Endocrine Conditions Flashcards
1
Q
Define Diabetes Mellitus
A
Syndrome of chronic hyperglycaemia due to relative insulin deficiency, resistance or both
2
Q
What is the principle organ of glucose homeostasis?
What is its role?
A
Liver
- Stores and absorbs glucose as glycogen
- Performs gluconeogenesis
- HIGH blood glucose - makes glycogen
- LOW blood glucose - splits glycogen, makes glucose
3
Q
What are the normal levels of blood glucose?
A
3.5-8.0mmol/L under all conditions
4
Q
How does the brain use glucose?
A
Major consumer.
Cannot use free fatty acids as cannot cross the blood brain barrier.
5
Q
How does muscle utilise glucose?
A
Stored as glycogen
OR
metabolised to lactate
OR
to CO2 and H2O
6
Q
How does adipose tissue utilise glucose?
A
Uses it as a substrate for triglyceride synthesis
7
Q
What are the two m ain regulators of blood glucose levels?
A
Insulin
Glucagon
8
Q
Describe the role of insulin as a regulator of blood glucose levels (2)
A
- Supresses hepatic glucose output
- Increases glucose uptake into insulin sensitive tissues
9
Q
Describe the role of glucagon as a regulator of blood glucose levels (5)
A
- Increases hepatic glucose output
- Reduces peripheral glucose uptake
- Stimulates peripheral release of gluconeogenesis precursors
- Simulates glycogenolysis and breakdown
- Stimulates lipolysis
10
Q
Describe biphasic release of insulin
A
B-cells sense rising glucose levels and aim to metabolise it by releasing insulin.
1st phase - rapid release of stored insulin
2nd phase (if levels still high) - more insulin synthesised (takes longer)
11
Q
Name 3 other counter regulatory hormones in blood glucose levels
What are their roles?
A
Adrenaline, cortisol and growth hormones
Increase glucose production in the liver and reduce its utilisation in fat and muscle
12
Q
How is insulin determined as natural or synthetic?
A
Presence of C peptide
13
Q
What is insulin coded on?
Where is it produced?
A
Chromosome 11
Beta cells of islets of Langerhans of the pancreas
14
Q
What is the main action of insulin in the fed state?
A
Regulate glucose release by the liver
15
Q
What is the main action of insulin in the post-prandial state?
A
Promote glucose uptake by fat and muscle
16
Q
What transporter allows glucose into cells
A
Glucose-transporter (GLUT) proteins
17
Q
What is the role of GLUT-1
A
Enables basal non-insulin stimulated glucose uptake into many cells
18
Q
What is the role of GLUT-2
A
Transport glucose into the beta cells.
Can detect high levels of glucose and release insulin as a response
19
Q
What is the role of GLUT-3
A
Enables non-insulin mediated glucose-uptake into brain, neurones and placenta
20
Q
What is the role of GLUT-4
A
Mediates much of the peripheral action of insulin
21
Q
Diabetes - name 3 microvascular complications
A
- Retinopathy
- Nephropathy
- Neuropathy
22
Q
Describe the microvascular complication of diabetes on the eye
A
High blood glucose and high BP can damage the eye blood vessels, causing retinopathy, cataracts and glaucoma
23
Q
Describe the microvascular complication of diabetes on the kidney
A
High blood pressure damages small vessels and excess blood glucose overworks the kidneys resulting in nephropathy
24
Q
Describe the microvascular complication of diabetes on the neuropathy
A
Hyperglycaemia damages nerves in the peripheral nervous system
This may result in pain and/or numbness
Feet wounds may go undetected and get infected and lead to gangrene
25
Describe the macrovascular complications of diabetes on the brain
Increases risk of stroke and cerebrovascular disease, including transient ischaemia attack, cognitive impairment etc.
26
Describe the macrovascular complications of diabetes on the heart
High blood pressure and insulin resistance increases risk of coronary heart disease
27
Describe the macrovascular effects of diabetes on extremities
Peripheral vascular disease results from narrowing of blood vessels increasing the risk for reduced or lack of blood flow to the legs
Feet wounds are likely to heel slowly contributing to gangrene and other complications
28
Diabetes - Name 4 macrovascular complications
1. Strokes
2. Renovascular disease
3. Limb ischaemia
4. Heart disease
29
Define type 1 diabetes
Metabolic autoimmune disorder characterised by hyperglycaemia due to an absolute deficiency of insulin.
30
What is type 1 diabetes caused by
Caused by autoimmune destruction of beta cells of the pancreas.
31
Define type 2 diabetes
Characterised by insulin resistance and less severe insulin deficiency
32
Define diabetic ketoacidosis
Acute metabolic complication of diabetes that is potentially fatal and requires prompt medical attention for successful treatment
33
Name the causes of DKA
Untreated type 1 diabetes (occasionally type 2 diabetes)
Undiagnosed diabetes
Exacerbations of type 1 diabetes
34
What are the possible causes for type 1 dm
Autoimmune
Idiopathic
Genetics
Enterovirus
35
Describe the pathophysiology of type 1 dm
Autoimmune destruction by autoantibodies of Beta-cells.
