Diabetes (IC12-14) + 11(DM) Flashcards
what are the values we must test for pre-diabetes?
impaired fasting glucose
impaired glucose tolerance
what are the lifestyle recommendations for ppl at risk of pre-DM
1) healthy lifestyle
- ≥ 150 minutes of moderate-intensity exercise or ≥75 min of vigorous- intensity exercise.
- healthy diet
2) metformin
- if unable to receive lifestyle modifications
- if not able to achieve glycaemic control despite healthy lifestyle
who are the patients at risk of pre-DM and should receive lifestyle modifications
if
BMI > 23
gestational women
<60 years old
what are the types of DM
t1dm
t2dm
gestational (50% might develop in the long term)
infection
drugs (hiv, steroids, immunosuppressants, etc)
endocrinopathy or pancreas destruction (no insulin production)
monogenic diabetes syndrome
profile of t1dm
t1dm = pancreatic b cell destruction
autoimmune disease
presence of autoantibodies:
- GAD65, tyrosine phosphotases (IA-2, IA2B), islet cell autoantiboides, ZnT8
typically manifest early on <30 years old and is abrupt
gradual loss of b cell mass (measured with C-protein levels) before a brief period of remission that ultimately leads to no b cell left.
individuals are often slim due to low or no sugar intake.
ketosis is more frequent as the body breaks down fats .
what is the LADA subtype of T1DM
late onset diabetes in adults
usually no need for glycaemic control in the first 6 months
similar characteristics to t1 and 2dm
profile of t2dm
progressive b cell loss with background of insulin resistance
c protein should still be normal to abnormal and insulin production should remain.
onset is later and gradual
patients are typically obese and ketosis is rare.
DM screening parameters and when to screen? (what to screen for and when to screen)
high risk factors or more than 40 years old
HbA1C and FPG
2 tests over consecutive days to confirm diagnosis
what are the glucose monitoring tests?
HbA1C = avg glucose for 3 months
FPG = after 8h of caloric intake
PPG = post pandrial, taken 2hours after food, or done with OGTT (75g oral glucose tolerance test)
what is the glucose monitoring regimen?
test HBA1C first
less than 6%c = low probability of glucose = maintain lifestyle control and diet and retest after 3 years
6.1-6.9% = test for FPG or OGTT (ALSO requires 2 confirmed tests) =
- FPG <6, OGTT<7.8 mmol/L = low probability
- FPG 6.1-6.9, OGTT 7.8-11 = pre DM
- FPG >7, OGTT >11.1 = DM confirmed
> 7 = DM confirmed
what are the complications of diabetes? include the screenings required for each
microvascular
1) retinopathy
Diabetic retinal photography (DRP)
- taken within 5 years for T1 and on diagnosis if T2
- if no complications (after ≥1 tests/glycemia controlled) = test every 1-2 years
- if complications = test at least annually (6 MONTHS)
2) nephropathy
- taken within 5 years for T1 and on diagnosis if T2
- 2 test types:
(a) = eGFR or SCr
normal SCr = 0.7 to 1.3 mg/dL (61.9 to 114.9 µmol/L) for men and 0.6 to 1.1 mg/dL (53 to 97.2 µmol/L) for women; eGFR > 60mL/min)
(b) = uACR or UPCr (<0.2mg/mg)
- albuminurea (normal levels= <30ug/mg or <3.3mg/mM)
- microalbuminuria (30-299 or 3.4-33.9)
- macro (>300, >33.9)
- test every 6 months oR annually depending on presence.
3) neuropathy
- DFS (annual by podiatrist, daily by patient)
- encourage patients to maintain foot care, quit smoking, optimal glycaemic control
MACRO
4) CVS
- no correlation between CVS mortality and HBA1C control (appears to fall initially before increasing again)
what other labs to check for DM
lipid panel, BP
lipid = every 3-6 mth if not controlled, annually if controlled
BP = every visitw
what is the target FPG and HBA1C for DM?
FPG = 5-7mmol/L
HBA1C =
(1) 6-6.5 if
- long life expectancy, no sig CVD, short disease duration
(2) 7.5-8
- hx of severe hypo, short life exp, advanced complications, extensive comorbidities, not responsive to treatment (and lifestyle mods)
Biguanides
indication and moa
Indication: Monotherapy with diet and exercise OR in combination with other agents/insulin for T2DM
- Off label: polycystic ovarian syndrome (PCOS).
