Endocrinology Flashcards
(126 cards)
1
Q
What is diabetes mellitus?
A
A disorder of carbohydrate metabolism characterised by hyperglycaemia
2
Q
What glucose levels define diabetes mellitus?
A
- Symptoms and random plasma glucose > 11 mmol/l
- Fasting plasma glucose > 7 mmol/l
- No symptoms: OGTT (glucose tolerance) (75g glucose) fasting > 7mmol/l or 2h value > 11 mmol/l (repeated on 2 occasions)
= HbA1c of > 48mmol/mol (6.5%)
3
Q
How is carbohydrate metabolism regulated in non diabetics?
A
- all glucose comes from liver (and a bit from kidney) either from breakdown of glycogen or gluconeogenesis
- Glucose delivered to insulin independent tissues, brain and red blood cells
- If insulin levels are low, muscle uses FFA for fuel
4
Q
What happens to glucose after feeding?
A
- Glucose stimulates insulin secretion and suppresses glucagon
- 40% of ingested glucose goes to liver and 60% to periphery, mostly muscle
- glucose replenishes glycogen stores in liver and muscle
- High insulin and glucose levels suppress lipolysis and levels of non-esterified fatty acids (FFA) fall
5
Q
What is the pathogenesis of T1DM?
A
- insulin deficiency characterised by loss of β cells due to autoimmune destruction
- may be triggered by viral infection
6
Q
What is the pathophysiology of T1DM?
A
- GLUT4 transporters require insulin to take up glucose from the blood and use it for fuel
- no insulin produced so glucose remains in blood
- cells think the body is being fasted so blood glucose levels keep rising causing hyperglycaemia
7
Q
What are the risk factors for T1DM?
A
- genetic predisposition
- northern European
- HLA DR3 or HLA DR4 human leukocyte antigens
8
Q
What are some signs and symptoms of T1DM?
A
- manifests in childhood and commonly presents with DKA
- polyuria
- polydypsia
- sudden unexplained weight loss
9
Q
Why is weight loss a sign/symptom of T1DM?
A
- Excess fluid depletion and accelerated breakdown of fat and muscle due to insulin deficiency.
- More common in T1DM as there is complete insulin deficiency so lipolysis and proteolysis occur more quickly
- No glucose can enter cells in T1 but insulin is still produced in T2
10
Q
What is the management of T1DM?
A
- monitoring dietary carbohydrate intake and monitoring blood sugar levels
- Subcutaneous insulin prescribed: background long acting insulin taken once a day and short acting insulin injected 30 mins before intake of carbs at meals
11
Q
What are the criteria for DKA?
A
- ketoacidosis: blood ketones > 3mmol/l
- hyperglycaemia: blood glucose > 11mmol/l
- acidosis pH < 7.3
12
Q
What is the aetiology of DKA?
A
- untreated/undiagnosed T1DM
- infection/illness
13
Q
What is ketoacidosis?
A
uncontrolled catabolism associated with insulin deficiency
14
Q
What is the pathophysiology of DKA?
A
- Insulin absence > unrestrained gluconeogenesis and dec peripheral glucose uptake > hyperglycaemia as higher blood glucose
- Hyperglycemia > osmotic diuresis > more water in urine > dehydration and electrolyte loss
- Peripheral lipolysis for energy > inc in circulating FFAs > oxidised to Acetyl CoA > ketone bodies (acidic) = Acidosis
15
Q
How does DKA present?
A
- Nausea + Vomiting
- dehydration > can cause hypotension
- Abdominal pain
- acetone breath smell
- lethargy
- respiratory compensation for acidosis leading to hyperventilation (Kussmaul breathing)
16
Q
Why is insulin treatment for DKA dangerous?
A
- Insulin decreases blood potassium levels by redistributing K+ via the sodium-potassium pump
- this causes low serum K+ leading to hypokalaemia
- can lead to arrhythmia, weakness
17
Q
How is DKA diagnosed?
A
- recognised from the clinical features
- confirmed by blood glucose and ABG
- U&E: raised due to dehydration
- urine dipstick - glycosuria and ketonuria
18
Q
How is DKA managed?
A
- ABC if unconscious
- fluid loss replaced with IV 0.9% saline
- give insulin and glucose (inhibits gluconeogenesis and therefore ketone production
- restore electrolytes
- treat underlying triggers e.g. infection
19
Q
What is a possible complication of DKA and why?
