Diabetes and Pituitary Flashcards
How does Diabetes Mellitus type 1 cause hyperglycaemia
pancreatic islet beta cells destroyed (autoimmune response)
ABSOLUTE insulin insufficiency leading to lipolysis and ketogenesis
how does diabetes mellitus type 2 cause hyperglycaemia
reduced peripheral sensitivity to insulin
reduced insulin production (over time)
which alleles are associated with type 1 diabetes
HLA DR3/4 (hoes in la diabetic aRound 3/4)
risk factors for t2d
obesity, HTN, inactivity, disturbed lipids
typical patient profile T1DM
<20 yrs
FH autoimmune
presents with polyuria and polydipsia
presents with weight loss and fatigue
DKA symptoms and signs
nausea and vomiting
abdo pain
kussmaul breathing (deep hyperventilation)
sweet-smelling breath (ketonaemia)
typical patient profile T2DM
> 40 yrs
often asymptomatic
polyuria, polydipsia
RF: obesity, hypertension, south asian/ afro-carribean
examination: acathosis nigricans, symptoms of micro/macrovascular complications of T2DM
How is a diagnosis of DM made
symptomatic + 1 test
asymptomatic + 2 different tests on two different days
tests specific for T1DM
urine dip for glucose and ketones
specific antibodies are useful to distinguish between T1 and T2 but not necessary for T1 diagnosis
Anti-GAD (80%) and islet cell antibodies (ICA) (70-80%)
tests for type 1 and 2
n= normal, d= diabetes, prediabetes is between
random glucose (n <11.1, d=>11.1)
fasting glucose (n <5.5, d=> 7.0)
2hr post prandial glucose (n< 7.8, d =>11.1)
HbA1c (n <42 [6%], d=> 48 [6.5%]
HbA1c should not be used in
children or young ppl
pt suspected of having T1DM
pt with symptoms of diabetes <2 months
pt at high risk and acutely ill
pt taking meds that cause rapid glucose rise (steroids, antipsychotics)
pt with acute pancreatic damage including pancreatic surgery
presence of factors that influence HbA1c
Management of T1DM
insulin
personalised to pt
monitored daily using capillary glucose and over time using HbA1c (3mo)
basal-bolus regime = long acting (subcut insulin glargine o.d) + short acting (subcut insulin lispro and aspart pre-meal)
T2D management summary
lifestyle mods
glycaemic control
lipid management
bp management
antiplatelets
lifestyle mods T2DM management
diet
exercise
education
glycaemic control T2DM management
If HbA1c > 48 on lifestyle modification start metformin
if HbA1c >58 metformin + another drug (DPP-4i, pioglitazone, sulfonylurea and sglt-2i)
if HbA1c still >58:
metformin + sulfonylurea + (DPP-4i or pioglitazone)
metformin + sglt-2i + (pioglitazone or sulfonylurea)
insulin based treatment
BP management T2DM
all BP management starts with ACEi/ARB rather than CCB even if patient is black or over age 55
step 1: ACEi or ARB (ARB preferred for black pts)
step 2: add CCB or thiazide
step 3: ACEi/ARB + CCB + thiazide
check potassium, consult specialist
step 4: if K<4.5, add spironolactone. of K>4.5, add b-blocker
lipid management T2DM
atorvastatin 20 mg o.d if 10-year cardiovascular event risk =>10%
atorvastatin 80 mg o.d if IHD/CVD/PAD
antiplatelet management (T2DM)
Aspirin 75mg for patients with IHD/CVD/CVD
A 65yr old man present to his GP for bp check. ambulatory bp constantly above 140/90. PMH shows gout and T2DM for which he takes metformin and allopurinol. He is black
which is the most appropriate drug
A: Amlodipine
B: Bendroflumethiazide
C: Irbesartan
D: Ramipril
E: Spironolactone
The correct answer is irbesartan. This medication is an angiotensin II receptor blocker (A2RB).
It is used to manage hypertension in diabetic patients, as it has a renoprotective effect.Black African and Afro-Caribbean patients are prescribed calcium channel blockers first-line for hypertension.
However, as the patient is diabetic, ACE inhibitors/A2RBs are preferred due to their renoprotective effect. In black African and Afro-Caribbean patients, A2RBs are preferred over ACE inhibitors.
