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Lipoproteins and Cholesterol Functions

Total questions: 165

Worksheet time: 2hrs 23mins

Name
Class
Date
1.

Cholesterol

What type of cholesterol is absorbed from the GI tract and consists of animal-based foods like meat, dairy, and eggs

(a)  

2.

Cholesterol

What type of cholesterol is naturally produced in the liver and is the primary source for circulating cholesterol in plasma

(a)  

3.

Lipid Transport

(a)   are formed when lipids bind to proteins for transport

4.

Lipoprotein functions

(a)   have the highest lipid content and lowest protein content

Primary function: transports dietary fats from small intestines

5.

Lipoprotein functions

(a)   has a high lipid content and low protein content

Primary function: delivers TGs to tissues from liver

6.

Lipoprotein functions

(a)   has both a moderate lipid and protein content

Primary function: Transports cholesterol to tissues

7.

Lipoprotein functions

(a)   has a low lipid content and has the highest protein content

Primary function: reverse cholesterol transport back to liver

8.

Lipid profile

Total cholesterol of (a)   mg/dL indicated desirable levels

9.

Lipid profile

LDL-C levels of (a)   mg/dL indicate optimal levels

10.

Lipid profile

HDL-C levels of (a)   mg/dL indicate low levels

11.

Lipid profile

Triglyceride levels of (a)   mg/dL indicates normal levels

12.

Lipid abnormalities are a primary risk factor for clinical...

(a)  

13.

Dyslipidemia etiology

Caused by inherited genetic abnormalities

(a)  

14.

Dyslipidemia etiology

Triggered by environmental including lifestyle, diet, medications, or underlying diseases

(a)  

15.

Hypercholesterolemia

Can occur independently or alongside genetic disorders (4D classification)

(a)  

16.

Medication etiology

Diuretics, Beta-blockers, Glucocorticoids can (a)   both LDL-C and triglycerides

17.

Patient group - LDL-C >190

Treatment:

(a)  

18.

Patient group - LDL-C >190

LDL-C goals:

(a)  

19.

Patient group - Diabetes (40-75 yrs)

Risk assessment:

(a)  

20.

Patient group - Diabetes (40-75 yrs)

Treatment:

(a)  

21.

Patient group - Diabetes (40-75 yrs)

LDL-C goals:

(a)  

22.

Patient group - >75 years

Risk assessment:

(a)  

23.

Patient group - >75 years

Treatment:

(a)  

24.

Patient group >75 years

LDL-C goals:

(a)  

25.

Patient group - 40-75 years

Risk assessment:

(a)  

26.

Patient group - 40-75 years

Treatment:

(a)  

27.

Patient group - 40-75 years

LDL-C goals:

(a)  

28.

Patient group - 40-75 years (WIthout T2DM)

LDL-C goal (<5% risk):

(a)  

29.

Patient group - 40-75 years (Without T2DM)

LDL-C goals (5% - 7.4% risk):

(a)  

30.

Patient group - 40-75 years (Without T2DM)

LDL-C goals (7.5% - 19.9% risk):

(a)  

31.

Patient group - 40-75 years (Without T2DM)

LDL-C goals (>20% risk):

(a)  

32.

Patient group - 40-75 years (With T2DM)

Treatment (ASCVD risk <7.5%):

(a)  

33.

Patient group - 40-75 years (With T2DM)

Treatment (ASCVD risk >7.5%):

(a)  

34.

Patient group - 40-75 years (With T2DM)

LDL-C goals (ASCVD risk <7.5%):

(a)  

35.

Patient group - 40-75 years (With T2DM)

LDL-C goals (ASCVD risk >7.5%):

(a)  

36.

Lipid parameters

Increasing soluble fiber intake and Phytosterol supplementation is used to...

(a)  

37.

Lipid parameters

Increasing physical activity and smoking cessation..

(a)  

38.

Lipid parameters

5-10% weight loss, increasing physical activity, abstain from alcohol, and reducing refined carbohydrates and sugars...

(a)  

39.

Thickening or hardening of the arteries caused by a buildup of plaque in the inner lining

(a)  

40.

Complications of atherosclerosis

Chest pain from reduced blood flow to the heart muscle

(a)  

41.

Complications of atherosclerosis

Heart attack

(a)  

42.