A
- cerebral oedema
- the blood is initially very concentrated with high salt levels and is rapidly diluted
- osmotic shifts occur and water moves from the blood into tissues
- causes swelling of the brain
20
Q
What is the definition of type 2 diabetes?
A
A progressive disorder characterised by inc insulin resistance and impaired insulin secretion due to a combination of genetic predisposition and environmental factors
21
Q
What is the aetiology of type 2 diabetes?
A
- age
- obesity
- family history
- genetics: determines whether or not you develop the disease, lifestyle factors determine when. genetic link stronger than in T1DM
22
Q
What is the epidemiology of type 2 diabetes?
A
Mainly found in Asians, men, elderly. Mostly in over 40s but prevalence increasing in teenagers
23
Q
What are the risk factors for type 2 diabetes?
A
smoking, obesity, hypertension, sedentary lifestyle, age, ethnicity, family history
24
Q
What is the pathophysiology of type 2 diabetes?
A
- Repeated exposure to glucose and insulin leads to insulin resistance > more insulin needed to produce response from cells for glucose uptake.
- β cells become fatigued and damaged > produce less insulin
- insulin resistance and pancreatic fatigue leads to chronic hyperglycaemia
25
What are the signs and symptoms of T2DM?
- polyuria
- polydypsia
- opportunistic infection
- slow healing
- lethargy
- glucose in urine (glycosuria)
- blurred vision
26
Why are polyuria and glycosuria symptoms of diabetes?
- glucose draws water into the blood by osmotic diuresis
- high levels of glucose in the blood and not enough glucose can be reabsorbed as kidneys have reached the renal maximum reabsorptive capacity of glucose.
- leads to excessive levels of glucose and water being excreted
27
What are the microvascular complications associated with diabetes?
- diabetic retinopathy > visual loss,
- nephropathy > end stage renal disease
- neuropathy > foot ulcers and amputation
28
What are the macrovascular complications associated with diabetes?
- stroke
- CVD/MI
29
What is the gold standard test for T2DM?
- HbA1c test > tells average blood glucose levels over the past 3 months
- > 48mmol/mol = diabetes
- >42-47 mmol/mol= pre-diabetes
30
What is 1st line management for T2DM?
- dietary changes, higher in complex carbs, low in fat and sugar
- smoking cessation and dec alcohol
- inc exercise
- blood glucose and HbA1c monitoring
31
What is 2nd line management for T2DM?
- metformin: inc insulin sensitivity
- if HbA1c remains high then add in either:
DPP4 inhibitor, sulphonylurea or thiazolidinedione
- if still high then add in insulin
32
What is the action of metformin?
- inc peripheral insulin sensitivity, decreases liver production of glucose
- reduces insulin resistance by modifying the glucose metabolic pathways
- lowers blood glucose levels
33
What is the action of sulphonylureas?
- stimulate insulin release by binding to β cell receptors
- don't prevent failure of insulin secretion and can cause hypoglycaemia
34
What is the action of thiazolidinediones?
- activate genes concerned with glucose uptake, utilisation and lipid metabolism
- improve insulin sensitivity but need insulin for a therapeutic effect
- can inc weight, risk of heart failure and fractures
35
Describe the pathogenesis of acromegaly
- Commonly caused by excess release of growth hormone from pituitary tumour
- GH binds to receptor in liver causing release of insulin-like growth factor 1 (IGF-1)
- IGF-1 stimulates soft tissue and skeletal overgrowth
36
What is the relationship between IGF-1, somatostatin and GH?
IGF-1 stimulates the release of somatostatin which inhibits GH production from the hypothalamus
37
What are some signs of acromegaly?
- prominent forehead and brow
- large hands, nose, feet, tongue
- bitemporal hemianopia (pressure on optic chiasm)
- profuse sweating
- larger jaw
- wide spaced teeth
38
What are some symptoms of acromegaly?
- headaches
- arthritis due to bony overgrowth
- fatigue
- carpal tunnel syndrome
39
What is the gold standard investigation for acromegaly?
OGTT: normally GH is inhibited by a rise in glucose, so should be undetectable but GH release is unsuppressed in acromegaly
40
What is the 1st line investigation for acromegaly?
IGF-1 test, levels will be increased correlating with increased levels of GH
41
What is the management of acromegaly?
- surgical removal of pituitary adenoma via transsphenoidal surgery
- if surgery isn't appropriate then:
- somatostatin analogues to block GH release
- GH receptor antagonists
- dopamine agonists which suppress GH
- radiotherapy
42
What are common complications of acromegaly?
