Academic Week 6 Flashcards

1
Q

What are the three types of hypertension in pregnancy and how are they defined?

A

Chronic hypertension (which exists before pregnancy)

Gestational hypertension (that develops after 20 weeks gestation without proteinuria)

Pre-eclampsia (which is hypertension that develops after 20 weeks gestation with proteinuria).

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2
Q

What are the complications of pre-eclampsia?

A

This is the leading cause of maternal death.

For the mother:
Pre-eclamptic seizures, HELLP syndrome, stroke, pulmonary oedema, renal failure, liver failure and disseminated intravascular coagulopathy.

For the foetus:
Intrauterine growth restriction, premature delivery and subsequent respiratory distress syndrome and even some stillbirths.

These children are at higher risk of heart disease, hypertension, stroke and diabetes.

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3
Q

What are the risk factors for pre-eclampsia?

A

Primiparous, family history, personal history, older mothers, obese mothers, multiple pregnancy, pre-existing conditions of diabetes, hypertension or antiphospholipid syndrome and coagulation disorders.

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4
Q

What genes are involved in the genetic predisposition to pre-eclampsia?

A

Factor V leiden, prothrombin gene variant, MTHFR and angiotensinogen 235THr.

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5
Q

How does the genetic predisposition lead to the development of pre eclampsia?

A

The genetic predisposition causes an abnormal immune response in pregnancy.

This causes deficient trophoblast invasion so spiral arteries in pre-eclamptic women are not as dilated and have a higher resistance than normal spiral arteries. Higher pressure is needed to perfuse the foetus and hence pre-eclampsia develops.

This hypo perfusion causes intrauterine growth restriction.

The proteinuria occurs as a result of the calculate endothelial cells of the renal arteries being damaged.

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6
Q

How is pre-eclampsia treated?

A

The only cure is delivery of the baby.

Treatment is aimed at minimising the risk to the mother and extending gestation when it is safe to do so. Blood pressure control is achieved with labetolol, nifedipine and methyldopa.

Timely antenatal steroids promote fetal lung development if premature delivery is likely to occur.

Women at high risk of pre-eclampsia should be given prophylaxis with magnesium sulphate. Women who have had pre-eclampsia in previous pregnancies should take 150mg aspirin OD for the first trimester.

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7
Q

What is eclampsia and how is this managed?

A

Eclampsia is defined as seizure activity unrelated to other cerebral conditions in a pregnant woman with pre-eclampsia. There is no cure other than removal of the placenta. The aim of treatment is to prevent death by stabilising the mother. Treatment involves lowering blood pressure with labetalol or hydralazine, anticonvulsants of magnesium sulphate and strict fluid resuscitation to prevent pulmonary oedema. Remember, hypertension is not the problem, fluctuations in blood pressure are!

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8
Q

What are the risk factors for gestational diabetes?

A

BMI over 30, previous macrocosmic baby over 4.5 kg, previous gestational diabetes, family history of diabetes, south asian ethnicity and any woman who has developed glycosuria during pregnancy.

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9
Q

What is the definition of gestational diabetes?

A

Gestational Diabetes is defined as any degree of glucose intolerance with its onset or first recognition in pregnancy. This definition is independent of the treatment regime or whether or not the condition persists after pregnancy. This affects 7% of pregnancies.

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10
Q

How is gestational diabetes diagnosed?

A

Oral glucose tolerance test is used (2-hour 75g glucose often performed at 24-28 weeks). Diagnosis is made if the woman has a fasting plasma glucose of 5.6 mmol/L or above or a 2-hour plasma glucose level of 7.8 mmol/L or above.

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11
Q

How is gestational diabetes treated?

A

Treatment of women with GDM is dependent on regular monitoring of capillary blood glucose. Diet and exercise control is used for women with a fasting glucose below 7 mmol/L at diagnosis, metformin is used if blood glucose targets are not met within 2 weeks of diet and exercise changes and insulin can be used if this is still ineffective or the patient cannot tolerate metformin.

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12
Q

What are the complications of gestational diabetes?

A

Complications of GDM for the mother include higher chance of C-section, miscarriage, gestational hypertension and pre-eclampsia and a higher risk of a pre-term birth. The complications for the fetus include macrosomia, polyhydramnios, birth trauma like shoulder dystocia, stillbirth, prematurity and neonatal hypoglycaemia.

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13
Q

What is the definition of obstetric cholestasis?

