Endocrine Flashcards
(179 cards)
1
Q
What is type 1 diabetes?
A
autoimmune destruction of the beta cells in the pancreas that produce insulin so there is an absolute deficiency in insulin and persistent hyperglycaemia state
2
Q
What are the risk factors for type 1 diabetes?
A
genetic predisposition
family history of autoimmunity e.g. thyroid disease, Addisons, coeliac, pernicious anaemia, vitiligo
3
Q
How does type 1 diabetes present?
A
- poluria
- polydipsia
- weight loss
- prolonged tiredness
+ blurred vision, increased skin infections, acutely unwell in DKA
4
Q
How is type 1 diabetes clinically diagnosed in adults and children?
A
ADULTS: hyperglycaemia + >1 of ketosis, weight loss, <50 y/o, BMI <25, FH of autoimmunity
CHILDREN: hyperglycaemia + polyuria/ polydipsia / weight loss/ tiredness
5
Q
How is type 1 diabetes diagnosed by hyperglycaemia?
A
random blood glucose >11.1 mol/l
fasting blood glucose >7 mmol/l
HbA1C >48
or urine dip (glucose ++)
6
Q
What are the microvascular complications of diabetes?
A
- RETINOPATHY - cataracts, diabetic maculopathy, glaucoma
- NEUROPATHY - “glove and stocking” distribution of peripheral neuropathy, vibration first sense to lose
- NEPHROPATHY - leads to HTN and CKD
7
Q
What are the macrovascular complications of diabetes?
A
- CARDIOVASCULAR DISEASE - high risk
- CEREBROVASCULAR DISEASE - stroke risk
- PERIPHERAL ARTERIAL DISEASE - cause “diabetic foot” , ulcers
8
Q
Apart from micro/macro vascular, what are the other complications of diabetes?
A
- autonomic dysfunction - ED, bladder retention, postural hypotension, diarrhoea, autonomic gastroparesis
- increased risk of infections e.g. vaginal thrush
- metabolic complications e.g. hypo, DKA, hyperosmolar lipidaemia, metabolic syndrome, dyslipidaemia
- psychological effects - depression, reduced QoL, eating disorders , anxiety
- other autoimmune conditions - coeliac, Addisons, vitiligo, pernicious anaemia, RA
9
Q
How is type 1 diabetes managed with medication?
A
INSULIN THERAPY
- need mix of short acting insulin (novorapid, actrapid) and long acting insulin (detemir)
- SE: weight gain, hypoglycaemia, lipodystrophy
- individual care plan
10
Q
What should be told to a type 1 diabetic when managing their care?
A
- attend DAFNE course (insulin education)
- testing random blood glucose 4 x a day and before each meal and before bed
- more frequent management if ill, exercise, stress, during pregnancy
11
Q
What is a type 1 diabetics target for blood glucose?
A
on waking up: 5-7 mmol/l
before meals and throughout the day: 4-7 mmol/l
12
Q
What is included in the annual review of type 1 diabetics?
A
- HbA1C (every 3-6 months) - target <48 mmol/l
- Blood pressure
- U&E
- ophthalmology eye check
- foot check
- assess for depression
- inspect injection sites
13
Q
What is defined as hypoglycaemia?
A
blood glucose < 4mmol/l
14
Q
List the risk factors for hypoglycaemia?
A
too much insulin
missed a meal / too few carbohydrates
unplanned exercise
15
Q
How does hypoglycaemia present?
A
sweating trembling anxious agitated/ restlessness pallor confused nausea drowsy blurred vision weakness
16
Q
How is hypoglycaemia managed?
A
- give 15g starchy carbohydrates / sugary drink
- repeat blood sugar in 15 minutes
- if still low and symptomatic, glucagon injection IM
17
Q
What is diabetic ketoacidosis?
A
- decreased insulin
- reduced uptake of glucose into the cells
- hyperglycaemic state
- osmotic diuresis -> potassium depletion
- increased protein catabolism
- increased lipolysis -> excess of free fatty acids -> converted to ketone bodies
18
Q
List the risk factors for ketoacidosis?
A
I - insulin missed
I - infection
I - intoxication
I - infarction/ ischaemia (MI)
+ pregnancy, surgery, periods, drugs (illegal, steroids)
19
Q
How does diabetic ketoacidosis present?
A
abdominal pain, nausea and vomiting polyuria, polydipsia confusion, loss of consciousness Kussmaul breathing acetone breath
20
Q
How is diabetic ketoacidosis confirmed?
A
- high plasma ketones >3mmol/L
- hyperglycaemia - plasma glucose >7 mmol/L
- metabolic acidosis
- urine dip: ketone ++, glucose ++
21
Q
How is diabetic ketoacidosis managed?
