finals 1 cardio/gynae/surigcal/gastro Flashcards

1
Q

When a thrombus forms in a fast-flowing artery what is it mainly made out of and hence what is the mainstay of treatment?

A

It is formed mainly of platelets.

This is why antiplatelet medications such as aspirin, clopidogrel and ticagrelor are the mainstay of treatment.

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2
Q

What are the 2 ECG changes found in a STEMI and and NSTEMI?

A

STEMI:
ST elevation
new LBBB

NSTEMI:
ST depression
T wave inversion

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3
Q

what does a pathological Q wave? (when the q wave dips greater than usual)

A

Pathological Q waves suggest a deep infarction involving the full thickness of the heart muscle (transmural) and typically appear 6 or more hours after the onset of symptoms.

Pathologic Q waves are a sign of previous myocardial infarction. They are the result of absence of electrical activity. (they are a marker of electrical silence).

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4
Q

which heart artery represent supplies each part of the heart and which ecg lead correlate

A

Right coronary artery
Inferior
II, III, aVF

Left anterior descending
Anterior
V1-4

lca/circumflex
the rest lateral
1, aVL, V3-6

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5
Q

Are troponin LEVELS required to diagnose a STEMI?

A

NO only nstemi

normally repeated on baseline then 3 hours, then should see a raise

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6
Q

nstemi vs unstable angina

A

NSTEMI is diagnosed when there is a raised troponin, with either:

A normal ECG
Other ECG changes (ST depression or T wave inversion)

Unstable angina is diagnosed when there are symptoms suggest ACS, the troponin is normal, and either:

A normal ECG
Other ECG changes (ST depression or T wave inversion)

NSTEMI is diagnosed when there is a raised troponin, with either:

A normal ECG
Other ECG changes (ST depression or T wave inversion)

Unstable angina is diagnosed when there are symptoms suggest ACS, the troponin is normal, and either:

A normal ECG
Other ECG changes (ST depression or T wave inversion)

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7
Q

managment of STEMI

A

M- Morphine
O- Oxygen
N- Nitrate (GTN) - vasodilatior
A- Aspirin 300mg
C- cloplidogrel

Patients with STEMI presenting within 12 hours of onset should be discussed urgently with the local cardiac centre for either:

-Percutaneous coronary intervention (PCI) (if available within 2 hours of presenting)

-Thrombolysis (if PCI is not available within 2 hours)

if you give Thomobolysis and it doesnt work try arange for PCI

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8
Q

What is PCI and thromobolysis?

A

Percutaneous coronary intervention (PCI) involves putting a catheter into the patient’s radial or femoral artery (radial is preferred), feeding it up to the coronary arteries under x-ray guidance and injecting contrast to identify the area of blockage (angiography). Blockages can be treated using balloons to widen the lumen (angioplasty) or devices to remove or aspirate the blockage. Usually, a stent is inserted to keep the artery open.

Thrombolysis involves injecting a fibrinolytic agent. Fibrinolytic agents work by breaking down fibrin in blood clots. There is a significant risk of bleeding, which can make thrombolysis dangerous. Some examples of thrombolytic agents are streptokinase, alteplase and tenecteplase.

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9
Q

what is post MI treatment

A

can remember as 4 A’s

Aspirin 75mg (forever) + SECOND antiplatelet either clopigogrel or trcagrelor - THIS IS CALLED DUAL ANTIPLATELET THERAPY - at least 12 months

Atorvastatin - A Statin (FOREVER)

Atenalol - A beta blocker normally is is bisoprolol (At least 12 months

ACE- inhibitor- normally ramipril (FOREVER)

or 6 A’s

Aspirin 75mg once daily indefinitely
Another Antiplatelet (e.g., ticagrelor or clopidogrel) for 12 months
Atorvastatin 80mg once daily
ACE inhibitors (e.g. ramipril) titrated as high as tolerated
Atenolol (or another beta blocker – usually bisoprolol) titrated as high as tolerated
Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily)

Dual antiplatelet therapy will vary following PCI procedures, depending on the type of stent that was inserted.

