WorksheetsMetasmart Final Test
Total questions: 50
Worksheet time: 25mins
Insulin is secreted by which cells of the pancreas?
Alpha cells
Beta cells
Delta cells
PP cells
Type 2 diabetes is primarily characterized by:
Absolute insulin deficiency
Autoimmune destruction of beta cells
Insulin resistance with relative insulin deficiency
Excess glucagon secretion alone
Incretin hormones are secreted from:
Pancreas
Liver
Intestine
Adrenal gland
Which is a microvascular complication of diabetes?
Stroke
Coronary artery disease
Diabetic retinopathy
Peripheral arterial disease
Diabetic nephropathy is best detected early by:
Serum creatinine
Blood urea
Microalbuminuria
Renal ultrasound
Diabetic foot ulcers are mainly due to:
Hyperglycemia alone
Neuropathy and ischemia
Infection only
Insulin deficiency
Which macrovascular complication has the highest mortality in diabetes?
Stroke
Peripheral arterial disease
Coronary artery disease
Retinopathy
Erectile dysfunction in diabetes is due to:
Psychological stress only
Hormonal imbalance only
Vascular and autonomic nerve damage
Excess insulin
Metformin primarily reduces blood glucose by:
Increasing insulin secretion
Reducing hepatic glucose production
Delaying gastric emptying
Increasing renal glucose excretion
Sulfonylureas act by:
Increasing insulin sensitivity
Closing K+ channels in beta cells
Activating GLP-1 receptors
Inhibiting DPP-4 enzyme
DPP-4 inhibitors work by:
Increasing insulin resistance
Destroying GLP-1
Prolonging endogenous incretin action
Inhibiting SGLT-2
SGLT-2 inhibitors reduce blood glucose independent of:
Insulin secretion
Kidney function
Glucose load
Calorie loss
Pioglitazone improves insulin sensitivity via:
PPAR-γ activation
GLP-1 stimulation
Insulin secretion
Alpha-glucosidase inhibition
Alpha-glucosidase inhibitors mainly affect:
Fasting glucose
Post-prandial glucose
Night glucose
HbA1c only
Combination therapy in diabetes is aimed at:
Increasing pill burden
Targeting multiple pathophysiological defects
Avoiding lifestyle changes
Replacing insulin
Semaglutide primarily acts by:
Increasing insulin resistance
Enhancing glucose-dependent insulin secretion
Blocking insulin receptors
Increasing glucagon secretion
A key effect of Semaglutide on appetite is mediated via:
Liver
Kidney
Brain (hypothalamus)
Pancreas only
Bioavailability of oral semaglutide is improved by:
Food intake
SNAC carrier
High-fat meals
Enteric coating
Semaglutide has which pharmacokinetic feature?
Short half-life
Once-daily injection
Long half-life allowing once-weekly dosing
Continuous infusion
Which effect is NOT seen with semaglutide?