A
- ABCDE
- IV fluids - 1L 0.9% saline in first hour -> 1L 0.9% saline with KCL over next 2 hours
- IV insulin 0.1 unit/kg/ hr + potassium
- once glucose <15 mmol/L, infusion of 5% dextrose added
22
Q
What is type 2 diabetes?
A
insulin resistance and insulin deficiency caused by destruction of beta cells in the pancreas
23
Q
List the risk factors for type 2 diabetes?
A
family history obesity sedentary lifestyle high calorific diet ethnic group - south asians, afro Caribbean hypertension PCOS history of gestational diabetes
24
Q
When is pre diabetes diagnosed and how is it managed?
A
if HbA1c 42-47, then diabetes is likely to develop in the next few years
“Impaired Glucose Tolerance “ confirmed by oral glucose tolerance test of 7.1 - 11.1 mmol/l
offer lifestyle advice: weight loss, reduce sugar in diet, exercise, smoking cessation, managed hypertension
25
How does type 2 diabetes present?
often incidental finding and symptoms less obvious
polyuria
polydipsia
tiredness
weight loss
recurrent/ prolonged infection and healing
26
When Is type 2 diabetes diagnosed?
random plasma glucose > 11mmol/l
| HbA1C >48 mmol/l
27
How is type 2 diabetes managed in terms of lifestyle and advice?
1. lifestyle: weight loss, reduce sugar in diet, exercise, manage BP, statin if cV risk
2. DESMOND course
3. blood glucose control: aim for 4-7 fasting glucose, HbA1C measured every 3-6 months
28
What is 1st line treatment for type 2 diabetes? (+ mechanism and side effects)
METFORMIN
= increases insulin sensitivity
SE: GI upset, lactic acidosis, impaired renal function
29
if metformin ineffective, what is added for dual therapy?
SULFONYLUREA e.g. gliclazide
= increases the amount of insulin produced by the pancreas
SE: weight gain, hypoglycaemia, peripheral neuropathy
aim: HbA1C <53 mmol/mol
30
What are 3rd line options in type 2 diabetic management?
PIOGLITAZONE
= increases insulin sensitivity
SE: weight gain, bladder cancer, osteoporosis , fluid retention (caution in HF)
DPP4 INHIBITORS e.g. gliptins
= increases incretin levels and inhibits glucagon secretion to increase insulin (decrease appetite)
SE: GI upset, flu like symptoms
31
if triple therapy is not tolerated/ ineffective in type 2 diabetes, what is used?
insulin therapy
indicated if BMI <35 and triple therapy ineffective
SE: weight gain, hypoglycaemia, lipodystrophy
32
What are the risk factors for hyperosmolar hyperglycaemic state?
```
infection
MI
dehydration
thiazide and loop diuretic
poor control
elderly
```
33
What is the pathology behind hyperosmolar hyperglycaemic state?
1. hyperglycaemia
2. osmotic diuresis
3. hyperosmolaltiy
4. causes fluid shift of water into intravascular compartment
5. severe dehydration
34
What is the criteria for hyperosmolar hyperglycamic state?
1. hypovolaemia
2. high serum osmolality >320 mosmol/kg
3. high hyperglycaemia >30
35
How does hyperosmolar hyperglycaemia present?
```
severe dehydration
confusion
altered mental state
LOC
+/- seizures, delirium, cerebral oedema
```
36
How is hyperosmolar hyperglycaemia managed?
1. MEDICAL EMERGENCY
2. ABCDE
3. IV fluids 3-6L over 12 hours of 0.9% saline
4. normalise blood sugars (insulin)
37
How is hyperthyroidism caused?
AUTOIMMUNE (graves disease) antibodies cause overstimulation of the thyroid gland so there is increased production of thyroid hormones T4 and T3 (but TSH suppressed)
38
List possible triggers for Graves disease?
smoking
e.coli infection
stress
high iodine intake
39
How does hyperthyroidism present?
GENERAL: sweating, heat intolerance, fatigue
HEART: palpitations, AF, heart failure
GYNAE: oligomenorrhoea
GI: diarrhoea, weight loss, increased appetite
NEURO/PSYCH: anxiety, tremors, restlessness
MSK: reduced bone mineral density
40
What are the signs of Graves disease?
1. EYE SIGNS - lid lad, ophthalmoplegia, exophthalmos (pop out eyes)
2. PRETIBIAL MYXOEDEMA (erythematous oedematous lesions above lateral malleolus)
3. THYROID ACROPACHY (clubbing)
41
What is aN emergency complication of hyperthyroidism?
THYROID STORM
| S+S: tachycardia, fever, sweating, trembling, agitation, confusion, confusion, goitre
42
How is a thyroid storm managed?
