Endocrinology Flashcards
for which 2 groups of ppl is BMI inaccurate
pregnant
ppl with large amount of muscle mass
how to calculate BMI
kg / m^2
underweight BMI
<18.5
normal BMI
18.5 - 24.9
overweight BMI
25 - 29.9
obese BMI class 1 2 3
class 1
30 - 34.9
class 2
35 - 39.9
class 3
40+
management for class 1 obese
1st line = lifestyle modifications
consider orlistat
Mech of action of osrlistat
pancreatic lipase inhibitor
management of class 2 obesity with comormidities / class 3 obesity / other Tx been ineffective
bariatric surgery
which classes of obesity qualify for bariatric surgery
management of class 2 obesity with comormidities / class 3 obesity / other Tx been ineffective
2 roles of cobalamin / vit b12
rbc synthesis
myelination
where is b12 absorbed
terminal ileum
which foods is b12 found in
animal products
4 causes of b12 deficiency
pernicious anaemia
gastrectomy
vegan diet
disease of terminal ileum: crohns or ileocaecal resection
which cancer does pernicious anaemia increase risk of
gastric
what are the 2 types of antibodies that can be found in pernicious anaemia
anti - IF antibodies
anti gastric parietal cell antibodies
clinical features of vit b12 deficiency
anaemia (fatigue, pallor, SOB etc)
peripheral neuropathy (tingling, numbness etc)
dementia
glossitis
b 12 deficiency management
IM supplementation of vitamin B12 (hydroxocobalamin)
should you replace b12 or folate first
b12
describe the rbc’s in b12/folate deficiency
Macrocytic, Megaloblastic Anaemia
→ decreased Hb,
increased MCV,
hyperchromic RBCs,
hypersegmented neutrophils
describe homocysteine levels in b12 and folate deficiency
elevated in B12 & Folate deficiency
describe Methylmalonic acid (MMA) levels in B12 and folate deficiency
elevated in B12 deficiency,
normal in folate deficiency
2 roles of folate
DNA synthesis and amino acid metabolism
which vitamin is folate
vit B9
which food is folate found in
green leafy veg
4 causes of folate deficiency
malabsorption (small bowel disease due to IBD or coeliac disease),
malnutrition (chronic alcohol use),
increased requirement (pregnancy),
drug related (methotrexate, antiepileptics)
clinical features of folate deficiency
anaemia
glossitis
fetal spinal bifida if mother is deficinet
what does the foetus get if the mother is folate deficient
fetal spinal bifida
anacephaly
main difference in clinical features between vit b12 and folate deficiency
folate deficiency does not result in neurological symptoms
Tx for folate deficiency
oral folate supplementation
how much folate should pregnant women take to prevent fetal neural tube defects
400mcg of folic acid until the 12th week of pregnancy
definition of hypothermia
< 35
definition of hyperthermia
> 40
what is mild hypothermia
35 - 32
features of mild hypothermia
tachycardia, tachypnoea, shivering, vasoconstriction
what is moderate hypothermia
28 - 32
features of moderate hypothermia
arrhythmias, hypotension, resp depression, cognitive impairment, may cease to shiver
what is severe hypothermia
< 28
features of severe hypothermia
loss of/reduced consciousness
coma
arrhythmia
apnoea
fixed dilated pupils
which temp do you measure for hypothermia
core body temp
ECG hypothermia features
J / Osborn waves
broad QRS complex
mild hypothermia management
passive external rewarming (remove wet clothing, cover with blankets, warm room)
moderate hypothermia management
active external rewarming (warm blankets, radiant head, forced warm air)
severe hypothermia management
IV warmed crystalloid
hypothermia complications
arrhythmias
hypoglycaemia
hyperkalaemia
GI disorders
rhabdomyolysis
which temp do you measure for hyperthermia
rectal temp
heat stroke vs heat exhaustion
heat stroke = hyperthermia with CNS dysfunction
heat exhaustion = hyperthermia without CNS dysfunction
what are the 2 types of heat stroke
classic (due to external environment)
exertional
heat stroke symptoms
confusion
seizures
loss of consciousness
delirium
heat stroke management
stabilisation (ABC, remove clothes)
rapid active cooling (full body immersion in ice water)
heat exhaustion symptoms
nausea
dizziness
weakness
muscle cramps
fatigue
headache
heat exhaustion management
oral isotonic fluids
active cooling
which LDL and HDL levels promote atherosclerosis
Elevated LDL and reduced HDL
familial hypercholestrolaemia inheritance pattern and mutation
Autosomal dominant inherited disorder
Caused by a mutation in the gene coding the LDL receptor
clinical features of hyperlipidaemia
Xanthomata → nodular lipid deposits in the skin and tendons
Xanthelasma → yellow, flat plaques on upper eyelids
(xanthelasma is a type of xanthomata)
Corneal Arcus → crescentic-shaped opacity at the periphery of the corne
Ix for hyperlipidaamia
Lipid Profile → total cholesterol, HDL, LDL and trigylcerides
Tests for Secondary Causes → HbA1c/Fasting glucose, TSH, LFTs, urinalysis, LFTs
QRISK2 → screens for risk of cardiovascular disease.