Causes insulin deficiency.
Eventual complete beta cell destruction
No transport of insulin into cells = hyperglycaemia = increased gluconeogenesis
36
What can be used to see how well beta cells are working
Serum-C peptide
37
In type 1 diabetes what will serum-C peptide be
Absent
38
When does type 1 diabetes tend to present
When only 10% beta cells remaining
39
Name 6 clinical manifestations of type 1 dm
Thirst
Polyuria
Weight loss and fatigue
Hunger
Pruritis vulvae and balitis
Blurred vision
40
Why is polyuria a manifestation of diabetes
Blood glucose > 10 mmol/L blood can no longer be absorbed
41
Describe the investigations of diabetes mellitus
Fasting plasma glucose > 7mmol/L (symptoms) or equal to
Random plasma glucose > 11.1 mmol/L (no symptoms x2) equal to
HbA1c > 48 mmol/mol (6.5%)
42
What is the management of type 1 diabetes
Insulin treatment
2x daily treatment short/medium acting insulin basal bolus and long acting insulin
43
What does monitoring of diabetes involve
HbA1c
Self-monitoring 4x a day
Annual checks
44
Name the risk factors of type 1 DM
Younger patients
Northern Europeans
Other autoimmune diseases
HLA-DR3-DQ2
HLA-DR4-DQ8
45
What are the serotypes for type 1 dm
HLA-DR3-DQ2
HLA-DR4-DQ8
46
Describe the causes of type 2 diabetes
Obesity
Lack of exercise
Calorie
Alcohol excess
Genetic link
47
Describe the pathophysiology of type 2 dm
Insulin levels tend to be higher than in non-diabetics, fall again months/years after - starling curve of the pancreas
Exhaustion of pancreas leads to hypoplasia and hypotrophy.
Hyperglycaemia and lipid excess are toxic to beta cells (glucotoxicity) = further beta cell loss
48
Name 7 symptoms of type 2 dm
Polydipsia
Polyuria
Blurred vision
Unexplained weight loss
Recurrent infections
Tiredness
Slow wound healing
49
Name a sign of type 2 diabetes
Acanthosis nigricans
50
Approx what % of beta cells are left at diagnosis of type 2 dm
50%
51
Describe the 1st line management for type 2 dm
1. Weight loss and exercise
150 mins moderate exercise over 3 days
DESMOND/xpert
52
Describe the pathophysiology of DKA
Complete lack of insulin = uncontrolled lipolysis = increased fatty acids = converted into ketones = metabolic acidosis
Increased FFA = increased acetyl-coA which synthesises ketone bodies.
53
What are the symptoms of DKA
Develop over days
Polyuria and polydipsia
Vomiting and nausea
Weight loss
Weakness
Abdominal pain
Drowsiness and confusion
54
What are the signs of DKA
Hyperventilation - Kussmaul breathing. Acetone smelling breath
Dehydration
Hypotension
Tachycardia
Coma
55
What are the risk factors for DKA
Incurrent illness
Treatment errors
Physiological stress
Previously undiagnosed diabetes
Unknown
56
What are the investigations for a DKA
Plasma glucose > 11 mol
Blood (serum) ketones > 3 mmol
Urine ketones > 2
Bicarbonate < 15 mmol
U&E
K+
57
What is the management for DKA
FIG PICK
Fluids 3L in 1st 3 hours
Insulin - sliding scale
Glucose (dextrose) + insulin
Potassium
Infection
Chart fluid balance
Ketone monitoring
58
Define hypoglycaemia
Lower than normal blood glucose concentration
< 3.9 mmol/L
59
Describe the pathophysiology of hypoglycaemia
Results from an imbalance between glucose supply and glucose utilisation and existing insulin
60
Name the 3 clinical features of hypoglycaemia
1. Autonomic
2. Neuroglycopenic
3. Non-specific
61
What is the value of hypoglycaemia
Blood glucose level < 3.9 mmol/L
62
Name the 5 steps of management in hypoglycaemia
1. Recognise symptoms
2. Confirm
3. Treat 15g fast acting carbohydrates to relieve symptoms
4. Re-rest in 15 minutes to ensure blood glucose > 4.0 mmol/L and re-treat if needed
5. Eat long acting carbohydrates to prevent recurrence
63
Define hyperosmolar hyperglycaemia state
Non-ketotic hyperglycaemic hyperosmolar syndrome, characterise by profound hyperglycaemia, hyperosmolality and volume depletion in the absence of significant ketoacidosis
Decreased insulin but not enough to cause ketogenesis
64
Describe the causes of hyperosmolar hyperglycaemic state
Most common reaction - infection
Cardiovascular insult
Chronic uncontrolled T2DM
Sedative drugs
Dementia
65
What are the clinical features of hyperosmolar hyperglycaemic state
Happens over days
Polyuria
Polydipsia
Weight loss
Dehydration
Tachycardia
Hypotension
Confusion
N&V
Severe case - shock
66
What are the investigations of hyperosmolar hyperglycaemic state
Hyperglycaemia > 30 mmol
Serum osmolality > 320 osmole/kg
No ketonuria
67
What is the management of hyperosmolar hyperglycaemic state
ABC approach
IV fluids - saline
LMWH
Restore electrolytes