1. iV Carbimazole / propiletheouracil (better in pregnancy)
2. resus: oxygen, fluids, NG tube
3. IV propanolol
4. IV hydrocortisone
43
How is hyperthyroidism confirmed?
1. low TSH
2. high T4 and T3
3. thyroid autoantibodies e.g. anti TPO, anti TSH
4. ultrasound of thyroid
44
How Is hyperthyroidism managed?
1. Carbimazole - inhibit production of thyroid hormones
2. propanolol - bloco circulating thyroxine and immediate relief of symptoms
3. lubricant eye drops - ease eye irritation
45
What are the side effects/ precautions with Carbimazole?
agranulocytosis, teratogenic, acute pancreatitis
46
what is the conservative management for hyperthyroidism?
1. refer to ophthalmology to assess eyes
2. annual thyroid function tests
3. follow up after starting medication
4. refer to thyroid specialist
5. advice to stop smoking
6. refer to endocrinologist if trying for baby
47
if medication is not working and relapse of symptoms in hyperthyroidism, how can it be managed?
1. radioiodine
| 2. thyroidectomy
48
What is hypothyroidism?
impaired production of thyroid hormone (T4 and T3)
49
What are the primary (95%) causes of hypothyroidism?
1. AUTOIMMUNE hashimotos thyroiditis **
2. deficiency of iodine **
3. radio iodine treatment or surgery
+ DeQuervains, atrophic hypothyroidism, riedels thyroiditis, postpartum thyroiditis, drugs (lithium, amiodarone)
50
What are the main features indicating hashimotos autoimmune hypothyroidism?
GOITRE * = painless, rubbery, irregular surface, nodular mass in thyroid
anti TPO and anti Tg autoantibodies
51
What are the features of de Quervains hypothyroidism?
subacute: PAINFUL goitre and raised ESR
after viral infection
first presents with hyperthyroidism and then drops
diagnosed by thyroid scintigraphy and reduced uptake of iodine 131
52
What are the secondary causes of hypothyroidism?
= insufficient production of TSH due to hypothalamic or pituitary problems
e.g. isolated TSH deficiency, neoplasia, radiotherapy or trauma to hypothalamus or pituitary,
53
How does hypothyroidism present?
B- bradycardia
R- reflexes slow (delayed tendon reflex)
A-ataxia
D- dry thin skin and hair
Y- yawn (fatigue)
C- cold intolerance
A- ascites, peripheral oedema
R- round face - weight gain, decreased appetite
D- depression
I- immobile
C- concentration loss
+ menorrhagia, fertility issues (still birth), carpal tunnel, CVD
54
When does myxoedema coma occur?
in elderly when primary hypothyroidism presents with adrenal insufficiency and too low T3/T4
seizures, hypothermia, decreased consciousness, hypoventilate
RX: IV levothyroxine + IV hydrocortisone + resp support
55
What would you see on TFTs in hypothyroidism?
primary: high TSH, low T3/T4, ANTI TPO and anti Tg
secondary: low TSH, low T3/T4
56
How is hypothyroidism treated?
levothyroxine (T4) 50-100mcg + annual TFTs
57
Which hormones does the anterior pituitary gland produce?
Growth hormone -> stimulates liver to produce IGF-1
Prolactin -> stimulates growth of mammary glands and lactation
FSH/LH -> stimulates release of testosterone and oestrogen from testes/ ovaries
ACTH -> stimulates adrenal cortex to release glucocorticoids and androgens
TSH -> acts of thyroid gland to produce thyroid hormones
58
Which hormones doe the posterior pituitary gland produce?
supraoptic nucleus -> vasopressin -> acts on kidneys
paraventricular nucleus -> oxytocin -> acts on breasts and uterus
59
How is the adrenal divided and what does it produce?
1. adrenal medulla (derived from ectodermal neural crest tissue)
- > contains phaeochromocytes which secretes adrenaline and noradrenaline -> control autonomic NS
2. adrenal cortex (derived from embryonic mesoderm)
- > produces steroid hormones (mineralocorticoids, glucocorticoids) and androgens
60
Where and which hormones are produced in the adrenal cortex?
renin/ angiotensin act on -> zona glomerulosa -> aldosterone -> electrolyte imbalance and regulate blood volume
ACTH act on -> zona fasciculata -> cortisol -> deals with metabolism and stress
ACTH act on -> zone reticularis -> DHEAS -> helps make sex hormones
61
What is acromegaly?
excess of growth hormone due to an anterior pituitary adenoma
62
How is growth hormone regulated?
1. hypothalamus produces somatostatin and GNRH
2. acts on anterior pituitary gland
3. produces growth hormone
4. acts on liver to produce IGF-1
5. this stimulates soft tissue and skeletal growth
63
What are the symptoms/ signs of acromegaly?