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10
Q

MANAGMENT ON NSTEMI

A

he medical management of an NSTEMI can be remembered with the “BATMAN” mnemonic:

B – Base the decision about angiography and PCI on the GRACE score
A – Aspirin 300mg stat dose
T – Ticagrelor 180mg stat dose (clopidogrel if high bleeding risk, or prasugrel if having angiography)
M – Morphine titrated to control pain
A – Antithrombin therapy with fondaparinux (unless high bleeding risk or immediate angiography)
N – Nitrate (GTN)

Unstable patients are considered for immediate angiography, similar to with a STEMI.

The GRACE score gives a 6-month probability of death after having an NSTEMI.

3% or less is considered low risk
Above 3% is considered medium to high risk

Patients at medium or high risk are considered for early angiography with PCI (within 72 hours).

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11
Q

2 main side affects of statins

A

muscle weakness/pain
Rhabdomyolysis (muscle damage – check the creatine kinase in patients with muscle pain)

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12
Q

which antibiotics interact with statins

A

Several common medications interact with statins. One key interaction to remember is with macrolide antibiotics. Patients being prescribed clarithromycin or erythromycin should be advised to stop taking their statin whilst taking these antibiotics.

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13
Q

1.what is the inheritance pattern of familial hypercholestrolemia
2. three important features for diagnosis?
3. management?

A

Familial hypercholesterolaemia is an autosomal dominant genetic condition causing very high cholesterol levels. Several genes have the potential to cause the disorder.

3 criterias for diagnosis
-FHX of CVD
-VERY High cholesterol - above 7.5
-Tendon xanthomata (hard nodules in the tendons containing cholesterol, often on the back of the hand and Achilles)

Management

-Specialist referral for genetic testing and testing of family members
-Statins

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14
Q

what is the Q- RISK score and threshold for treatment?

A

he percentage risk that a patient will have a stroke or myocardial infarction in the next 10 years.

if above 10%, they should be offered a statin, initially atorvastatin 20mg at night.

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15
Q

why should you monitor renal patients on ACE inhibitors and aldosterone antagonists.

A

Both can cause hyperkalaemia (raised potassium). The MHRA issued a safety update in 2016 that using spironolactone or eplerenone (aldosterone antagonists) plus an ACE inhibitor or angiotensin receptor blocker carries a risk of fatal hyperkalaemia.

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16
Q

what is dressler’s syndrome, how does it present and how is it managed?

A

AKA POST MI SYNDROME

happens 2-3 weeks after an MI, caused by local inflammatory response. Resulting in inflammation of the pericardium - pericarditis.

presentation:
pleuritic chest pain, low grade fever, pericardial rub on auscultation (rubbing and scratching sounds)

  • it can causes a pericadial effusion and rarely a cardiac tamponase

A diagnosis can be made with an ECG (global ST elevation and T wave inversion), echocardiogram (pericardial effusion) and raised inflammatory markers (CRP and ESR).

Management is with NSAIDsand, in more severe cases, steroids (e.g., prednisolone). Pericardiocentesis may be required to remove fluid from around the heart, if there is a significant pericardial effusion.

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17
Q

complications post MI an be remembered with the “DREAD” mnemonic:

A

D – Death
R – Rupture of the heart septum or papillary muscles
E – “oEdema” (heart failure)
A – Arrhythmia and Aneurysm
D – Dressler’s Syndrome

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18
Q
A
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18
Q

You are starting a patient on sublingual glyceryl trinitrate (GTN) for angina.

What should you tell them before commencing treatment?

A

you may get a headache and dizziness after using it

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19
Q

what are the reversible causes of cardiac arrest 4 Ts 4 Hs?

A

T- Thrombosis, Tension pneumothorax, tamponade, toxins
H-Hypoxia, hypovoalemia Hypothermia, Hyperkalemia/Hypoglycaemia (and other metabolic abnormalities),

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20
Q

what are the shockable rhythms? defibrilation

A

Ventricular tachycardia
Ventricular fibrillation

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21
Q

How to treat sinus tachycardia ?

