Steroids and Cholesterol Flashcards

1
Q

Discuss the actions of oestrogens

A
Anabolic
Increased HDL
Water and Sodium Retention
Decreased Bone Resorption
Increased Blood Coagulability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Discuss the side effects of oestrogen

A
Breast tenderness
Nausea
Decreased glucose tolerance
Vomiting
Water retention
Thromboemolism
Endometrial hyperplasia -> Cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Discuss the actions of progesterone/progestogen

A
Secretary endometrium
Anabolic
Increased mineral density
Fluid retention
Mood change
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Discuss the side effects of progesterone/progestogen

A
Weight gain
Fluid retention
Acne
PMS
Depression
Irritability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Discuss the actions and side effects of testosterone

A

Secondary sex characteristics, anabolic, voice changes
Acne
Aggression
Adverse metabolic effects on lipids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Discuss the problem with 21-hydroxylase deficiency.

A

Converts 17α-OH progesterone to cortisol to provide negative feedback to hypothalamus and pituitary.
Absence causes excessive conversion to testosterone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the activation of testosterone in the body

A

5α-Reductase converts to 5α-dihydrotestosterone which is more potent than testosterone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Discuss the transport of gonadal steroids in the body

A

Bound to sex hormone binding globulin (SHBG)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Discuss the metabolism, excretion and action of sex steroids

A

Metabolised in liver (prog metabolised by 1 passage through liver).
Renal excretion as glucuronides and sulphates.
Binding to nuclear receptors to stimulate transcription.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Discuss the different types of COCP

A

Monophasic, Triphasic or Daily (+placebo)
20->50mg/day oestrogen (ethinylestradiol or mestranol)
Progestogens (drospirenone or norelgestromin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the mechanism of action of the COCP?

A

Suppression of ovulation by inhibition of FSH and LH.
Adverse effect on cervical mucus to reduce sperm penetration.
Adverse effect on endometrium to prevent implantation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Discuss the metabolism of COCP

A

Metabolised in the liver by CYP450 enzyme.

Efficacy is reduced by inducers (carbamazepine and phenytoin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the side effects of taking the COCP?

A
Venous thromboembolism
MI
Hypertension
Decreased glucose tolerance
Increased risk of stroke with focal migraine
Headaches
Mood swings
Cholestatic jaundice
Precipitate porphyria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Discuss the use and action of the progestogen only pill

A

28 day course of levonorgestrel, norethisterone or etynodiol diacetate
Cervical mucus ‘plug’
Adverse effect on myometrium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the major disadvantage with pop?

A

Poor cycle control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What other forms can progestogen be in other than the PoP?

A

Implanon or vaginal ring

MPA and Etonogestrol

17
Q

Discuss the types of emergency contraception

A

Levonorgestrel (1.5mg) in 72 hours or Ullipristal Acetate (30mg) in 120 hours

18
Q

What is the main aim of post menopausal HRT?

A

Symptom control

Preventing osteoporosis a bonus

19
Q

What is the general make up of HRT medication?

A

Oestradiol 1-2mg daily + Premarin 0.625-1.25mg daily

May be combined with medroxyprogesterone acetate, norethisterone and duphaston

20
Q

What are the two main routines for HRT? And what are the advantages of each?

A

Sequential combined = bleed every month (protective)

Continuous combined = no period but less protective

21
Q

What are the main risks of HRT?

A
Endometrial and Ovarian Cancer
Breast cancer
IHD
Stroke
Thromboembolism
Uterine bleeding
22
Q

A 55 year old patient is post menopausal. What questions should be asked before prescribing hormone replacement therapy?

A

Has she had a hysterectomy? If so unopposed oestrogen is fine
Still has womb? NO unopposed oestrogen

23
Q

Discuss use of anti i) oestrogens; ii) progesterone; iii) androgens.

A

i) weak oestrogens that block receptors (clomiphene and tamoxifen).
ii) mild agonist -> sensitise uterus to prostaglandins for use in termination of pregnancy or inducing of labour.
iii) competes with dihydrotestosterone found in COCP (ciproterone).

24
Q

Discuss the effects of SERM

A

Selective oEstrogen Receptor Modulators (Raloxifen)
Prevent osteoporosis
No proliferation in endometrium or breast
Decreased risk of invasive breast cancer in post meno women
Increased hot flushes

25
Q

Describe the damaging effects of oxidised LDLs

A

Inhibit macrophage motility
Enhance platelet aggregation
Induce T cell activation
Endothelial cell toxicity

26
Q

What is the mechanism of action of statins?

A

Inhibit HMG-CoA Reductase
Inhibit cholesterol synthesis
Increased clearance of IDL and LDL
Decreased production of VLDL and LDL

27
Q

Discuss the adverse effects of statins

A
Increase in transaminase levels
Myopathy
GI disturbance
Arthralgias
Headaches
28
Q

What are the secondary/indirect benefits of statins?

A

Anti inflammatory
Plaque reduction
Decreased thrombotic risk
Improved function of endothelial cells

29
Q

What criteria suggests statin use should be recommended?

A

> 20% 10 year risk of cardiovascular disease

30
Q

Discuss the use of fibric acid derivatives

A

PPARα (peroxisome proliferator activated receptor agonist)
Increased lipoprotein lipase, fa uptake and oxidation. Direct vascular effects and decreased TAG production.
Given to patients with low HDL who don’t respond to NA.

31
Q

What are the side effects and contraindications of fibric acid deriavtive use?

A

GI upset, Cholelithiasis and Myositis.

Hepatic/Renal dysfunction or pre-existing gall bladder disease.

32
Q

What are the benefits of Nicotinic Acid use?

A

👇VLDL and 👆HDL at high doses.
Best to raise HDL-c.
Inhibition of lipoprotein synthesis.

33
Q

Discuss the side effects and contraindications associated with use of nicotinic acid.

A

Flushing, itching, headache, hepatotoxicity, peptic ulcer, hyperglycaemia and decreased insulin sensitivity.
Liver disease and peptic ulcer disease

34
Q

What is the action of ezetimibe?

A

Inhibit intestinal cholesterol absorption, 👇intestinal delivery to liver, 👆expression of LDL receptors.
Circulates enterohepatically so delivers directly to site of action.

35
Q

What are the side effects of ezetimibe?

A

Headaches
Abdo pain
Diarrhoea

36
Q

Discuss the benefits and problems with statin and PPAR-α co-prescription.

A

Good control of triglycerides, LDL and HDL.

Increased myopathy and rhabdomyolysis.

37
Q

Suggests dietary advice for control of cholesterol

A

👆👆👆 Fish oil, fibre, vitamin c/e and alcohol (HDL).

👇👇👇 Dietary cholesterol/fat and alcohol (triglycerides).