FACIAL FEATURES: prominent nasolabial folds, large nose, large jaw, large tongue, prominent supraorbital ridge, enlarged head circumference, interdental spaces, frontal bossing
spade like hands and feet, wide feet/ increase in shoe size
SKIN: excessive sweating, oily skin
NERVE: peripheral neuropathy, carpal tunnel
GU: sexual dysfunction, galactorrhea
64
What are the signs of a pituitary tumour?
```
headache
bitemporal hemianopia (compression of optic chiasm)
hypopituitarism (abdo pain, thirst, fatigue, anaemia, loss of libido)
```
65
What are the possible complications of acromegaly?
hypertension
diabetes , glucose intolerance (GH is anti-insulin so insulin resistance develops)
cardiomyopathy, CV disease (most common cause of death)
osteoarthritis
sleep apnoea
66
How is acromegaly diagnosed?
1) oral glucose tolerance test * -no suppression of GH (rapid increase in blood glucose should depress GH secretion)
2) pituitary MRI* - diagnose pituitary adenoma
3) random GH levels
4) serum IGF1 raised
67
How is acromegaly managed?
1. transphenoidal surgery
| 2. somatostatin analogue e.g. octreotide - directly inhibit release of GH
68
What is cushings syndrome?
chronic excess glucocorticoids (cortisol)
69
How is cushings syndrome caused?
1. CUSHINGS DISEASE - pituitary adenoma stimulating adrenal cortex to secrete excess cortisol and loss of negative feedback system (+ pigmented skin **)
2. prolonged treatment with steroids e.g. IBD, asthma, RA, post transplant
3. small cell lung cancer - ectopic ACTH production
4. adrenal adenoma - ACTH independent
70
When can pseudo cushings occur and how can you differentiate between cushings disease?
caused by: alcohol excess, severe depression
| insulin stress test differentiates
71
What are the main features of cushings syndrome?
weight gain: central obesity, buffalo hump, moon face, purple striae , hyperglycaemia
hirsutism: acne, facial hair, red cheeks,
steroids: thin skin, thin skin, easy bruising, proximal muscle weakness, slow wound healing
72
What are the complications of cushings?
```
osteoporosis
diabetes
depression, insomnia
hypertension
heart failure
metabolic syndrome
impaired immunity
```
73
How is cushings syndrome diagnosed?
1. overnight dexamethasone suppression test **
if cortisol not suppressed: steroid therapy, ACTH syndrome likely
if cortisol suppressed by high doses dexamethasone: cushings disease
2. 24 hr urinary free cortisol high
3. plasma ACTH
if low= adrenal cause -> CT adrenal glands
74
How is cushings disease managed?
transphenoidal pituitary adenomectomy or pituitary irradiation?
SE: NELSONS SYNDROME (enlargement of pituitary gland and development of adenomas)
75
What is Addisons disease?
primary insufficiency of the adrenal cortex characterised by deficient secretion of glucocorticoids (cortisol) and mineralocorticoids (aldosterone)
76
What are the causes of insufficiency of corticosteroids and mineralocorticoids?
PRIMARY: autoimmune Addisons disease => progressive autoantibody destruction of the adrenal cortex so reduced cortisol and aldosterone produced
SECONDARY: tumour, TB, meningococcal septicaemia, autoimmune adrenalitis => inadequate secretion of pituitary hormones so decrease stimulation of adrenal glands
77
What are the clinical features of Addisons disease?
" thin tanned tired tearful and tumbling"
GI: nausea and vomiting, abdo pain , crave salty foods, anorexia, weight loss
NEURO: depression, lethargy, dizziness
POSTURAL HYPOTENSION
SKIN/MSK: bronze pigmentation, vitiligo, loss of pubic hair, skeletal muscle weakness
78
describe the features of addisonian/ adrenal crisis ?
cause: stress, infection, long term steroid therapy WITHDRAWAL
acute deficiency of gluocorticoids and mineralocorticoids
1. hypovolaemia
2. hypoglycaemia
3. hypotensive shock
79
How is an addisonian crisis managed?
1. iV hydrocortisone - then continue 6 hourly until stable
2. IV fluids (FLUID BOLUS)
3. cardiac and electrolyte monitoring
80
How is Addisons diagnosed?