A

treat underlying cause

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22
Q

How to treat supraventricular tachycardia ?

A

FIRST vagal manoeuvres- massage carotid and blowing against force into tube

IF UNSUCCESSFUL
adenosine

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23
Q

How to treat Atrial Fibrilation? - atrial flutter basically the same

A

treated with rate control or rhythm control.

Options for rate control:

Beta blocker first-line (e.g., atenolol or bisoprolol)
Calcium-channel blocker (e.g., diltiazem or verapamil) (not preferable in heart failure)
Digoxin (only in sedentary people with persistent atrial fibrillation, requires monitoring and has a risk of toxicity)

Rhythm control aims to return the patient to normal sinus rhythm. This can be achieved through:

Cardioversion
Long-term rhythm control using medications
e.g. Flecainide, Amiodarone (the drug of choice in patients with structural heart disease)

Most patients will end up on a beta blocker for rate control, often bisoprolol, plus a DOAC for anticoagulation. If you remember one thing about the treatment of atrial fibrillation, remember this combination.

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24
Q

what is the CHA2DS2-VASc score and opposite scoring systems?

A

CHA2DS2-VASc is a mnemonic for the factors that score a point:

C – Congestive heart failure
H – Hypertension
A2 – Age above 75 (scores 2)
D – Diabetes
S2 – Stroke or TIA previously (scores 2)
V – Vascular disease
A – Age 65 – 74
S – Sex (female)

NICE (2021) recommends, based on the CHA2DS2-VASc score:

0 – no anticoagulation
1 – consider anticoagulation in men (women automatically score 1)
2 or more – offer anticoagulation

bleeding risk score - ORBIT (also HAS BLED) which is less accurate.

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25
Q

what is the criteria for a narrow complex tachycardia and name the 4 main types ?

A

A QRS complex duration of less than 0.12 seconds or 3 small squares.

-Sinus tachycardia
-Supraventricular tachycardia
-Atrial fibrillation
-Atrial flutter

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26
Q

In both broad and narrow complex tachycardia’s how do you treat patients with life-threatening features, such as loss of consciousness (syncope), heart muscle ischaemia (e.g., chest pain), shock or severe heart failure ?

A

synchronised DC cardioversion under sedation or general anaesthesia. Intravenous amiodarone is added if initial DC shocks are unsuccessful.

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27
Q

Difference between cardioversion and defibrillation ?

A

C- ELECTIVE D- EMERGENCY
C- Synchronised D- Unsyncronised
C- lower energy D-high energy

Unlike defibrillation, which is used in cardiac arrest patients, synchronized cardioversion is performed on patients that still have a pulse but are hemodynamically unstable.

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28
Q

what is the criteria for a broad complex tachycardia and name the 4 main types and treatment

A

Ventricular tachycardia or unclear cause (treated with IV amiodarone)
Polymorphic ventricular tachycardia, such as torsades de pointes (treated with IV magnesium)
Atrial fibrillation with bundle branch block (treated as AF)
Supraventricular tachycardia with bundle branch block (treated as SVT)

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29
Q

cause of atrial flutter ?

A

Atrial flutter is caused by a re-entrant rhythm in either atrium. The electrical signal re-circulates in a self-perpetuating loop due to an extra electrical pathway in the atria.

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30
Q

what is Paroxysmal atrial fibrillation and how it it investigated ?

A

Paroxysmal atrial fibrillation refers to episodes of atrial fibrillation that reoccur and spontaneously resolve back to sinus rhythm. These episodes can last between 30 seconds and 48 hours.

Patients with a normal ECG and suspected paroxysmal atrial fibrillation can have further investigations with:

  • 24-hour ambulatory ECG (Holter monitor)
  • Cardiac event recorder lasting 1-2 weeks
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31
Q

what are the 3 key causes of pancreatitis?