Careful monitoring
68
Why is LMWH given in the management of hyperosmolar hyperglycaemic state
Due to increased risk of thrombolytic events (blood viscosity)
69
Describe the pathophysiology of hyperosmolar hyperglycaemic state
Medical emergency - due to chronic T2DM
Decreased insulin - but not enough that ketogenesis happens
Overtime causes
- osmotic diuresis
- dehydration
- electrolyte deficiency - hyperglycaemia, diuresis causing hyperosmolality
- mild/no ketones
70
Name 5 features of an ECG seen in a DKA
Tall peaking T waves
Prolonged QT interval
Widening QRS complex
Prolongation of the ST interval
ST segment elevation
71
Define hyperthyroidism (Grave's)
Thyroid stimulating hormone receptor antibodies stimulate the thyroid gland
Overproduction of T3/T4
72
Describe the presentation of hyperthyroidism (Grave's)
Weight decrease
HR increase
Painless goitre
Exothalamous (protrusion of eyes out of the orbit)
Pretibial myxedema
Thyroid acropachy
73
What is the GS investigation of hyperthyroidism (Grave's)
Measurement of TSH receptor antibody
74
What condition would this be seen in
TSH - low
T3 - high
T4 - high
Hyperthyroidism (Grave's)
75
What would be the thyroid function tests of hyperthyroidism (Grave's)
TSH - low
T3 - high
T4 - high
76
What is the 1st line management in hyperthyroidism (Grave's)
Block - carbimazole
Treat - levothyroxine
77
What is 2nd line management in hyperthyroidism (Grave's)
Propylthiouracil
Reduction of thyroid gland
78
Name the conditions which can cause hyperthyroidism
GIST
Graves disease
Inflammatory (thyroiditis)
Solidary toxic thyroid nodule
Toxic multinodular goitre
79
Define hypothyroidism (Hashimoto's thyroiditis)
Autoimmune causing antithyroid antibodies to damage the thyroid = decreased production of T4/T3
80
Describe the presentation of hypothyroidism (Hashimoto's thyroiditis)
Dry skin, hair and brittle nails
Fatigue
Weight gain
Cold sensitivity
Constipation
Heavy or irregular periods
81
What is the GS investigation for hypothyroidism (Hashimoto's thyroiditis)
Thyroid function tests
Anti-thyroid peroxide antibodies
82
What condition would this be seen in
TSH high
T4 normal/low
T3 normal/low
hypothyroidism (Hashimoto's thyroiditis)
83
What would be the thyroid function test in hypothyroidism (Hashimoto's thyroiditis)
TSH high
T4 normal/low
T3 normal/low
84
What is the 1st line management in hypothyroidism (Hashimoto's thyroiditis)
Levothyroxine
85
Describe thyroid cancer
Genetic alterations + mutations
4 types
- papillary
- follicular
- anaplastic
- medullary
86
Name a key presentation of thyroid cancer
Palpable thyroid nodule
87
What is the GS investigation in thyroid cancer
Ultrasound neck + fine needle biopsy
88
What is the 1st line management of thyroid cancer
Thyroidectomy + radioactive iodine
89
What is the 2nd line management of thyroid cancer
Ablation + suppression of TSH
90
What are the risk factors of thyroid cancer
Head and neck irradiation
Female
91
Name 2 complications of thyroid cancer
Increased risk of laryngeal nerve damage
Increased risk of hypoparathyroidism
92
Define cushing's syndrome
Excess cortisol
93
Define cushing's disease
Caused by endogenous cortisol - ACTH-producing pituitary adenoma
94
Describe the presentation of cushing's syndrome
Central obesity
Hirsutism
Purple abdominal striae
Buffalo hump
Moon face
Hyperpigmentation
95
What is GS investigation of cushing's syndrome
Dexamethasone suppression test (low dose)
96
What is a 2nd line investigation in cushing's syndrome
High dose dexamethasone test - diagnose pituitary adenoma
24-hour urinary free cortisol
MRI pituitary
CT chest and abdomen
97
What test is used to diagnose cushings disease (caused by a pituitary adenoma)
High dose dexamethasone suppression test
98
What is GS management for cushing's syndrome
Trans-sphenoidal surgery for pituitary adenoma
99
What is 2nd line management for cushing's syndrome
Cessation of steroids
100
What is the most common cause of cushing's syndrome (disease)
Pituitary adenoma
101
What are the causes of cushing's syndrome
Pituitary adenoma
Small cell lung cancer
Exogenous steriods
102
Define acromegaly
Exocrine disorder
Excessive secretion of growth hormone
103
Describe the clinical features of acromegaly
Bitemporal hemianopia
Large spade hands and feet
Acroparathesia
Back pain
Arthralgia
Oily skin
Amenorrhoea
104
What is the GS investigation for Acromegaly
Oral glucose tolerance test
105
What is the 1st line investigation for acromegaly
Insulin-like growth factor-1
106
What is a possible extra investigation for acromegaly
MRI brain
107
What is the GS management for acromegaly