Complications of atherosclerosis

Blockage to blood flow in brain

(a)  

43.

Complications of atherosclerosis

Plaque in arteries of the extremities, especially legs

(a)  

44.

Complications of atherosclerosis

Weakened/bulging area of the wall of the aorta, which may rupture or dissect

(a)  

45.

ASCVD risk enhancing factors

Waist circumference (inches)

(a)  

46.

ASCVD risk enhancing factors

Family history of premature ASCVD (first degree relative)

(a)  

47.

ASCVD risk enhancing factors

Primary hypercholesterolemia

(a)  

48.

ASCVD risk enhancing factors

Chronic kidney disease

(a)  

49.

ASCVD risk enhancing factors

History of (a)  

50.

ASCVD risk enhancing factors

Premature (a)  

51.

ASCVD risk enhancing factors

____ ____ ancestry

(a)  

52.

ASCVD risk enhancing factors

Chronic inflammatory conditions

(a)  

53.

ASCVD risk enhancing factors

Elevated triglycerides

(a)  

54.

ASCVD risk enhancing factors

Elevated blood pressure

(a)  

55.

ASCVD risk enhancing factors

Elevated blood glucose

(a)  

56.

CAC scoring

CAC = 0

(a)  

57.

CAC scoring

CAC 1-99

(a)  

58.

CAC scoring

CAC >100

(a)  

59.

Efficacy monitoring

Short-term evaluation leads to lipid panel reading in (a)   after initiation

60.

Efficacy monitoring

Long-term evaluation on lipid panel every (a)  

61.

SAMS

(a)   statins MAY be better tolerated as they are less likely to be to be taken up into the muscles

62.

SAMS

(a)   statins are more distributed through the body and more often linked to SAMS

63.

Thyroid

Hypothalamus produces...

(a)  

64.

Thyroid

Pituitary produces...

(a)  

65.

Thyroid

TSH forms...

(a)  

66.

Thyroid

Cold, stress, leptin, norepinephrine, and MSH promote

(a)  

67.

Thyroid

Inhibitors that block TRH release

(a)  

68.

Stimulus and release of TRH (Stage 1: Hypothalamus)

"Stimulators” activate the

(a)  

69.

Stimulus and Release of TRH (Stage I: Hypothalamus)

GPCRs are linked to Gs which activates

(a)  

70.

Stimulus and Release of TRH (Stage I: Hypothalamus)

cAMP activates ______ which activates _____

(a)  

71.

Stimulus and Release of TRH (Stage I: Hypothalamus)

CREB = cAMP response element-binding protein that binds to ____ receptors on DNA which activates the hypothalamus to make ____

(a)  

72.

TRH and TSH Production (Stages I-II)

TRH formed in hypothalamus is transported down the portal
system to the pituitary where it binds to (a)   receptors

73.

TRH and TSH Production (Stages I-II)

THR receptors are GPCR linked to ___ which
forms ___ and ___

(a)  

74.

TRH and TSH Production (Stages I-II)
DAG and IP3 stimulates (a)   release

75.

Thyrotropin (TSH) and GPCRs (Gs) – Stage II

TSH increases expression of Na+/I- iodine uptake pumps, TPO
genes, efflux pumps and stimulates (a)   growth

76.

Iodination

TPO catalyzes two DITs which combines to form

(a)  

77.

Iodination

TPO catalyzes an MIT and DIT to combine to form

(a)  

78.

Endocytosis and release

The (a)   secretes T4/T3 hormone to maintain peripheral thyroid hormone levels

79.

Substances that inhibit T4/T3 secretions (Name two)

(a)  

80.

Overview of T4/T3 Biosynthesis and Release

Storage of T4 and T3 in the ______ gland

Binding of T4/T3 by _______ ______

(a)  

81.

The body is producing normal quantities of substances to stimulate those receptors in the hypothalamus involved in TRH biosynthesis, but no TRH is being produced. Propose several possible explanations for these abnormalities.

a)

Receptor, G-protein, cAMP not formed

b)

Enzymes produce TSH that are functional

c)

Drug could block steps in processes

d)

TSH is produced but not functional

e)

Creb not binding or not forming

82.

