Pathophysiology Summary:

DIABETES MELLITUS
● Insulin resistance is the hallmark of T2DM,
exacerbated by obesity, inflammation, and genetic
STATION 1: RISK FACTOR ANALYSIS predisposition
● Beta-cell dysfunction leads to insufficient insulin
Non-Modifiable Risk Factors:
production and secretion
● Age > 40 years: T2DM incidence increases with age, ● Increased hepatic glucose production contributes to
particularly after 45 years fasting hyperglycemia
● Family history: Having a first-degree relative with ● These changes result in hyperglycemia, which if
T2DM increases the risk uncontrolled, leads to complications such as
● Ethnicity: Higher risk among Asian, Hispanic, and cardiovascular disease, nephropathy, and retinopathy
African American populations

Modifiable Risk Factors:

STATION 2: HEALTHCARE NEEDS, GOALS,
● BMI ≥ 25 kg/m²: Overweight and obesity are the most INTERVENTIONS
significant risk factors
● Abdominal obesity: Central obesity is particularly Primary Healthcare Need:
associated with insulin resistance
● Sedentary lifestyle: Lack of physical activity ● Control hyperglycemia and prevent complications
contributes to insulin resistance of diabetes such as neuropathy, nephropathy,
● High-carb diet: High intake of refined carbs increases retinopathy, and cardiovascular disease
the risk of developing T2DM
Clinical Goals:
● Smoking: Smoking impairs insulin sensitivity and
worsens metabolic control
● HbA1c < 7% (or individualized based on comorbidities
● Dyslipidemia: High LDL cholesterol and low HDL
and risk of hypoglycemia)
cholesterol levels
● Fasting blood glucose (FBG): 80–130 mg/dL
● Hypertension: BP ≥ 140/90 mmHg is a major
● 2-hour postprandial glucose (2h PPG): < 180 mg/dL
cardiovascular risk factor for T2DM
● Prevent micro- and macrovascular complications
● Maintain quality of life
Recommended Drugs:

1. First-line therapy: 3. Add-on therapies:

○ Metformin: Start at 500 mg/day, titrate up to a ○ DPP-4 inhibitors: (e.g., linagliptin 5 mg/day)
max of 2 g/day ■ Mechanism: Increases incretin
■ Mechanism: Increases insulin hormones, which enhances insulin
sensitivity, reduces hepatic glucose secretion and decreases glucagon
production release
■ Adverse Effects: GI upset (nausea, ■ Adverse Effects: Mild, well-tolerated;
diarrhea), rare lactic acidosis (especially rare risk of pancreatitis
in renal impairment) ○ Sulfonylureas: (e.g., gliclazide MR 30–120
2. If ASCVD (Atherosclerotic Cardiovascular Disease), mg/day)
HF (Heart Failure), or CKD (Chronic Kidney ■ Mechanism: Stimulates insulin
Disease): secretion from beta-cells
○ SGLT2 inhibitors: (e.g., dapagliflozin 10 ■ Adverse Effects: Hypoglycemia, weight
mg/day) gain
■ Mechanism: Reduces glucose 4. Insulin:
reabsorption in the kidney, promotes
glucosuria ○ Start if HbA1c > 10% or symptomatic
■ Benefits: Cardiovascular and renal hyperglycemia (e.g., significant polyuria,
benefits, reduces hospitalization for polydipsia)
heart failure ○ Consider rapid-acting insulin for meal-time
■ Adverse Effects: Genital infections, risk coverage and long-acting insulin for basal
of dehydration, hypotension control
○ GLP-1 Receptor Agonists: (e.g., liraglutide
1.2–1.8 mg SC/day)
■ Mechanism: Increases insulin
secretion, reduces glucagon secretion,
delays gastric emptying
■ Adverse Effects: Nausea, vomiting, risk
of pancreatitis
 STATION 3: DRUG-RELATED PROBLEMS (DRPs)
4. Dosage Too Subtherapeutic Titrate dose gradually to
Low metformin dose an effective level (max 2
DRP Example How to Counter / (e.g., 500 mg g/day); monitor FBG and
Interventions once daily) HbA1c to track efficacy
and adjust dose
1. Patient on insulin Reassess the need for
Unnecessary and full-dose oral insulin or oral drugs based 5. Dosage Too Glimepiride 6 Reduce dose or switch to
Drug Therapy hypoglycemics on glycemic control and High mg/day causing a drug with a lower
despite controlled risk of hypoglycemia; hypoglycemia hypoglycemia risk (e.g.,
HbA1c taper or discontinue DPP-4 inhibitor); educate
unnecessary agents (e.g., patient on meal timing to
oral hypoglycemics) to prevent hypoglycemia
avoid polypharmacy
6. Adverse GI upset from For metformin: Take with
2. Need for No statin despite Initiate statin therapy Drug Reaction metformin; food or switch to
Additional cardiovascular (e.g., atorvastatin 20–40 (ADR) genital infections extended-release form;
Drug Therapy risk; no ACEi in mg/day) for patients with from SGLT2 For SGLT2i: Reinforce
microalbuminuria ASCVD or high inhibitors hygiene practices, monitor
cardiovascular risk; add for signs of genital
ACEi (e.g., enalapril 5–20 infections (yeast
mg/day) in patients with infections), consider
microalbuminuria to discontinuation if recurrent
reduce the progression of
nephropathy 7. Skipping insulin Provide patient
Non-Adherenc due to fear of counseling; consider
3. Ineffective Metformin in Switch to alternative e/ injection using pens or smaller
Drug patient with agents: Add GLP-1 RA or Noncomplianc needles to improve
eGFR <30; poor SGLT2i for better e comfort; explore
glycemic control glycemic control, or fixed-dose combination
on monotherapy initiate insulin if oral options if appropriate
necessary; discontinue
metformin in cases of 8. Drug Corticosteroids Monitor glucose closely,
severe renal impairment Interactions raising glucose; adjust antidiabetic doses
(eGFR <30) beta-blockers (e.g., increase insulin or
masking oral hypoglycemics);
hypoglycemia consider alternative
 necessary to achieve glucose control and prevent
medications for conditions
like asthma or complications.
hypertension if possible
R – Recommendation:
9. Monitoring No HbA1c check Educate on importance of
Problems in 6 months; regular monitoring: ● Discontinue glimepiride if it is causing hypoglycemia
metformin use schedule routine HbA1c or switch to a DPP-4 inhibitor (e.g., linagliptin 5
without renal tests every 3–6 months; mg/day)
monitoring monitor renal function
(serum creatinine, eGFR)
every 6–12 months to ● Add SGLT2 inhibitor (e.g., dapagliflozin 10 mg/day)
ensure drug safety for better glycemic control and potential
cardiovascular protection