A

Obstetric Cholestasis is also known as intrahepatic cholestasis of pregnancy and is a multifactorial condition characterised by pruritis in the absence of a rash with abnormal LFTs. Neither of these findings have an alternative cause and both resolve after delivery. This condition has a higher prevalence in Indian or Pakistani Asian communities and is associated with genetics and environmental factors.

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14
Q

How is obstetric cholestasis diagnosed?

A

Obstetric Cholestasis is diagnosed when otherwise unexplained pruritis occur in pregnancy and abnormal LFTs or raised bile acids occur in the pregnant woman and resolve after birth. This typically occurs in the third trimester and the pruritis normally affects the palms and soles and is worse at night. The differential diagnosis is Hepatitis A, B and C, Epstein Barr Virus, Cytomegalovirus, autoimmune liver disease and primary biliary sclerosis.

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15
Q

What are the risks of obstetric cholestasis?

A

Prematurity, meconium staining, increased chance of reoccurrence and possibly miscarriage

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16
Q

How is obstetric cholestasis managed?

A

Symptomatic relief with chlorphenamine for the itching and surveillance of the fetus.

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17
Q

Define a biological medicine

A

A biological medicine is defined as a medication whose active substance is made by or derived from a biological source. Any substance made in a laboratory from a living organism. These include insulin, vaccines, stem cells and tissue therapies. Biological drugs are usually of a high molecular weight and immunogenic.

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18
Q

Define biosimilars

A

Biosimilars is a biological medicine which is highly similar to another already approved biologic. It has a similar structure, biological activity, efficacy, safety and immunogenicity. These are not exact replications of biologic agents. A biosimilar can be considered for approval for one or more indications for which the reference product is approved, without itself being subjected to clinical testing for every indication.

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19
Q

What are the adverse reactions to biologics?

A

Standard infusion reactions occur within the first hour of infusion. the symptoms include fever, shaking chills, musculoskeletal pain, nausea, vomiting, diarrhoea and skin rashes. They are usually moderate in intensity but can be fatal.

Hypersensitivity reactions include degranulation of muscles and basophils, pruritis, urticaria and angioedema. They do not usually occur on 1st infusion but are triggered on subsequent infusions. All immediate reactions should be managed on an individual basis.

Non-immediate reactions include high cytokine release, cytokine storm, autoimmunity as seen in SLE, atopic dermatitis and depression. Biologics inhibit the immune system so increase the risk of infections such as TB, especially if they have latent TB. Live vaccines should be avoided such as BCG, MMR and Rubella. Risk of malignancy is unknown.

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20
Q

How is pre-term birth sub-categorised?

A

Pre-term is defined as babies born alive before 37 weeks of pregnancy are completed. There are sub-categories of pre-term birth based on gestational age:

  • Extremely pre-term (<28 weeks)
  • Very Pre-term (<32 weeks)
  • Moderate to late preterm (32-37 weeks)
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21
Q

What are the causes of pre-term birth?

A

Causes of pre-term birth include uterine overdistention, cervical disease, breakdown of maternal-fetal tolerance, stress, decidual senescence, vascular disorders and infections.

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22
Q

What are the consequences to the baby in pre-term birth?

A

Cerebral palsy, impaired learning, vision problems, dental problems, behavioural and psychological illness and chronic health conditions.

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23
Q

When should vaginal progesterones be given?

A

When a patient has a cervix shorter than 25mm pre-term.

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24
Q

What infections can cause pre-term birth?

A

Infection in pregnancy which can cause pre-term birth include bacterial vaginosis, chlamydia, vaginal candidiasis and trichomonas vaginalis. Asymptomatic bacteriuria is a significant cause of pre-term birth meaning pregnant women are the only patient group who should receive antibiotics for asymptomatic bacteriuria.

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25
Q

How should a patient who is suspected to be pre-term be managed?

A

Treatment can be with a cervical cerclage, a purse strings suture that strengthens the cervix mechanically. Hormonal treatments with progesterone as this has an anti-inflammatory effect and reduces some tocolytic such as silent contractions. The cervical pessary is a mechanical silicon pessary which fits around the cervix to strengthen it.

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26
Q

How should threatened pre-term birth be managed?

A

Threatened pre-term labour is a diagnostic challenge and difficult therapeutically. If confirmed then it should be treated with corticosteroids and magnesium sulphate. This is very effective. Tocolytics are used to suppress contractions and temporarily arrest labour to give steroids and magnesium to improve outcomes for the baby.

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27
Q

What are the biochemical properties of the combined hormonal contraceptive pill and what are there effects?

