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Diabetes pt 2 and Estrogen and Progesterone Agents

Total questions: 60

Worksheet time: 30mins

Name
Class
Date
1.

According to treatment guidance, initial combination therapy should be considered when A1C is:

a)

0.5% above target

b)

1% above target

c)

1.5–2.0% above target

d)

3.0% above target

2.

Which medication combination should NOT be used together?

a)

SGLT2 inhibitor + GLP-1 receptor agonist

b)

Metformin + SGLT2 inhibitor

c)

Sulfonylurea + insulin

d)

GLP-1 agonist + TZD

3.

Which therapy class is recommended for cardiorenal risk reduction, relevant in MASLD management?

a)

DPP-4 inhibitors

b)

Sulfonylureas

c)

GLP-1 receptor agonists & SGLT2 inhibitors

d)

TZDs only

4.

Which of the following is a common trigger for DKA or HHS?

a)

Chronic stable exercise

b)

Missed insulin doses

c)

Metformin initiation

d)

Carbohydrate-restricted diet

5.

Which treatment is shared in both DKA and HHS management?

a)

IM glucagon

b)

High-dose IV insulin only

c)

IV fluids + electrolytes + insulin

d)

DPP-4 inhibitor therapy

6.

According to ADA treatment recommendations, medication regimens and adherence should be reassessed at what interval to avoid delays in intensification?

a)

Every month

b)

Every 3–6 months

c)

Once annually

d)

Only when A1C rises by ≥2%

7.

Which combination reflects a contraindicated/avoid pairing?

a)

GLP-1 agonist + SGLT2 inhibitor

b)

Metformin + GLP-1 agonist

c)

GLP-1 agonist + DPP-4 inhibitor

d)

TZD + SGLT2 inhibitor

8.

When managing diabetes, treatment goals must address both glycemic and which additional clinical domain?

a)

Hepatic fibrosis score

b)

Immunization compliance

c)

Weight management

d)

Hospital readmission rate

9.

A patient using metformin monotherapy remains above A1C goal after 3 months of adherence. According to treatment guidance, what is the next appropriate step?

a)

Increase monitoring frequency but delay therapy change

b)

Add an additional agent based on comorbid needs

c)

Switch to insulin immediately

d)

Repeat A1C in 12 months

10.

Which of the following is prioritized for type 2 diabetes patients with ASCVD or high ASCVD risk?

a)

Sulfonylureas

b)

GLP-1 receptor agonists or SGLT2 inhibitors

c)

DPP-4 inhibitors alone

d)

TZDs alone

11.

Which patient profile is the best match for insulin pump therapy?

a)

Performs SMBG <2 times daily

b)

Motivated and checks glucose ≥4 times daily

c)

Refuses diabetes self-management training

d)

Only requires basal insulin

12.

A 59-year-old patient with T2DM on metformin and lifestyle modification continues to have an A1C above goal. BMI is 35 kg/m². No ASCVD, CKD, or HF. She asks for medication that will help with glucose AND weight and wants to avoid hypoglycemia.

Which is the best next step?

a)

Add sulfonylurea

b)

Add GLP-1

c)

Begin basal insulin

d)

Add DPP-4 inhibitor

13.

A 63-year-old patient has T2DM, obesity, and suspected MASLD based on elevated ALT and ultrasound findings. Which diabetes therapy class supports liver-related AND cardiorenal benefits?

a)

DPP-4 inhibitors

b)

SGLT2 inhibitor

c)

Sulfonylureas

d)

Regular insulin

14.

A 42-year-old patient presents with recent unintentional weight loss, elevated glucose, and symptoms of polyuria and polydipsia. Current therapy is metformin only.

Which recommendation aligns with guidelines?

a)

Increase metformin to maximum dose

b)

Add GLP-1 RA and reassess in 6 months

c)

Start insulin due to catabolic state

d)

Begin DPP-4 inhibitor

15.

Which statement best describes the link between diabetes treatment and MASLD management?

a)

Hepatic outcomes improve only with insulin

b)

Therapies that improve metabolic and cardiac risk are preferred

c)

MASLD treatment is not affected by diabetes therapy choice

d)

DPP-4 inhibitors are the first-line medication for MASLD

16.

A patient is newly diagnosed with diabetes after showing elevated A1C and symptoms of hyperglycemia. They also have obesity and elevated ASCVD risk. After metformin, which therapy class best aligns with pathophysiology, weight benefit, and cardiometabolic protection?

a)

Sulfonylurea

b)

GLP-1

c)

Regular insulin

d)

Premixed insulin

17.

A T2DM patient with persistent hyperglycemia despite basal insulin has post-meal elevations. Which adjustment best aligns with both intensification strategy and DKA prevention?

a)

Increase basal insulin dose only

b)

Add rapid-acting insulin at meals

c)

Switch to DPP-4 inhibitor monotherapy

d)

Discontinue insulin and start SGLT2 inhibitor

18.

A patient is experiencing possible DKA symptoms (polyuria, fatigue, abdominal pain) after missing insulin due to illness. Which treatment principle combines acute management and pathophysiologic correction?

a)

Rehydrate and initiate IV fluids, electrolytes, and insulin

b)

Administer sliding-scale insulin and restrict fluids

c)

Start oral antihyperglycemics

d)

Increase carbohydrate intake

19.