1. ACTH (synacthen) stimulation test - confirms Addisons if cortisol doesn't rise rapidly (<550nmol/l after 30 mins)
2. U&E: hypoglycaemia, Hyperkalemia, hyponatraemia
3. adrenal autoantibodies e.g. anti 21 hydroxyls
4. 9am serum cortisol levels
81
How is Addisons treated?
hydrocortisone and fludrocortisone lifelong
patient education: carry steroid cards, how to adjust in illness (double hydrocortisone, same fludrocortisone as cortisol increases in stress response)
82
What are the side effects of long term steroid therapy?
easy bruising, thin skin, weight gain, osteoporosis, hyperglycaemia
83
What are the causes of hyperaldosteronism?
PRIMARY: Conns syndrome : adenoma of the zona glomerulosa which secrets aldosterone
SECONDARY: renal artery stenosis, excess diuretic therapy, congestive heart failure, nephritic syndrome, cirrhosis with ascites
84
What are the clinical features of conns syndrome?
hypertension
hypernatraemia
hypokalaemia - muscle cramps, weakness, paraesthesia
metabolic alkalosis
+ polyuria, polydipsia
85
How is conns syndrome diagnosed?
1. U&E - hypernatraemia, hyponatraemia
2. high blood pressure
3. raised aldosterone
4. low renin levels ---> aldosterone: renin >800 confirms diagnosis
86
How is conns syndrome managed?
surgery to remove adenoma + spironolocatone 4 weeks prior to surgery
87
What are the causes of raised prolactin?
1. prolactinoma: benign adenoma associated with MEN1
2. hypothyroidism
3. physiological: pregnancy, stress, exercise
4. drugs: anti psychotics *, TCA, SSRI
88
How does a prolactinoma present in women?
galactorrhea
oligomenorrhoea, amenorrhoea
hirsutism: male pattern hair growth, increase muscle bulk
+ headache, bitemporal hemianopia, visual loss, hydrocephalus, loss of appetite
89
How does a prolactinoma present in men?
reduced libido
reduced hair growth
ED
+ headache, bitemporal hemianopia, visual loss, hydrocephalus, loss of appetite
90
How is a prolactinoma diagnosed?
1. raised prolactin levels
2. MRI pituitary
3. TFTs to exclude hypothyroidism
91
How is a prolactinoma managed?
1. dopamine agonist e.g. bromocriptine
dopamine has inhibitory effect on prolactin production
2. transphenoidal surgery
92
What are the side effects of dopamine agonists?
impulsive behaviours
sleepiness
hypotension
93
What is diabetes insipidus?
deficiency of ADH secretion preventing osmotic control of kidneys
94
Explain how ADH is secreted, where and its actions
1. osmoreceptors in the hypothalamus detect an increased serum osmolality (concentration of solutes)
2. ADH is secreted by supraoptic nucleus in the hypothalamus
3. ADH released by the posterior pituitary gland
4. travels to kidneys and binds to ADH receptors on distal convulated tubules
5. causes Aquaporin2 channels to be inserted into the tubules
6. causes more water reabsorption back into the circulation and bloodstream
7. concentres the urine and decreases serum osmolality
95
What are the possible causes of diabetes insipidus?
CRANIAL DI: deficiency of ADH due to damage of hypothalamus or pituitary
idiopathic, head injury, pituitary surgery, craniopharyngiomas, haemochromatosis , Sheehans syndrome (pituitary infarction after PPH)
NEPRHOGENIC DI: insensitivity to ADH in the kidneys
tubulo interstitial disease ( pyelonephritis, sickle cell disease), genetic, drugs (lithium), Hypercalcaemia, CKD
96
How does diabetes insipidus present?
```
polyuria
polydipsia
dehydration
nocturia
distended bladder
```
97
How is diabetes insipidus diagnosed?
1. high plasma osmolality
| 2. ADH stimulation test - distinguish between cranial and nephrogenic DI CAUSES
98
How is nephrogenic diabetes insipidus managed?
1. thiazide diuretics
| 2. low salt and protein diet
99
What is SIADH (syndrome of inappropriate ADH secretion)
excessive secretion of ADH causing excessive water retention and dilution of blood and hyponatraemia
100
What are the causes of SIADH?
1. malignancy - small cell lung cancer ***, pancreas, prostate
2. neurological - stroke, meningitis, SAH, encephalitis
3. infection - TB, pneumonia
4. hypothyroidism
5. drugs - carbamazepine, sulfonylureas, SSRI, amitriptyline, vincristine
101
How does SIADH present?
symptoms of hyponatraemia (more symptomatic when acute, chronic hyponatraemia asymptomatic mostly)
MILD: nausea, vomiting, malaise, headaches
MODERATE: weakness, muscle cramps, lethargy, ataxia
SEVERE: coma, seizures, loss of consciousness, confusion
102
How is SIADH diagnosed?