MOA:
Primary: decrease hepatic glucose production (inhibits gluconeogenesis in liver = increase AMP-activated protein kinase)
Secondary: increase peripheral/muscle glucose uptake and utilization (increase insulin sensitivity)
Biguanides
(Dosages and administration)
Metformin IR
250mg 500mg 850mg 1000mg
Start with 500-850mg OD
Increase by 500-850mg OD every 1-2 weeks in divided doses.
Max dose 2500 – 2550 mg OD.
Metformin XR
500mg 750mg 1000mg
Start with 500mg OD
Increase by 500mg weekly.
Max dose 2000mg OD. May divide dose to 1000mg BD if glycaemic control not achieved with OD dosing.
If dose >2000mg needed, switch to IR
Biguanides
PD PK
PD
Onset within days max 2 weeks
PK
A: Oral, F 40-60%, DOA: 8-12h
D: Rapidly distributed, minimal plasma protein binding. T1/2 3h
M: NA
E: Renal elimination, 90% in urine unchanged.
Biguanides
ADR
Common:
GI disturbances (diarrhoea, N/V, indigestion), anorexia, loss of appetite, metallic taste.
Usually transient and to take with food and increase dose regularly to minimise GI disturbance.
Long term:
May decrease serum B12.
Consider periodic measurement esp in those with anemia, peripheral neuropathy, or symptoms such as numbness, tingling.
Rare but fatal:
Lactic acidosis (3/100,000 patients/year)
Symptoms – N/V, abdominal pain, shallow/labored breathing, mental confusion.
Biguanides
Contra
DDI
Contraindications
Severe renal impairment (GFR <30ml/min)
Hypoxic states/hypoxia risk (increased risk of lactic acidosis)
E.g.,
HF (avoid use in acute decompensated heart failure), sepsis, respiratory failure, liver impairment, alcoholism, ≥80 yo
DDI
EtOH/alcohol:
Increase risk of lactic acidosis.
Iodinated contrast material (for radiologic procedures e.g., x-rays, CT scan):
Temporarily withhold metformin for ≥48 hours after administration. Restart when renal function is stable and acceptable post procedure.
(Metformin may accumulate)
Organic cationic transporters (OCT) inhibitors/inducers e.g., cimetidine, dolutegravir, ranolazine):
May increase metformin by decreasing its renal elimination.
Biguanides
Special population
May be considered for pregnancy patients with T2DM (low risk)
Require renal dose adjustment.
Metformin IR suitable for children ≥10 years; metformin XR not suitable for children.
Biguanides
Comments
Decreases A1c by 1.5%.
Negligible weight gain and hypoglycaemia.
- Good for obese patients (loss of appetite) and elderly patients (low risk of hypoglycaemia)
Possible reduction in CV with T2DM.
Prevent and delay T2DM.
OK for pregnancy.
thiazolidinediones
MOA
Peroxisome proliferator activated receptor gamma ( PPARgamma ) agonist to promote
glucose uptake into target cells (skeletal muscle/adipose tissue)
- ↓insulin resistance; ↑ increase insulin sensitivity
- No effects on insulin secretion
thiazolidinediones
(Drug Dosage Administration PD PK
Pioglitazone 15mg , 30mg (tablet)
Start with 15mg or 30mg OD
Increase dose by 15mg
Max 45mg OD
PD
Up to one month for max effect
PK
Liver elimination
thiazolidinediones
(ADR)
Hepatotoxicity
Monitor LFT prior to initiation and periodically thereafter.
Do not initiate therapy/discontinue if ALT > 3xUNL.
If ALT > 1.5xULN during therapy, repeat LFT weekly until normal.
Discontinue if s/sx of hepatic dysfunction regardless of ALT level.
Fluid retention
Caution use in NYHA Class I and II HF
Monitor s/sx of HF after initiation/dose adjustment.
Monitor weight gain from fluid retention.
Fracture (increased risk, esp women)
Risk of bladder cancer
Increased risk of hypoglycaemia with insulin therapy.
thiazolidinediones
(Contraindications DDI Special population )
Contraindications
Active liver disease
Symptomatic or history of HF (esp class III to IV)
Active/history of bladder cancer.
DDI
CYP3A4 AND CYP2C8 inhibitors and inducers
thiazolidinediones
(comments)
Decreases A1c by 0.4 - 1.4%.
Appears beneficial to patients with fatty liver disease (NAFLD and NASH)
CV effects
Potential reduction in risk of stroke
Increase risk of HF
Progression of diabetes kidney disease (neutral)
has some weight gain effects
sulfonylureas
MOA
Primary: stimulate insulin secretion by blocking K+ channel of b-cells in pancreas islets (NEED BETA CELLS TO WORK).