The hypothalamus is producing normal quantities of TRH to stimulate pituitary TRH receptors, but no TSH is being secreted. Propose several possible explanations for these
abnormalities

a)

Disease related such as infection, cancer, or even trauma

b)

DAG and IP3 not formed

c)

IP3 releases Ca++

d)

Genetic defects

e)

TRH can reach the pituitary

83.

The thyroid gland is producing normal quantities of thyroid hormones, but peripheral tissues are not responding as they normally do to thyroid hormone stimulation. Propose several possible explanations for these abnormalities.

a)

Receptor has low affinity (MCAT binding to THR)

b)

Genetic abnormality (DNA)

c)

Protein synthesis compromised (mutation)

d)

Functional MCAT

84.

The hypothalamus, pituitary and thyroid gland are all functioning normally, but plasma T4 levels are well below normal. Propose several possible explanations for these abnormalities

a)

MCAT hyper activity

b)

Patient may be hyperthyroid

c)

Phenytoin excreted at an abnormally high rate

d)

Patient may be hypothyroid

85.

A patient on lithium therapy has lower than normal plasma thyroid hormone levels, signs and symptoms of hypothyroidism and has developed a goiter. Why are plasma thyroid hormone levels low and why has the patient developed a goiter?

a)

Lithium competition with Na/K pump and indirectly blocks the Na/I pump

b)

Lithium can block the release of T4/T3

c)

T4/T3 plasma levels are low so the HP increase TRH and TSH

d)

TSH over stimulates the thyroid gland

e)

Lithium blocks the release of TSH

86.

The hypothalamus is under-producing TRH and the pituitary gland is under-producing TSH (lower than normal levels of both TRH and TSH). However, plasma levels of T4 are normal (not high!). Propose several possible explanations for these abnormalities.

a)

Deiodinase problem (T4 levels are normal but not T3)

b)

Possible autonomous nodules

c)

T4 levels are unstable while T3 levels are stable

d)

T4 is turning off hypothalamus

87.

The liver is producing significantly higher than normal levels of thyroxine binding globulin, but plasma free (unbound) thyroid hormone levels are normal and hypothalamus, pituitary and thyroid gland function is normal. What would cause thyroxine binding globulin levels to rise and how could plasma free T4 levels be normal?

a)

Maybe a patient is on high dose estrogen and the liver produces more binding proteins

b)

Measuring TH hormone level in blood

c)

HPT system can correct for some variation in plasma proteins

d)

Androgens tend to raise binding globulin levels

88.

Hypothyroid causes

Many disease that directly target the thyroid is known as

(a)  

89.

Hypothyroid Causes

Diseases that directly target the hypothalamus and pituitary are known as

(a)  

90.

Hypothyroid causes

Issues related directly to the T4/T3 diffusion in target tissue is known as

(a)  

91.

What is a cause of peripheral hypothyroidism

(a)  

92.

Biochemical defects

Chronic autoimmune thyroiditis (Hashimoto's disease) is

(a)  

93.

Subclinical hypothyroidism outcomes

More than 10 mIU/liter of thyrotropin leads to a stronger risk of

a)

Congestive heart failure

b)

Stroke

c)

Coronary heart disease

d)

Cognitive decline

94.

Foods such as cauliflower, cabbage, bok choy, broccoli, brussel sprouts can inhibit

(a)  

95.

Medications that can induce or worsen thyroid disorders - HOW?

Parkinson’s Disease patient on carbidopa/levodopa

(a)  

96.

Medications that can induce or worsen thyroid disorders - HOW?

Patient with schizophrenia treated with risperidone

(a)  

97.

Medications that can induce or worsen thyroid disorders - HOW?

Patient with bipolar disease treated with lithium?

(a)  

98.

Medications that can induce or worsen thyroid disorders – HOW?

Patient with cardiovascular disease treated with amiodarone

(a)  

99.

Medications that can induce or worsen thyroid disorders – HOW?

Patient with cardiovascular disease treated with propranolol?

(a)  

100.

Medications that can induce or worsen thyroid disorders – HOW?

Seizure patient on phenytoin (CYP inducer)

(a)  

101.

Hypothyroid major signs and symptoms

Cardiovascular:

a)

Hypertension

b)

Hypotension

c)

Bradycardia

d)

Tachycardia

102.

Hypothyroidism major signs and symptoms

Dermatologic:

a)

Cool, dry skin

b)

Coarse hair

c)

Brittle nails

d)

Nail overgrowth

e)

Warm, clammy skin

103.