- insulin resistant diabetes
- htn and heart disease
- cerebrovascular events
- arthritis
- sleep apnoea
43
What is hypothyroidism?
A clinical syndrome resulting from the deficiency of thyroid hormones resulting in a slowing of metabolic processes
44
What is the epidemiology of hypothyroidism?
- way more common in women than men
- mean age of diagnosis around 60
45
What is the aetiology of hypothyroidism?
- Hashimoto's thyroiditis
- iodine deficiency
- medications for hyperthyroidism (carbimazole)
- lithium and amiodarone
46
Describe the pathophysiology of Hashimoto's thyroiditis
- autoimmune destruction by cell and antibody mediated processes
- formation of antithyroglobulin and antithyroid peroxidase (anti-TPO) antibodies that attack the thyroid tissue causing progressive fibrosis
47
Describe the pathophysiology of hypothyroidism
- 1º hypothyroidism: in peripheral thyroid disorder, T3 or T4 isn't produced and to compensate, TSH levels rise
- 2º hypothyroidism: pituitary disorder causes decreased TSH levels which leads to lowered T3/T4 levels
48
Describe the presentation of hypothyroidism
- Weight gain
- Depression/low mood
- Menstrual disturbance
- Fatigue
- Muscle cramps
- Cold intolerance
Presentation
- bradycardia
- goitre
- slow reflexes
49
What investigations are done for hypothyroidism, what are the relevant TSH, T3 & T4 levels and where does the problem lie according to these levels?
- thyroid function tests (TFTs)
- High TSH and Low T3/T4 = 1º hypothyroidism = thyroid
- Low TSH and Low T3/T4 = 2º hypothyroidism = pituitary
- can check for elevated TPO levels indicating autoimmunity
50
How is hypothyroidism managed?
- Replacement of thyroid hormone by levothyroxine
- is synthetic T4 that metabolises to T3 in the body
- If TSH is too low then the dose needs to be increased and vice versa
51
What is the difference between hyperthyroidism and thyrotoxicosis?
- hyperthyroidism: overproduction of thyroid hormone by the thyroid gland
- thyrotoxicosis: excessive T3 + T4 in circulation
52
Describe the aetiology of hyperthyroidism
- Grave's disease
- iodine excess
- toxic multinodular goitre
- thyroiditis
53
Describe the pathophysiology of hyperthyroidism
- High T3 AND T4, low TSH
- 1º: thyroid producing excess thyroid hormone
- 2º: thyroid producing excess due to overstimulation by TSH - pathology in hypothalamus or pituitary
54
How does hyperthyroidism present?
- Weight loss
- feverish
- tachycardia
- anxiety
- heat intolerance
- diarrhoea (inc bowel metabolism)
- menstrual disturbance
- everything increases
55
How is hyperthyroidism managed?
- 1st line: anti-thyroid drug: carbimazole
- 2nd line: propylthiouracil
- radioiodine therapy: radioactivity destroys thyroid cells
- β blockers
- surgery
56
What is Grave's Disease?
- autoimmune condition
- TSH receptor antibodies cause primary hyperthyroidism
- abnormal antibodies produced by the immune system that mimic TSH and stimulate the TSH receptors on the thyroid
57
What is the difference between Cushing's syndrome and Cushing's disease?
- Cushing's syndrome: signs and symptoms which develop after prolonged, abnormal elevation of cortisol
- Cushing's disease: a pituitary adenoma secretes excessive ACTH
- Cushing's disease can cause Cushing's syndrome but the syndrome isn't always caused by the disease
58
What is the aetiology + epidemiology of Cushing's?
- ACTH independent: iatrogenic e.g. steroids (most common) or adrenal adenoma
ACTH dependent: Cushing's disease (most common dependent) or ectopic ACTH (small cell lung/neuroendocrine tumour
- more likely in women
59
What is the presentation of Cushing's?
- round moon face
- central obesity
- abdominal striae
- proximal limb muscle wasting
- fat pad on upper back
- hypertension
- hyperglycaemia
- depression
- insomnia
60
What is the investigation of Cushing's?
- 1st line: raised plasma cortisol
- CT/MRI for tumours
- Low dose dexamethasone test initially
61
What is the low dose dexamethasone test?
- patient takes 1mg at night and cortisol and ACTH are measured in the morning
- normal: dexamethasone suppresses cortisol release by -ve feedback on hypothalamus and pituitary
- hypothalamus reduces CRH, pituitary reduces ACTH
- Cushing's: cortisol not suppressed
62
What is high dose dexamethasone test?