A

Combined Hormonal Contraception contains ethinyl oestradiol (EE) which is a synthetic oestrogen. EE suppresses LH and FSH and inhibits ovulation. EE can stimulate hepatic production of sex hormone binding globulin (SHBG). The Combined Hormonal Contraceptive pill also used one of several progesterone which prevent over-proliferation of the endometrium, thicken cervical mucus and suppress ovulation.

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28
Q

How does the combined transdermal patch work?

A

The combined transdermal patch (CTP) is given through the brand Evra. It uses EE with norelgestromin. The patch is changed weekly, and hormones are absorbed through the skin. It is less effective in women who weigh more than 90kg.

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29
Q

What are the non-contraceptive benefits of the combined contraceptive methods?

A

There are many non-contraceptive benefits of the combined contractive methods. These include reduction of heavy menstrual bleeding, reduced menstrual pain, benefits for premenstrual syndrome symptoms (PMS), continuous CHC can reduce the risk of recurrence of endometriosis after surgical management, management of acne, management of hirsutism, management of irregular menstrual cycles associated with PCOS, reduction in headaches, mood changes, bloating, cramps, nausea, and breast discomfort and reduction in endometrial, ovarian and colorectal cancer risks.

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30
Q

Describe the mechanism of action of some progesterone only pills

A

Progesterone only methods include progesterone only pills and LARC (Long-acting reversible contraception) methods which require administration less than once per cycle such as injectable progesterones, sub dermal implants and intrauterine systems.

Desogestrel (DSG) containing the POP is taken daily with no hormone free interval. Brands include Cerazette and Zelleta. The must be taken daily within the same 12-hour window. They work by increasing the volume and viscosity of cervical mucus to prevent sperm penetration and ovulation is suppressed in 97% of cycles. It may also hinder implantation in the endometrium and reduce fallopian tube cilia activity.

The traditional POP is also taken daily with no hormone free interval. They have to be taken daily in the same 3-hour window. Examples include norethisterone and levonorgestrel. They work by increasing the volume and viscosity of cervical mucus and ovulation is suppressed in 50% of cycles. It may also hinder implantation and reduce fallopian cilia activity. This may increase the chance of an ectopic pregnancy.

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31
Q

Describe how progesterone only injectable contraception can be used

A

Progesterone only injectable contraception is with depot medroxyprogesterone acetate (DMPA) every 12-13 weeks. It can be IM or SC and its primary action is inhibition of ovulation, but it also causes thickening of the cervical mucus and thinning of the endometrium to create an unfavourable environment for implantation.

This is beneficial for some patients as it has no interaction with the GI tact, does not interact with enzyme inducers, causes amenorrhoea and reduces dysmenorrhoea however there is a delay in the return of fertility and risks of weight gain and osteoporosis.

32
Q

Describe the use of progesterone only implants

A

Progesterone only implants are with etonogestrel implants such as Nexplanon. This can be used for three years and it works by preventing ovulation, altering cervical mucus and thinning the endometrium. Side effects include bleeding which has an unpredictable pattern.

33
Q

Describe the use of Intrauterine Contraception (IUS) such as Levonorgestrel

A

Intrauterine Contraception (IUS) is levonorgestrel (LNG-IUS) such as Mirena and Levosert. This is a LARC that can be used for 5 years. Locally it causes cervical mucus thickening, endometrial thinning and atrophy and has the foreign body effect which prevents implantation of the ovum. There is minimal absorption systemically and so does not affect the HPA axis and over 75% of these women continue to ovulate. Progesterone symptoms are usually minimal.

These are used for contraception, management of heavy menstrual bleeding, reduce pain associated with primary dysmenorrhoea, endometriosis and adenomyosis and they offer endometrial protection during oestrogen replacement therapy (Mirena).

34
Q

Describe emergency contraception

A

Emergency Contraception is dependent on the stage of the cycle and the predicted ovulation. The Gold Standard is always an intrauterine device of a copper IUD. Oral emergency contraception includes Ulipristal acetate (UPA) progesterone receptor modulators (EllaOne) and levonrgestrel 1.5/3mg depending on weight (Levonelle).

35
Q

What drug interactions should contraceptive methods be used cautiously with?

A

Drug interaction are important for all contraceptive methods. Absorption from the GI tract is vital as EE and Progesterones are absorbed in the small intestine and therefore any drugs affecting gut transit or gastric pH are important. EE is excreted through the urine after being reabsorbed in the colon. There is no enterohepatic circulation of progesterones. Activation is dependent on Cytochrome P450 so ant drug which interferes with P-450 will cause toxicity, increased side effects or too little drug.