Small changes in T4/T3 levels produce _______ changes in ___ levels

(a)  

104.

Interpretation of TFTs and Site of Pathology

High T4/T3 + low TSH targets

(a)  

105.

Interpretation of TFTs and Site of Pathology

High T4/T3 + High TSH targets

(a)  

106.

Interpretation of TFTs and Site of Pathology

Low T4/T3 + Low TSH targets

(a)  

107.

Interpretation of TFTs and Site of Pathology

Low T4/T3 + High TSH targets

(a)  

108.

Hypothyroid Problem #1

Low TRH

Low TSH

Low T4

Low T3

What is happening?

a)

TRH is produced and secreted, the pituitary cells are stimulated to produce TSH. TSH production means the thyroid gland cannot be activated to synthesize and release T4/T3.

b)

TRH is not being produced and secreted, the pituitary cells cannot be stimulated to produce TSH. No TSH production means the thyroid gland cannot be activated to synthesize and release T4/T3.

c)

TRH is not being produced and secreted, the pituitary cells can be stimulated to produce TSH. TSH production means the thyroid gland cannot be activated to synthesize and release T4/T3.

109.

Hypothyroid Problem #2

High TRH

Low TSH

Low T4

Low T3

What is happening?

a)

Low levels to T3 lead to no negative feedback so the hypothalamus continues to produce TRH

b)

The hypothalamus is producing excessive amount of TRH

c)

The hypothalamus is producing an excessive amount of TSH

d)

T4 negative feedback causes hypothalamus to produce TRH

110.

Hypothyroid Problem #3

High TRH

High TSH

Low T4

Low T3

What is happening?

a)

Both hypothalamus and pituitary are over producing hormones

b)

Thyroid gland is dysfunction and not responding to TSH

c)

Thyroid gland is producing enough T4/T3 to send negative feedback to promote TRH secretion

d)

Low levels of T3 means no negative feedback

111.

Hypothyroid Problem #4

Normal TRH

Normal TSH

High T4

Low T3

What is happening?

a)

T4 is not being converted to T3 in peripheral tissues

b)

T3 is not sending negative feedback

c)

T3 can be treated with cytomel

d)

Hypothalamus and pituitary are not working

112.

Raphe Nucleus is the site where (a)   is synthesized

113.

Locus coeruleus is the site where (a)   is synthesized

114.

Substantia nigra is the site where (a)   is synthesized

115.

VTA is the site where (a)   is synthesized

116.

GPCR signaling

Gs _______ adenylyl cyclase and also _______ cAMP activity

(a)  

117.

GPCR signaling

Gi ______ adenylyl cyclase and _______ cAMP activity

(a)  

118.

GPCR signaling

Gq ______ Ca++ and ______ activity

(a)  

119.

________ quickly increases BDNF whereas __________ take longer to work

(a)  

120.

= Activity of the natural ligand (10 cAMP)

(a)  

121.

60% of natural ligand activity, blocks 40% of activity (6 cAMP)

(a)  

122.

Blocks natural ligand activity but no basal activity (2 cAMP)

(a)  

123.

Block natural ligand and basal activity (0 cAMP)

(a)  

124.

Pharmacologic action defined as "inverse agonism" can only exist at a receptor that exhibits..

a)

inhibitory activity upon natural ligand binding

b)

Constitutive activity in the absence of natural ligand binding

c)

Gs-mediated GPCR signaling upon natural ligand bonding

d)

An influx of positively charged ions upon natural ligand binding

125.

Selective Serotonin Reuptake inhibitors (SSRIs) _______ synaptic levels of ________

(a)  

126.

Name the drugs (core concept only) that increase synaptic levels of serotonin

a)

Sertraline (Zoloft)

b)

Fluoxetine (Prozac)

c)

Venlafaxine (Effexor)

d)

Paroxetine (Paxil)

e)

Amitriptyline (Elavil)

127.

Serotonin Norepinephrine Reuptake Inhibitors (SNRIs) _______ synaptic levels of ______ and _______

(a)  

128.

What might have caused an individual to have elevated blood pressure when on MAO?

a)

Activation of MAO lead to too little monoamine causing hypotensive crisis

b)

Non-adherence with blood pressure medication

c)

Too much serotonin in the blood stream causing serotonin syndrome

d)

Inactivation of MAO enzyme caused to much monoamine leading to elevated blood pressure

129.

