ENDOCRINE: DIABETES, THYROID, Flashcards
drug causes dysglycemia
glucocorticoids BB atypical antipsychotics fluoroquinolone protease and calcineurin inhibitors statins ( HMG-CoA Reductase inhibitors)
the diagnosis of diabetes in Canada is established by
a random plasma glucose ≥11.1 mmol/L
a fasting plasma glucose (FPG) ≥7 mmol/L
2hPG in a 75-g OGTT ≥11.1 mmol/L
an HbA1c ≥6.5% (in adults)
what is the target for diabetes
FPG 4-7 mmol/L
2HPG 5-10 mmol/L OR 5-8 if A1C target not met
HBA1C <7% or <6.5% if patient has low hypoglycemia risk to reduce CKD & retinopathy
when is higher <8.5% A1C target indicated?
<8.5% in patient with history of severe hypoglycaemia, limited life expectancy, frail and/elderly with dementia
when is higher <8.0% A1C target indicated?
functionally dependent ( to avoid hypoglycaemia)
diabetes+ ASCVD ( acute MI, Coronary/ arterial vascularization, stroke, TIA, PAD)–> add?
GLP1 ( liraglutide, dulaglutide or SQ semaglutide)
SGLT2 ( empa, cana)
Diabetes + HF?
Dapa or empa
CKD+ DIABETES
SGLT 2 ( cana ( most evidence) then daga or empa)
ESRD + diabetes, what agent ??
ESRD < 15ml/min
DPP4 ( alogliptin, linagliptin, sitagliptin) or dulaglutide or repaglinide or SU (gliclazide) )insulin (low dose)
Which diabetes agent has benefit on weight loss
GLP1 and SGLT2I
which diabetes agent have reduce risk of hypoglycaemia
GLP1
SGLT2
acarbose or pioglitazone
when is appropriate to add insulin?
symptomatic hyperglycaemia, metabolic decompensation or antihyperglycemics insufficient
A1C >10%
Glucose >16.7 mmol/L
what is the recommended insulin basal starting dose
0.1-0.2 units/kg/day OR 5-10 units/ day , titrate 1 unit/day to taget BG ( FP <7 mmol/L
when it is appropriate to initiate bolus insulin?
how should bolus insulin be initiated?
BG not control despite being on basal + SGLT2 or GLP1 OR gylcemic values extremely high, may start basal/bolus right away
then add bolus
what is the renal cutoff in metformin, SGLT2-inhibitor
eGFR <30 ml/min
what is the MOA of biguanides and AE?
AI: increasing peripheral glucose uptake and insulin sensitivity and decreasing hepatic production
AE: upset stomach, N/V/, metallic taste, rhinitis, acidosis, B12 deficiency
MOA of a-glucosidase inhibitor and AE?
acarbose; inhibit a-glucosidase enzyme in SI, less glucose in absorbed since carbohydrates are B/D
AE: flatulence, diarrhea, abdominal pain ( dose related), hepatitis
sulfonylureas MOA and AE
gliclazide, glyburide, glimepiride, tobutamide
Meglitinides ( repaglnide)
depolarizes beta cells to stimulate insulin
hypoglycaemia ( higher with glyburide and eGFR <60 ml/min) weight gain headache dizziness GI effects
MOA of thiazolidinediones and AE
pioglitazone and rosiglitazone
increase PPAR-y sensitivity to insulin and decrease hepatic glucose production
ae: exacerbations/cause of HF, fluid retention, weight gain ( 2-2.5 kg), fractures, macular edema (rare), URI, headache
what are the CI of thiazolidinediones
HF, liver failure, bladder cancer( pioglitazone-rare), MI ( rosiglitazone- controversial)
DPP-4 inhibition MOA and adverse effects
“liptin” drug, sitagliptin, saxagliptin, linagliptin, alogliptin