- Targets the b-cell ATP-sensitive potassium (K ATP) channel, which controls the b-cell membrane potential.
- Binds to the SU receptor protein subunits of the K ATP channel inhibits K ATP channel mediated K+ efflux depolarisation opens voltage gated Ca channel trigger calcium dependent exocytosis of insulin granules from b-cells.
Secondary: decrease hepatic glucose output and increase insulin sensitivity.
glipizide
(Drug Dosage Administration PD PK )
Glipizide
5mg 10mg (tablet)
5 mg BD (max dose 40mg/day)
Onset 12-24 hours
Inactive metabolite
A: F>95%
Onset: 1/2h
DOA: 12-24h
D: Binds extensively (99%) to plasma proteins (primarily albumin)
T1/2 4h
M: Hepatic 90%, hydroxylation
E: <10% excreted unchanged in urine + faeces. metabolites are excreted in urine + faeces.
sulfonylureas
ADR
Hypoglycaemia
Use with caution in patients with irregular meal schedules.
Use with caution in elderly patients as more likely to have kidney failure titrate dose.
Weight gain (appx 2-5kg)
Exercise to minimise weight gain.
sulfonylureas
Contraindications DDI
Contraindications
Hypersx due to SUs
DDI
Betablockers
May mask the signs and symptoms of hypoglycaemia.
EtOH/alcohol
Disulfiram-like reactions
(1st gen»> 2nd/3rd gen)
Flushing, tremors. Usually, 1-2 glasses a day is okay, however if patient drinks a lot, to avoid dosing.
CYP2C9 inhibitors e.g., amiodarone, 5FU, fluoxetine)
sulfonylurea comments
Decreases A1c by 1.5%.
No apparent benefits other than blood glucose lowering.
Take 15-30min before meal.
Glipizide has lowest risk of hypoglycaemia compared to other SUs.
Glipizide and tolbutamide recommended for renal impairment, however still need to watch for kidney function in glipizide as overdose can cause hypoglycaemia.
vitagliptin special population instructions
Hepatic dose adjustment:
CrCL ≥50ml/min: 50mg BD CrCL <50ml/min: 50mg daily
Use with caution if ≥75 years old.
linagliptin special population + DDI
DDI
CYP3A4 inducers
Decreases linagliptin concentration.
Special populations
No renal or hepatic dose adjustment
DPP4i
MOA
Inhibit DPP4 enzyme
- Decrease enzymatic degradation of GLP1.
- Prolong action of endogenous incretins.
- Stimulates B cell to increase glucose stimulated insulin release.
- Suppress alpha cell mediated glucaogon release and hepatic glucose production.
Sitagliptin
Dosage Administration PD PK
DDI
Special population
100mg OD
Take regardless of meals.
A: oral
F 87%
D: T1/2 10-12h
M: low liver metabolism
E: 80% excreted unchanged in urine, rest in faces.
DDI Digoxin
Increase digoxin conc (minimal).
Special population
Renal dose adjustment:
eGFR ≥ 30 to < 45 mL/min/1.73 m2: 50mg OD
eGFR < 30 mL/min/1.73 m2: 25mg OD
doses for the dpp4i agents?
SITAGLIPTIN 100MG OD
VILDAGLIPTIN 50MG BD (IF METFORMIN/TZD), 50MG OD (IF SU)
LINAGLIPTIN 5MG OD
DPP4i
ADR contra
ADR
Generally mild side effects
GI disturbances
Severe joint pain that can be disabling (persist even after stopping treatment)
Flu like symptoms: headache, running nose, sore throat.
Acute pancreatitis
Hypersx reaction
Bullous pemphigoid, skin rash
Start on prednisolone
Contra
Pancreatitis
Hypersensitivity
DPP4i
(Comments)
Decreases A1c by 0.5 – 0.8% (monotherapy).
Limited human data for pregnancy.
2nd or 3rd combination therapy due to no benefits.
Weight neutral
alpha glucosidase inhibitor
(Drug Dosage Administration PD PK ADR Contraindications DDI Special population Comments)
Acarbose
25mg 50mg 100mg (tablets)
Weight based dosing.
Start 25mg BD/TDS, take with meals.
Increase by 25mg/day every 2-4 weeks.
Max dose
150mg/day (≤60kg)
300mg/day (>60kg)
Rapid onset with each meal.