QRISK < 10% management for hyperlipidaemia
lifestyle modifications
QRISK >= 10% management for hyperlipidaemia
atorvastatin 20mg
or simvastatin
or if they have IHD/PAD/cerebrovascular disease give atorvastatin 80mg
or if statin intolerant:
ezetimibe
in which pts is atorvastatin C/I
pregnant
Mech of action of ezetimibe
cholesterol absorption inhibitor
when should statins be taken to be most effective
last thing at night
when should statins be discontinued
if serum transaminase concentrations rise to and persist at 3 times the upper limit of the reference range
what is an important drug interaction of statins
with erythromycin/clarithromycin (macrolides) (can cause myopathy, increased likelihood of rhabdomyolysis)
which medication can cause both hypo and hyperthyroidism
amiodarone
list some side effects of amiodarone
hypothyroidism
hyperthyroidism
corneal deposits
Steven Johnsons syndrome
grey discolouration of the skin
liver failure
pneumonitis + pulmonary fibrosis
what type of medicine is aledronic acid
bisphosphonate
in which disease should bisphosphonates be avoided
advanced kidney disease
side effects of bisphosphonates
severe reflux disease
peptic ulceration
jaw necrosis
what med should be started in women with osteoperosis confirmed by DEXA scan or over 75yrs with 2+ risk factors for fracture / have had a previous fragility fracture
bisphosphonates eg aledronic acid
which side effect can spironolactone cause in men
gynaecomastia
symmetrical aches and pains
proximal muscle weakness
bone wearing fracture
waddling gait
likely diagnosis
osteomalacia
4 causes of osteomalacia
insufficient dietary calcium
vit D deficiency due to poor UV light exposure
CKD (causes low vit D which can cause low calcium)
malabsorption
what is osteopetrosis
defect in osteoclasts which means they cannot break down bone
results in denser bones and thickened bone cortices –> brittle bones
have stunted growth, bone pain, and bright hyper dense bones on imagining
joint and bone pain
stunted growth
in a child
likely diagnosis
rickets (childhood vit D deficiency)
bone pain
fractures
nausea
vomiting
constipation
high calcium, high PTH and ALP, low phosphate
likely diagnosis
hyperparathyroidism causing osteitis fibrosa csytica (excessive PTCH activates osteoclasts leading to increased bone resorption
weak deformed hyper vascular bones
normal calcium / phosphate / PTH
increased ALP
bone pain
symptoms in one bone only
likely diagnosis
pagets disease
–> is caused by deformed bone remodelling
MEN I symptoms
Parathyroid hyperplasia / adenoma
pituitary prolactinoma or GH secreting tumour (acromegaly)
Pancreas endocrine tumour (insulinoma, gastrinoma)
MEN IIa symptoms
thyroid cancer
parathyroid hyperplasia
bening and bilateral phaechromocytoma
MEN II b symptoms
Phaechromocytoma
Medullary thyroid cancer
mucosal neuroma
marfanoid appearance
tall stature
hypogonadism
gynaecomastia delayed puberty
likely diagnosis
Klinefelter’s syndrome (47 XXY)
what is the Rotterdam criteria for PCOS
2/3 of the below are needed for a diagnosis to be made
- presence of multiple ovarian cysts
- oligomenorrhoea or amnehorrhoea
- clinical/biochemical signs of hyperandrogenismeg acne/hirsutism/alopecia
oligomenhorroea
amenhorrea
galactorrrhoea
decreased libido
infertility
decreased bone mass
likely diagnosis
hyperprolcatinaemia
decsreased bone mass is due to decreases in oestrogen (hypogonadism)
oligomenhorrea
infertility
hirsutism
ambiguous genitalia
salt losing addisonian crisis
late onset congenital adrenal hyperplasia
(21 hydroxylate deficiency so can’t make cortisol and aldosterone, so make lots of androgens - high testosterone)
what diagnosis does recurrent chest infections and azoospermia point to
CF
(azoospermia is due to genesis of the vas deferens)
what effects does amiodarone withdrawal have on the thyroid
thyrotoxicosis
most common cause of hypopituitarism
pituitary adenoma
1st line investigation to confirm Addisons
measure cortisol.
if its low then do a short synthacten test - synthacten should stimulate cortisol production form the adrenal glands, this will not happen in Addisons
does parathyroid adenoma cause visible neck swelling
no
what is measured in the screening tests for medullary thyroid carcinoma
serum calcitonin
what is the effect of reduced Gh and gonadotrophin secretion on the bones
osteoporosis
1st line and definitive treatment for phaechromocytoma
alpha blockers eg Phenoxybenzamine
(then can add beta blocker to manage tachycardia/arrhythmias caused by alpha blockers, if needed)
then would do a phaechromocytoma resection (definitive management)
main side effect of phenoxybenzamine
reflex tachycardia
what is Waterhouse friderishcen syndrome (WS)
a severe, often fatal, disorder characterized by adrenal hemorrhage and failure, resulting from disseminated intravascular coagulation (DIC) triggered by a bacterial infection
presents initially with a nonspecific infection progressing into a macular, petechial, and subsequently purpuric rash, along with septic shock
most common cause of Waterhouse friderishcen syndrome (WS)
Neisseria meningitides
strep pneumonia
first line diagnostic test for phaechromocytoma
plasma free metenephrines
pt had cushings then had a bilateral adrenalectomy to treat it
they start to develop headaches and visual field defects
Nelsons syndrome
–> bilateral adrenalectomy causes loss of feedback to brain
therefore increased CRH release form hypothalamus
increased stimulation of pituitary causes enlargement and formation of pituitary adenoma
what is sick euthyroid syndrome
commonly seen during a period of illness
deranged low thyroid function tests despite normal functioning thyroid
will recover as the illness improves
which medications can cause a rise in prolactin levels
SSRI
cimetidine
BBs
how to manage galactorrhoea due to a certain drug, where the pt can’t stop taking the drug
co prescribe a dopamine agonist eg cabergoline to counteract the side effect - but manage with care bc cabergoline may reduce the effectiveness of the medication that they’re on
how to manage post partum thyroiditis
watch and wait
–> post part thyroiditis consists of hyperthyroidism then hypothyroidism. so if you give an antithyroid medication and then they become hypothyroid anyway, you could worsen things
what is made in each layer of the adrenal gland
Going deeper:
zona glomerulosa: aldosterone (salt)
zona fasciculata: glucocorticoids, cortisol (sugar)
zona reticularis: androgens (sex)
what medication is bromocriptine
dopamine agonist
what is li-fraumeni syndrome
a hereditary cancer predisposition syndrome associated with cancers such as leukaemia and sarcoma
first step in investigation/management of a pt with signs of cushings who is on long term steroid therapy currently
wean their steroid use