DPP-4 inhibition leads to increase incretin levels
AE: headache, N/V/D, nasopharyngitis,
what should we be cautious of when initiating DPP-4 inhibition
**caution with history of pancreatitis or pancreatic cancer
what diabetic agent should we avoid in HF patient
DPP-4 I ( saxagliptin only)
thiazolidinediones,
what are the MOA of GLP-1 agonist and adverse effects
“tide drug”- exenatide, dulaglutide, liraglutide, lixisenatide, semaglutide
increased incretin concentrations
AE: N/V/D, weight loss
rare: acute pancreatitis, gallbladder
GLP-1 agonist Contraindication
pregnancy, personal/family hx of MTC or MENS, caution with history of pancreatitis or pancreatic cancer
**gastric emptying ( give agents requiring rapid GI absopr
what is the MOA of SGLT2 inhibitor and adverse effect
inhibits glucose reabsorption in the kidneys
AE: UTI, yeast infection. hypotension, hyperkalemia and diabetic ketacidosis (rare)
what are the CI of SGLT2
bladder cancer ( dapagliflozin) EGFR < 30ML/MIN
Adverse effects of insulin
weight gain, hypoglycaemia, lipohypertrohy ( must rotate site)
what is a significant side effects of rosiglitazone
increased cardiovascular event risk, NEED WRITEN CONSENT FROM PATIENT
MOA of lipase inhibitor and AE
Orlistat ( decreases fat and breakdown and absorption by 30%) used as weight loss agent
AE: N/V/D, increased bowel movement, flatulence
CI of lipase inhibitor
pregnancy, chronic malabsorption syndrome, cholestasis
what counselling point should be mentioned when taking meglitinides
take 15-30 mins prior to meals or right before, Delay or skip dose if delayed or skipped ** quicker onset compared to SU and less risk of hypoglycaemia
which class of diabetic meds can you NOT combine with GLP1 agonist
DPP 4 INHIBITOR
which diabetic class have weight gain potential
insulin, SU, meglitinides, TZD,
which insulin is basal ?
which is bolus
Insulin NPH, glargine 100u/ml + glargine 300 u/ml, degludec, determir
bolus: insulin glulisine (apidra) , lispro ( humalog), aspart (novorapid)
regular: Humulin-R, Entuzity
what is the difference between ultra-rapid analogues and regular insulin
ultra rapid has less hypoglycaemia than regular insulin, take right before eating (lispro, aspart, glulisine)
Regular: take 30 min prior to eating (Novolin R)
basal insulin longest to shortest acting
degludec>glargine>determir/levemir> Humulin N, Novolin
Which insulin is cloudy
INTERMEDIATE BASAL NPH ( Humulin N,
drug of choice for pregnancy
rapid acting insulin or regular insulin,
lisper and aspart have decreased risk of hypoglycaemia compared to regular insulin
if Insulin is CI, metformin or glyburide can be used ( off labels)
is ACE, ARB or STATINS safe in pregnancy?
no
what are the recommended target for pregnancy?
FPG <5.3
2HRPG < 6.7
HBA1C: <6.5& OR <6.1% if safely achievable
what is the chronic adverse effect of metformin
vitamin B12 deficiency
What is the difference between dawn phenomenon and Somogyi effect?
If the blood sugar level is low at 2 a.m. to 3 a.m., suspect the Somogyi effect. If the blood sugar level is normal or high at 2 a.m. to 3 a.m., it’s likely the dawn phenomenon.
what is diabetic ketoacidosis? signs and symptoms? how to treat?