STATION 4: SBAR FORMAT ● Initiate statin therapy (e.g., atorvastatin 20 mg/day)

for primary prevention of cardiovascular events
S – Situation:
Mr. Juan Dela Cruz, a 55-year-old male, presents with T2DM,
● Monitor glucose closely, especially with
uncontrolled HbA1c of 9.2% despite current therapy of
corticosteroids; consider a lower dose of prednisone
metformin 1000 mg/day and glimepiride 4 mg/day. He is
or alternative therapy if appropriate
also on prednisone for autoimmune disease.
● Regularly check HbA1c every 3 months and renal
B – Background:
function every 6–12 months
Patient has HTN (BP 145/90 mmHg), dyslipidemia, and a
family history of T2DM. His current therapy is suboptimal,
with significant hyperglycemia and elevated blood pressure.
His renal function is normal (eGFR 90), but corticosteroid
therapy may worsen blood glucose control.

A – Assessment:
The patient has uncontrolled hyperglycemia and requires
adjustment of his regimen. The glimepiride dose may
contribute to hypoglycemia, and corticosteroids are
increasing his blood glucose. Additional therapy is
First-Line Treatment: Metformin (Glumet, Glumet-XR) Sulfonylureas

● Advantages ● Second-generation drugs:

- Minimal hypoglycemia ○ Gliclazide (Diamicron MR) 60mg.
- high efficacy ○ Glipizide (Minidiab OD) 5mg, 10mg.
- cost-effective ○ Glimepiride (Solosa) 1mg, 2mg, 3mg.
● Strengths: 500mg, 850mg, 1000mg (XR tab ● Dosing: OD, 15-30 minutes before a main meal.
available). ● Common Side Effects:
● Dosing: ○ Hypoglycemia (pharmacist’s advice: do not skip
○ Start at a low dose (minimum 1,000 mg/day), meals).
gradually increase. ○ Weight gain (1-2kg) (pharmacist’s intervention:
○ Maximum daily dose: 2,550 mg/day. avoid in overweight or obese patients).
● Common Side Effects: Metallic taste, diarrhea,
severe nausea, abdominal pain, weight loss. 1ST gen: chlorpropamide, tolazamide, and tolbutamide are no
● Administration: Take after meals to reduce side longer used due to low potency and AE: liver disease
effects.
● Metformin causes B12 deficiency Other Antidiabetic Agents
- Peripheral neuropathy (microvascular
Meglitinides: Nateglinide (Starlix), Repaglinide (Novonorm).
complication) is common in DM2 and can be
worsened with low B12
● Advantages: Faster onset and shorter duration than
- Pharmacist’s advice: B12 supplementation
sulfonylureas.
● Serious Adverse Effect: Lactic acidosis (symptoms:
● Best for: Patients with renal insufficiency or erratic
abdominal discomfort, weakness, muscle pain).
meal schedules.
○ Hold use if SCr >1.5 or eGFR <30.
● TID, 15-30 mins BEFORE MEALS
α-Glucosidase Inhibitors Glucagon-like Peptide-1 Receptor Agonists