Trans-sphenoidal surgery for pituitary tumour
108
What type of condition is acromegaly
Benign
109
What is the 2nd line management of acromegaly
Somatostatin analogues e.g. octreotide
110
What is the 3rd line management of acromegaly
Growth hormone receptor antagonists e.g. Pegvisomant
111
Name the cause of acromegaly
Anterior pituitary adenoma
112
Describe the pathophysiology of acromegaly
Excessive production of GH = excessive production of insulin like growth factor (IGF-1) = stimulates bone and soft tissue growth
113
Define prolactinoma
Benign lactotroph adenoma expressing and secreting prolactin
114
What type of condition is the hypersecretion of prolactin
Secondary hypogonadism
115
What are the clinical features of prolactinoma in females
Amenorrhea
Oligomenorrhea
Infertility
Galactorrhoea
Low libido
116
What are the clinical features of prolactinoma in males
Low testosterone
Erectile dysfunction
Reduced facial hair
Low libido
117
What is the GS investigation in prolactinoma
Serum prolactin levels = elevated
Followed by a pituitary MRI
118
What is the GS management in prolactinoma
Dopamine agonist e.g. oral cabergoline/bromocriptine
119
What is prolactinoma caused by
Pituitary adenoma
120
Describe the pathophysiology of prolactinoma
Hormone made by lactotrophs in the anterior pituitary gland - milk in the breast
121
Define carcinoid syndromes
Release of serotonin and other vasoactive particles into the systemic circulation from a carcinoid tumour
122
Define a carcinoid tumour
Neuroendocrine tumour growing from neuroendocrine cells
123
Describe the clinical features of carcinoid tumours and syndromes
Flushing
Diarrhoea
Wheeze
Palpitations
Telangiectasia (vessels visible on the skin)
Abdominal pain
124
What is the GS investigation for carcinoid tumours and syndromes
Urinary 5-hydrozyincholeacetic acid = elevated levels
125
What is the GS (cure) of carcinoid tumours and syndromes
Surgery
126
What is the 2nd line management of carcinoid tumours and syndromes
Somatostatin analogues e.g. octreotide
= blocks the release of tumour mediators and counter peripheral effects
127
Where do the most common carcinoid tumours arise from
GI tract
then
lungs
liver (common site of metastases)
ovaries thymus
128
Describe GI carcinoid tumours
Hormone is secreted - enters enterohepatic circulation - live activated hormone = no symptoms
129
Describe liver metastases carcinoid tumours
Hormone is secreted - released into the circulation due to liver dysfunction = symptoms
130
Name the risk factors of Graves (hyperthyroidism)
Strong association with other autoimmune conditions - DM1, Addison's disease, vitiligo
Females
40-60
131
Describe post-partum thyroiditis
Presents transient acute phase of thyrotoxocosis followed by a period of hypothyroidism
2-6 months after birth or miscarriage
132
What is Grave's disease (hyperthyroidism) mediated by
Autoimmune condition via TSH-receptor antibodies (anti-TSHR)
133
Describe the pathophysiology of Grave's disease
Bind to TSH-receptors on the thyroid gland + stimulate increased T3 + T4 from the thyroid gland = results in thyrotoxicosis
134
Describe iatrogenic causes of thyrotoxicosis
Amiodarone + levothyroxine
135
Describe the pathophysiology of iatrogenic causes of thyrotoxicosis
Contains iodine - increases iodine levels = increases follicular thyroid hormone production
136
What is causes De Quervain's thyroiditis
Viral infections
137
Describe the pathophysiology of De Quervain's thyroiditis
Cause transient rise in thyroid hormone production due to inflammation of the thyroid gland
Subsequent excessive excretion of thyroid hormones into the circulation
138
How does subacute De Quervain's thyroiditis present
Painful lump in neck
139
What are the risk factors of Hashimoto's disease (hypothyroidism)
Women
30-50
Other autoimmune conditions
140
What is Hashimoto's disease (hypothyroidism) mediated by
Anti-TPO (anti-thyroid peroxidase) attack the thyroid gland
141
Describe the pathophysiology of De Quervain's thyroiditis
Transient inflammation of the thyroid gland causing 3 stages - thyrotoxicosis, hypothyroidism, euthyroidism
142
What is the treatment of De Quervain's
Self-limiting
143
Describe lithium as a cause of hypo (more common) or hyperthyroidism
Inhibits uptake, iodination and release of thyroid hormones
144
Name 4 risk factors of cushing's syndrome
Long term use of corticosteroids
Tumour
Familial
Increased stress
145
Name the risk factors for Acromegaly
Sporadic (most common)
Middle aged
Familial - younger.
- MEN-1, McCune-Albright syndrome, Carney complex.