acute and fetal metabolic complication due to severe insulin deficiency. more common in type 1
- decreased consciousness
- depleted Na+ K+ Cl- H2O
- hospitalization
- fluid
how to treat diabetic ketoacidosis
- ICU
- fluid resuscitation and K+ replacement
- insulin and dextrose infusion (10u bolus IV until BG 5-7)
- bicarbonate ( beneficial when pH <7)
what is consider mild and moderate to severe hypoglycaemia
mild <4 mmol/ L + autonomic symptoms: sweating, trembling, palpitations, anxiety, tingling, hunger
moderate to severe <2.8 mmol + neuroglycopenic symptoms: LOC, drowsiness, confusion, weakness, visual disturbances, speech impairment
how to treat hypoglycaemia
15g of carbohydrate ( 4 glucose tabs OR 3 tsp of table sugar (15ml) or 1 tbsp of honey (15ml) ), check BG in 15 mins and if BG <4, 6 life savers repeat treatment
what is consider microvascular and macrovascular complications
macro: cerebrovascular, CAD, PVD
micro: retinopathy, neuropath, nephropathy
symptoms of hyPOgylcemia and hyPERgylcemia
hypo: sweating, trembling, LOC, drowsiness, confusion, weakness
hyper: polydipsia, polyuria, kussmaul breathing (hyper-ventilation), acetone breath
what is the most common cause of hyperthyroidism
graves disease ( thyroid-stimulating immunoglobulin stimulate TSH receptor on thyroid gland ** overproduction of thyroid hormone
clinical presentation of hyperthyroidism
nervousness, palpitation hand tremors, increased appetite, weight loss, goitre, nodules
which drug can cause hyper-t
levothyroxine ( over replacement , amiodarone, lithium ( rare), interferon, Tyrosine kinase inhibitors ( TKIs), SU (glyburide)
what are laboratory for hyper-t
increase RAIU, decreased TSH and increased FT4
What are treatment option for hyper-t
radioactive iodine
methimazole
propylthiouracil
propanolol
what are the MOA of radioactive iodine? adverse effects?
CI?
radioactive damages thyroid tissue
N/V/D/ metallic taste, sore neck, worsen graves opthalmopathy
CI: pregnancy and breastfeeding
important counselling point for radioactive iodine
drug interaction?
wait at least 6 months before conceiving
lithium prolongs RAI
1) MOA of methimazole?
2) ae?
3) CI
Blocks conversion of T4 to T3
arthralgia, rash, nausea, sore throat and fever
GI
rare: bone barrow suppression, agranulocytosis
CI: 1st trimester of pregnancy ( MMI) ** d/c at least 5 days before diagnostic test
Propylthiouracil MOA,
indication?
adverse effects?
inhibits peripheral T4 to T3 conversion
ae: same same as Methimazole + higher risk of hepatotoxicity and agranulocytosis with propythiouracil
significant DI between methimazole and propylthiouracil?
clozapine ( risk of agranulocytosis)
which agent can be used in children and which in pregnancy for hyperthyroid
methimazole: can be used in children
propylthiouracil: preferred in 1st trimester of pregnancy, avoid in children due to risk of hepatotoxicity
what drug is used in management of severe hyper-t ( thyroid storm)
lug’s solution
which disease is classified as primary hypo-t
hashimoto thyroiditis
autoimmune destruction of thyroid cells due to overproduction of antibodies against thyroid gland
laboratory for primary hypo-t, secondary and tertiary
primary: Increased TSH and decreased fT4
2 + 3: decreased TSH and decreased fT4
what the difference b/w 2 and 3 hypo-t
2: pituitary gland disorder ( neoplasm or trauma
3: hypothalamus disorder ( neoplasm or trauma
what value is subclinical hypo-t
increased TSH, normal T3T4
what are clinical presentation and symptoms of hypo-t
fatigue, cold intolerance, weight gain, bradycardia
is female at an increased risk of hypo-t
yes
what medication can cause hypo-
lithium, amiodarone, thionamides,
is there non-pharm therapy for hypo-t
no, thyroid hormone replacement is mainstay of therapy
pharmacotherapy for hypo-t
levothroxine (synthetic t4)- drug of choice
liothyronine ( synthetic T3)- replaces endogenous T3 ( shorter acting)
AE of synthroid
symptoms of hyper-t and may worsen angina
dose of synthroid
1.6 mcg/kg/ day ( dose titration of 12.5-25 mcg q 4-8 weeks) PRN
consider 12.5-25 mcg/day for elderly or those with cardiac disease
what are counselling points for synthroid
- take 1/2 hr before food
- space at least 4 hrs from calcium and iron containing products
what is the indication of liothronine
short term management in thyroid cancer patients off synthroid therapy
when should u check TSH after dose changes?