● Drug: Acarbose (Glucobay) 50mg tablet, taken TID. ● Dulaglutide (Trulicity®), exenatide(Byetta®),
● Common Side Effects: Flatulence, abdominal pain, lixisenatide(Soliqua®), liraglutide (Victoza®), and
diarrhea. semaglutide
● Give after first bite of a main meal to maximize effect ● Administered subcutaneously, except semaglutide
on the breakdown of carbohydrates (oral); twice daily to once weekly
● Low HbA1c effect; high GI side effects; considered ● Direct effect on the stomach through the autonomic
when other medications are contraindicated or not nervous system to slow gastric emptying, thereby
tolerated. reducing meal-related glucose excursions
● Crosses blood-brain barrier to increase satiety
Thiazolidinediones (TZD)
Dipeptyl Peptidase-4 (DPP-4) Inhibitors
● Drugs: Pioglitazone (Prialta, Actos), Rosiglitazone
(Avandia). ● Sitagliptin (Januvia®) 50mg &100mg; combination:
● Common Side Effects: Edema, worsening heart Sitagliptin+metformin (Janumet XR)
failure, weight gain (3-4kg), bone fractures. ● Saxagliptin (Onglyza®) 2.5mg & 5mg
● Pharmacist’s Advice: Take calcium + Vitamin D. ● Linagliptin (Trajenta®) 5mg; combination:
● Not advised for: Heart failure patients, linagliptin+metformin (TrajentaDuo)
postmenopausal women, overweight/obese patients. ● No nausea, no significant effects on satiety, neutral
● Glycemic-lowering onset is slow; maximal effects seen impact on weight but more expensive compared to the
after 3 - 4 months; do not stop medication despite little older antidiabetic agents
changes in blood sugar levels initially ● Linagliptin it does not require renal dose adjustment
● Pioglitazone decreases plasma triglyceride, increases due to its nonrenal mode of excretion; may be used in
HDL moderate-to-severe renal insufficiency
● Rosiglitazone increases LDL and HDL ● Post-marketing warning: heart failure, pancreatitis, and
joint pain
Sodium-Glucose Cotransporter-2 (SGLT-2) Inhibitors

● canagliflozin (Invokana®) 100mg and 300mg ● Preferred in Type 2 DM: Basal insulin.
● dapagliflozin (Forxiga®) 5mg and 10mg ● Required in Type 1 DM: Combination of basal and
● empagliflozin (Jardiance®) 10mg and 25mg bolus insulin.
● acts in the kidneys; causes urinary glucose excretion of ● The abdomen provides the most consistent absorption
75 to 85 g/day by inhibiting reabsorption of filtered for insulin
glucose
● effective even in the absolute absence of insulin Basal and prandial insulin
● Common SE: genitourinary infections → good hygiene
● May increase LDL and HDL Basal insulin (background insulin): Long-acting insulin that
regulates by suppressing hepatic glucose production and
Watch out for SGLT2-I use in maintaining near-normal glycemic levels in the fasting state.

● Patients taking diuretics – orthostatic hypotension and Bolus insulin (prandial insulin): Short or rapid-acting insulin
electrolyte imbalance that covers meals.
● Older adults – poor thirst response may lead to
dehydration Basal insulin is the preferred and most convenient initial
● CKD 4 and 5 patients insulin formulation in patients with type 2 DM, while
patients with type 1 DM require a combination of basal and
Insulin Therapy bolus insulin to achieve adequate glycemic control.