Common enzyme inducing drugs to avoid include antiepileptics, antibacterial, antiretrovirals, ritonavir, some antidepressants like St John’s wart and lumacaftor. When stopping enzyme inducing drugs, P-450 may take up to 4 weeks to return to their normal levels of activity.

36
Q

What are the causes of erectile dysfunction?

A

The main causes of erectile dysfunction are vascular, psychological, endocrine, neurological and secondary to drugs. The pathophysiology of erectile dysfunction can be subdivided into failure to initiate (psychological or neurogenic), arterial insufficiency or a venous leak.

Vascular disease one of the most common causes of erectile dysfunction and erectile dysfunction can even be a predictor of cardiovascular disease. All men with erectile dysfunction should have a cardiovascular screen. Vascular disease is a disorder of endothelial function caused by the build-up of cholesterol plaques. It affects the penis first because there are many microvascular structures in the penis. Risk factors for vascular erectile dysfunction include diabetes, smoking, alcohol use, hypertension, hypercholesterolaemia, age, obesity and low testosterone.

37
Q

What drugs can cause erectile dysfunction?

A

Testosterone and an intact nervous system are key to initiating and sustaining an erection. Some drugs which interfere with these systems can cause erectile dysfunction. These include diuretics, antihypertensives, antihistamines, antidepressants, Parkinson’s disease drugs, antiarrhythmics, tranquilizers, muscle relaxants, histamine H2 receptor antagonists, some hormone, NSAIDs, chemotherapy and prostate cancer drugs.

Illicit drugs are also problematic with alcohol, amphetamines, barbiturates, cocaine, marijuana, methadone, nicotine and opiates responsible for erectile dysfunction.

38
Q

How can psychogenic erectile dysfunction and organic ED be differentiated?

A

Psychogenic erectile dysfunction is often sudden onset and is well remembered. It is situational and there may be other psychological complaints. It is often with a new partner, but they can masturbate as normal on their own. Organic erectile dysfunction has a more gradual onset and occurs every time. They will not have a morning erection and cause may be apparent from their history. They may get a secondary loss of their libido.

Always assess the cardiovascular risk of any patient presenting with ED, check secondary characteristics and their peripheral pulses. Gross neurology including lower limb reflexes and anal tone may be indicated. DRE may be needed if prostate is suspicious, it is unlikely that prostate cancer is the primary cause for ED.

39
Q

What is the management of erectile dysfunction?

A

Lifestyle modification is incredibly important in the management of ED secondary to cardiovascular disease. Weight loss, increased exercise, smoking cessation and diabetes risk factors can have a dramatic effect on their ED and their general quality of life.

Oral treatment is with phosphodiesterase inhibitors such as sildenafil (Viagra) Tadalafil (Cialis) or Vardenafil (Levitra). These are not aphrodisiacs and need therefore need sexual stimulation to work. Multiple doses should be tried to assess which is the best dose for the patient. Alprostadil is an injectable vasodilator which is injected into the urethra.

The mechanism of action of PDE51 is by preventing the breakdown of cyclic GMC to reduce calcium and hence arterial smooth muscle relaxation. This can only occur in response to nervous stimulation. Alprostadil is independent of stimulation. They cause a rise in Cyclic AMP causing calcium reduction and smooth arterial muscle relaxation.

A penile prosthesis is a permanent solution but should only be done as a last resort. Testosterone supplementation must only be given in patient proven to have low testosterone in their biochemistry. This form of treatment is rarely successful on its own and the clinician should assess testosterone associated illness.

Psychosexual interventions are offered to some with explanation of normal sexual activity, couple therapy and sensate focus.

40
Q

What are the contraindications and side effects of phosphodiesterase inhibitors?

A

The contraindications of phosphodiesterase inhibitors include people who are not fit enough for sexual activity, hypotension or uncontrolled hypertension, severe hepatic impairment, retinitis pigmentosa, interactions with other drugs such as nicorandil, nitrates and alpha blockers, cocaine and take care with drugs which are P450 dependent or grapefruit juice.

Side effects include facial flushing, headache, nasal congestion, dizziness due to hypotension, indigestion, back/leg pain and visual disturbances.

41
Q

What is the definition of premature ejaculation and how is it classified?