—> he first step would NOT be high/low dexamethasone suppression tests in this case as they would provide us with no further info, since she’s already on steroids and has high cortisol
treatment of subacute thyroiditis aka de quervains thyroiditis
supportive care and pain relief if needed (the condition will go from thyrotoxicosis, to hypothyroidism to euthryoidism)
antithyroid drugs dont work bc the thyrotoxicosis is due ti release of reframed hormones from the thyroid gland
at what age are boys with no pubertal development classed as having delayed puberty
14
which gene is associated with MEN 2a
RET gene
acute thyroiditis vs subacute thyroiditis
acute aka suppurative thyroiditis = caused by bacterial infection
presents with fever
presents quicker than subacute
rare
subacute thyroiditis aka de quervians = caused by viral infection
presents with painful neck, malaise
more common
initial screening test and result fro conns syndrome (primary hyperaldosteronism)
aldosterone to renin ratio
- elevated aldosterone causes sodium and therefore water retention. this increases renal perfusion, so inhibits renin secretion
high aldosterone, low renin
= high aldosterone: renin ratio
what is the aldosterone: renin ratio in primary vs secondary hyperaldosteronsim
high in primary eg conns syndrome
low in secondary - bc the aldosterone is elevated bc of the renin itself being elevated
best initial investigation in a young pt with poorly controlled HTN and hypokalaemia
aldosterone: renin ratio –> check for conns syndrome
what is the gold standard “challenge” test which is used ti clarify the diagnosis of hypopituitarism
insulin tolerance test
- stimulates hypoglycaemia wich aggravates a stress respinse
how does PTH act on bone to increase serum calcium levels
binds to osteoblasts which stimulate osteoclasts via porcine signalling
phaechromocytoma symptoms
episodic hypertension
palpitations
sweating
which hormones does a phaechromocytoma produce
it is a catecholamine producing tumour
potassium levels in conns syndrome vs Addisons
conns = hypokalaemia
Addisons = hyperkalaemia
which conditions are anti TPO antibodies found in
hashimotos or graves
how does PTh affect intestinal absorption of calcium and phosphate
increases intestinal absorption of both
carbimazole mech of action
inhibits TPO
palpitations, sweating, malignant hypertension
likely diagnosis
phaechromocytoma
which condition results in 2 or more specific neruoendocrine tumours (medullary thyroid cancer, phaechromocytoma, adenoma, parathyroid hyperplasia)
MEN 2a
what kind stature do MEN 2b sufferers have
marfanoid stature
what is the most likely cause of hyperprolactinamyia in young females with mental health problems
anti psychotics eg rsiperidone, tricyclic antidepressants, SSRIs, haloperidol
first line diagnosis test for cushings
overnight dexamethasone suppression test
first line investigation for delayed puberty
measure FSH and LH levels
what type of hypogonadism does kleinfleter’s cause
primary hypogonadism
what type of hypogonadism does kallman’s cause
secondary hypogonadism
what type of hypogonadism does cryptorchidism cause
primary hypogonadism
high TSH, normal T4
diagnosis
subclinical hypothyroidism
in what type of hyperaldosteronism are both renin and aldosterone raised
secondary hyperaldosteronism
causes of secondary hyperaldosteronism
nephrotic syndrome
liver cirrhosis
congestive heart failure
renal artery stenosis
young pt with high bp, sweating, headaches and anxiety
diagnosis
phaechormocytoma
an asymptomatic thyroid mass which is gradually getting larger in elderly pt
diagnosis
thryroid cyst / colloid nodule
what is involved on MEN1, MEN2a and MEN2b
MEN 1- (3 P’s) pancreas, parathyroid, pituitary
MEN 2A - (1M, 2P’s) Medullary thyroid cancer, pheochromocytoma, parathyroid
MEN 2B - (3M’s, 1P) Medullary thyroid cancer, Marfanoid, pheochromocytoma, mucosal neuroma
first line Tx for hypogonadism in men
testosterone therapy
first line investigation for hyperaldosteronism
aldosterone: renin ratio
(will be high in hyperaldosteronism)
gold standard for locating source of excess aldosterone in hyperaldosteronism
Selective adrenal venous sampling
treatment for hyperaldosteronism caused by bilateral adrenal disease
aldosterone antagonsists (Spironolactone, Eplerenone)
Then surgical resection
likely diagnosis for polyuria / polydipsia / headaches with osteoporosis
hyperaldosteronism
what is a well known heart complication of hyperthyroidism
atrial fibrillation
which condition is RET gene mutation associated with
MEN 2
male secondary sexual characteristics
the growth of pubic hair, and facial hair and the voice deepens
female secondary sexual characteristics
breasts develop, hips widen, and pubic hair begins to grow
long boy with small testicles, delayed puberty, gynaecomastia and no secondary sexual characteristics
likely diagnosis
kleinfelters
common cause of tingling after thyroid surgery
hypocalacemia - surgery may have affected the parathyroid glands
best investigation when looking for the cause of diabetes insipidus
MRI brain
(DI could be due to pituitary adenoma which is causing suppression of ADH secretion)
what is a neck lump which moves on swelling but not tongue protrusion suggestive of
a thyroid mass
most common cause of thyrotoxicosis in younger vs older pts
younger = graves
older = toxic multi nodular goitre
describe the thyroid and associated symptoms of subclinical ( de quervians) thyroiditis
thyroid is small and tender to palpation
pt recently experinced infectious symptoms
pt is initially hyperthyroid, then euthyroid, then hypothyroid, then euthyroid again
carbimazole mech of action
inhibits TPO
what is Waterhouse-Friderichsen’s syndrome
adrenal haemorrhage and consequent adrenal failure
if cortisol is high after overdose dexamethasone suppression test but is suppressed after high dose dexamethasone suppression test, which investigation needs to be conducted next
MRI of pituitary
- if they respond to his dose dexamethasone suppression test, its cusihings disease (due to pituitary adenoma), if they dont respond its ectopic ACTH production
give examples of potassium sparing diuretics
sprionolcatone
amiloride
Eplerenone
Triamterene
what type of diuretic is furosemide
loop diuretic
which medication is given to someone with hypertension, hypokalaemia and bilateral adrenal disease
potassium sparing diuretic
eg sprionolcatone
amiloride
Eplerenone
Triamterene
what kind of goitre would a non functioning adenoma cause
nodular goitre
what is the main complication of any decrease in FSH/LH and oestrogen/testosterone
osteoporosis
which scan is used to detect oestoperosis
DEXA scan
what is Waterhouse friderichsen syndrome
adrenal gland failure due to bleeding in the adrenal gland, usually caused by severe meningitis or bacterial infection