146
Describe the difference between acromegaly + gigantism
Acromegaly - post-epiphyseal fusion
Gigantism - condition of childhood due to excessive growth hormone secretion prior to epiphyseal growth plate fusion
147
What are the risk factors for prolactinoma
More common in women
Genetic - MEN-1, FIPA
Male 30-60
Female 20-50
Oestrogen therapy
148
What is the full name for MEN-1
Multiple endocrine neoplasia-1
149
What is the full name for FIPA
Familial isolated pituitary adenoma
150
What are the normal levels of prolactin
< 400 mU/L in males
< 500mU/L in females
151
Define Conn's
Adrenal glands produce too much aldosterone
152
Define Conn's syndrome
Adrenal adenoma secreting aldosterone
153
Describe the clinical features of Conn's
Often asymptomatic
Hypertension
Headache
Hyperkalaemia
Muscle cramps
Paraesthesia
Polyuria
Nocturia
Polydipsia
154
Name the risk factors of Conn's
30-40
Obesity
Family history
Female
Increased BP
155
What is the GS investigation of Conn's
Selective adrenal venous sampling
156
Name the 1st investigation of Conn's
Serum renin low = supressed
157
What is the GS management of Conn's
Aldosterone antagonist
158
What are possible management of Conn's
Treat underlying cause
Adrenalectomy
Percutaneous renal artery angioplasty
159
What type of hyperaldosteronism is Conn's
Primary hyperaldosteronism caused by adrenal adenoma
160
Define Adrenal insufficiency
Adrenal glands do not produce enough steroid hormones - particularly cortisol and aldosterone
161
What is the key symptom of adrenal insufficiency
Hyperpigmentation
162
Name the risk factors of adrenal insufficiency
Female
Other autoimmune disorders
Presence of adrenocortical antibodies
Sepsis - cause adrenal haemorrhage
163
Name the GS investigation for adrenal insufficiency
Short Synacthen - failure to double
164
Describe the Short Synacthen test
Measures response to cortisol levels to a synthetic ACTH
165
Describe blood test results in adrenal insufficiency
Decreased Na+
Increased K+
Low cortisol
166
In adrenal insufficiency caused by primary what would ACTH be
High
167
In adrenal insufficiency caused by secondary what would ACTH be
Low
168
What test can be used to differentiate adrenal insufficiency with primary or secondary causes
ACTH
Primary - high
Secondary - low
169
Name the GS management of adrenal insufficiency
Hydrocortisone (cortisol)
Fludrocortisone (aldosterone)
170
What hormone can hydrocortisone replace
Cortisol
171
What hormone can fludrocortisone replace
Aldosterone
172
Describe primary adrenal insufficiency
Addison's disease
Adrenal glands are damaged
173
What is the most common cause of primary adrenal insufficiency
Autoimmune adrenalitis
174
What is the most common cause of adrenal insufficency
Autoimmunity
175
Describe secondary adrenal insufficiency
Inadequate ACTH stimulating the adrenal glands
176
What is the cause of secondary adrenal insufficiency
Loss or damage to the pituitary gland
177
What is a complication of adrenal insufficiency
Addison's crisis - acute adrenal insufficiency
178
What is the full name of SIADH
Syndrome of inappropriate antidiuretic hormone secretion
179
Define SIADH
Inappropriate secretion of ADH
180
Describe the clinical features of SIADH
Largely due to hyponatraemia
Seizures
Reduced consciousness
181
What is diagnosis of SIADH
Usually diagnosis of exclusion
182
Name 4 clinical signs of SIADH
Euvolemic hyponatraemia
Increased urine osmolality
Increased urine sodium
183
Describe the treatment of acute SIADH
Treat cause
Fluid restriction - 500mL/1L
184
Describe the treatment of chronic SIADH
Vasopressin receptor antagonist e.g. tolvaptan
185
Describe the pathophysiology of SIADH
ADH produced by hypothalamus - secreted by posterior pituitary gland
Stimulates water reabsorption from collecting ducts in kidneys
186
Name a complication of SIADH
Central pontine myelinolysis
187
Describe central pontine myelinolysis
Osmotic demyelination
188
Name the risk factors of SIADH
CNS disorders
Small-cell lung cancer
Medication - SSRIs + amitriptyline
Surgery - postoperative
189
Define arginine vasopressin deficiency
Lack of ADH - hypothalamus does not produce
190
Define arginine vasopressin resistance
Lack of response - collecting ducts do not respond
191
Name the clinical features of arginine vasopressin deficiency/resistance
Polyuria - > 3L urine
Polydipsia
Dehydration
Postural hypotension
No glycosuria
192
What is the GS investigation for arginine vasopressin deficiency/resistance
Water deprivation test - desmopressin stimulation test
193
What would be the results of water deprivation test then desmopressin test for arginine vasopressin deficiency
Water deprivation test - urine osmolality low
Desmopressin test = urine osmolality high
194
What would be the results of water deprivation test then desmopressin test for arginine vasopressin resistance
Water deprivation test - urine osmolality low
Desmopressin test = urine osmolality low
195
Name the risk factors of arginine vasopressin deficiency
Genetic problem in chromosome 20
Damage/dysfunction of hypothalamus/pituitary gland
196
Name the risk factors of arginine vasopressin resistance
Genetic predisposition
Medication use e.g. lithium
Kidney condition e.g. PKD, sickle cell anaemia, Sjogren's syndrome
197
Name the GS management in arginine vasopressin deficiency
Desmopressin - replace ADH
198
Name the GS management in arginine vasopressin resistance
High dose desmopressin
199
Name 2nd line management in arginine vasopressin deficiency
Sort underlying cause
Serum sodium monitored
200
Name multiple 2nd line management in arginine vasopressin resistance
Thiazide diuretics
NSAIDS
Avoid precipitating drugs
201
Define the clinical diagnosis using biochemistry of arginine vasopressin deficiency/resistance
Inappropriate dilute urine for plasma osmolality.