A

This is defined as when a man ejaculated sooner during sexual intercourse than he or his partner would like. Features include always or nearly always ejaculating within one minute of penetration, unable to delay ejaculation during intercourse and feeling distressed or frustrated and avoiding sexual intimacy as a result.

It is classified as either primary (lifelong and beginning with first sexual encounters) or secondary (acquired after previous normal sexual activity).

42
Q

What are the causes of premature ejaculation?

A

Causes are debated by psychological elements, erectile dysfunction, relationship problems, hormonal dysfunction or chronic inflammation may be a factor. Some evidence suggests it is linked with anxiety or lifelong premature ejaculation is related to central 5-HT receptor sensitivity as it runs in families.

43
Q

How is premature ejaculation treated?

A

Treatment is with a combined approach with psychosexual support such as pelvic floor exercises and the squeeze technique. The use of condoms or topic anaesthetics to reduce the sensation and enable the man to last longer or oral medications such as Dapoxetine that have a recognised side effect of delaying ejaculation. If ED is a problem then that will need to be addressed as well.

44
Q

What is Peyronie’s disease?

A

This is an abnormal curvature of the penis when erect. This is caused by a plaque formation in the fascia layer of the tunica albuginea. This effects 9% of the population and is often seen congenitally with hypospadias. Young onset may be associated with a raised HbA1c in diabetes.

The classic history is an area of penile pain when the penis is erect followed by a bend. The plaque may or may not be palpable and ED may also occur. It has been associated with Dupuytren’s contracture, Lederhosen’s disease, DM, hypertension and some procedures which involved catheterisation. This is a clinical diagnosis but should be confirmed with evidence from witnessing an erection.

45
Q

What is the management of Peyronie’s disease?

A

Management is with explanation of the condition. Many will resolve naturally, and most will stabilise. If it continues to progress over 24 months then surgery may be required. Stretching can be done with vacuum or traction devices but surgery is with plication, excision of the plaque or prosthesis. Always remember to try and maximise erectile function.

46
Q

What is the pathophysiology of endometriosis?

A

Endometriosis is a common benign condition where endometrial tissue is found outside of the uterine cavity and continues to respond to oestrogen. The pathogenesis that is most widely accepted is retrograde menstruation. This suggests that when the endometrium is menstruated via the vagina, some endometrium moves through the fallopian tubes into the pelvic cavity causing endometriosis. This cannot be the only reason that endometriosis occurs as retrograde menstruation happens in most cycles.

47
Q

What are the symptoms of endometriosis?

A

The classical symptoms of endometriosis include dysmenorrhoea, dyschezia (painful defaecation when on period), dysuria, dyspareunia, chronic pelvic pain and subfertility. Other symptoms include lower back pain, rarely diaphragmatic symptoms such as shoulder tip pain and pneumothorax (even haemoptysis), fatigue and irritability.

48
Q

What are the differentials for endometriosis?

A

The differentials include MSK pain, irritable bowel syndrome, chronic fatigue, nerve related pain and other gynaecological pathology such as fibroids, ovarian cysts and adenomyosis.

49
Q

How is the diagnosis of endometriosis made?

A

Diagnosis is made upon a classical history with cyclical pain, on examination patients may have erythema ab igne caused by scolding from hot water bottles being used to manage the pain. Also signs of umbilical endometriosis, rectal nodules and endometriomas.

50
Q

How should endometriosis investigated?

A

Investigation includes transvaginal ultrasound and MRI pelvis. There are no blood tests required. Management can be non-surgical or surgical. Non-surgical management is with explanation, reassurance, analgesia and lifestyle advice. This is aimed to reduce foods that are high in oestrogens such as red meat. Hormonal management with COCP, POP, IUS, implant or GnRHa can be very helpful if the side effects are not debilitating.

Surgical management is very effective for symptomatic patients who have failed non-surgical management or who are trying to conceive. Excision of deep endometriotic lesions can improve the symptoms and preserve reproductive function. The last resort is hysterectomy.

The GOLD standard diagnostic tool is with a diagnostic laparoscopy. Stage 4 endometriosis is when there are multiple organs involved such as bowel, bladder, ureters and other structures. This requires complex surgical management for widespread excision of endometriomas.

51
Q

What are the risk factors for STI?

A

Risk factors for STI include people with multiple sexual partners, men who have sex with men, being under 25, IVDU, recreational drugs use, excessive alcohol use, sex workers and their partners, not using condoms and having a sexual partner outside Europe.