● Advantages: Achieves wide glucose targets, ● PK/PD differences must be evaluated for clinical
individualized dosing. significance in patient outcomes.
● Disadvantages: Hypoglycemia risk, injections ● Longer-acting basal insulins reduce hypoglycemia
required, weight gain. risk (especially nocturnal hypoglycemia) and glucose
● Initial Dose: 0.2 units/kg/day. variability but have higher costs.
● Types: ● Ultra-Long Acting Insulins: Glargine U-300 (Toujeo®
○ Basal Insulin: Long-acting, maintains fasting Solostar), Degludec (Tresiba®).
glucose levels. ● Rapid and Ultra-Rapid Insulins: Mimic prandial
○ Bolus (Prandial) Insulin: Short/rapid-acting, endogenous insulin release, crucial for type 1 DM to
covers meals. mimic pancreatic function.
Diabetes with Co-morbidities CBS Sliding Scale
Sliding scale insulin is when the prescriber orders a specific
Hypertension Treatment amount of insulin to be given based on a capillary blood
glucose level.
● First-line: ACE inhibitors & ARBs.
● Additional agents: Thiazide diuretics, calcium channel The following rule of thumb may also be followed:
blockers, beta-blockers (caution: masks hypoglycemia
symptoms → palpitations ). ● Blood glucose <230 mg/dL - continue with current
dosage
Dyslipidemia Management ● Blood glucose 230 to 390 mg/dL - +2 units per
injection, even if unable to eat
● LDL target: <100 mg/dL. ● Blood glucose greater than 390 mg/dL - + 4 units per
● Statin therapy recommended, regardless of baseline injection, even if unable to eat
lipid levels. ● Return dose to normal when blood glucose returns to
normal
Cardiovascular Risk Reduction

● Aspirin therapy (75–162 mg/day) recommended for: Sulfonylureas Stimulate insulin release 1-2%
○ Men >50 years, women >60 years with HbA1C
additional risk factors. lowering
● Not recommended for low-risk individuals. Meglitinides Short-acting insulin 0.5-1.5%
secretagogue
Weight Management
Biguanides Decreases glucose by the liver, 1-2%
● Target BMI: Below 23. increases insulin sensitivity
● Recommended weight loss rate: 0.5-1 kg/week.
TZDs Stimulates PPARy receptor 0.5-1.4%
improving insulin sensitivity
Sick Day Management
AGIs Breaks down complex carbs 0.5-0.8%
● Increased insulin needs due to stress. into absorbable form
● Sulfonylurea dose reduction if decreased carbohydrate
intake. DPP4-inhibitor Increases GLP-1 levels causing 0.5-1%
● Stop metformin if dehydration occurs. increase in insulin secretion
Comparison of Antidiabetic Drugs
Class Indication Examples (Root Side Effects Benefits Over Others When to Shift
Word Highlighted)

Biguanides 1st-line for T2DM, Metformin (met-) GI upset (diarrhea, Weight neutral, low GI intolerance, lactic
insulin resistance nausea), lactic hypoglycemia risk acidosis risk
acidosis

SGLT2 Inhibitors T2DM with CV Empagliflozin UTIs, genital CV and renal benefits, Recurrent UTIs,
disease, CKD (gliflozin), infections, weight loss dehydration, eGFR <
Dapagliflozin dehydration, 30 mL/min
ketoacidosis

DPP-4 Inhibitors Postprandial Sitagliptin (gliptin), Headache, Weight neutral, low Ineffective in severe
hyperglycemia Linagliptin nasopharyngitis, hypoglycemia risk hyperglycemia
pancreatitis

GLP-1 Agonists Obesity, T2DM, CV Liraglutide (glutide), Nausea, vomiting, Weight loss, CV GI intolerance, high
protection Exenatide pancreatitis benefits cost

Sulfonylureas T2DM without renal Glimepiride (gli-), Hypoglycemia, weight Inexpensive, effective Recurrent
impairment Gliclazide gain, CV risk for insulin secretion hypoglycemia, weight
gain

Meglitinides Postprandial Repaglinide (glinide), Hypoglycemia (less Short-acting, less Meal skipping,
hyperglycemia Nateglinide than sulfonylureas), hypoglycemia frequent dosing issues
weight gain

Thiazolidinediones Insulin resistance, Pioglitazone Weight gain, edema, Improved insulin Heart failure,
T2DM (glitazone), heart failure, fractures sensitivity, long-acting excessive weight gain
Rosiglitazone

Alpha-Glucosidase Postprandial Acarbose (carb-) Bloating, flatulence, No hypoglycemia, Poor tolerance due to
Inhibitors hyperglycemia diarrhea weight neutral GI effects
How One Class Is Better Than Others:

● Metformin: Preferred for newly diagnosed T2DM due to efficacy and safety.
● SGLT2 Inhibitors: Great for patients with heart failure or chronic kidney disease (CKD).
● DPP-4 Inhibitors: Suitable for elderly patients due to low hypoglycemia risk.
● GLP-1 Agonists: Best for those needing weight loss and cardiovascular protection.
● Sulfonylureas: Effective when cost is a concern but may cause weight gain and hypoglycemia.
● Meglitinides: Good for managing post-meal glucose spikes with flexible dosing.
● Thiazolidinediones: Helpful when insulin resistance is prominent.
● Acarbose: Ideal when the goal is to manage postprandial hyperglycemia without hypoglycemia.