Complications for DM
Acute metabolic:
hypoglycaemia
DKA
hyperosmolar hyperglycaemic state
Long term microvascular:
retinopathy
neuropathy
nephropathy
long term macrovascular:
ischaemic heart disease
cerebrovascular disease
peripheral artery disease
plasma glucose hypoglycaemia
<3.6 mmol/L
cause of hypoglycaemia
inappropriate insulin regime
missed meals
drugs (sulfonylureas, SGLT-2 inhibitors etc)
signs of hypoglycaemia
tachycardia
tremor
sweating
pallor
anxiety
drowsiness
confusion
altered behaviour (aggression)
coma
Treatment of hypoglycaemia
give sugar
conscious - oral glucose and complex carb
impaired consciousness - IM glucagon 1mg
IV 10% dextrose infusion if glucagon fails to improve symptoms
A 20yr old man with T1DM brought into A+E following a seizure after a heavy night out yday. Injected insulin this morning but fell back asleep before eating. Drowsy in ambulance but now cannot be roused. Ambulance staff performed cap glucose which was 1.8 mmol
what is most urgent step in the management of this pt
A: IV insulin
B: IM glucagon
C: IL 0.9% saline
D: feed sugary foods
E: 500 mL 50% IV dextrose
This patient is experiencing severe hypoglycaemia with neuroglycopaenic effects of seizures and reduced consciousness
B: administration of IM glucagon 1mg is the initial management for hypoglycaemic patients with reduced consciousness. It will stimulate the liver to convert glycogen to glucose and release this into the blood therefore increase hepatic glucose output and increasing blood sugar levels. If this does not bring glucose >4mmol/L after 10 mins, IV dextrose at 10% or 20% should be administered
Is DKA more common T1 or T2
T1
DKA triad
hyperglycaemia, ketonaemia and metabolic acidosis
high levels of glucose cause polyuria which causes dehydration (treat with IV fluids)
high levels of ketones (treat with insulin) is highly acidic which leads to enzyme dysfunction resulting in coma and death
DKA treatment
rehydrate with IV fluids and reduce ketones with insulin
hyperosmolar hyperglycaemic state is more common in which type of diabetes
t2dm
difference in pathophysiology is DKA and HHS
DKA- absolute lack of insulin and increased stress hormones causing hyperglycaemia, ketonaemia and metabolic acidosis
HHS- hyperglycaemia but no ketonaemia as still some insulin to suppress ketogenesis
difference in causes dka and hhs
both- infection, other acute illness and non-adherence to diabetes meds
signs and symptoms DKA and HHS
dka- collapse/confusion, abdo pain, nausea, vomiting, kussmaul breathing, dehydration
hhs- same minus abdo pain
Ix results for DKA and HHS
dka: ketones > 3mmol/L, pH < 7.3, plasma glucose > 11
hhs: ketones <3mmol/L, pH normal, plasma glucose > 30
Mx for dka and hhs
fluids started first (normal saline) + potassium chloride (is k+ < 5.5)
IV insulin after fluids and only when K+ not <3.5
include dextrose if fluids falls < 14
treat underlying cause
13 yr old boy presents to a+e with generalised abdo pain. nauseous and vomited 4 times. progressively getting drowsier. groans when you palpate his abdomen
what is the most appropriate initial management option?
A. fixed rate insulin infusion
B. variable-rate insulin infusion
C. 10 U actrapid STAT
D. 10 ml 10% calcium gluconate
E. IL IV 5% dextrose
A. DKA treatment is IV fluids, fixed-rate insulin infusion
background retinopathy: findings and management
blot and dot haemorrhages/ hard exudates
mx: improve glycaemic control
pre-proliferative retinopathy: findings and management
background retinopathy findings + cotton wool spots
mx: pan-retinal laser photocoagulation
proliferative retinopathy: signs and management
non-proliferative + new vessels on disk (neovascularisation)
neovascularisation is often associated with retinal detachment and vitreous haemorrhage which leads to vision loss
mx: pan-retinal laser photocoagulation
maculopathy retinopathy: signs and management
hard exudates happens to be near macula
mx: intravitreal VEGF (vascular endothelial growth factor) inhibitors
nephropathy signs, ix and mx
signs: oedema, polyuria, lethargy, hypertension
ix: 1st line urinalysis. increased ACR = microalbuminuria
gold standard - renal biopsy showing Kimmelstiel Wilson nodules
mx- ACEi/ARB (renoprotective)
- improve glycaemic control
what do you find in peripheral neuropathy
glove and stocking distribution
loss of sensation esp feet
monofilament on lower limb exam
loss of ankle jerk/vibration sense/fractures (Charcot’s joint)
what do you find in mononeuropathy
sudden motor loss usually eg wrist drop, foot drop, 3rd nerve palsy
what do you find with autonomic neuropathy
difficulty swallowing, delayed gastric emptying, bladder dysfunction
postural hypotension
cardiac autonomic supply
mx of neuropathy
glycaemic control
if painful use neuropathic pain agent (duloxetine, pregabalin, gabapentin)
what is diabetes insipidus
inadequate secretion or sensitivity to vasopressin (ADH)
hypotonic polyuria
2 types of diabetes insipidus
cranial - lack of vasopressin release from posterior pituitary
nephrogenic - collecting ducts insensitive to vasopressin
causes of cranial and nephrogenic DI
cranial: pituitary tumour/surgery, traumatic brain injury, infection (meningitis), sarcoidosis/TB, subarachnoid haemorrhage