52
Q

Give some examples of bacterial STIs

A

Bacterial STIs include Chlamydia, Gonorrhoea and Syphilis. Chlamydia is the most common STI and is usually asymptomatic. It infects mucous membranes and incubates for between 7-14 days. Gonorrhoea is often asymptomatic but causes urethral discharge in men and vaginal discharge plus dysuria in women. It can also cause rectal, pharyngeal and eye infections.

Syphilis (Treponema Pallidum) is known as the great imitator. In the primary stage is cause Chancre which are single, painless firm ulcers. In secondary syphilis there is a generalised rash including the palms and soles. Latent syphilis has no symptoms. Tertiary syphilis causes gummatous, neurological and cardiovascular complications.

53
Q

Give some examples of viral STIs

A

Viral STIs include HIV, genital herpes and genital warts. Initially HIV causes non-specific, flu like symptoms such as fever, sore throat, skin rash, lymphadenopathy, weight loss, headache and generalised aches and pains. This will resolve after 1-2 weeks. This may progress to AIDS.

Herpes Simplex virus 1 and 2 causes multiple painful blisters and should be treated with acyclovir. Genital warts caused by HPV are painless and are treated topically with podophyllotoxin or imiquimod. They can also undergo cryotherapy, cautery and curettage.

54
Q

What are the indications for renal imaging in urological trauma?

A

Indications for renal imaging are visible haematuria, non-visible haematuria with an episode of hypotension, history of rapid deceleration injury, any penetrating trauma or clinical signs such as flank pain, abrasions, broken ribs or palpation of an expanding mass. The investigation of choice is with CT.

There are three phases of a CT in renal trauma. The first phase (arterial) is used to assess any vascular injury or presence of active extravasation of contrast, nephrogenic phase optimally demonstrates parenchymal contusions and lacerations, and the delayed phase identifies any collecting system or ureteric injuries.

55
Q

How should kidney trauma be acutely managed?

A

Management depends on the renal injury grading scale 1-5. Initially it should be managed with A-E and polytrauma should be managed at a major trauma centre. Aim is to limit the damage and prevent secondary injuries through hypothermia, coagulopathy and acidosis.

Blunt trauma with a patient who is haemodynamically stable should be managed conservatively with bed rest, serial Hb and renal function, regular observations and repeat imaging. Primary conservative management is associated with lower rate of nephrectomy and no increase in immediate or long-term morbidity. Grade 4 injuries may require stenting or nephrostomy and grade 5 will generally have haemodynamic instability and will need a nephrectomy.

Penetrating renal injuries can be managed conservatively but often require nephrectomy. Surgical management is indicated if there is persistent haemodynamic instability or grade 5 vascular injury. They may require a nephrectomy or debridement and partial nephrectomy.

56
Q

What are the complications of renal trauma?

A

Complications of renal trauma include recurrent episodes of bleeding, abscess, sepsis, urinary fistula, hypertension, urinary extravasation and urinomas. Delayed complications include bleeding, hydronephrosis, calculus formation, chronic pyelonephritis, hypertension, arteriovenous fistulae and pseudo-aneurysms.

57
Q

How are bladder and ureter injuries classified?

A

Bladder trauma can be classified into intraperitoneal, extraperitoneal or combined. It can also be defined by whether it was iatrogenic or not.

Extraperitoneal injuries are associated with pelvic factures, shearing of the anterolateral border near the bladder base, and rarely caused by perforation from a sharp bony fragment. Intraperitoneal causes include sudden rises in intravesical pressure of a full bladder (dome ruptures) and penetrating injuries seen in wars and conflicts.

Iatrogenic injuries are far more common and can be seen in any operation in the pelvis.

58
Q

What are the indications for imaging in bladder or ureter trauma?

A

Indications for imaging in a trauma setting include visible haematuria and a pelvic fracture or non-visible haematuria combined with a high risk pelvic fracture. Inability to void or inadequate urine output, abdominal tenderness or distention due to urinary ascites or other suspicion of urinary ascites, uraemia and elevated creatinine level due to intraperitoneal re-absorption or any exit or entry wound in the lower abdomen, peritoneum or buttocks.

Iatrogenic injuries often present with visible lacerations to the bladder. There may also be blood or gas in the urine bag during a laparoscopic procedure. During TURBT and TURP it would be indicated by cystoscopy identification of fatty tissue, dark space, or bowel, inability to distend the bladder, low return of irrigation fluid or abdominal distention.