Serum osmolality > 100
AND
Urine osmoality < 200
Normothermia
Hypernatremia
202
Define hyperparathyroidism
Excessive secretion of parathyroid by parathyroid glands
203
Name the reasons for hyperparathyroidism clinical features
Symptoms of hypercalcaemia
204
What are the key investigation results for primary hyperparathyroidism
Increase PTH
Increase calcium
Decrease phosphate
205
What are the key investigation results for secondary hyperparathyroidism
Increase PTH
Decrease/normal calcium.
Normal phosphate
206
What are the key investigation results for tertiary hyperparathyroidism
Increase PTH
Increase calcium
Increase phosphate
(everything is high)
207
Which hyperparathyroidism would this be
Increase PTH
Increase calcium
Decrease phosphate
Primary
208
Which hyperparathyroidism would this be
Increase PTH
Decrease/normal calcium.
Normal phosphate
Secondary
209
Which hyperparathyroidism would this be
Increase PTH
Increase calcium
Increase phosphate
Tertiary
210
Name the risk factors for hyperparathyroidism
Women > 60
Prolonged/severe calcium or vitamin D deficiency
CK Failure
MEN-1
211
What is the GS management for hyperparathyroidism
Surgical removal
212
What is 2nd line management for hyperparathyroidism
Vitamin D or transplant (depending on cause)
213
What is the 3rd line management for hyperparathyroidism
Total/sub parathyroidectomy
Calaminetic
214
What is the role of calaminetic (cinacalcet)
Increased sensitivity to parathyroid cells to Ca2+ = causes less PTH secretion.
215
Name the cause of primary hyperparathyroidism
Tumour (solitary adenoma)
Hyperplasia of parathyroid glands
216
What is the most common hyperparathyroidism
Primary
217
Name the cause of secondary hyperparathyroidism
Insufficiency vitamin D or chronic renal failure
218
Name the cause of tertiary hyperparathyroidism
Prolonged secondary (CKD)
Does not respond to negative feedback
219
What the level of calcium in primary hyperparathyroidism
Hypercalcaemia
220
What is level of calcium is secondary hyperparathyroidism
Hypocalcaemia
221
Name the risk factors of hypoparathyroidism
Surgery - damage or removal of parathyroid gland
Autoimmune or endocrine conditions e.g. Addison's
Family history
Radiation therapy
Magnesium deficiency
222
Define hypoparathyroidism
Reduced PTH production
223
Name the clinical features of hypoparathyroidism
Hypocalcaemia
224
Name 2 signs of hypoparathyroidism
Chvostek's sign
Trousseau's sign
225
Name 2 signs of low calcium
Chvostek's sign
Trousseau's sign
226
Describe Chvostek's sign
Low Ca2+
Facial nerve induces spasm
227
Describe Trousseau's sign
Low Ca2+
BP cuff causes wrist flexion and fingers to pull together
228
What is the GS investigations in hypoparathyroidism
Bone profile
ECG
229
What is seen in a bone profile of hypoparathyroidism
Low calcium
Low/normal phosphate
Low PTH
230
Describe the ECG of hypoparathyroidism
Prolonged QT/ST segment
231
Name the GS management in hypoparathyroidism
IV calcium
232
Name the 2nd line management in hypoparathyroidism
AdCalD3 (calcitriol)
Synthetic PTH if required
233
Describe primary hypoparathyroidism
Gland failure
Autoimmune destruction, congenital DiGeorge syndrome (22q11del)
234
Describe secondary hypoparathyroidism (2)
Surgical removal or decrease magnesium (required for PTH production)
235
Define hypercalcaemia
> (or equal to) 2.6 mmol/L
236
Name the risk factors of hypercalcaemia
Disease - TB, sarcoidosis
Immobility
Severe dehydration
Hyperparathyroidism
Cancer
237
Name the cancers which can cause hypercalcaemia
Multiple myeloma
Breast cancer
Renal cancer
Ovarian cancer
Endometrial cancer
Squamous cell carcinoma
238
Name the clinical features of hypercalcaemia
Renal stones
Painful bones
Abdominal groans
Psychiatric moans
239
Name the GS investigation of hypercalcaemia
Fasting serum calcium and phosphate
240
What would be seen on a fasting serum calcium and phosphate in hypercalcaemia
Decreased PTH
Decreased calcium
241
Name 2nd line investigations in hypercalcaemia
ECG
24-hour urinary calcium - to exclude familial hypocaloric
242
What would be seen on an ECG of hypercalcaemia
Short QT
243
Name the management of hypercalcemia
1st - rehydration with normal saline
2nd - biphosphates
244
What is the 2 main causes of hypercalcaemia
Hyperparathyroidism or malignancy
245
Define hypocalcaemia
< 8.5 mg/dl
< 2.2 mmol/L
246
What 2 mnemonics can be used for the clinical features of hypocalcaemia
SPASMODIC