What is the mechanism of action for the blood pressure elevation? MAO

a)

Norepinephrine cannot be broken down because of enzyme inhibition and causes elevated blood pressure

b)

Serotonin cannot be broken down because of enzyme inhibition and causes elevated blood pressure

c)

Dopamine cannot be broken down because of enzyme inhibition and causes blood pressure elevation

d)

Acetylcholine cannot be broken down because of enzyme inhibitions and causes blood pressure elevation

130.

What adverse effect do you suspect is the cause of this patients dry mouth, blurred vision, constipation, and urinary retention?

a)

Antidopaminergic activity

b)

Antiserotonergic activity

c)

Anticholinergic activity

d)

Antinoradrenegic activity

131.

What antidepressant class causes the greatest risk of anticholinergic activity?

a)

Serotonin antagonists and reuptake inhibitors (SARIs)

b)

Monoamine oxidase inhibitors (MAOls)

c)

Norepinephrine dopamine reuptake inhibitors (NDRIs)

d)

Tricylic antidepressants

e)

Serotonin norepinephrine reuptake inhibitors

132.

Antidepressant associated arrhythmias are associated with blocking which of the following?

a)

Acetylcholine receptors

b)

Alpha adrenergic receptors

c)

Voltage gated sodium channels

d)

Noradrenergic receptors

133.

Can any of the patients medications cause an increase in blood pressure? If so, which one(s)?

a)

None of these medications increase blood pressure

b)

Angiotensin-converting enzyme inhibitors increase blood pressure

c)

Serotonin norepinephrine reuptake inhibitors increase blood pressure

d)

Both of this patients medications can potentially increase blood pressure

134.

What is the mechanism of action of this patients increase in blood pressure?

a)

Increase in 5HT

b)

Decrease in 5HT

c)

Increase in NE

d)

Decrease in NE

135.

Why would this patient be looking for a medication to help with sleep?

a)

Diuretic is keeping him up because he has to go to the bathroom

b)

Depression causes insomnia

c)

NDRI induced activation

d)

Because he is not sleeping well

136.

Is an NaSSA a good choice for this patient? Why?

a)

No, it will cause weight loss

b)

Yes, it will cause weight gain

c)

No, it will cause insomnia

d)

Yes, it will help with sleep

137.

Why would this patient have difficulty with sleeping?

a)

Depression causes insomnia

b)

SSRIs cause insomnia

c)

SSRIs cause insomnia

d)

SSRIs cause sedation

138.

Why did the clinician add a serotonin antagonist and reuptake inhibitor?

a)

SARI causes activation

b)

SSRI causes activation

c)

Depression causes activation

d)

SSRI causes sedation

139.

What is the mechanism of action of this patients sexual dysfunction?

a)

Its just natural because he is over age 20

b)

Anticholinergic activity

c)

5HT2C antagonism

d)

Sigma 1 receptor activity

e)

Nitric oxide synthetase (NOS) inhibition

140.

AB is a 20 year old male who is having his first episode of depression. He is started on an SSRI today. How long should he take the SSRI?

a)

4 to 6 weeks

b)

A minimum of one year

c)

Indefinitely

d)

Until symptoms are better and then stop

141.

What is the goal of treating depression?

a)

Response

b)

Relapse

c)

Recurrence

d)

Remission

142.

A 46-year-old female complains of sedation, weight gain, lack of energy, lack of focus, and anxiety. These are her only symptoms and she has had them for about 8 weeks. Does she have depression? Why or why not?

a)

Yes, because she has 5-symptoms

b)

Yes, because she has had symptoms for 8 weeks

c)

No because she needs to have more than 5-symptoms

d)

No because she does not have depressed mood or anhedonia

143.

AB is now having a second episode of depression and his doctor initiates an SNRI antidepressant today. How long should you use the antidepressant and why?

a)

4 to 6 weeks

b)

Minimum treatment is 12 months

c)

Indefinitely

d)

4 to 9 months

144.

AB is now having a third episode of depression. He is initiated on an NRDI. How long do you recommend that he take this drug?

Why?

a)

4 to 6 weeks

b)

A minimum of 12 months

c)

Indefinitely

d)

4 to 9 months

145.