- 8mg dexamethasone
- low cortisol: Cushing's disease
- High cortisol, low ACTH: Adrenal Cushing's
- High cortisol, high ACTH: ectopic ACTH
63
What is the management of Cushing's?
- transsphenoidal removal of pituitary adenoma
- surgical removal of adrenal tumour or tumour producing ectopic ACTH
- iatrogenic: stop steroids
64
What is primary adrenal insufficiency and what is it caused by?
- Also called Addison's disease
- adrenal glands are damaged
- cortisol and aldosterone production impaired
- autoimmune or caused by TB
65
What is secondary adrenal insufficiency and what is it caused by?
- damage to or loss of the pituitary gland
- inadequate ACTH stimulating adrenals
- leads to low cortisol release
66
What is tertiary adrenal insufficiency and what is it caused by?
- results from inadequate CRH release from the hypothalamus
- iatrogenic: long term use of steroids (+ 3 weeks) > hypothalamus suppression
- sudden steroid withdrawal doesn't allow hypothalamus to regain normal functioning
67
How does adrenal insufficiency present?
- Fatigue
- Vitiligo
- Abdo pain + nausea
- postural hypotension (dec aldosterone)
- hyperpigmentation
68
In which type of adrenal insufficiency does hyperpigmentation present and why?
- In primary
- ACTH stimulates melanocytes to produce melanin
- hyperpigmentation seen in palmar creases
69
How is Addison's investigated?
- Gold standard: Short synacthen: give patient synacthen (synthetic ACTH) in morning (9am)
- failure of cortisol to rise after 30 mins indicates Addison's
- U&E > hyponatraemia, hyperkalaemia,
- low glucose
70
How is Addison's managed?
- hydrocortisone to replace cortisol
- fludrocortisone to replace aldosterone > inc Na and dec K to correct postural hypotension
- double dose in acute illness for stress response
71
What is SIADH?
- syndrome of inappropriate ADH
- condition where there are inappropriately large amounts of ADH
72
What is the pathophysiology behind SIADH?
- ADH produced in hypothalamus and secreted by posterior pituitary
- Stimulates water reabsorption in collecting ducts
- water dilutes sodium > hyponatraemia
- leads to euvolaemic hyponatraemia (normal body sodium, inc in total body water)
- patients have high urine osmolality and high urine sodium
73
What is the aetiology of SIADH?
- iatrogenic: post operative/medication (SSRIs, NSAIDs, carbamazepine)
- infection e.g. pneumonia, lung abcess
- head injury
- meningitis
- ectopic production of ADH e.g. from small cell lung
74
How does SIADH present?
- nausea + vomiting
- headache
- fatigue
- muscle aches and cramps
- confusion
- mild/severe hyponatraemia (115-125/<115mmol/L)
75
How is SIADH investigated?
- diagnosis of exclusion
- clinical exam: euvolaemia
- U&E: hyponatraemia
- urine sodium and osmolality: high
- serum osmolality: low
76
How is SIADH managed?
- stop the cause (if meds)
- fluid restriction: 0.5-1L
- Tolvaptan: ADH receptor blocker > causes inc in sodium levels
77
What is nephrogenic diabetes insipidus and what are some causes?
- Collecting ducts don't respond to ADH
- lithium
- mutations in gene coding for ADH receptor
- electrolyte disturbance
78
What is diabetes insipidus?
- lack of ADH (cranial) or lack of response to ADH (nephrogenic)
- prevents kidneys being able to concentrate urine > polyuria or polydipsia
79
What is cranial diabetes insipidus and what are some causes?
- hypothalamus doesn't produce ADH
- idiopathic
- brain tumour, infection, surgery, head injury
80
How does diabetes insipidus present?
- polyuria
- polydipsia
- dehydration
- postural hypotension (BP drops on standing after sitting/lying down)
- hypernatraemia
- nocturia: waking in night to urinate
81
How is diabetes insipidus investigated?
- low urine osmolality
- high serum osmolality
- water deprivation test (gold standard)
82
What is the water deprivation test?
- patient avoids taking in fluids for 8hrs
- urine osmolality measured and desmopressin administered
- urine osmolality measured 8hrs later
- in CDI > urine osmolality: low > high
- in NDI > urine osmolality: low > low
83
How is diabetes insipidus managed?