Eliminated 50% via faeces as unabsorbed drug.
ADR
GI disturbances:
Flatulence, abdominal pain, diarrhoea (most common cause of drug discontinuation)
Contra
GI diseases (obstruction, IBD)
Liver cirrhosis
DDI
Intestinal adsorbents and digestive enzyme preparations
Decrease effects of drug.
Renal impairment: CrCl <25ml/min/1.73m2 DO NOT recommend.
Comments
Decreases A1c by 0.4 - 1.4%.
alpha glucosidase inhibitor MOA
(acts locally) by delaying glucose absorption and decreasing PPG by competitively inhibiting brush border alpha-glucosidase enzymes required for breakdown of complex carbohydrates.
SGLT2i
(Drug Dosage
Canagliflozin (Invokana)
100mg
300mg
Empagliflozin (Jardiance)
10mg
25mg
Dapagliflozin (Forxiga)
5mg
10mg
SGLT2i
Administration
Canagliflozin (Invokana)
100mg OD before first meal of the day
Increase to 300mg if eGFR >60ml/min and need further BG control.
Empagliflozin (Jardiance)10mg OD, taken in the morning with or without food.
Max dose 25mg OD.
Dapagliflozin (Forxiga) 5mg OD, taken in the morning with or without food.
Max dose 10mg OD.
SGLT2I ADR
Hypotension, urinary urgency
Increases water excretion in urine.
Check BP and down titrate HTN lowering agents before starting.
Hypoglycaemia, renal impairment, increased LDL.
Genital mycotic infection/UTI (>5%) (higher in females).
Sugar in urine increases risk of UTI/infection.
Check history for both before starting. Counsel good toilet hygiene, changing undergarments regularly to discourage pathogen breeding.
Increased risk of DKA (esp euglycemic DKA)
Precipitated by severe stress, dehydration, undereating, alcohol use, illness stop drug.
Fournier’s gangrene (necrotising fasciitis of the perinium)
Canagliflozin specific: lower limb amputation, hyperkalemia, fractures.
SGLT2i contra
cana = <30
empa and dapa = <45
when to initiate SGLT2i if renal imp?
if jUST glycemic control
<45 do not initiate
discontinue if <45 persistently
if cardiorenal also
<25 for dapa, <20 for empa DO NOT initiate
discontinue if starting dialysis
SGLT2i dose adjustment
empa and dapa no need dose adjustment above 45 egfr
for cana, eGFR 30 to 60 ml/min: 100 mg OM
SGLT2i comments
Decreases A1c by 0.8-1.0%.
Limited human data for pregnancy.
Neutral for hypoglycaemia.
Slight weight loss benefits
ASCVD: canagliflozin and empagliflozin ONLY.
HF: shorten hospitalisation (all)
CKD: prevent/delay microalbuminuria (all)
Empagliflozin PK
A: Oral,
F 60-80%
Cmax 1-2h
D: T1/2 12h
90% plasma protein bound
M: minimal metabolism by liver (glucuronidation)
E: ~40% unchanged in faeces, ~27% unchanged in urine
SGLT2i MOA
MOA: Inhibition of SGLT2 glucose transporters located in the proximal tubules of kidneys decrease renal threshold for glucose and hence increased renal glucose excretion AND decreased reabsorption of filtered glucose decreased blood glucose.
GLP1i
MOA
GLP1 is an incretin, which is a naturally occurring hormone released from the GI tract. GLP-1 inhibitors act as receptor agonists/endogenous GLP1 and binds to the receptors on B cells,
Incretin=↓gastric emptying,↑glucose-dep insulin biosynth, ↓glucagon, ↑b-cell function, and ↓appetite
Activate GLP1 receptor on pancreatic b-cell= stimulates adenylate cyclase = increase cAMP = stimulate PKA = increase insulin secretion and decrease glucagon release.
Insulin secretion decreases as blood glucose concentration decreases and approaches euglycemia.
GLP1i
(Drug Dosage Administration
1) Liraglutide (Victoza®)
Initiate at 0.6mg SC injection OD regardless of meals.
Titrate to 1.2mg after 1 week.
Max 1.8mg
2) Dulaglutide (Trulicity®)
Initiate at 0.75mg SC injection once weekly regardless of meals.
Titrate to 1.5mg after 4 weeks.
Max 3 – 4.5mg
3) Semaglutide (Ozempic®) Initiate at 0.25mg SC injection once weekly regardless of meals.