nephrogenic: lithium therapy, electrolyte imbalance (high Ca, low K), idiopathic, ureteric obstruction, inherited (AVPV2 gene)
control of osmolality following water deprivation
water deprivation
increased serum osmolality
osmoreceptors stimulated
posterior pituitary releases vasopressin (ADH)
increased water reabsorption from renal collecting ducts
reduced urine volume, increased urine osmolality and reduced serum osmolality
presentation for DI
polyuria (incl nocturia)
polydipsia
dehydration: tachycardia/reduced tissue turgor, dry mucous membranes
signs of the cause (eg bitemporal hemianopia)
Ix for DI
U+Es (Ca/K for cause, Na (rarely raised), increased urea)
glucose to exclude DM
plasma osmolality = high
urine osmolality = low (>700 excludes DI)
diagnostic test for types of DI
water deprivation test
water restricted fr 8 hrs
plasma and urine osmolality measured every hour
after 8 hrs give desmopressin and measure urine osmolality
management of DI
treat the cause
cranial: intranasal desmopressin (should not drink large amounts of water on this med)
nephrogenic: thiazide diuretic, low salt/protein diet
SIADH Ix
serum Na low
urine Osm high
urine Na high
causes of SIADH
CNS: Subarachnoid haemorrhage, tumour, TB
pulmonary: pneumonia, bronchiectasis
malignancy: small cell lung cancer
drugs: carbamazepine, SSRI
idiopathic
management for mild SIADH
treat cause
immediate fluid restrict for hyponatraemia
if ineffective: oral demeclocycline, IV vaptan
normal serum sodium
135-145 mEg/L
hypovolaemic hyponatraemia causes and management
causes: diarrhoea, vomiting, diuretics
management: IV fluids
euvolaemic hyponatraemia causes and management
causes: SIADH, hypothyroidism, adrenal insufficiency
1.TFTS - if normal then
2) do a shorty synacthen test to look for adrenal insufficiency
3) if normal look for cause, eg drug history, breast exam, CXR to look for lung pathology, brain scan
hypervolaemic hyponatraemia causes and Mx
causes: liver failure, renal failure, heart failure
Mx: fluid restrict
what to do in case of urinary sodium <20
if very severe hyponatraemia (seizures, reduced consciousness), give slow hypertonic saline (too fast can cause central pontine myelinolysis)
sodium levels for hypernatraemia
serum Na > 145 mEg/L
causes of hypernatraemia
unreplaced water loss
- GI losses, sweat loss
- renal losses: osmotic diuresis (eg HHS), diabetes insipidus
sodium overload (rare)
- Cushing’s, primary aldosteronism, iatrogenic (hypertonic saline)
hypernatraemia presentation
lethargy
irritability
thirst
signs of dehydration
confusion
coma
fits
management of hypernatraemia
correct water deficit - 5% dextrose
correct ECF volume depletion - 0.9% saline
measure Na+ every 4-6hrs
types of pituitary adenoma
non-functional
-do not release hormones
-test visual fields
- brain MRI with contrast
functional
- acromegaly (GH secreting)
- prolactinoma (prolactin secreting)
- Cushing’s disease (ACTH secreting)
pituitary adenomas of either type can compress other parts of the pituitary gland (hypopituitarism)
can compress optic chiasm causing bitemporal hemianopia
what are the causes of hyperprolactinaemia
physiology:
-pregnancy
-breast feeding
pathological:
-prolactinoma
-other pituitary adenoma (stalk compression)
-primary hypothyroidism
presentation of men with hyperprolactinaemia
loss of libido, erectile dysfunction, infertility, galactorrhoea (uncommon)
mass effect of tumour: headaches/visual field defect
presentation of women with hyperprolactinaemia
galactorrhoea, secondary amenorrhoea/oligomenorrhoea, loss of libido, infertility
mass effect of tumour: headaches/visual field defect
how does hyperprolactinaemia affect GnRH
high prolactin suppresses GnRH pulsatility
Ix for hyperprolactinaemia
pregnancy tests (exclude physiological hyperprolactinaemia)
TFTs
Basal serum prolactin
MRI preferred imaging
Prolactinoma management
1st line- Dopamine receptor (D2) agonists eg bromocriptine, cabergoline > reduce prolactin secretion and tumour size
2nd line- Surgery
when to suspects T2DM in adult
if they present with persistent hyperglycaemia plus clinical features eg polydipsia, polyuria, blurred vision, unexplained weight loss, recurrent infections, tiredness, acanthosis nigricans
what is persistent hyperglycaemia defined as
HbA1c of 48 mmol/mol (6.5%) or more
fasting glucose of 7.0+
random plasma glucose pf 11.1mmol/L or more in presence of clinical features
how is t2dm diagnosed
symptomatic: one abnormal HbA1c or plasma glucose result
asymptomatic: repeat testing
metformin use has increased risk of which vitamin deficiency
b12
which drug class to offer diabetic patients with cvs disease
SGLT-2 inhibitor
what class of drug are gliclazide, glimepiride, glipizide and tolbutamide
sulfonylureas
associated with hypoglycaemia, weight gain
what class of drugs are alogliptin, linagliptin, sitagliptin, saxagliptin and vildagliptin
DPP-4 inhibitors
what class of drugs are canagliflozin, dapagliflozin, empagkiflozin and ertygliflozin
SGLT2 inhibitor
promote weight loss, improve cardiovascular outcomes
what class of drugs are dulaglutide, exenatide, liraglutide, lixisenatide and semaglutide
GLP-1
should be reserved for combination therapy when other options failed