likely diagnose: pot and meningitis then developed persistently low glucose levels and increased skin pigmentation
Waterhouse friderichsen syndrome
what advice should be given with regards to steroids and intercurrent illness
double steroid dose
which features make graves eye disease be classed as more severe
lid retraction > 2mm
significant soft tissue involvement
exophthalmos > 3mm
diplopia
optic neuropathy
corneal breakdown
what does tds mean
three times a day
what does bd mean
twice a day
what does qid mean
4 times a day
which antithyroid drugs cause agranulocytosis
PTU
carbimazole
methimazole
what kind of hyperaldosteronism does a renin producing tumour cause
secondly hyperaldsteronism
what sort of ph class does conns syndrome cause
metabolic alkalosis (bc it increases urinary acidification)
which cancers most comply release ectopic ACTH
small cell lung cancer
carcinoid tumours
which cause of hyperthyroidism would present with reduced uptake on a radioisotope scan
de quervain’s thyroiditis
which cause of hyperthyroidism would present with diffuse uptake on a radioisotope scan
graves
which cause of hyperthyroidism would present with patchy uptake on a radioisotope scan
toxic multi nodular goitre
which cause of hyperthyroidism would present with uptake in only one area on a radioisotope scan
toxic thyroid adenoma
whats the difference between hot and cold nodules on an iodine 123 thyroid scan
hot = functional eg causes hyperthyroidism
cold = non functional - malignant
best investigation to do for pt with a thyroid mass who has abnormal TSH and T3/4
fine needle aspiration- could be a malignancy
which thyroid cancer has the worst prognosis
anapaestic thyroid cancer - most case lead to rapid death
where does a medullary thyroid cancer metastasis to
lymph nodes, liver, bones, and lungs
which cause of hyperthyroidism classically presents as a painful smooth goitre
de quervain’s thyroiditis
which cause of hyperthyroidism classically presents as a painful nodular goitre
toxic solitary adenoma
which cause of hyperthyroidism classically presents as a painless smooth goitre
graves
someone who is usually on long term steroids collapses and is found to have hyponatraemia, hypokalaemia and hypoglycaemia - likely diagnosis
adrenal crisis
likely diagnosis: high cortisol in low dose dexamethasone suppression test
high cortisol and low ACTH in high dose dexamethasone suppression test
adrenal adenoma
likely diagnosis: high cortisol in low dose dexamethasone suppression test
high cortisol and high ACTH in high dose dexamethasone suppression test
topic source of ACTH (eg small cell lung cancer or carcinoid tumour)
likely diagnosis: high cortisol in low dose dexamethasone suppression test
low cortisol and low ACTH in high dose dexamethasone suppression test
cushings disease
medication prescribed in post partum thyroiditis
propanolol
- just like with de quervain’s thyroiditis, the hyperthyroidism is transient, so you down give anti thyroid drugs, just symptomatic relief
Tx for tertiary hyperparathyroidism
parathyroidectomy
which is the most common antibody in graves
TSHr antibodies
(anti TPO antibodies are also present but are less common)
aldosterone mech of action on nephron
increases Na reabsorption into blood
increases K and H+ secretion into urine
what does a high aldosterone: renin ratio indicate
conns syndrome
[t has low calcium, high phosphate and short 4/5th metacarpal
diagnosis?
pseudohypopituitarism (autosomal dominant contain, reisstance to PTH)
which T3/4 and TSH pattern would a poor compliance with levothyroxine show
normal T3/4
raised TSH
(T4 replacement has been intermittent so has been unable to suppress the TSH)
which type of thyroid cancer is the most rapidly and aggressively growing and invades local structures
anaplastic thyroid cancer
pt presents with thyroid mass that has appeared 2 weeks ago and has been rapidly growing, they also have some cervical lymphadenopathy
likely diaganosis?
anaplastic thyroid cancer
first investigation and confirmatory investigation do to if suspect primary hyperaldosteronism
aldosterone: renin ratio first (high ratio is suggestive)
then fludrocortisone suppression test to confirm- fludrocortisone ownt suppress aldosterone production in primary hyperaldosteronism
4 causes of primary hyperaldosteronism
Adrenal adenoma (Conn’s Syndrome): Often associated with primary hyperaldosteronism.
Bilateral adrenal hyperplasia: Common cause of Conn’s Syndrome.
Familial hyperaldosteronism: Rare genetic conditions leading to excessive aldosterone production.
Adrenal carcinoma: A rare malignant growth within the adrenal gland
which blood test should e done if you are worried a pt on carbimazole has developed sepsis due to agranulocytosis
FBC and blood culture
what levels of calcium and PTH would be seen in malignant hyperparathyroidism
high calcium with low parathyroid hormone (as parathyroid hormone-related protein mimics parathyroid hormone but is not detected in the assay)
what is myxoedema crisis a complication of
untreated hypothryoidism
history of visual problems
sudden onset retro orbital headache
nausea / vomiting
likely diagnosis
pituitary apoplexy
(a rare emergency and is defined as bleeding into the pituitary gland that occurs in patients who have pituitary tumours)
patients >50 years old associated with a raised ESR, jaw and tongue claudication and visual change
temporal artery thickening , loss of pulsation and tenderness and may have proximal stiffness
likely diagnosis
giant cell arteritis
what medication should be prescribe to treat vit D deficiency
ergocalciferol
what are the 4Ds of vitamin B3 (niacin) deficiency
diarrhoea
dermatitis - brown scaly rash on hands and neck (Casal necklace)
dementia
death
vegetarian starts to experience reduced sensation and pins and needles
which vitamin is she likely to be deficient in
B12
(vitamin B12 comes from animal products such as meat, fish and eggs. Vitamin B12 deficiency causes neurological symptoms, including peripheral neuropathy, visual changes and cognitive changes)
deficiency of which vitamin are white spots (“bitot’s spots”) on the conjunctiva suggestive of
vit A
what should be checked before a pt is started on levothyroxine
serum cortisol level
This is because patients with primary hypothyroidism may have additional autoimmune conditions such as hypoadrenalism and replacement of thyroid hormones may precipitate an adrenal crisis.
child with DKA complains of headache, has a deterioration in neurological status and bradycardia. what condition should be urgently checked for
cerebral oedema (swelling of brain parenchyma)
ABs for hashimotos
anti TPO ab
UK guidlines for diagnosing DKA
blood ketone levels ≥ 3.0 mmol/L
hyperglycaemia
(blood glucose > 11.0 mmol/L)
acidosis
(bicarbonate < 15.0 mmol/L and/or venous pH < 7.3).