HbA1c reduction
Weight loss
Increased hypoglycemia risk (monotherapy)
CV risk reduction
The SUSTAIN trials primarily evaluated:
Insulin therapy
Metformin combinations
Injectable semaglutide
Oral antidiabetics only
SUSTAIN-6 demonstrated benefit in:
Renal failure reversal
Cardiovascular outcomes
Neuropathy reversal
Beta cell regeneration
Typical starting dose of injectable semaglutide is:
1 mg weekly
0.5 mg weekly
0.25 mg weekly
2 mg weekly
Most common side effects of semaglutide are:
Hypotension
GI symptoms (nausea, vomiting)
Renal failure
Hypoglycemia
Semaglutide is contraindicated in patients with:
Hypertension
Type 2 diabetes
Medullary thyroid carcinoma
Obesity
Oral semaglutide should be taken:
With food
At bedtime
Fasting with water only
After breakfast
Semaglutide-induced weight loss is primarily due to:
Diuresis
Fat malabsorption
Appetite suppression and satiety
Muscle breakdown
Compared to insulin, semaglutide has:
Higher hypoglycemia risk
Weight gain
Glucose-dependent action
Need for titration based on SMBG
The biggest clinical advantage of semaglutide is:
Only glucose control
Weight loss with CV benefit
Cheap cost
Replacement of lifestyle changes
In Type 2 diabetes, fasting hyperglycemia is mainly driven by:
Reduced peripheral glucose uptake
Increased hepatic gluconeogenesis
Delayed gastric emptying
Reduced renal glucose clearance
Advanced glycation end products (AGEs) cause tissue damage mainly by:
Increasing insulin secretion
Cross-linking proteins and activating inflammatory pathways
Enhancing glucose oxidation
Reducing oxidative stress
The most common cause of hospitalization in diabetics is:
Nephropathy
Hypoglycemia
Cardiovascular disease
Retinopathy
Metformin improves insulin sensitivity primarily by activating:
AMPK pathway
PPAR-γ receptors
GLP-1 receptors
SGLT-2 transporters
Sulfonylureas cause hypoglycemia mainly because they:
Increase insulin sensitivity
Stimulate insulin release irrespective of glucose levels
Reduce hepatic glucose output
Delay carbohydrate absorption
DPP-4 inhibitors have low hypoglycemia risk because they:
Do not affect insulin secretion
Increase insulin only during hyperglycemia
Act mainly on kidneys
Reduce insulin levels
Which patient would benefit most from SGLT-2 inhibitors?
Lean young diabetic
Diabetic with recurrent UTIs
Diabetic with heart failure
Diabetic with frequent hypoglycemia
A unique advantage of SGLT-2 inhibitors over other OADs is:
Pancreatic beta cell protection
Insulin-independent glucose lowering
Central appetite suppression
Reduction of gastric emptying
Semaglutide differs from native GLP-1 mainly because it:
Has higher receptor affinity only
Is resistant to DPP-4 degradation
Acts on insulin receptors
Is rapidly cleared by kidneys
Which structural modification allows semaglutide to have a long half-life?
PEGylation
Fatty acid side-chain enabling albumin binding
Enteric coating
Enzyme inhibition
SUSTAIN-6 was designed primarily as a:
Glycemic superiority trial
Weight loss trial
Cardiovascular outcomes trial
Renal outcomes trial
Which patient profile is MOST suitable for semaglutide?
Lean Type 1 diabetic
Obese Type 2 diabetic with CV risk
Elderly with recurrent hypoglycemia
Advanced renal failure patient
Compared to insulin, semaglutide offers which major clinical advantage?
Faster glucose reduction
Weight loss with low hypoglycemia risk
No need for titration
Lower GI side effects
Semaglutide should be avoided or used cautiously in patients with:
Mild hypertension
History of pancreatitis
Dyslipidemia
Obesity
Why is semaglutide not a replacement for insulin in Type 1 diabetes?
Ineffective on beta cells
Causes ketoacidosis
Requires endogenous insulin presence
Short duration of action
If semaglutide is stopped abruptly, the most likely outcome is:
Severe hypoglycemia
Rebound hyperglycemia and weight regain
Ketoacidosis
Permanent GI damage
Time in Range (TIR) in CGM refers to the percentage of time glucose remains:
Below 70 mg/dL
Above 250 mg/dL
Between 70–180 mg/dL
Between 100–140 mg/dL
HFpEF (Heart Failure with Preserved Ejection Fraction) is commonly associated with Type 2 diabetes because of:
Reduced myocardial contractility
Diastolic dysfunction due to myocardial stiffness
Acute ischemic injury
Valvular heart disease
The hypothalamus contributes to glucose and weight regulation primarily by:
Producing insulin
Regulating appetite, satiety, and energy expenditure
Increasing renal glucose excretion
Controlling pancreatic beta-cell mass
The SNAC carrier used in oral semaglutide mainly:
Inhibits CYP450 enzymes
Neutralizes gastric acid and enhances transcellular absorption
Acts as an enzyme inhibitor
Delays gastric emptying
A bioequivalence study is primarily conducted to establish:
Clinical efficacy superiority
Safety in special populations
Comparable rate and extent of absorption between two products
Long-term cardiovascular outcomes