1. serum osmolality low
2. urine osmolality high
3. hyponatraemia
4. high Na in urine
103
How is SIADH managed?
correct slowly as want to prevent central pontine myelinolysis
1. fluid restrict 1-1.5L/ day
2. Na given and monitored every 2 hours
104
What is a pheochromocytoma?
neuroendocrine tumour (usually unilateral and benign) of the adrenal medulla which produces catecholamines (adrenaline and noradrenaline)
105
What is associated with pheochromocytoma?
MEN 2
familial
Von Hippel Lindau syndrome
neurofibromatosis
106
How does pheochromocytoma present?
excess secretion of adrenaline and noradrenaline so...
dangerous hypertension ** causing headaches **
sweating
trembling
palpitations
tachycardia
anxiety
107
What are the complications of pheochromocytoma?
```
heart failure
arrhythmias e.g. SVT
MI
dilated cardiomyopathy
stroke
death !
```
108
How is pheochromocytoma diagnosed?
1. 3x 24 hr urinary samples of plasma free catecholamines
| 2. high levels of VMA in urine
109
How is pheochromocytoma managed?
1. alpha blockers e.g. phenoxybenzamine
2. then beta blockers given
3. surgical excision of benign tumour
110
What is carcinoid syndrome?
due to carcinoid tumour or mets in the liver releasing SEROTONIN into the circulation
111
what are the features of carcinoid syndrome?
```
flushing **
diarrhoea
hypotension
bronchospasm
R side heart failure/ valve stenosis
```
112
How is carcinoid syndrome managed?
somatostatin analogues e.g. octreotide
113
What are the causes of hypocalcaemia?
with a low PTH: hypoparathyroidism , parathyroid surgery
with a high PTH: pseudohypoparathyroidism, vitamin D deficiency , hypomagnesaemia
other: CKD, pancreatitis, rhabdomyolysis
114
What are the symptoms of hypocalcaemia?
```
paraesthesia - tingling in fingers, toes, mouth
muscle cramps
depression
carpopedal spasm
tetany - severe sign
```
115
What are the signs of hypocalcaemia?
Trousseaus sign - when inflate BP cuff, look for carpopedal spasm
Chvosteks sign - tap over facial nerve and induce facial spasm
116
How is hypocalcaemia diagnosed and assessed?
1. U&E - low adjusted calcium
2. ECG - prolonged QT
3. serum PTH
4. serum magnesium
117
How is hypocalcaemia managed acutely?
if severe/ seizures/ tetany -> IV calcium gluconate 10ml 10%
| if mild/ moderate - oral calcium
118
How is hypocalcaemia managed long term?
oral calcium and vitamin D
119
What are the causes of Hypercalcaemia?
1. primary hyperparathyroidism *
2. malignancy * - squamous cell lung cancer, bony mets, breast, myeloma
+ sarcoidosis, TB, Addisons, pheochromocytoma, dehydration, pagets disease of the bone, drugs (thiazines, vit D)
120
What are the symptoms of hypercalcaemia?
ABDOMINAL MOANS - constipation, nausea and vomiting, abdominal pain
THRONES - polyuria, polydipsia, dehydration
STONES - renal colic and stones
PSYHIC OVERTONES - depression, confused, memory loss
+ weakness, proximal myopathy, fatigue, osteoporosis, arrhthymias
121
How is hypercalcaemia investigated?
1. U&E - high serum Ca
2. ECG - short QT interval
3. serum PTH - high in hyperparathyroidism
4. alk phos - high in bony mets, low in myeloma
+ x ray, albumin, calcitonin ( high in B cell lymphoma)
122
How is acute hypercalcaemia managed?
1. IV fluids 3-4 L 0.9% saline
2. loop diuretic
3. IV bisphosphonates
4. treat cause
123
What are the causes of hyperkalaemia?
```
AKI, CKD
renal tubular acidosis
DKA (metabolic acidosis)
Addisons
drugs - potassium sparing diuretics, ACE-I, ARBs, NSAIDs, digoxin, ciclosporin
blood transfusion
rhabomyolysis
```
124
How does hyperkalaemia present?
fatigue
weakness
flaccid paralysis
palpitations and chest pain
125
How is hyperkalaemia investigated?
1. U&E - high potassium
2. ABG- metabolic acidosis
3. review medications
4. ECG
126
List the ECG changes in hyperkalaemia?
tall tented t waves
absent p waves
wide QRS
VF !!!!***
127
How is hyperkalaemia managed?