When to Shift Medications:

● From Metformin: GI intolerance → Shift to DPP-4 Inhibitors or GLP-1 Agonists.

● From Sulfonylureas: Recurrent hypoglycemia or weight gain → Shift to SGLT2 Inhibitors or DPP-4 Inhibitors.
● From TZDs: Heart failure or excessive weight gain → Shift to Metformin or SGLT2 Inhibitors.
● From SGLT2 Inhibitors: Recurrent UTIs or dehydration → Shift to DPP-4 Inhibitors or GLP-1 Agonists.
● From Acarbose: GI intolerance → Shift to DPP-4 Inhibitors.
● From GLP-1 Agonists: Persistent nausea or high cost → Shift to DPP-4 Inhibitors.
● From Meglitinides: Difficulty with frequent dosing → Shift to long-acting sulfonylureas.
 ● Inflammation, oxidative stress, and endothelial
STATION 1: RISK FACTOR ANALYSIS dysfunction are central mechanisms linking
dyslipidemia to ASCVD
Common Risk Factors for Dyslipidemia
STATION 2: HEALTHCARE NEEDS, THERAPEUTIC
● Demographic: GOALS, INTERVENTION
○ Age ≥45 years
○ Male sex, Postmenopausal women Identifying Healthcare Needs
● Lifestyle:
○ High-fat, high-cholesterol diet ● Elevated LDL-C or non-HDL-C
○ Sedentary lifestyle ● Presence of diabetes, CKD, ASCVD, or FH
○ Cigarette or vape smoking ● Persistent triglyceride elevation (≥200 mg/dL)
● Medical Comorbidities: ● Statin intolerance or suboptimal response
○ Diabetes mellitus (Type 1 or 2)
○ Hypertension Therapeutic Goals
○ Obesity (BMI >25 kg/m²)
○ Chronic kidney disease ● LDL-C
○ Left ventricular hypertrophy ○ Individuals w/ DM → <100 mg/dL
○ Proteinuria ○ No linical ASCVD → <130 mg/dL
● Family & Genetic: ○ With clincal ASCVD → <55 mg/dL
○ Family history of premature coronary artery ○ With ASCVD → <55 mg/dL
disease ○ FH w/ ASCVD or w/ major risk factor/target
○ Familial hypercholesterolemia (FH) organ damage → <55 mg/dL
○ > 1 risk factor/target organ damage → <70
Pathophysiological Link to Cardiovascular Disease (CVD) mg/dL
○ Familial Hypercholesterolemia (FH) → <70
● Elevated LDL-C promotes atherosclerotic plaque mg/dL
formation ● HDL-C
● Diabetes, obesity, and CKD exacerbate lipoprotein ○ >40 mg/dL in males; >50 mg/dL in females
metabolism abnormalities ● Triglycerides
● FH causes lifelong elevation of LDL-C, accelerating ○ <150 mg/dL
atherosclerosis
 ● Secondary Targets:
ACS or ASCVD Early initiation of high-intensity statin
○ Non-HDL-C: 30 mg/dL above target LDL-C
(e.g., atorvastatin 40–80 mg or
○ Apo B-100: consider in high-risk patients after
rosuvastatin 20–40 mg)
LDL goal is reached
LDL not at goal Add ezetimibe
Recommended Interventions despite statin

1. Non-Pharmacologic (For All Risk Groups) Diabetic men, low May consider adding fibrates
HDL + high TG
● Low-fat, low-cholesterol diet (e.g., Pinggang Pinoy)
● Regular aerobic physical activity (≥150 minutes/week) Persistently high May consider EPA (omega-3) on top of
● Smoking/vaping cessation TG (150–499 statin
● Weight loss if overweight/obese mg/dL)

2. Pharmacologic Interventions Pediatric with risk Screen with fasting lipid profile
factors
Clinical Context Recommendation