CATS GO NUMB
247
Define the mnemonic SPASMODIC
Spasm
Perioral, Parathesis
Anxious
Seizure
Muscle contractions (increased)
Orientation impaired and confusion
Dermatitis
Impetigo herpetiformis
Chvostek's sign/cardiomyopathy
248
Define mnemonic CATS GO NUMB
Convulsions
Arrythmia
Tetany
Spasms/stridor
Numbness in fingers
249
What are the investigations in hypocalcaemia
Low calcium
ECG
250
What would be seen on an ECG of hypocalcaemia
Prolonged QT interval
251
Name the risk factors of hypocalcaemia
Vitamin D deficiency
Thyroidectomy
Hypomagnesemia
Hypoalbuminemia
Hyperphosphatemia
Parathyroid disorder
Family history
252
What is the 1st line management in acute hypocalcaemia
IV calcium gluconate (10mL of 10% solution over 10 mins)
253
What is the management of hypocalcaemia if it persists after 1st line management
Vitamin D supplements
254
What is the main cause of hypocalcaemia
Hypoparathyroidism
255
Name the complications of hypocalcaemia
Seizures
Cardiac arrests
Decreased HR and contractility = medical emergency = low QT syndrome
256
Define hyperkalaemia
Serum > (or equal to) 5.5 mmol/L
257
When is hyperkalaemia severe
serum > (or equal to) 6.5 mmol/L
OR
ECG changes
= emergency
258
Describe the clinical features of hyperkalaemia
Muscle weakness
Numbness + tingling
N&V
Irregular heart rhythm
SOB
Palpitations
Chest pain
Fatigue
259
Describe the ECG changes in hyperkalaemia
Tall tented T waves
Small p waves
Wide QRS
Complex ventricular fibrillation
Sine wave
260
What does a sine wave on an ECG mean
Severe hyperkalaemia
261
Name the risk factors of hyperkalaemia
Renal failure
Diabetes
Adrenal disease
Use of - ACEi, ARBs, potassium sparing diuretics
262
What is the 1st line management in hyperkalaemia if there are ECG changes
Stabilise cardiac membranes
IV calcium gluconate/chloride
It will not lower K+ levels
263
What is the 1st line management in hyperkalaemia if there are no ECG changes
Shift K+ into cells (EC-IC)
Insulin + dextrose + nebulised salbutamol
264
Name the causes of hyperkalaemia
Increased uptake (exogenous)
Increased production (endogenous)
Decreased excretion
Redistribution - shift from intracellular to extracellular
265
Define hypokalaemia
Serum < 3.5 mmol/L
266
Name the clinical features of hypokalaemia
Weakness
Fatigue
Muscle cramps
Constipation
Arrythmias
Leg cramps
Tingling and numbness
267
What is seen on an ECG in hypokalaemia
Small or inverted T waves
Prominent U waves
Long PR interval
Deep ST segments
268
What is severe hypokalaemia
< 2.5 mmol/L
269
What is the treatment of severe hypokalaemia
IV replacement - 40 mmol KCl in IL 0.9 NaCl
270
What is the treatment for mild hypokalaemia
3-3.4 mmol/L
Oral replacement - consider IV
271
Describe the causes of hypokalaemia
Decreased K+ intake
Increased K+ entry into cells
Increased K+ excretion - sweat, urine, Gi tract
Magnesium depletion
Hyperaldosteronism
272
Name the risk factors of hypokalaemia
Bulimia
Hyperhidrosis
Diuretics
Excessive alcohol
Diaorrhea and vomiting
273
Define thyroid storm
Severe end spectrum of thyrotoxicosis characterised by compromised organ function
274
Name the clinical features of thyroid storm
Fever
Cardiovascular dysfunction
Profuse sweating
Tachycardias
N&V
275
What would be the investigation findings in thyroid storm
Free T4 (thyroxine)
TSH completely supressed
276
What is the GS management for thyroid storm
Thyroidectomy
277
What is 2nd line management of thyroid storm
Antithyroid treatment - carbimzaole + hydrocortisone
278
What are the risk factors of thyroid storm
Untreated hyperthyroidism
Damage to thyroid gland
Infections
Surgery
Trauma
Stroke
279
What is the 1st line medical management of T2DM
Metformin
+ (if at high risk of CVD) SLGT-2 inhibitor
280
What is the 2nd line management of T2DM
Add one of the 4
GLP-1 inhibitors
SGLT2-inhibitors
Sulfonylurea
Pioglitazone
281
What is the 3rd line management of T2DM
Add another of the 2nd line drugs
or
start insulin based treatment
282
What is the 4th line management of T2DM
If triple therapy not effective
Switch one of the GLP-1 mimetic
283
When would insulin be contradicted in the treatment of T2DM
if BMI > (or equal to) 35 kg^2 would have occupational implications
284
What is the mnemonic used to remember the treatment of DKA
FIG PICK
285
Describe FIG PICK
Treatment of DKA
Fluids first - 3L in 1st 3 hours
Insulin - sliding scale
Glucose (dextrose) + insulin
Potassium
Infection
Chart fluid balance