1. ABCDE
2. IV 10ml 10% calcium gluconate - stabilises cardiac membrane
3. insulin actrapid / 10% dextrose infusion in 250ml over 15 mins - shift potassium from extracellular to intracellular
4. nebulised salbutamol
128
What are the causes of hypokalaemia?
vomiting (alkalosis)
thiazide and loop diuretics (alkalosis)
diarrhoea (acidosis)
cushings and conns syndrome
129
How does hypokalaemia present?
muscle weakness
constipation
hypotonia
130
What are the signs on ECG of hypokalaemia?
prominent u waves
prolonged PR interval
ST depression
131
How is hypokalaemia managed?
mild/ moderate: oral sandoK supplements 2040mmol x2/4 daily
severe: IV potassium + ECG monitoring
132
What are the causes of hypernatraemia?
dehydration - diarrhoea, vomiting, severe burns, inadequate fluid intake, excessive exercise/ sweating
diabetes insipidus
drugs and excess saline - IV abx, IV sodium bicarbonate, hypertonic dialysis, loop diuretics
133
How does hypernataemia present?
```
lethargy
irritable
doughy skin
hyperreflexia
myoclonic jerk
confusion
signs of dehydration
```
134
How is hypernatraemia managed?
1. treat cause
2. correct 0.5 mmol/hour and fluids
3. monitor fluid status and monitor electrolytes
135
List drugs that can cause weight gain?
```
A- anti psychotic
A - anti depressants e.g. TCA, mirtazepine
A - anti histamines e.g. certrizine
A - anti convulsants e.g. lithium
B - beta blocker
C - corticosteroids
C - contraceptives e.g. depo-provera
D - diabetic medication e.g. insulin, sulfonylurea, pyoglitazone
```
136
Which conditions cause weight Gain / obesity?
hypothyroidism
Cushings syndrome
PCOS
137
what are the possible complications of obesity?
```
type 2 diabetes **
hypertension **
CVD - MI, angina , stroke
pregnancy risks - infertility, gestational diabetes, macrosomia, shoulder dystocia
endometrial, breast and colorectal cancer
sleep apnoea
GORD
gallstones , fatty liver disease
osteoarthritis
```
138
How is obesity managed?
1. diet advice - 600 kcal deficit, low fat, high wholewheat carbs, low sugar, limit alcohol
2. exercise - 30 mins moderate 5x/week
3. medication - orlistat
4. bariatric surgery - gastric band, bypass
139
Which medication is used to help weight loss in obesity and when is it given?
ORLISTAT= pancreatic lipase inhibitor
indicated if BMI >30, BMI >28 + RF
stopped after 3 months if not lost 5% of body weight
140
what are the side effects of orlistat?
flatulence, diarrhoea, incontinence, abdo pain, oily stool
141
What is the criteria for metabolic syndrome?
1. truncal obesity/ BMI >30
2. blood pressure: systolic >130, diastolic >85
3. reduced HDL
4. high triglycerides
5. fasting glucose >6.1 mmol/l -> prediabetes
142
what are the causes of metabolic syndrome?
OBESITY ***
sedentary lifestyle
smoking
143
What are some of the causes of gynaecomastia?
LOW TESTOSTERONE
klinefelters, mumps
HIGH OESTROGEN
obesity, seminoma , oestrogen secreting tumour, hyperthyroid
prolactinoma
MEDICATION
finasteride (inhibit testosterone), anabolic steroids, anti psychotics, digoxin, spironolactone
144
Describe parathyroid hormones action when serum calcium is low
1. calcium in the blood is low
2. chief cells in the parathyroid gland secrete parathyroid hormone which have 3 actions:
- BONE: stimulate osteoclasts and inhibit osteoblasts so bone is broken down and releases Ca into the blood
- KIDNEY: decreases Ca excretion in the urine and also activates vitamin D which increases Ca absorption
- INTESTINE: calcitriol stimulates intestine to absob more Ca from the food
3. results in calcium levels raising
145
Describe what happens if serum calcium is high
1. parafollicular cells in the thyroid gland activated to release calcitonin
2. acts on the BONE to inhibit osteoclast and stimulate osteoblast so Ca is removed from blood and used to build new bone
3. calcium leves decrease
146
What is the cause of primary hyperparathyroidism?
benign adenoma of the parathyroid gland (85%) **
| + carcinoma of the parathyroid gland, hyperplasia
147
Who is primary hyperparathyroidism associated with?
post menopausal elderly women
MEN 1/2
hypertension
148
How does primary hyperparathyroidism present?