projectile non-bile-stained vomiting following feeds, usually within the first 6 weeks of life and rarely in older children
diagnosis?
pyloric stenosis
what is the effect of calcium carbonate on levothyroxine
Calcium carbonate decreases the absorption of oral Levothyroxine. They should be taken 4 hours apart
what is diabetic ketosis
Hyperglycaemia and raised ketones in the absence of acidosis
which antibodies are seen in post partum thryoditis
anti TPO antibodies
which quick investigations can one done to assess for DKA
capillary blood gas (quicker, less distressing and just as beneficial as ABG)
capillary blood ketones
what VBG result does diarrhoea cause
Normal Anion Gap Metabolic Acidosis.
what VBG result does hypokalaemia cause
Metabolic alkalosis
what VBG result does Addisons disease cause
Normal Anion Gap Metabolic Acidosis
what VBG does vomiting cause
metabolic alkalosis
a cause of raised anion gap (>16) metabolic acidosis
diabetic ketoacidosis
what is the DVLA guidance surrounding hypoglycaemia
if a patient has more than one severe episode of hypoglycaemia whilst awake or one episode of severe hypoglycaemia (ie the pt required help from another person to mange it) whilst driving then they must stop driving immediately and inform the DVLA
what is hypoglycaemic unawareness
patient is having a hypoglycaemic attack but does not show the normal symptoms of hypoglycaemia such as shaking, sweating, tremor
how to treat hypoglycaemic attack in a pt with hypoglycaemic unawareness
glucogel
levothyroxine dose for over 65 / adults with history of CVD
25-50 ug
best first line Ix for pt presenting with hair loss
Thyroid function tests and ferritin
diagnosis if a pregnant women presents with normal TSH but low t3/t4
normal physiology - Low free T3 and T4 levels in the second and third trimester of pregnancy is normal
what is pandered syndrome
an inherited disorder where there is a defect in thyroxine synthesis leading to hypothyroidism. This tends to present at an early age
most likely cause of deterioration a few hours into treatment for DKA
cerebral oedema
best test for differentiating an endogenous from an exogenous cause of hypoglycaemia
Serum C peptide
Serum C-peptide is a byproduct of insulin production. Therefore, if it is raised this indicates that there is excessive endogenous insulin production. In contrast, if it is not raised then this indicates that the patient has administered herself insulin
most common cause of hypothyroidism with negative antibodies
iodine deficiency
which parts of the world have high prevalence of iodine deficiency
Middle East, Nepal (for the purposes of exams) and parts of South America
how long should a dehydrated child with DKA (but not in shock) be given 10ml/kg 0.9% NaCl fluids for
30 mins
which anti hyperglycaemic drug is most likely to cause a hypoglycaemic event
sulphonylureas eg gliclazdie
difficulty concentrating, hair loss and joint pain, heavy menstrual periods
likely diagnosis?
hypothyroidism
effect of hypothyroidism on periods
causes heavy menstrual periods
effect of hyperthyroidism on periods
irregular, lighter or missed periods
if a patient is unconscious with hypoglycaemia in a hospital ward, do you give IM glucagon or IV dextrose
IV dextrose (10%)
this is a more rapid way of treating hypoglycaemia and the pt is likely to have IV access as its in the hospital
IM glucagon is suitable in treating hypoglycaemia, but it has a slower duration of action (hours instead of minutes). Therefore, IM glucagon is preferred only when IV access cannot be established.
what is losing the lateral third of eyebrow suggestive of
hair loss due to possible hypothyroidism
diagnostic test for insulinoma
72 hr fast
A 72 hour supervised fast is key to observing a monitored drop in blood glucose levels and then at the moment of proper hypoglycaemia taking the correct hormonal blood profile which would include plasma insulin levels, pre-insulin, pre-pro insulin and ketones amongst others
which drugs can affect the absorption of levothyroxine
ferrous sulphate
calcium chloride,
digoxin
Hormone Replacement Therapy
side effect of levothyroxine
osteoporosis
contrast the mechanism and causes of CDI and NDI
Central DI (More common)
insufficient levels of ADH from posterior pituitary.
Causes:
pituitary tumour/surgery,
traumatic brain injury,
infection (meningitis),
sarcoidosis,
TB,
SAH,
hereditary haemochromatosis
Nephrogenic DI
defective ADH receptors in the distal tubules and collecting ducts.
Causes:
lithium therapy,
electrolyte imbalances (hypercalcaemia or hypokalaemia),
idiopathic,
inherited (AVP2 gene)
which receptors in the collecting duct does ADH work on
increases water reabsorption into blood in collecting duct via V2 receptors
symptoms of DI
polyuria with very DILUTE URINE
nocturia
polydipsia
dehydration
no symptoms suggestive of DM
what is the urine and plasma osmolality in DI
Low urine osmolality + High serum osmolality
contrast plasma/urine osmolality and sodium levels in DI and psychogenic polydipsia
DI:
low urine osmolality
high plasma osmolality
hypernatraemia (and hypokalaemia)
PP:
low urine osmolality
high plasma osmolality
hyponatraemia
glucose levels in DI
normal
sodium and potassium conc in DI
high sodium conc
low potassium conc
(bc dehydrated)
which test can be used to differentiate PP, CDI and NDI
1) low plasma osmolality, low urine osmolality –> PP
high plasma osmolality, low urine osmolality –> DI
2) do water deprivation test
If osmolality corrects itself then more sure it’s psychogenic polydipsia
3) If no correction, after 8 hours administer desmopressin to differentiate between CDI and NDI.