- treat underlying cause
- desmopressin (synthetic ADH)
84
What is prolactinoma?
- lactotrophs in anterior pituitary produce and release prolactin
- type of pituitary adenoma
- presents most in biological females aged 20-40
85
What is the pathophysiology of prolactinoma?
- hypersecretion of prolactin causes secondary hypogonadism > due to inhibitory effects on GnRH
86
How does prolactinoma present in females and why?
- decreased release of GnRH > decrease in LH and FSH > decrease in oestrogen and progesterone
- amenorrhoea or oligomenorrhoea
- infertility
- galactorrhoea
- low libido
87
How does prolactinoma present in males and why?
- decreased release of GnRH > decreased testosterone
- low testosterone
- erectile dysfunction
- reduced facial hair
- low libido
- can have galactorrhoea
88
How is prolactinoma investigated?
- serum prolactin levels
- pituitary MRI to detect adenoma
89
How is prolactinoma managed?
- 1st line: dopamine agonists e.g. oral bromocriptine
- dopamine inhibits prolactin and shrinks the prolactinoma
- 2nd line: HRT e.g. oestrogen (if fertility and galactorrhoea aren't issues
90
What is Conn's syndrome?
- primary hyperaldosteronism
- excess of aldosterone
- serum renin is low as it is suppressed by high bp
91
What is the aetiology of primary hyperaldosteronism?
- Adrenal adenoma (only actual cause of Conn's, others are hyperaldosteronism)
- bilateral adrenal hyperplasia
92
What is secondary hyperaldosteronism and its aetiology?
- excessive renin stimulating adrenal glands to produce more aldosterone
- serum renin is high
- renal artery stenosis/obstruction
- heart failure
93
How does Conn's present?
- often asymptomatic
- hypertension (Conn's + hyperaldosteronism are usually indistinguishable unless measuring renin + aldosterone)
- headaches
- hypokalaemia (excretion of K+)
- weakness, cramps, polyuria, polydipsia, thirst
94
How is Conn's investigated?
- high aldosterone, low renin = 1º
- high aldosterone, high renin = 2º
- CT/MRI to look for adrenal mass
- selective adrenal venous sampling (gold)
95
How is Conn's managed?
- aldosterone antagonists to control BP and low K+ e.g. Spironolactone
- adrenalectomy
- percutaneous renal artery angioplasty for 2º hyperaldosteronism
96
What is the physiology of the parathyroid?
- 4 parathyroid glands
- chief cells produce PTH
- PTH increases serum Ca by:
- inc osteoclast activity, Ca reabsorption in kidney, vit D activity > more Ca absorbed in intestines
97
What is primary hyperparathyroidism?
- uncontrolled parathyroid hormone produced by a tumour of the parathyroid gland
- leads to hypercalcaemia
- treated by surgical removal of the tumour
98
What is secondary hyperparathyroidism?
- insufficient vitamin D or chronic renal failure leads to low calcium absorption
- causes hypocalcaemia
- more PTH excreted in response to low serum calcium
- leads to hyperplasia of glands
- therefore, low/normal serum calcium and high PTH
- management: treat vit D deficiency/renal transplant
99
What is tertiary hyperparathyroidism?
- 2º continues for a long time
- hyperplasia of glands so PTH baseline increases dramatically
- PTH levels remain high even after 2º is treated
- high PTH and absent previous pathology > high calcium absorption + hypercalcaemia
- treated by surgical removal of PTH tissue
100
What is the presentation of hyperparathyroidism?
- hypercalcaemia: stones, bones, groans, moans
- renal stones
- painful bones
- groans: constipation, nausea, vomiting
- moans: fatigue, depression, psychosis
101
How is hyperparathyroidism investigated?
- bones: DEXA scan for osteoporosis
- stones: ultrasound
- groans: abdo X-ray
- moans: radioisotope scanning for adenoma
102
What is hypokalaemia and how is it caused?
- low serum potassium
- dec potassium intake, dec entry into cells, inc excretion through sweat, urine, GI, hyperaldosteronism
103
What is the hyperosmolar hyperglycaemic state (diagnosis criteria)?
- life-threatening emergency characterised by:
- hyperglycaemia: ≥30mmol/L
- hyperosmolality: ≥320mOsm/kg (due to inc serum glucose and potassium
- no ketoacidosis
104
What is the pathophysiology behind hyperosmolar hyperglycaemic state?