No ASCVD, ≥2 Start statin

STATION 3: IDENTIFICATION OF DRUG-RELATED
risk factors, LDL
PROBLEMS (DRPs)
≥130
Common Statin-Related DRPs
Diabetes, no Start statin; LDL goal <100 mg/dL
ASCVD
● Statin-Associated Muscle Symptoms (SAMS)
Diabetes + risk LDL goal <70 mg/dL ○ Risk ↑ with high doses, drug interactions (e.g.,
factors/TOD fibrates, cytochrome P450 inhibitors)
● Liver Toxicity
FH (any type) Statin strongly recommended; consider ○ Monitor liver enzymes; hepatotoxicity is rare but
high-intensity serious
● New-Onset Diabetes
CKD not on Start statin ○ Slightly increased risk; outweighed by CV
dialysis benefit
 ● Cognitive Effects and Hemorrhage Advantages of Specific Drugs
○ No strong evidence linking statins to dementia
or intracerebral hemorrhage Drug Advantages

Rosuvastatin High potency, long half-life, minimal CYP

Management of Statin Side Effects
metabolism
● For SAMS:
Atorvastatin Effective for high-intensity needs,
○ Check CK levels; discontinue statin if
cost-effective
rhabdomyolysis suspected
○ Restart with low dose or alternate-day dosing Ezetimibe Add-on for patients not reaching LDL goal
○ Consider switching to a different statin
○ Use non-statin therapy if intolerant to multiple EPA-only May reduce CV risk in patients with high
statins omega-3 TG

Other Drug-Related Considerations Fibrates Considered only in specific diabetic lipid

profiles
● Avoid Fibrates + Statins in general population due to
myopathy risk; consider only in specific diabetics Non-statin Useful in statin-intolerant patients (e.g.,
● Monitor adherence and therapeutic response options ezetimibe, PCSK9 inhibitors – not in
○ Repeat lipid profile 6–8 weeks after starting or guidelines but clinically relevant)
changing therapy
● Consider renal function when prescribing fibrates
● Omega-3: EPA-only products may benefit selected
high TG patients; avoid DHA-containing omega-3s in
general ASCVD patients

CLINICAL PEARLS AND HIGH-YIELD FACTS

Populations to Screen or Treat Aggressively

● Filipino adults ≥45 years with ≥2 CVD risk factors

● Patients with diabetes, CKD, ASCVD, or FH
● Children with family history of FH or premature CVD
 Pathophysiological Linkage
STATION 1: RISK FACTOR ANALYSIS
● Hyperuricemia is central (SUA > 7 mg/dL in men, > 6
Common Risk Factors for Gout mg/dL in women)
● Leads to urate crystal deposition in joints
Demographic: ● Triggers inflammatory response → acute gout attack
● Obesity, Metabolic Syndrome → ↓ renal excretion of
● Age (≥40 years), Male sex
uric acid
● Postmenopausal women
● Renal dysfunction → impaired urate clearance
Lifestyle & Social History: ● Genetic polymorphisms can influence urate
metabolism
● High meat, seafood, and alcohol (esp. beer)
consumption STATION 2: HEALTHCARE NEEDS, GOALS, AND
● Sedentary lifestyle INTERVENTION

Comorbidities: Identify Healthcare Needs

● Hypertension ● Elevated SUA

● Obesity ● Acute joint pain/inflammation
● Dyslipidemia ● Recurrent flares
● Diabetes mellitus ● Presence of tophi
● Renal disease ● Comorbidities (HTN, CKD, DM, CVD)
● Psoriasis
● Cardiovascular disease

Genetic/Family History:

● Family history of gout or hyperuricemia

Therapeutic Goals 2. Chronic Gout / SUA Control:

Acute Gout: Allopurinol:

● Relieve pain & inflammation within 24–48 hours ● Start at 100 mg/day after acute flare subsides
● Titrate every 2–4 weeks up to 300 mg/day max
Chronic/Intercritical Gout: ● Monitor SUA & serum creatinine
● Maintain SUA < 6 mg/dL
● Reduce SUA to < 6 mg/dL
● Prevent flares and joint damage Colchicine 0.5 mg OD-BID:
● Manage comorbidities (e.g., BP, glucose, renal
function) ● Prophylaxis for flare prevention during ULT initiation
(3–6 months)
Recommended Interventions
Lifestyle:
1. Acute Gout:
● Weight loss, low-purine diet, hydration, alcohol
○ Colchicine (max 4 tabs/day) — avoid in renal avoidance
impairment
○ NSAIDs (e.g., indomethacin) — unless GI/renal Comorbidity-Focused:
contraindication
○ COX-2 inhibitors (e.g., etoricoxib) — fewer GI ● Losartan for HTN: uricosuric effect
side effects ● Fenofibrate for dyslipidemia: lowers SUA
○ Corticosteroids: Prednisone 30 mg tapered over
6 days
○ Ice Compress as adjunct for symptom relief
STATION 3: DRUG-RELATED PROBLEMS (DRPs) BONUS: HIGH-YIELD CLINICAL PEARLS