The primary hypothesis for depression is the monoamine hypothesis. Why is this theory flawed?

a)

Monoamines rise immediately but depression is not treated for a minimum of 4 to 6 weeks

b)

The monoamine hypothesis is not flawed

c)

The primary hypothesis is not the monoamine hypothesis

d)

Monoamines take 4 to 6 weeks to rise correlating with treatment of depression

146.

A PHQ-9 score of 25 is associated with:

a)

Mild depression

b)

Moderate depression

c)

Moderately severe depression

d)

Severe depression

147.

Which of the following medications can cause symptoms of depression?

a)

Isotretinoin

b)

Oral contraceptives

c)

Beta blockers

d)

Benzodiazepines

148.

How long does it take for antidepressants to treat depressive symptoms?

a)

4-6 days

b)

1-2 weeks

c)

2-4 weeks

d)

4-6 weeks

149.

What kind of information is placed in the subjective portion of a SOAP? What kind of information is placed in the objective portion of a SOAP?

a)

Social history, Rating scales scores

b)

Rating scale scores, medications

c)

History of present illness, family history

d)

Laboratory values, vital signs

150.

Suicidal thinking is a potential adverse effect that must be managed for which of the antidepressants?

a)

None of the antidepressants

b)

TCAS

c)

MAOIs

d)

All of the antidepressants

e)

SSRIS

151.

Serotonin norepinephrine reuptake inhibitors (SNRIs) are the most dangerous class of antidepressants in overdose.

a)

True

b)

False

152.

Which rating scale is clinician rated?

a)

Patient health questionaire-9

b)

Beck Depression Inventory

c)

Hamilton Depression Scale

d)

Zung Depression Scale

153.

Which is a risk factor for developing depression?

a)

Being male

b)

Being in your 30's (i.e. 30 -40 years old)

c)

Having a job making decent money

d)

Being divorced

154.

What drugs do not cause this adverse effect (decreased libido/inability to maintain an erection)?

a)

MAOI

b)

NDRI

c)

SARI

d)

NaSSa

e)

SNRI

155.

Which of the drug classes that we discussed this week decrease libido?

a)

SSRI

b)

SNRI

c)

TCA

d)

NDRI

156.

Which antidepressants initially make anxiety worse in the first week of use, but treat anxiety with long term use?

a)

SSRIs

b)

SNRIs

c)

NDRIs

d)

MAOIs

157.

Which of the following drug classes has an antidepressant that can lead to hypertension?

a)

Serotonin reuptake inhibitors

b)

Serotonin norepinephrine reuptake inhibitors

c)

Serotonin antagonists and reuptake inhibitors

d)

Serotonin modulators

158.

Which PHQ-9 score is associated with severe depression?

a)

20-27

b)

15-19

c)

10-14

d)

5-9

159.

Which PHQ-9 score is associated with a moderate depression

a)

20-27

b)

15-19

c)

10-14

d)

5-9

160.

Which of the following effects is caused by antagonism of muscarinic (acetylcholine) receptors?

a)

Anxiety, nausea, headache

b)

Dry mouth, constipation, urinary retention

c)

Hypertension, orthostatic hypotension, QTinterval prolongation

d)

Sedation, sexual dysfunction, weight gain

161.

An increase in norepinephrine in the synaptic cleft leads to which of the following adverse effects?

a)

Postural hypotension

b)

Hypertension

c)

Arrhythmia

d)

QT prolongation

162.

Which of the following drugs block reuptake of norepinephrine and dopamine?

a)

Mirtazapine (Remeron)

b)

Bupropion (Wellbutrin)

c)

Tricyclic antidepressants

d)

Citalopram (Celexa)

163.

Tricyclic antidepressants (TCA's) and Specific Serotonin Norepinephrine Reuptake Inhibitors (SNRI's) cause which mutual adverse effects when taken in overdose?

a)

Prolongation of the QTc interval

b)

Central nervous system depression

c)

Seizures

d)

Hypertension

164.

It takes 5 months to see which of the following with the use of antidepressants?

a)

Response

b)

Recurrence

c)

Remission

d)

Recovery

165.

Which of the following medications are associated with a risk of developing depression?

a)

Isotretinoin

b)

Benzodiazepines

c)

Beta blockers

d)

Oral contraceptives