4 weeks
TSH is produced by
pituitary gland
Which compound is necessary for the production of T3 and T4?
iodine
Which of the following drugs may block the conversion of T4 to T3?
amiodaone and PTU
what is the role of beta blocker in thyroid disease
elieve the thyrotoxic symptoms such as palpitations, anxiety, tremor and heat intoleranc
what is the interaction b/w warfarin and synthroid ?
increases warfarin. ( decrease in the dose of anticoagulant may be warranted with correction of the hypothyroid state or when the levothyroxine sodium dose is increase)
The cause of the hyperthyroidism is the production of an antibody that does which of the following?
Activates the thyroid gland TSH receptor and stimulates thyroid hormone synthesis and release
Which of the following is a drug that is a useful adjuvant in the treatment of thyroid storm?
In thyroid storm, beta blockers such as propranolol are useful in controlling the tachycardia and other cardiac abnormalities, and propranbolol also inhibits peripheral conversion of T4 to T3.
What hormone is produced in the peripheral tissues when levothyroxine is administered?
T3
When should screening for type 2 diabetes using a fasting plasma glucose (FPG) be performed in the average adult patient?
Every 3 years for individuals ≥ 40 years.
which diabetic medication can prevent progression from prediabetes to diabetes
metformin + acarbose
when is ketone testing indicated
all individuals with type 1 diabetes during periods of acute illness accompanied by elevated BG, when preprandial BG levels remain elevated (>14.0 mmol/L), or when symptoms of diabetic ketoacidosis (DKA) (such as nausea, vomiting or abdominal pain) are present
when should SMBG be done in type 1 and type 2 diabetes
type 1: 3 times daily
2: once daily on basal + oral antihyperglycemic agents
IF not on insulin- individualized (usually 1 to 2 times per week)
What is the duration of effect of long-acting basal insulin analogues?
42 hours ( degludec)
What is the recommended treatment of an unconscious patient with hypoglycemia?
1 mg glucagon SC or IM
Which of the following would be considered as alternatives to NPH insulin in someone prone to hypoglycemia?
Use of long-acting basal insulin analogues (insulin detemir, insulin glargine, insulin degludec) in those already on antihyperglycemic agents reduces the relative risk of symptomatic and nocturnal hypoglycemia compared to treatment with NPH insulin
When should you realistically expect to attain a target A1C in patients with type 2 diabetes who are using antihyperglycemic agents?
3-6 months
in DKA, is serum bicarb decreased or increased
decreased serum bicarbonate level
what are the common carbbohydrate ratio?
1:10 to 1:15
1 unit per 10 g CHO
when is post prandial BG testing done?
2 hours after a meal
what site is best for injecting bolus and basal insulin
bolus: abdomen for rapid reabsorption
basal: abdomen or thigh or arms since rapid absorption is not critical
** note switching between sites will lead to variability in BG control.
Anatomical areas ranked in decreasing order of absorption rate are:
adomen, arm, thigh, buttock
how should patient administer insulin
hort term re-use of needles/syringes are not recommended (unless there is an emergency situation). Most patients should use a 90 degree angle (45 degrees is reserved for very thin people
which insulin can be mixed and which cannot
LANTUS CANNOT be mixed with other insulin
regular short insulin can be mixed with NPH with no problem
rapid analogues have onset of?
Apidra / Humalog / NovRapid have onset of 10-15 minutes
NPH peak?
long acting insulin onset???
5- 8 hours
90 mins
when would insulin pump CSII be indicated for patient with type 1 diabetes
CSII can be considered in people with type 1 diabetes who do not reach glycemic targets despite optimized basal-bolus injection therapy, as well as in the following individuals: those with significant glucose variability; frequent severe hypoglycemia and/or hypoglycemia unawareness; significant “dawn phenomenon” with rise of blood glucose early in the morning;
increasing breakfast aspart dose will decrease the—- meal preprandial glucose readings, and increasing the lunchtime aspart dose will decrease the —- r meal preprandial glucose readings.
lunch, dinner
*** Adjustment of fast-acting insulin doses will affect the preprandial glucose levels at the following meal
which GLP1 is dose weekly
semaglutide, dulaglutide
exenatide 2mg
which GLP-1 RA what CV benefit
liraglutide