4)Urine osmolality will rise in CDI but remain low in NDI.
how to mange hypernatraemia in DI, and what should you be cautious about
manage with oral or IV fluids (prevent dehydration)
(be careful, as correction of chronic hypernatraemia too fast predisposes to cerebral oedema)
CDI Tx
intranasal desmopressin
NDI Tx
discontinue causative agent if medication induced (lithium),
Thiazide Diuretics,
sodium restriction
whipple’s triad for hypoglycaemia
low blood glucose concentration,
hypoglycaemic symptoms
resolution of symptoms after raising blood glucose concentration to normal
causes of hypoglycaemia in diabetics
insulin or sulfonylurea use,
fasting/missing meals
drugs which cause hypoglycaemia
sulfonylureas and insulin,
SGLT-2 inhibitors,
DPP-4 inhibitors
hormone deficient which cause hypoglycaemia
hypopituitarism
adrenal insufficiency (Addisons)
malignant cause fo hypoglycaemia
Insulinoma (excessive secretion of insulin due to tumour in pancreas)
3 categories of symptoms in hypoglycaemia
- Increased Sympathetic Activity
sweating, anxiety, tachycardia, tremor, palpitations, pallor - Increased Parasympathetic Activity
hunger, nausea, vomiting, paraesthesia - Neuroglycopenic
confusion, seizures, agitation
which glucose levels cause neuroglycopenic symptoms and autonomic symptoms in hypoglycaemia
<2.8 mmol/L causes neuroglycopenic symptoms,
<3.3 mmol/L causes autonomic symptom
what can be measured to determine whether hypoglycaemia is due to endogenous or exogenous insulin
C peptide - high C peptide = endogenous insulin eg insulinoma
what is the cause of hypoglycaemia if C peptide and insulin are high
insulinoma
what is the cause of hypoglycaemia if cortisol is low
adrenal insufficiency (Addisons)
what should you always measure in any patient presenting with confusion/neurological symptoms
measure blood glucose
insulinoma Tx
surgical excision
hypoglycaemia Tx in conscious pt who is able to swallow
oral glucose 15-20g (liquid, gel or tablet)
fast-acting carbohydrates (glucose tablets, candy, juice)
hypoglycaemia Tx in unconscious pt
IM Glucagon (takes hours to work)
IV Dextrose (20% Glucose) (more rapid or if glucagon doesn’t improve symptoms)
if have access to IV, use Iv dextrose, if in community use IM glucagon in meantime
describe the process of developing DKA
1)infection / inadequate insulin therapy / undiagnosed T1DM / MI
2)no insulin to suppress lipolysis
3) ketone formation
4) acidosis
how could infection cause DKA and what are the sick day rules
Infection/illness
→ increased cortisol (antagonist of insulin)
→ bodies insulin requirements increase
⇒ hence type 1 diabetics should make sure they continue taking insulin when they are unwell to prevent DKA
‘Sick Day Rules’
⇒ continue normal insulin dose,
check blood glucose more regularly,
aim to drink 3L of fluid over 24hrs,
self-monitor ketones regularly through day.
DKA symptoms
N&V
severe abdo pain
Kussmauls breathing - hyperventilation
Dehydration → dry mucous membranes, decreased skin turgor, slow CRT, tachycardic, hypotensive
reduced consciousness
fruity breath
rapid onset <24hrs
VBG in DKA
metabolic acidiosis with raised anion gap (>16), with partial respiratory compensation (hyperventilation)
glucose level in DKA
HIGH
sodium and potassium in DKA
low sodium
high potassium
due to lack of insulin
UK guidlines for DKA diagnosis
blood ketone levels ≥ 3.0 mmol/L
hyperglycaemia (blood glucose > 11.0 mmol/L)
acidosis (bicarbonate < 15.0 mmol/L and/or venous pH < 7.3
what should be given in DKA if there is severe metabolic acidosis
IV bicarbonate
how should regular insulin medication be adjusted after DKA
continue long acting insulin, stop short acting insulin
2 key parts of DKA Tx
- Rehydrate → IV Fluids (Isotonic Saline - 10ml/kg 0.9% NaCl)
important complication of fluid resuscitation in DKA = cerebral oedema (may cause headache, reduced consciousness, rise in BP, seizures)
With Electrolyte repletion (especially K+ as insulin will drive it into cells) → Potassium Chloride
- Reduce Ketones → fixed rate IV Insulin (0.1 units/kg/hour) (AFTER FLUIDS)
Once glucose falls, give 5% dextrose
in which people does HHS commonly occur
older people with T2DM
why is DKA prevented in HHS
there is still smalll amounts of insulin being secreted by the pancreas
RF for HHS
infection (most commonly pneumonia or UTI),
surgery,
inadequate insulin therapy,
acute illness(MI, sepsis, stroke),
non-adherence to diabetes medications
what are the main components of HHS
hyperglycaemia (>30),
hyperosmolality (>320),
volume depletion (dehydration)
in the absence of significant ketoacidosis
DKA vs HHS
both have
N&V,
features of dehydration,
weight loss/polyuria/polydipsia
DKA =rapid onset <24hs, HHS = more insidious onset over days
DKA = abdominal pain, HHS = no abo pain
DKA = fruity breath odour and kussmaul respirations)
^ not seen in HHS
DKA = normal serum osmolality, HHS = significantly risen serum osmolality
ketones in HHS
negative
what is the key parameter to monitor in HHS
serum osmolality - is significantly raised in HHS
how to estimate serum osmolality in HHS
Estimated Serum Osmolality = 2(Na+K) + Glucose + Urea
Tx for HHS
Fluid Resuscitation (IV Fluids) → Isotonic Saline solution (0.9% NaCl)
- Excessive infusion of NaCl
⇒ can cause hyperchloraemic acidosis (hence hartmann’s solution may be preffered when large volumes of fluid are to be administered). - Excessive infusion of any IV fluid can cause pulmonary oedema and potentially cardiac failure.