Common DRPs in Gout Management Populations at Higher Risk

Incorrect Dosing: ● Filipino males, 40–60 y/o

● Patients with:
● Allopurinol: not adjusted in renal insufficiency ○ Poor dietary habits (high purine intake)
● Colchicine: risk of toxicity in renal/hepatic impairment ○ CKD, metabolic syndrome
○ Family history of gout
Drug-Drug Interactions:
Drug-Specific Benefits
● Allopurinol + Azathioprine → severe toxicity (xanthine
oxidase inhibition)
Drug Advantage
● NSAIDs + antihypertensives → ↓ effectiveness, ↑ renal
risk Allopurinol Cost-effective, cornerstone ULT
Therapeutic Duplication: Colchicine Rapid flare resolution, also prophylactic

● Concurrent NSAIDs and COX-2 inhibitors Etoricoxib NSAID efficacy with lower GI risk

Inappropriate Medication Use: Losartan Antihypertensive + urate-lowering

● NSAIDs in CKD or peptic ulcer disease Fenofibrate Lipid control + urate reduction
● Long-term colchicine for prophylaxis without monitoring
Key Side Effects to Watch
Recommendations
● Colchicine: GI upset, diarrhea, myopathy (esp. in renal
● Adjust allopurinol dose based on renal function
disease)
● Avoid NSAIDs in renal impairment; use steroids instead
● Allopurinol: Rash, rare but serious hypersensitivity
● Replace colchicine with alternative if GI side effects
syndrome
occur
● NSAIDs: GI bleeding, nephrotoxicity
● Educate patient on adherence, side effects, lifestyle
● Steroids: Hyperglycemia, fluid retention
 STATION 2: HEALTHCARE NEEDS, GOALS,
CKD INTERVENTIONS

Primary Healthcare Need:

STATION 1: RISK FACTOR ANALYSIS
● Delay CKD progression
Non-Modifiable Risk Factors: ● Prevent and manage complications (e.g., CVD,
electrolyte imbalance, anemia)
● Age: Risk increases >60 years
● Genetics / Family History: Especially if 1st-degree Clinical Goals (Based on PH CPG and KDIGO):
relatives have CKD, hypertension, or T2DM
● Maintain BP < 130/80 mmHg (especially if albuminuria
Modifiable Risk Factors: >30 mg/day)
● Stabilize or slow decline of eGFR
● Type 2 Diabetes Mellitus (T2DM): Major cause of
● Reduce albuminuria (UACR <30 mg/g if possible)
CKD in the Philippines
● Hypertension (HTN): Contributes to glomerular
damage and nephrosclerosis Pharmacologic Interventions:
● NSAID Use: Causes afferent arteriolar vasoconstriction
→ decreased GFR 1. ACE inhibitor (e.g., enalapril 5–20 mg/day)
● Smoking: Accelerates progression of CKD and ○ Especially if proteinuria or HTN is present
worsens albuminuria ○ Initiate at low dose, titrate while monitoring
potassium and creatinine
Pathophysiology Summary: 2. ARB (e.g., losartan 50–100 mg/day) – alternative to
ACEi if cough develops
● Chronic injury → nephron loss
3. SGLT2 inhibitor (e.g., dapagliflozin 10 mg/day)
● Glomerulosclerosis and tubulointerstitial fibrosis
○ Recommended even in non-diabetic CKD
● Compensatory hyperfiltration → further nephron
with eGFR ≥25 mL/min/1.73 m² and albuminuria
damage
○ Reduces CKD progression and cardiovascular
● Decline in GFR, increase in albuminuria →
events
progressive CKD
4. Avoid nephrotoxins:
○ NSAIDs, aminoglycosides, IV contrast (if
avoidable)
 Non-Pharmacologic Interventions: General Recommendations:

● Smoking cessation, weight control, low-salt diet, limit ● Adjust all medications based on renal function
protein intake (0.8 g/kg/day), glycemic control (HbA1c ● Monitor: eGFR, serum creatinine, potassium every
<7% in DM) 1–3 months depending on stage
● Use eGFR calculators (e.g., CKD-EPI) for accurate
STATION 3: DRUG-RELATED PROBLEMS (DRPs) staging

Drug DRP Intervention

Metformin Risk of lactic Discontinue if eGFR

acidosis if eGFR <30; consider dose
<30 reduction or safer
alternatives if 30–45

NSAIDs (e.g., Nephrotoxicity, Avoid in CKD; use

ibuprofen) decreased renal paracetamol for pain or
perfusion refer to a specialist