- some insulin still produced by pancreas
- sufficient to inhibit hepatic ketogenesis (preventing ketogenesis)
- insufficient to inhibit hepatic glucose prod
- leads to osmotic diuresis, loss of Na and K
- hyper viscosity of blood + volume depletion
105
What is the presentation of the hyperosmolar hyperglycaemic state?
- dehydration, polyuria, polydypsia
- lethargy, nausea, vomiting
- altered level of consciousness (low GCS)
- focal neurological deficits
- hyperviscoscity
106
How is the hyperosmolar hyperglycaemia state managed?
- fluid replacement: IV 0.9% NaCl solution
- insulin: should NOT be given unless blood glucose falls while giving IV fluids
- venous thromboembolism prophylaxis
107
What is pheochromocytoma?
- neuroendocrine tumour of the chromatin cells in the medulla of the adrenal glands
- secretes large quantities of the catecholamine hormones noradrenaline and adrenaline
- stimulates the SNS and fight or flight response
108
What is the presentation of pheochromocytoma?
- anxiety
- sweating
- headache
- htn
- palpitations, tachycardia, paroxysmal AF
109
How is pheochromocytoma diagnosed and managed?
- 24hr urine catecholamines
- plasma free metanephrines: breakdown product of adrenaline with a longer half life
- α blockers first (phenoxybenzamine), β blockers, surgical management is definitive
110
What are the causes and pathophysiology behind hyperkalaemia?
- Causes: AKI, spironolactone, Addison's, DKA
- inc K+ decreases action potential threshold leading to easier depolarisation and abnormal heart rhythms
111
How is hyperkalaemia diagnosed?
- high K+ on U&Es
- serum potassium >5.5mmol/L
- ECG: absent P wave, prolonged PR interval, tall T waves, widened QRS complex
112
How is hyperkalaemia treated?
- urgent: calcium gluconate to stabilise the cardiac membrane then insulin and dextrose
113
What are differential diagnoses for hyperkalaemia?
- CKD, DKA, HHS
- uncommon: AKI, Addison's
114
How is hypoparathyroidism diagnosed and treated?
- decreased PTH, decreased Ca2+, inc phosphate and long QT
- treatment: calcium supplements and vit D3
115
What is the presentation of hypoparathyroidism/hypocalaemia?
- Cats go numb: convulsions, arrhythmias, tetany (involuntary muscle contraction), numbness in hands, feet and around mouth
- Chvostek's sign: facial spasm when tapping over CN7
- Trousseau's sign: carpopedal spasm
- calcium <8.5mg/dL
116
What are the causes of hypoparathyroidism?
- 1º: DiGeorge and idiopathic
- 2º: surgical
117
What is the role of ghrelin?
- stimulates hunger
- produced by P/D1 cells in stomach and epsilon cells in pancreas
- levels inc before meals and dec after meals
118
What is the role of leptin?
- regulates body weight
- produced by adipose tissue so more adipose = more leptin
- acts on satiety centres in hypothalamus and decreases appetite
- stimulates release of melanocyte-stimulating hormone and CRH
119
How is obesity managed?
- conservative: diet + exercise
- Orlistat: pancreatic lipase inhibitor
- Liraglutide: glucagon-like peptide-1 (GLP-1) used in T2DM
120
How is hypercalcaemia managed?
- rehydration with saline and bisphosphonates
- calcitonin
- steroids if sarcoidosis
121
What is the cause of hypercalcaemia?
- primary hyperparathyroidism
- malignancy: PTHrP from tumours, bone metastases or myeloma
- sarcoidosis, acromegaly, thyrotoxicosis
122
What is the definition of hypoglycaemia?
- glucose below the normal fasting glucose levels
- blood glucose levels below 3 mmol/L
123
What is the pathophysiology behind hypoglycaemia?
- when glucose is taken up by cells, blood glucose levels drop
- this stimulates α islet cells to produce glucagon and reduces the production of insulin
- glucagon increases liver gluconeogenesis and glycogenolysis
- production of adrenaline, GH, cortisol
- interruption of one or more mechanisms causes hypoglycaemia
124
What are the symptoms of hypoglycaemia?
- sweating, shaking, hunger, anxiety, nausea
- weakness, vision changes, confusion, dizziness
125
How is hypoglycaemia treated?
- oral glucose
- IM/SC injection of glucagon
- IV 20% glucose solution last resort hospital setting
126
What is De Quervain's thyroiditis?
- subacute granulomatous thyroiditis
- occurs post viral infection
- presents with hyperthyroidism
- treated with NSAIDs