Missed iatrogenic bladder trauma is diagnosed by haematuria, abdominal pain, abdominal distention, ileus, peritonitis, sepsis, urine leakage from the wound, decreased urine output or increased serum creatinine. A CT cystogram is used to show where urine is in the abdomen.

59
Q

How should bladder and ureter injuries be managed?

A

Initial management is to prevent it with catheterisation, and in TURBT general anaesthetic to avoid movements and muscle relaxation to prevent an obturator kick which would cause damage to the bladder when operating.

Extraperitoneal ruptures can generally be managed with catheterisation and antibiotic prophylaxis. Intraperitoneal ruptures may require closure with absorbable sutures. They should have a catheter for 5-10 days.

Ureteric trauma is rare in major trauma as the structures are so small and so iatrogenic injury is the main cause. Post-operative signs include flank pain, urinary incontinence, vaginal or drain urinary leak, haematuria, fever, uraemia or urinoma on CT scan. A CT Urogram is the best way to investigate this possibility. A retrograde pylogram can be done in surgery if there are concerns about the ureter where contrast is sent up the ureter under CT surveillance.

Initial management is to manage small injuries with STENTING. This is for injuries such as small fistulae and ligation injuries. If the injury is more severe then an immediate repair is needed or nephrostomy if it was not recognised in surgery. Transureteroureterostomy can be done if one ureter is badly damaged whereby the damaged ureter is resected to the undamaged level and then plumbed into the other ureter.

60
Q

What is the mechanism of injury for urethra injuries?

A

Urethral trauma can be caused anteriorly by compression against the public symphysis such as an astride injury (falling onto bike), kick, stab or animal bite. Iatrogenic injuries often occur in catherization. Posterior urethral injury is caused by deceleration events where the prostate is lifted off the pelvic floor.

In women the main cause of urethral damage is childbirth and occasionally in pelvic fractures. Iatrogenic injuries are less common than in men.

61
Q

How should urethral injuries be investigated?

A

Urethral injuries should be investigated if there is blood at the urethral meatus, the patient cannot void after the injury or there is oedematous fluid in the scrotum. On DRE if the prostate is higher than you would expect and feel boggy then there may be a posterior injury. Investigations are with urethrography, flexible cystoscope and USS for insertion of a suprapubic catheter.

62
Q

How should urethral trauma be managed?

A

Management is with bladder drainage. This should be attempted with a gentle urethral catheter or insertion of a suprapubic catheter but beware of haematoma, haemodynamic shock and rupture so use an USS to guide this. Small injuries can be repaired early on, especially in women.

63
Q

What are the common mechanisms of injury in scrotum trauma?

How should this be investigated and managed?

A

Testicular trauma is usually caused by blunt trauma such as compression against the public symphysis. The main issue is intratesticular haematoma or rupture of the tunica albuginea. Testicular trauma often presents with immediate pain, nausea, vomiting and fainting. Ultrasound is the main tool for investigation. Initial management is surgical exploration to preserve any viable tissue.

64
Q

What is the mechanism of injury for penis fracture, how is this investigated and managed?

A

Penile trauma is most commonly caused when the penis is erect in sexual intercourse, forced flexion, masturbation or rolling over in bed, this is penile fracture. It may also be seen in other major trauma.

The history of a penile fracture includes sudden cracking or popping, pain, immediate detumescence, local swelling and bruising. MRI scan should be done. Immediate loss of erection suggests are more serious blood vessel has been damaged. Management is to surgically close the tunica albuginea as there is an increased risk of erectile dysfunction and urethral injuries.

65
Q

What is endometrial hyperplasia and describe the process of endometrial hyperplasia

A

Endometrial Hyperplasia is the absolute or relative increase in the amount of oestrogen, with consequent hyperplasia of the endometrial glands. There are many classifications, but they are classified on architecture and atypia.

There is a progression from proliferative endometrium, PTEN mutation takes it to hyperplasia without atypia, H-MLH1 mutation take it to hyperplasia with atypia and finally beta-catenin PI3K mutation will produce uterine endometrial carcinoma.

66
Q

What are the types of endometrial cancer?

A

Endometrial carcinoma can be type 1 which makes up the majority and is seen in excess osteogenic stimulation with a background of endometrial hyperplasia. Risk factors for type 1 endometrial carcinoma include obesity, diabetes, hypertension, failure of ovulation, long oestrogen use and functioning ovarian tumours.

Type 2 occurs in 20% of cases. It is De novo and is not associated with hyperplasia. There is often p53 over-expression. Papillary serous adenocarcinoma, high grade endometroid carcinomas and clear cell carcinomas are seen. These are much more aggressive tumours.