Titrate to 0.5mg after 4 weeks.
Max 1mg
4) Semaglutide (Rybelsus®)
Initiate at 3mg PO once daily 30 mins before first meal of day.
Titrate to 7mg after 30 days.
Max 14mg
Can consider dosing in the morning on empty stomach OR atleast ½ hour before other meds/food/drink WITH NO MORE THAN 120ML WATER for adequate absorption.
Can also consider taking with PPI/H2PA to reduce stomach acidity.
PK of liraglutide
A: F 55%
D: C16 fatty acid binds to plasma proteins. T1/2 13hr (extended due to plasma protein binding)
M: endogenous metabolism like polypeptides without specific organ as major route of elimination.
E: little/none excreted unchanged.
ADR and contra of GLP1RA
ADR
- Headache, Nausea (common),
-Vomiting (common),
-Acute pancreatitis,
- Acute cholecystitis,
- Injection site reactions
Contra
- Patients with history of pancreatitis or family history of thyroid cancer.
special population for GLP1RA
BLACK BOX
WARNING: Thyroid
C-cell tumors in
animals. Human
relevance unknown.
Counsel patients
regarding the risk of
medullary thyroid
carcinoma and the
symptoms of thyroid
cancers.
DO NOT USE IN PREGNANT MOTHERS (liraglutide)
comments for GLP1RA
Decreases A1c by 1-2 %.
Weight loss benefits.
Neutral hypoglycaemia
Expensive
Recommended as 1st line before insulin when greater glucose lowering is needed.
ASCVD benefits (liraglutide, duraglutide, semaglutide)
Minimal CKD benefits (some benefit in reducing macroalbuminuria in SC agents)
Neutral HF benefit
special formulation of semaglutide Rybelsus
Co-formulated with absorption enhance SNAC to protect it as it passes through the GI tract SNAC increases pH reversibly to protect drug from proteolytic degradation and enhancing its BA.
what is HBA1C affected by
because it is affected by binding of glucose to the RBCS, conditions that affect RBC can affect levels
lifespan increase = anemia
decrease RBC = blood loss eg mensturation
which SUs can take once daily
gliclazide and glimepiride
when to initiate insulin despite oral ?
INSULIN CONSIDERED WHEN
- Ongoing catabolism (weight loss)
- Symptoms of hyperglycaemia e.g., polyuria, dysuria.
- A1c > 10%
- BG > 16.7 mmol/L
comorbidity oral agents?
Hx of comorbidities (consider the following agents independent of A1c level)
1) ASCVD: GLP1 agonist OR SGLT2
2) HF: SGLT2
3) CKD: SGLT2 > GLP1 agonist
insulin PK?
Exogenous insulin: mainly kidneys.
Endogenous insulin: mainly liver.I
insulin needle lengths?
Pen needle (4mm to 12.7mm)
Syringe needles (for vials) (6mm to 12.7mm)
- Usually, no medical reason to recommend needles >8mm as skin thickness does not differ among BMI, race, or age.
- Average skin thickness only around 2.4mm at insulin injection sites.
insulin stability
Unopened
If refrigerated (2-8ºC), good until expiration date, otherwise non-refrigerated = good for 28 days.
Non-refrigeration (<30ºC ideal).
Put in fridge; DO NOT put in freezer.
Opened
28 days, regardless of refrigeration.
SQ insulin admin
Step 1: Pinch the area to be injected (? depends)
- Patients with 6, 8, or 12.7mm needles need to pinch a skinfold for medication to reach the intended absorption site.
- 4-5mm needles can be used for lean or obese children and adults = no need to punch a skinfold for this length. These lengths are usually only seen in injection pens. UNLESS patient has less SC fat and use arms/thigh for injection.
Step 2: Needle should be inserted at a 90º angle, unless frail elderly/cachexic adults or children, then 45º, at the centre of the injection site.
Step 3: Release the pinch.
Step 4: Press the plunger to inject insulin.
Step 5: Hold the syringe or device in the area for 5-10 sec to ensure full delivery of insulin.
Step 6: Remove the syringe or device.
counselling/additional instructions for proper SQ insulin admin?
rotate sites to avoid lipohypertrophy eg abdomen, around the belly button area
comparing the absorption sites for SQ insulin?
abdomen > outer upper arms > top and outer thighs > butt
ADR of insulin?