80% asymptomatic and found on bloods
HYPERCALCAEMIA - "abdominal groans, stones, thrones and psychotic moans" (constipation, thirst, abdo pain, renal stones, peptic ulcers, osteoporosis, confusion, memory loss, polyuria)
149
What is seen on the bloods for primary hyperparathyroidism?
high PTH
high Ca
low phosphate
x-ray: pepper pot skull
MRI scan
150
How is primary hyperparathyroidism treated?
watch and wait if mild: monitor PTH and Ca levels, increase fluids, low Ca diet , Cincalet
if HIGH calcium, symptomatic: surgical excision of adenoma
151
What are the possible complications with parathyroid surgery?
damage of the recurrent laryngeal nerve
hypothyroidism
symptomatic hypocalcaemia
"hungry bone syndrome"
152
How is secondary hyperparathyroidism caused?
as a result of low calcium (usually due to CKD*, vitamin D deficiency, inadequate Ca in diet) there is parathyroid gland hyperplasia
153
What would you see on the bloods for secondary hyperparathyroidism?
high pTH
low Ca
high phosphate
low vitamin D
154
How does secondary hyperparathyroidism present?
CKD + bone pain
low vitamin D + osteomalacia + fracture
155
How is secondary hyperparathyroidism treated?
1. correct Vit D deficiency
2. phosphate binders
3. cinacalet
156
what causes tertiary hyperparathyroidism ?
after secondary hyperparathyroidism and correction of calcium, there is still parathyroid gland hyperplasia so continues secreting parathyroid hormone at high levels
157
what would you see on the bloods of tertiary hyperparathyroidism?
high PTH
high Ca
high phosphate
high Alk Phos
158
What are the causes of hypoparathyroidism?
1. PRIMARY HYPOPARATHYROIDISM
= surgery to thyroid/ parathyroid gland, DiGeorges syndrome, alcohol, Wilsons/ hereditary haemochromatosis
2. PSEUDO HYPOPARATHYROIDISM
= target cells insensitive to PTH
low IQ, short stature, short 4th and 5th metatarsal
3. PSEUDOPSEUDO HYPOPARATHYROIDISM
similar to pseudo but normal biochemical
159
What would you do to diagnose pseudo hypoparathyroidism?
urinary cAMP and phosphate levels after a PTH infusion - will not rise
160
How does primary hypoparathyroidism present?
hypocalcaemia features (tetany, carpopedal spasm, paraesthesia, muscle cramps, depression, Trousseaus sign, Chvosteks sign)
161
What would you see on bloods for primary hypoparathyroidism?
```
low PTH
low Ca
high phosphate
low Mg
ECG - prolonged QT
```
162
How is primary hypoparathyroidism treated?
diet rich in calcium and vit D
| calcium and vIt D suppléments
163
How does nephropathy occur in T1DM?
hyperglycaemia damages and causes thickening of the glomerular basement membrane and increase in mesangial cells
164
How does glucagon work?
increases the concentration of glucose in the blood by promoting glycogenolysis and gluconeogenesis
165
which antibodies are found in hyperthyroidism?
anti TPO
| anti TSH
166
which antibodies are found in hypothyroidism?
anti TPO
| anti Tg
167
How does goitre occur?
increase in TSH so increases cellularity and hyperplasia of thyroid gland
168
list the tissues derived from ectoderm?
```
adrenal medulla
CNS
hair, teeth
nose
eyes
nails
```
169
List the tissues derived from endoderm?
```
stomach
intestines
liver
pancreas
bladder
respiratory epithelium
```
170
List the tissues derived from mesoderm?
```
adrenal cortex
muscle
bone
cartilage
kidneys
heart
testis
```
171
list the functions of cortisol
```
gluconeogenesis
lipolysis
reduce stress
anti inflammatory
protein synthesis
```
172
List the functions of aldosterone
1. vasoconstriction
| 2. up regulate Na/K pump at DCT to increase Na and water reabsorption and excrete K
173
Summarise MEN and its associations
MEN 1 - (3 P's) - Parathyroid (hyperparathyroidism), Pancreas (insulinoma, gastrinoma), Pituitary -> MEN1 gene
MEN 2A/B - parathyroid, phaemochromocytoma, medullary thyroid cancer -> RET oncogene
174
How is toxic multi nodular goitre treated?
radioactive iodine
175
List the different types of steroids?
HIGH mineralocorticoid activity, MINIMAL glucocorticoid -> fludrocortisone
HIGH mineralocorticoid, HIGH glucocorticoid -> hydrocortisone
LOW mineralocorticoid activity , HIGH glucocorticoid -> prednisolone
MINIMAL mineralocorticoid activity , HIGH glucocorticoid -> dexamethasone
176
What are the electrolyte disturbances in cushings syndrome?
hypokalaemia
| metabolic alkalosis
177
where is thyroid derived from embryonically?
foramen caecum
178
describe the oral glucose tolerance test?
1. pt fasts overnight
2. given drink of 75g sugar in morning
3. BM taken before and 120 mins after drink
4. blood glucose >11.1 mmol/L after drink = diabetes
179
If taking regular steroids, what advice should be given?
carry steroid cards
wear medic alert bracelet
side effects of long term steroids
know how to adjust steroids in infection