67
Q

What are the common types of ovarian cysts?

A

Ovarian cysts are very common and are physiological if corpus luteum or follicular cysts. Benign cysts include cystadenoma and benign cystic teratomas. Also beware of endometriomas. Borderline tumours are pre-invasive tumours and cystadenocarcinomas are the malignant form. Benign lesions are often larger than malignant lesions.

Borderline serous tumours will have some papillary architecture when opened by histology. Teratomas are benign tumours which arise from the stem cells in the ovary.

High grade serous papillary carcinomas account for the majority of ovarian carcinoma diagnoses and related deaths. It is more common in Western nations with an increased risk in Caucasians. Risk is reduced with increased parity, later age of menarche, earlier age of menopause, use of the contractive pill. There is an increased risk with use of the oestrogen only hormonal therapy, combined oestrogen and progestin regimes. There is also a hereditary predisposition with BRCA1 and BRCA2.

68
Q

What are the risk factors for endometriosis?

A

Risk factors include retrograde menstruation, increased menstruation (pregnancy and OCP protective) and genetics have been hypothesised. Obesity and oestrogen stimulation increase the risk. Endometriomas in the ovaries are cysts lined by endometrial tissue which bleed, this causes the chocolate colour known as a chocolate cyst.

69
Q

Give an overview of cervical neoplasia

A

Cervical neoplasia is almost always associated with high-risk HPV infection. High risk HPV types are 16, 18, 31, 45 and 56 whereas low risk types include 6 and 11. 6 and 11 are associated with benign lesions such as condylomata. P16 immunochemistry is used as a marker for high-risk HPV infection. Other risk factors include early age at first sexual intercourse, multiple sexual partners, increased parity, male partner with previous partners and oral contraceptive and nicotine.
This should be treated with excison of the cervix.

70
Q

What are the risk factors for ectopic pregnancies?

A

Ectopic Pregnancies are lifethreatening. Risk factors include tubal damage through infections (PID) or salpingitis or damage through abdominal or pelvic surgery/tubal ligation. Congenital abnormalities and previous ectopic pregnancies are also huge risk factors. Other risk factors include smoking, alterted tubal motility, multiple sexual partners, intrauterine device and history of infertility.

71
Q

What is pelvic inflammatory disease?

A

Pelvic inflammatory disease is a polymicrobial infection in women characterised by inflammation of the upper genital tract, including endometritis, salpingitis, pelvic peritonitis and occasionallt leadng to tubo-ovarian abscess. It is most commonly due to gonorrhoea, chlamydia and enteric bacteria or puerperal infections (from end of third stage of labout until the uterus completely involutes at 3-6 weeks).

72
Q

What does the acronym IBD mean for obstetric histories?

A

I: Infection risk in pregnancy such as GBS or maturnal pyrexia
B: Birthweight
D: Delivery including method, duration, problems and gestation

73
Q

What does the acronym CRUST mean for paediatric family histories?

A
Family History acronym of CRUST:
C: Consanguinity
R: Relevant Conditions
U: Unusual things – Something running in the family
S: Sibling health
T: Family Tree
74
Q

What are the red flags on the paediatric traffic light system?

A
  1. Pale mottled skin
  2. No response to social cues
  3. Does not wake or if roused does not stay awake
  4. High pitched continuous cry
  5. Grunting
  6. Tachypnoea over 60
  7. Moderate or severe chest indrawing
  8. Reduced skin turgor
  9. Ages under 3 months with a temperature greater than 38
  10. Non-blanching rash
  11. Bulging fontanelle
  12. Neck stiffness
  13. Status epilepticus
  14. Focal neurological signs
  15. Focal seizures
75
Q

What are the amber flags on the paediatric traffic light system?

A
  1. Pale
  2. Not responding to normal social cues
  3. No smile
  4. Wakes only with prolonged stimulation
  5. Decreased activity
  6. Nasal flaring
  7. Tachypnoea over 50 (6-12 months) or 40 (>12 months)
  8. O2 sats less than 95%
  9. Crackles on the chest
  10. Tachycardia 160 (under 1), 150 (1-2) or 140 (2-5)
  11. CRT over 3 seconds
  12. Dry mucous membrane
  13. Poor feeding
  14. Reduced urine output
  15. Temperature over 39 at ages 3-6 months
  16. Fever for longer than 5 days
  17. Rigors
  18. Swelling of a limb or joint
  19. Non-weight bearing