1) hypoglycemia = counsel on 15 15 15 rule
2) weight gain (more than SU)
3) lipodystrophy
- hypertrophy if no rotation of injection site
- atrophy if pork or beef insulin
4) local allergy = redness, itching
5) rare = systemic allergic reaction, insulin resistance
what is the 15-15-15 rule
15-15-15 rule
- 15g of fast acting carbs
- Wait 15min.
- Check BG, if still < 4.0mmol/L, then another 15g of fast acting carbohydrates.
Examples of fast acting carbs
- Commonly found: Fruit juices (4oz or ½ cup), Raisins (2tbsp), Sugar (3 cubes or 1 tbsp), Hard candies (5-6 pieces), Regular soft drinks (4oz or ½ cup) (Not sugar free!), Honey (1tbsp).
- Commercially manufactured: glucose tablets or gels.
insulin vial size
what is in U-100
means 1ml = 100UI
what are the diff types of insulin
rapid acting:
lispro, aspart, glulisine
short acting:
regular
intermediate acting:
NPH
long acting
glargine, detemir
considerations about oral therapy when insulin is started?
metformin = continue
TZD = discontinue or reduce
SU = if basal, discontinue or reduce by 50%. if pre-meal, discontinue completely
SGLT2i = continue
DPP4i = discontinue if GLP1 initiated
what is the insulin dosing conversion for diff scenarios?
if NPH mix to NPH mix
= keep to the same regimen
if NPH to basal
= reduce by 20%
if U300 to another basal
= reduce by 20%
how to manage diabetic emergencies?
IV insulin, among others
signs and symptoms of the two types of diabetic emergencies
DKA
(type 1) Hyperglycaemic hyperosmolar state (HHS)
Type 1 does not have insulin ketones formed.
- Ketones found in blood and urine.
- Fruity breath odour
- Acidosis (blood acidic)
Usually still alert.
- BG > 14mmol/L.
(type 2)
Type 2 usually have some residual insulin production, so they are protected against excessive lipolysis and ketone production no acidosis.
- Usually extremely dehydrated hence BG can be > 33mmol/L (dehydration due to osmotic gradient).
- Usually stupor (confusion).
causes of diabetic emergencies
Usually infection (due to water loss and release of catecholamines).
- Others: MI, stroke, inadequate insulin therapy, pancreatitis.
parameters for DKA vs HHS?
Arterial/venous pH Bicarb (normal 22-32 mmol/l) Urine/blood acetoacetate Urine/blood Beta- hydroxybutyrate (measures ketosis) (normal <0.4-0.5mmol/L) Effective serum osmolality Anion gap (normal 4-12 mmol/L) Mental status
usually all are normal, slight change in HHS except the hypersomolarity
DKA lab values are more drastic
urine/blood acetoacetate is positive while in HHS it is negative/slight positive
what are the bP goals and treatment for DM HTN
<130/80 is the goal
1st line agents
ACEi or ARBs
enalapril 5mg od-bd (10-40)
lisinopril 10mg od (20-40)
lorsartan 50mg od-bd (50-100)
what are the risk factors for ASCVD in DM?
50 YEAR old patient (with diabetes) with any of the following
- HTN
- LDL >2.6
- smoking
- CKD
- albuminuria
- fam history of ASCVD
when is treatment indicated for ASCVD in DM (include regimen)
aspirin is recommended for primary and secondary prevention
consider age >70 as a potential risk factor to taking aspirin, may want to weight risk vs benefits
for secondary prevention, clopidogrel 75mg/day also indicated
what are the goals and regimen for hyperlipidemia in DM?
primary prevention
goal 1.8mmol/L
- atorvastatin 10mg = 39% reduction
- simva 20mg = 38% reduction
- rosuva 5mg = 45% reduction
secondary prevention
goal 1.4mmol/L
- rosuva 40mg = 63% reduction
note every double dose = 6-7% increase in reduction
ideally both around 50% reduction from baseline
what is the clinical presentation of DKD
1) albuminuria in gross hematuria
2) absence of other signs causing CKD
others
3) worsening eGFR
4) retinopathy especially in T1DM
5) long duration of diabetes (= worsening kidney damage)
what are the treatment options for CKD in DM
1) ace and arb
- not for primary prevention in patients with normal BP
- reducing BP and BG one of the goals to reducing CKD
2) SGLT2i
- recall eGFR criteria (empa <20, dapa<25 = contra)
3) finerenone
- beneficial in reducing CKD progression
- also reduce risk of kidney failure and ASCVD + mortality
side effects of finerenone? and contra
gynaecomastia, hyperkalemia, HTN
x egfr<25