A patient using a GLP-1 RA + metformin still has A1C above goal after 6 months. Which next step aligns with treatment reassessment frequency, insulin strategy, and hypoglycemia risk minimization?

a)

Continue current therapy without change

b)

Reassess and consider adding basal insulin

c)

Add DPP-4 inhibitor for incretin synergy

d)

Switch directly to premixed insulin

20.

A patient is on metformin and basal insulin, but A1C remains elevated due to post-prandial hyperglycemia. Which adjustment aligns with insulin kinetics, intensification principles, and hyperglycemia crisis prevention?

a)

Increase basal dose by 10–20%

b)

Add rapid-acting mealtime insulin

c)

Switch to NPH at bedtime

d)

Discontinue insulin and use DPP-4 inhibitor instead

21.

A 57-year-old with T2DM is on metformin 1000 mg BID and glargine 28 units QHS. Fasting glucose averages 95–115 mg/dL, but post-meal readings remain 220–260 mg/dL. A1C is still above goal.

Which adjustment is most appropriate?

a)

Increase glargine to 40 units nightly

b)

Add rapid-acting insulin before the largest meal

c)

Switch glargine to NPH BID

d)

Add sulfonylurea

22.

A 42-year-old has severe hyperglycemia, polyuria, recent 12-lb weight loss, and ketones in urine.

Best action:

a)

Start dual oral therapy

b)

Start GLP-1 RA

c)

Initiate insulin therapy immediately

d)

Add DPP-4 inhibitor

23.

A clinician wants to add sitagliptin to a patient already receiving dulaglutide.

Appropriate response:

a)

Proceed to enhance incretin synergy

b)

Avoid due to overlapping mechanism and limited benefit

c)

Switch dulaglutide to basal insulin

d)

Add SGLT2 inhibitor also

24.

A patient’s TDD is 36 units/day.
What is the approximate CF (mg/dL drop per 1 unit of rapid-acting insulin)?

a)

30 mg/dL/unit

b)

40 mg/dL/unit

c)

50 mg/dL/unit

d)

60 mg/dL/unit

25.

Current BG 275 mg/dL, target 110 mg/dL
CF = 1:50 mg/dL

How many correction units are needed?

a)

1 unit

b)

3 units

c)

5 units

d)

7 units

26.

Which estrogen is considered the most potent endogenous estrogen in women?

a)

Estriol

b)

Estrone

c)

Ethinyl estradiol

d)

Estradiol

27.

Which of the following correctly describes the carbon structure of estrogens and progestins?

a)

Estrogens are C21 steroids; progestins are C18 steroids

b)

Estrogens are C18 steroids; progestins are C21 steroids

c)

Both are C19 steroids

d)

Estrogens are C17 steroids; progestins are C20 steroids

28.

Which of the following increases with estrogen therapy according to metabolic effects?

a)

LDL

b)

Bone resorption

c)

HDL

d)

Plasma antithrombin III

29.

Which enzyme is responsible for converting androgens into estrogens?

a)

17,20-lyase

b)

Estradiol dehydrogenase

c)

Aromatase

d)

5-α reductase

30.

Which estrogen formulation is a prodrug that undergoes hepatic O-demethylation to form ethinyl estradiol?

a)

Estradiol valerate

b)

Mestranol

c)

Quinestrol

d)

Sodium equilin sulfate

31.

Which mechanism explains how estrogens exert their physiological action?

a)

Bind cell surface G-protein coupled receptors

b)

Activate tyrosine kinase receptors

c)

Bind SHBG then act via nuclear receptors

d)

Act only through membrane-bound receptors

32.

Which adverse effect is specifically associated with unopposed estrogen therapy?

a)

Venous ulcers

b)

Endometrial carcinoma

c)

Pulmonary fibrosis

d)

Rheumatoid arthritis flare

33.

What clinical effect results from the GI bacterial hydrolysis of EE conjugates?

a)

Increased hepatic toxicity

b)

Increased clearance of EE

c)

Reabsorption and enhanced efficacy of EE

d)

Increased protein binding and reduced activity

34.

Which anti-estrogen competitively inhibits estrogen receptors and is used to treat anovulatory infertility?

a)

Fulvestrant

b)

Clomiphene

c)

Ethinyl estradiol

d)

Drospirenone

35.

Which type of aromatase inhibitor is steroid-based and irreversible?

a)

Triazole derivatives

b)

Mestranol

c)

Exemastane

d)

Quinestrol

36.

Which of the following describes the primary contraceptive mechanism of progesterone?

a)

Inhibition of androgen synthesis

b)

Suppression of GnRH → ↓ LH/FSH release

c)

Increased endometrial proliferation

d)

Blocking aromatase enzymes

37.

Which of the following progesterone adverse effects occurs due to androgen receptor binding?

a)

Osteoporosis

b)

Hyperthyroidism

c)

Acne and hirsutism

d)

Hypoglycemia

38.

