonin into the systemic circulation from a carcinoid tumour
219
Where do carcinoid tumours commonly arise from
GI tract (SI)
Lungs
Liver - most common for metastasis
Ovaries
Thymus
220
How does carcinoid syndrome present
Flushing
Diarrhoea
Abdo cramps
221
Define hypokalaemia
Serum K level <3.5 mmol/L
222
What causes hypokalaemia with alkalosis
Vomiting
Thiazide and loop diuretics
Cushing's syndrome
Conn's
223
What causes hypokalaemia with acidosis
Diarrhoea
Renal tubular acidosis
Partially treated DKA
Decreased intake
224
How does hypokalaemia present
Muscle weakness
Hypotonia
Arrhythmias
Hyporeflexia
225
Describe the ECG presentation of someone with hypokalaemia
Small/ inverted T wave
Prominent U wave
Long PR interval
ST depression
226
Investigations for hypokalaemia
Decreased [K+]
Urine electrolytes - differentiate between renal and non-renal causes of hypokalaemia
ECG
227
Treatment for hypokalaemia
Mild: oral K+ replacement
Severe (<2.5mmol/L): IV replacement 40mmol KCl in 1L 0.9 NaCl
228
Give 2 complications of hypokalaemia
Long QT syndrome
Chronic heart failure
229
Define hyperkalaemia
Serum K value >5.5mmol/L
230
Causes of hyperkalaemia
Acute kidney injury
Addison's
DKA
NSAIDs
ACEi
231
Symptoms of hyperkalaemia
Fast irregular pulse (AF)
Muscle aches and pains
Chest pain
Ventricular fibrillation
232
Describe the typical ECG presentation of hyperkalaemia
Tall tented T waves
Small/ absent p waves
Wide QRS
233
Diagnosis and investigations of hyperkalaemia
U+E - high [K+]
ECG
234
Treatment for hyperkalaemia with ECG changes
Stabilise cardiac membrane via IV Ca gluconate/chloride
235
Treatment for hyperkalaemia if no cardiotoxic changes are seen
Shift K+ ECF to ICF by giving combined insulin and dextrose infusion with nebulised salbutamol
236
What can be used to remove potassium from the body
Calcium resonium
Loop diuretics
Dialysis
237
Define severe hyperkalaemia
Serum K value > 6.5mmol/L
238
Describe the dexamethasone suppression test
Low dose test: 1mg dexamethasone given
* normal response = low cortisol
* Cushing’s syndrome = normal/high cortisol
High dose test: 8mg dexamethasone given
* low cortisol = Cushing’s disease
Normal/high cortisol:
* low ACTH = adrenal adenoma
* high ACTH = ectopic ACTH
239
What are normal levels of blood glucose
Between 3.5-8.0mmol/L
240
What are the effects of T3/T4 on the body
* Increases basal metabolic rate
* Anabolic (form) effects at low serum levels and catabolic (breakdown) effects at higher levels
* Increases release and effect of GH and IGF-1
* Increases HR and contractility through increasing sensitivity to catecholamines
241
Which part of the adrenal gland secretes catecholamines (e.g Adr)
Adrenal medulla
242
Describe the layers of the adrenal cortex and state which hormone is secreted
* Zona glomerulosa - secretes mineralocorticoids e.g. aldosterone
* Z. fasciculata - secretes glucocorticoids e.g. cortisol
* Z. reticularis - secretes androgens (sex hormones)
243
Action of aldosterone
* Works on kidneys to increase blood volume and BP
* Can cause hypernatremia
244
Action of cortisol
* Suppresses immune system
* Inhibits bone formation
* Increases metabolism - protein catabolism, lipolysis, gluconeogenesis
* Increases alertness