Electrolyte Repletion (if needed) → add potassium (KCl) to infusion
- IV Insulin (0.05 units/kg/hr)
→ not given first, as can result in cerebral oedema due to quick shift in glucose. - If Glucose falls
→ 5% Dextrose
2 things to be cautious about during fluid resuscitation in HHS
excessive infusion of NaCl can cause hyperchloraemic acidosis - so can use Hartmanns solution when need to infuse a large volume
excessive infusion of any IV fluid can cause pulmonary / cerebral oedema and cardiac failure –> monitor for this (cerebral oedema will present as headache/pain, the deterioration)
order of progression of the types of diabetic eye disease
Background Retinopathy → Pre-Proliferative Retinopathy → Proliferative Retinopathy (Also Maculopathy)
which 2 things can cause complete loss of vision in diabetic eye disease
retinal detachment
vitreous haemorrhage
retinal detachment vs vitreous haemorrhage
retinal detachment:
- sudden painless loss of bison
flashers
floaters
dense shadow starts peripherally and moves central
vitreous haemorrhage
- bleeding into nitrous humour
sudden blurring
dark spots
floaters
NO flashers
fundoscopy findings in background / pre proliferative / proliferative retinopathy and maculopathy
○ Background → microaneurysms, blot haemorrhages, hard exudates (lipid deposits)
○ Pre-Proliferative → background + cotton wool spots (soft exudates)
○ Proliferative → non-proliverative + neovascularisation (new vessels on disk)
Maculopathy → hard exudates (ie. background retinopathy) that happens to be near macula
background retinopathy Tx
improve glycaemic control and regular observation
pre proliferative and proliferative retinopathy Tx
pan-retinal laser photocoagulation
maculopathy Tx
VEGF inhibitors
what is diabetic neuropathy caused by
blockage of vasa nervorum
how does chronic hyperglycaemia cause diabetic neuropathy
causes glycation of axons
features of diabetic neuropathy
MOSTLY AFFECTS SENSORY AXONS, BUT CAN AFFECT A SOME MOTOR AXONS TO A LESSER EXTENT
Peripheral Neuropathy:
* Pain (Peripheral) → described as burning/sticking/aching. Often worse at night and may disturb sleep. * Loss of Sensation (Peripheral) → at early stage affects tips of toes or fingers. Eventually causes a symmetrical distal sensory loss in a 'glove and stocking distribution’. * Dysaesthesia (Peripheral) → burning sensation in feet * Reduced/Absent Ankle Reflexes (Peripheral) * Painless Injuries (Peripheral) → occur at pressure points. Infection is a common complication, followed by gangerene if vascular compromise.
Mononeuropathy
→ sudden motor loss (eg. wrist drop, foot drop, 3rd nerve palsy - down and out eye)
Autonomic
→ resting tachycardia,
urinary frequency/urgency/nocturia/incontinonence/hesitency/weak stream/retention,
erectile dysfunction,
constipation,
difficulty swallowing,
postural hypotension
Gastroparesis (GI Autonomic Neuropathy)
what treatment should be initiated if someone with diabetic neuropathy begins to experience N&V, abdo pain, bloating, loss of appetite, refleux
metoclopramide
(Gastroparesis)
mech of action of metoclopramide
pro-kinetic that improves gastric emptying
Ix for diabetic neuropathy
Test sensation using 10g monofilament
Tuning fork (decreased vibration sense), Pinprick assessment (decreased sensation)
where are neuropathic ulcers often seen in diabetic neuropathy
over pressure points eg
plantar surface of metatarsal head
plantar surface of hallux
Tx for pain associated with diabetic neuropathy
1st line = duloxetine
2nd line = amitriptyline, gabapentin or pregabalin
Avoid amitriptyline in patients with BPH as can cause urinary retention
which pts should amitriptyline be avoided in
Avoid amitriptyline in patients with BPH as can cause urinary retention
3 major histological changes of diabetic nephropathy
mesangial expansion,
glomerular basement membrane thickening,
Glomerulosclerosis
symptoms of diabetic nephropathy
- Hypertension
- Oedema → in advancing diabetic nephropathy
- Polyuria
- Lethargy
first line Ix for diabetic nephropathy
urinalysis
(ACR >2.5 = microalbuminuria)
how and how often should pts be screened for diabetic nephropathy
anual screening
using urinary ACR (ACR >2.5 = microalbuminuria)
gold standard Ix for diabetic nephropathy
- Gold Standard: Renal Biopsy
→ shows kimmelstiel-wilson nodules (also mesangial expansion and GBM thickening)
eGFR level in diabetic nephropathy
GFR raised in early disease but reduced in late disease
management of diabetic nephropathy
Antihypertensive Treatment
→ ACE inhibitors or ARBs are first line (renoprotective effect).
Add CCB or Thiazide Diuretic as 2nd line.
Tight Glycaemic Control
Control Dyslipidaemia
→ Statins (atorvastatin)
Dietary Modification
→ reduce protein and salt intake
Smoking Cessation
what is seen on renal biopsy for diabetic nephropathy
kimmelstiel-wilson nodules
which medication can cause diabetes
corticosteroids
metformin side effects
lactic acidosis
Gi effects
- diarrhoea
- N&V
- abdo discomfort
Metallic taste in mouth
–> weight NEUTRAL
what is recommended for pts with a fasting glucose of >5.6mmol/L but <7mmol/L
2 week trial fo diet and exercise
which antidiabetic drugs can cause acidosis and whats the difference n the acidosis they cause
metformin. - lactic acidosis (NO KETONES)
SGLT2 inhibitor - ketoacidosis
which anti HTN drugs are teratogenic
ACE inhibitors
metformin mech of action
increases insulin sensitivity
reduces hepatic gluconeogenesis
when can metformin be prescribed
if HbA1C ≥48 despite lifestyle advice
which conditions are type 1 diabetes pts checked for due to the common association between them
autoimmune thyroid disease
coeliac disease
autoimmune gastrotis
pernicious anaemia
vitiligo
criteria for diagnosing T2DM
If symptomatic, one of the following results is sufficient for diagnosis:
- Random blood glucose ≥ 11.1mmol/l
- 2-hour glucose tolerance ≥ 11.1mmol/l
- HbA1C ≥ 48mmol/mol (6.5%)
If the patient is asymptomatic, two results are required from different days.
or
2 abnormal fasting glucose results
* Fasting plasma glucose ≥ 7mmol/l
what type of drug is glimepiride
sulphonylurea
which microorganism is commonly found in diabetic foot ulcers
Pseudomonas
what is the honeymoon period in T1DM
Immediately after diagnosis, insulin requirements may be very low if the pancreas is still able to produce a significant amount of insulin. This is known as the ‘honeymoon period’. It is important that children are closely monitored during this time. This is because insulin requirements can suddenly increase as the remaining beta cells are destroyed. Additionally, as the blood glucose may be normal in this period on very low insulin doses, parents may incorrectly think that the condition has gone away.