Which progesterone agent is classified as a 19-nor progesterone derivative?

a)

Norgestrel

b)

Estradiol

c)

Quinestrol

d)

Equilin sulfate

39.

Which phase of the menstrual cycle is primarily driven by estrogen-mediated endometrial rebuilding?

a)

Secretory phase

b)

Follicular (proliferative) phase

c)

Luteal phase

d)

Menstrual phase

40.

Which estrogenic effect on bone contributes to decreased risk of osteoporosis?

a)

Increased osteoclast proliferation

b)

Stimulating osteoblast apoptosis

c)

Promoting osteoclast apoptosis

d)

Increased calcium excretion

41.

Which factor makes ethinyl estradiol significantly more potent than estradiol?

a)

Increased water solubility

b)

C17 alkylation

c)

Greater SHBG binding affinity

d)

Reduced plasma half-life

42.

Which of the following estrogens is derived from pregnant mares and used orally?

a)

Estradiol valerate

b)

Sodium equilin sulfate

c)

Quinestrol

d)

Estriol sulfate

43.

Which of the following is TRUE regarding estrogen receptor subtypes?

a)

ER-α is the only receptor activated by endogenous estrogens

b)

Both ER-α and ER-β are G-protein coupled receptors

c)

Both ER-α and ER-β are ligand-activated transcription factors

d)

ER-β is only active during pregnancy

44.

Which delivery system provides slow, sustained systemic estrogen levels with fewer peaks and troughs?

a)
Oral contraceptive
b)
Intramuscular injection
c)

PR suppository estrone

d)
Transdermal patch
45.

Which statement best explains why antibiotics may reduce oral contraceptive efficacy?

a)

They displace estrogen from SHBG

b)

They inhibit liver conjugation enzymes

c)

They destroy gut bacteria that hydrolyze conjugates needed for EE reabsorption

d)

They increase estrogen renal excretion

46.

Fulvestrant differs from clomiphene because it is described as:

a)

A partial estrogen agonist

b)

A pure estrogen receptor antagonist

c)

An aromatase substrate

d)

A triazole derivative

47.

Which of the following causes menstruation at the end of the cycle?

a)

Estrogen surge

b)

Progesterone receptor saturation

c)

Decline in both estrogen and progesterone levels

d)

Aromatase inhibition

48.

Which clinical use of progesterone is specifically related to patients taking estrogen in post-menopause?

a)

Treating PMS

b)

Reducing endometrial hyperplasia

c)

Contraception

d)

Treating vasomotor hot flashes

49.

Which progesterone receptor isoforms exist and mediate genomic signaling?

a)

PR-α and PR-γ

b)

PR-α and PR-β

c)

PR-A and PR-B

d)

PR-B and PR-D

50.

Which of the following endogenous estrogens is considered the weakest in potency?

a)

Estradiol

b)

Estrone

c)

Estriol

d)

Mestranol

51.

Which estrogen structural feature is essential for estrogenic activity according to SAR?

a)

C21 steroid backbone

b)

Aromatic A-ring + C3 hydroxyl group

c)

Alkyne at C17

d)

Sulfation of estrone

52.

Which estrogen source becomes the primary contributor in post-menopausal women?

a)

Ovaries

b)

Adrenal cortex

c)

Placenta

d)

Adipose tissue

53.

Which adverse effect of estrogen is most directly linked to thromboembolism risk?

a)

Increased HDL

b)

Increase in clotting factors II, VII, IX, and X

c)

Breast tenderness

d)

Hyperpigmentation

54.

Which anti-estrogen is indicated for tamoxifen-resistant breast cancer?

a)

Clomiphene

b)

Mestranol

c)

Fulvestrant

d)

Drospirenone

55.

Which best describes the feedback effect of clomiphene on the HPO axis?

a)

Enhances estrogen negative feedback

b)

Blocks estrogen receptors → ↑ GnRH → ↑ LH/FSH

c)

Direct inhibition of aromatase

d)

Suppression of follicular development

56.

Which progesterone-mediated reproductive effect is responsible for maintaining pregnancy?

a)

Stimulation of endometrial proliferation

b)

Transition to secretory endometrium + reduced uterine contractility

c)

Inducing luteolysis

d)

High-dose inhibition of implantation

57.

Which drug has an aminoalkyl ether side chain important for its anti-estrogenic activity?

a)

Drospirenone

b)

Fulvestrant

c)

Clomiphene

d)

Equilin sulfate

58.

Which adverse effect of progesterone is explained by its interaction with androgen receptors?

a)

Osteoporosis

b)

Vaginal dryness

c)

Acne and hirsutism

d)

Hypertension

59.

What is the primary SAR purpose of adding an ethinyl (≡C–H) group at C17 to estradiol?

a)

Increase receptor affinity only

b)

Convert it into a prodrug

c)

Prevent metabolic inactivation and increase oral potency

d)

Increase water solubility for IV administration

60.

Mestranol differs structurally from ethinyl estradiol due to which modification?

a)

C17 esterification

b)

C3 methylation (-OCH₃) forming a prodrug

c)

Removal of aromaticity

d)

Fluorination of the A ring

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