Allopurinol Risk of toxicity Dose adjustment

due to renal required (e.g., start at
excretion 50–100 mg/day if eGFR
30–59)

RAAS blockers Risk of Initiate cautiously,

(ACEi/ARB) hyperkalemia monitor serum K+ and
and acute rise in SCr within 1–2 weeks of
creatinine starting

Others (e.g., Potential for AKI, Avoid or closely monitor

aminoglycosides, hypomagnesemia renal function
PPIs)
 Pathophysiology Summary:
OSTEOPOROSIS
● Postmenopausal estrogen deficiency leads to
increased bone resorption by osteoclasts, causing
STATION 1: RISK FACTOR ANALYSIS an imbalance between bone resorption and formation
● Reduced bone mineral density (BMD) leads to
Non-Modifiable Risk Factors:
increased fracture risk, especially in the spine, hip,
● Female sex: Women have a higher risk, especially and wrist
postmenopausal
● Age > 65 years: Aging accelerates bone loss, STATION 2: HEALTHCARE NEEDS, GOALS,
particularly after menopause INTERVENTIONS
● Genetics/family history: A family history of
osteoporosis or fractures increases risk Primary Healthcare Need:

Modifiable Risk Factors: ● Prevent fractures and minimize the risk of falls
● Manage bone mineral density (BMD) and treat
● Low calcium/Vitamin D intake: Essential for bone symptoms of osteoporosis
health; deficiency increases risk of fractures
● Smoking: Reduces bone density and interferes with Clinical Goals:
bone healing
● T-score > -2.5 (indicating normal bone density)
● Chronic corticosteroid use: Increases bone
● Prevent new fractures or worsening of existing ones
resorption and decreases bone formation
● Improve overall bone health and quality of life
● Excessive alcohol consumption: Impairs calcium
absorption and bone formation
● Physical inactivity: Weight-bearing exercises help
maintain bone strength
Pharmacologic Interventions: Non-Pharmacologic Interventions:

1. Bisphosphonates: ● Weight-bearing exercises (e.g., walking, weight

○ Alendronate 70 mg weekly or Risedronate 35 training)
mg weekly ● Fall prevention strategies: Remove tripping hazards,
i. These help decrease bone resorption ensure good lighting, use mobility aids
and increase bone density ● Smoking cessation and reducing alcohol intake
ii. Adverse effects: GI upset, esophagitis,
jaw osteonecrosis (rare)
○ Counseling: Instruct patient to remain upright
for at least 30 minutes after administration to
reduce esophageal irritation

2. Vitamin D and Calcium supplementation:

○ Vitamin D: 800–1000 IU/day
○ Calcium: 1000–1200 mg/day (based on age
and risk)
○ Important for optimal bone health and function

3. Teriparatide (20 mcg SC/day) or Denosumab (60 mg

SC every 6 months):
○ Indicated for severe osteoporosis or patients
at high risk of fracture
○ Teriparatide: Stimulates new bone formation,
typically given for up to 2 years
○ Denosumab: A monoclonal antibody that
inhibits osteoclast activity
 STATION 3: DRUG-RELATED PROBLEMS (DRPs)
bisphosphonates or
Drug DRP Intervention Denosumab after 2
years of therapy
Bisphosphonate GI disease Instruct to remain
s (e.g., upright for 30 Denosumab Infection risk Monitor for signs of
esophagitis, minutes post-dose; (e.g., infections; ensure
gastritis) consider alternatives osteonecrosis good oral hygiene,
like Denosumab if of the jaw, consider dental
intolerance occurs infections) examination prior to
starting treatment
Steroid-induced Risk of Prophylactic
osteoporosis increased therapy: Calcium General Recommendations:
bone loss and Vitamin D
supplementation; ● Evaluate fracture risk using FRAX tool to assess
consider 10-year fracture risk
bisphosphonates
(e.g., alendronate) ● DEXA (Dual-energy X-ray absorptiometry) scan
for long-term steroid monitoring every 1–2 years to track BMD and
use treatment efficacy

Calcium and Hypercalcemia Monitor serum ● Adjust treatment based on BMD changes and patient
thiazide diuretics calcium levels; tolerance, including possible transition from one
adjust calcium intake therapy to another
if necessary;
consider reducing ● Ensure proper patient education on drug
thiazide dosage administration and lifestyle modifications to optimize
outcomes
Teriparatide Cost and Limit use to 2 years
long-term use due to cost and risk
of osteosarcoma
(rare); transition to