Ketone monitoring
286
What is a risk factor in the management of DKA
Risk of cerebral oedema - due to rapid fluid replacement
287
Why is dextrose given in the management of DKA
Risk of hypo
288
Why is potassium given in the management of DKA
insulin caused K+ into cells - cause hypokalaemia (levels must be checked)
289
Define the values of pre-diabetes
42-47 mmol/mol
Fasting 6.1-6.9 mmol/L
290
What is the aim of HbA1c in diabetes
48%
Measured every 6 months
291
Name the risk factors of hypoglycaemia
Long duration diabetes
Increased age
Use of drugs - prescribed/alcohol
Sleeping
Increase in physical activity
292
When may hypoglycaemia be caused when not below 3.9 mmol/L
If poor glycaemic control may be experiences at > 3.9 mmol/L
293
When is hypoglycaemia screened for
In those at high risk
294
Name the risk factors of hyperosmolar hyperglycaemic state
Type 2 diabetes
65+
Infection
Illness
Heart failure
Stroke
Trauma
Medications
Poor diabetes control
295
Define hyponatraemia
< 135 mmol/L serum sodium
Severe < 120 mmol/L
Acute < 48 hours or chronic
296
Name the symptoms of hyponatraemia
Anorexia
Headache
N&V
Lethargy
Ataxia
Seizures
Cerebral oedema
297
Name the signs of hyponatraemia
Cognitive impairment
Drowsiness
Signs of seizures
298
Name the risk factors of hyponatraemia
Older age
Medications e.g. diuretics, antidepressants
CKD
Heart disease
SIADH
Extreme physical activity
Warmer climates
299
What is the GS investigation for hyponatraemia
U&E
300
Name potential investigations for hyponatraemia
Bloods/urine - identify cause
Urine osmolality = confirm diagnosis of SIADH
Urine sodium - renal vs extrarenal causes
301
How is serum osmolality calculated
2Na + Glu + Urea (all in mmol/L)
302
What is the management of hyponatraemia
IV hypertonic saline bolus with close monitoring of serum sodium
No more than 6 mmol/L in 6 hours
No more than 10 mmol/L in 1st 24 hours
303
What is the most common electrolyte abnormality
Hyponatremia
304
How can hyponatraemia be a life threatening condition
Due to cerebral fluid shift
305
Name 3 causes of hyponatraemia
Hypovolaemic - dehydrated
Hypervolemic - overloaded
Euvolemic
306
Define hypernatremia
Serum sodium > 146 mmol/L
Severe > 160 mmol/L
307
Name the symptoms of hypernatremia
Excessive thirst
Extreme fatigue
Lack of energy
Confusion
308
Name the signs of hypernatremia
Muscle twitching or spasm
Restlessness
Seizures
309
Name the risk factors of hypernatremia
Advanced age
Medications
CKD
SIADH
Extreme physical activity
310
What is the GS investigation for hypernatremia
U&E
311
Name extra investigations you could do in hypernatremia
Blood test
Urine osmolality
Clinical history
Venous blood gas
312
Describe the management of hypernatremia
Iv hypotonic fluids without sodium
313
Describe the correction of hypernatremia
Should not be corrected
> 0.5 mmol/L per hour
OR
> 10 mmol in 24 hours
Check sodium within 2-4 hours of initiating treatment
314
What is the most common cause of hypernatremia
Dehydration
315
What is a side effect of rapid correction of hypernatremia
Intracerebral fluid shift
316
Define pheochromocytoma
Tumour of the adrenal glands that secrete unregulated and excessive amounts of catecholamine (adrenaline)
317
Describe how signs and symptoms of pheochromocytoma present
Fluctuate relating too when tumour is secreting
318
Name the symptoms of pheochromocytoma
Anxiety
Headache
Palpitations
319
Name the signs of pheochromocytoma
Hypertension
Tachycardia
Tremor
Sweating
320
Name the risk factors of pheochromocytoma
MEN 2
Neurofibromatosis type 1
Von Hippel-Lindae disease
321
What is the 1st line investigation of pheochromocytoma
Plasma free metanephrilnes
24-hour urine catecholamines
322
Why is serum catecholamine or adrenaline not measured in pheochromocytoma
Unreliable
Levels fluctuate
323
Name 2 other investigations other than 1st line which can be used in the investigation of pheochromocytoma
CT or MRI - for tumour
Genetic testing
324
What is GS management of pheochromocytoma
Surgically remove tumour
Control symptoms medically before surgery to reduce risks
325
What medications can be used in pheochromocytoma
Alpha blockers e.g. phenoxybenzamine or doxazosin
Beta blockers - only once established on alpha blockers
326
Describe the pathophysiology of pheochromocytoma
Tumour of chromaffin cells (in medulla) secrete unregulated and excessive amounts of adrenaline
Tends to be secreted in bursts