first lien Tx for T1DM
basal bolus insulin, or if pt has good self-management skills may prefer to use an Insulin pump
which pts can receive fixed dose insulin
if they cannot manage 3-4 insulin injections daily, or have trouble mixing the insulin
what should be the target bp for diabetic pts
140/90
what counts as an impaired fasting glucose
6.1-6.9 mol/L
what counts as a diabetic fasting glucose
7+ mmol/L
what counts as impaired glucose tolerance (2hr OGTT)
7.8-11 mmol/L
what counts as a diabetic glucose tolerance (2hr OGTT)
11.1+ mmol/L
can C peptide levels be used to diagnose diabetes
no, can be used to differentiate between type 1 and 2 diabetes
when can just a random blood glucose result be sued to diagnose diabetes
One measurement of blood glucose >11.1mmol/L in a symptomatic patient is sufficient to diagnose diabetes mellitus
which anti diabetic medication can cause weight gain
sulphonylurea
(and pioglitazone)
what is a high risk contributor to the development of gestational diabetes
maternal obesity (BMI>30)
type 2 diabetic pt presents with hypoglycaemia, which medication could have caused this
sulphonylurea eg gliclazide
what kind of diabetic drug is glibenclamide
sulpohonylurea
what will pulses and foot temp be like in the case of an arterial leg ulcer vs neuropathic foot ulcer
palpable pulses and warm foot in neuropathic not arterial
moat appropriate initial Ix for diabetic retinopathy
fundoscopy
target HbA1c for diabetic pt managed by diet / lifestyle / single drug
48
target HbA1c for diabetic pt managed by 2+ drugs / sulphonylurea
53
T1DM diagnosis
If symptomatic, one of the following results is sufficient for diagnosis:
Random blood glucose ≥ 11.1mmol/l or Fasting plasma glucose ≥ 7mmol/l
2-hour glucose tolerance ≥ 11.1mmol/l
HbA1C ≥ 48mmol/mol (6.5%)
If the patient is asymptomatic, two results are required from different days.
To confirm T1DM, the following investigations can be done:
Autoantibody testing: Identification of specific antibodies (e.g. anti-GAD, ICA, IAA) contributes to confirming the autoimmune nature of T1DM.
C-peptide levels: Evaluation of C-peptide production helps assess endogenous insulin secretion.
Urine ketone testing: Presence of ketones may suggest concurrent DKA.
best initial Ix for T1DM
glucose - faster and more accurate than HbA1c - takes longer and level can be affected by other things
what type of medicine is indapamide
diuretic
recommendation for pt taking metformin when fasting during ramadan
Continue on 500mg, take the morning dose before Suhoor (pre-sunrise meal), combine afternoon dose with dose taken at Iftar (after sunset meal)
most common autoantibodies associated with T1DM
ICA (islet cell autoantibodies) —> MOST COMMON
anti GAD antibodies (glutamic acid decarboxylase)
IAA (insulin autoantibodies)
what is balanitis
inflammation of glans penis
what should be prescribed if a T2DM pt has symptomatic hyperglycaemia,ia
insulin or a sulphonylurea
after starting medication for diabetes what should be checked at 3-6 monthly intervals
check HbA1c at 3-6 monthly intervals until it is stable on a set diabetes treatment plan.
how often should diabetic retinopathy / nephropathy / neuropathy be screened for in diabetic pts
at diagnosis, and then annually
what is allodynia
pain due to a stimulus that does not normally provoke pain.
An example would be a light feather touch (that should only produce sensation), causing pain.
which condition presents with ascending cure bilateral motor loss
Guillain-barre (auto-immune condition against nerves)
which ulcers are commonly found above the medial or lateral malleolus
venous ulcers
first course of action in gastroparesis due to diabetic neuropathy
stabilise blood glucose levels
what is listeriosis
serious infection caused by eating food contaminated with listeria bacteria eg cold cooked sliced meats
normal / average birth weight
2.5 kg - 4kg
what is AGPAR score and what is a normal score
test given to newborns a few minutes after birth - checks HR, muscle tone etc to check baby’s stability
normal = 7-10
what is macrosomia
birth weight > 4kg
what does macrosomia and neonatal seizures suggest
gestational diabetes in the mother
how does pre eclampsia affect weight of babies
lower birth weight due to reduced placental blood flow
what do neonatal seizures, microcephaly, petechial rash, jaundice and low birthweight suggest
CMV transmitted vertically from mother to foetus
diagnostic criteria for gestational diabetes
either:
a fasting plasma glucose level of ≥5.6 mmol/L;
or
a 2-hour post-oral glucose tolerance test plasma glucose level of ≥7.8 mmol/L
when would you use short/rapid acting subcutaneous insulin vs fixed rate insulin infusion
fixed rate insulin infusion: hyperglycaemic crisis eg HHS
rapid acting subcutaneous insulin: patient develops hyperglycaemia, has been present fro several hours and is not resolving, pt is not critically unwell
which anti diabetic medications should be stopped when a pt is reaching the last phase of heir life
medications which can cause hypoglycaemia eg Sulphony;ureas
risk of mother under 25 yrs w T1DM passing it onto child
1/25
3 reasons for immediate referral to an ophthalmologist in the case of diabetic retinopathy
proliferative retinopathy - angiogenesis / neovascularisation
vitreous haemorrhage
retinal detachment
urine osmolality after fluid deprivation n and after desmopressin in partial cranial DI
A urine osmolality of 300-800mOsm/kg after fluid deprivation
and
<800mOsm/kg after desmopressin
which cells produce insulin
beta cells
how can bendroflumethiazide cause elevated blood sugars
Bendroflumethiazide works on the distal convoluted tubule to reduce both sodium and potassium reabsorption.
Insulin release from Beta cells is mediated in part by membrane ATP-sensitive potassium channels.
Due to low serum potassium there is therefore decreased insulin release and therefore worsening blood sugars
what type of DI does lithium cause
nephrogenic DI
what is Wolfram syndrome
aka DIDMOAD syndrome
DI (diabetes insipidus)
DM (diabetes mellitus)
OA (optic atrophy)
D (deafness)
what is acarbose used for ad what is side effect
cam be used for T2DM but not as effective as other meds
Sid effects of GI upset / flatulence / bloating
best Tx for postural hypotension
increase dietary NaCl
next step in gestational diabetes if fasting palms glucose remains uncontrolled on diet, exercise and metformin
insulin