A

gallstones
alcohol
post-ERCP

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32
Q

causes of pancreatitis IGET SMASHED

A

Idiopathic
Gallstones
Ethanol
Trauma

Steroids
Mumps
Autoimmune
Scorpion bite
Hyperlipidemia
ERCP
D (furosemide, thiazide diuretics and azathioprine)

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33
Q

Glasgow score - PANCREAS NUEMONIC

A

The criteria for the Glasgow score can be remembered using the PANCREAS mnemonic (1 point for each answer):

P – Pa02 < 8 KPa
A – Age > 55
N – Neutrophils (WBC > 15)
C – Calcium < 2
R – uRea >16
E – Enzymes (LDH > 600 or AST/ALT >200)
A – Albumin < 32
S – Sugar (Glucose >10)

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34
Q

What is the most common cause of chronic pancreatitis and what are the symptoms?

A

alcohol
and same as acute but longer lasting and less intense

Key complications are:

-Chronic epigastric pain
-Loss of exocrine function, resulting in a lack of pancreatic enzymes (particularly lipase) secreted into the GI tract
-Loss of endocrine function, resulting in a lack of insulin, leading to diabetes
-Damage and strictures to the duct system, resulting in obstruction in the -excretion of pancreatic juice and bile
Formation of pseudocysts or abscesses

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35
Q

Management of chronic pancreatits

A

-Stop alcohol and smoking

-Replacement pancreatic enzymes (Creon) may be required if there is a loss of pancreatic enzymes (i.e. lipase). Otherwise, a lack of enzymes leads to malabsorption of fat, greasy stools (steatorrhoea), and deficiency in fat-soluble vitamins. (A,D,E,K)

Subcutaneous insulin regimes may be required to treat diabetes.

ERCP with stenting can be used to treat strictures and obstruction to the biliary system and pancreatic duct.

Surgery may be required by specialist centres to treat:

Severe chronic pain (draining the ducts and removing inflamed pancreatic tissue)
Obstruction of the biliary system and pancreatic duct
Pseudocysts
Abscesses

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36
Q

What type are the majority of pancreatic cancers? and where are they mostly?

A

adenocarinomas
head of pancreas

TOM TIP: It is worth noting that a new onset of diabetes, or a rapid worsening of glycaemic control type 2 diabetes, can be a sign of pancreatic cancer. Keep pancreatic cancer in mind if a patient in your exams or practice has worsening glycaemic control despite good lifestyle measures and medication.

only cancer where u can refer directly for ct - not everyone though

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37
Q

Courvoisier’s law

A

Courvoisier’s law states that a palpable gallbladder along with jaundice is unlikely to be gallstones. The cause is usually cholangiocarcinoma or pancreatic cancer.

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38
Q

what do these tumour markers relate to?
CA 125
CA 19-9
CA 15-3
Alpha-feto protein (AFP)
Carcinoembryonic antigen (CEA)

A

CA 125 - Ovarian cancer
CA 19-9 - Pancreatic cancer
CA 15-3 - Breast cancer
Alpha-feto protein (AFP) Hepatocellular carcinoma, teratoma
Carcinoembryonic antigen (CEA) Colorectal cancer

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39
Q

what treatments can be offered for endometriosis before establishing a definitive diagnosis with laparoscopy?

A

Cyclical pain can be treated with hormonal medications that stop ovulation and reduce endometrial thickening. This can be achieved using the combined oral contraceptive pill, oral progesterone-only pill, the progestin depot injection, the progestin implant (Nexplanon) and the Mirena coil.

GnRH agonists- to induce menopause but you also get menopause sympotoms e.g. hot flushes and risk of osteoperosis

40
Q

investigation for adenomyosis?

A

Transvaginal ultrasound of the pelvis is the first-line investigation for suspected adenomyosis.

MRI and transabdominal ultrasound are alternative investigations where transvaginal ultrasound is not suitable.

The gold standard is to perform a histological examination of the uterus after a hysterectomy. However, this is not usually a suitable way of establishing the diagnosis for obvious reasons.

41
Q

how does adenomyosis affect pregnancy?

A

Adenomyosis is associated with:

Infertility
Miscarriage
Preterm birth
Small for gestational age
Preterm premature rupture of membranes
Malpresentation
Need for caesarean section
Postpartum haemorrhage

42
Q

what is the treatment for adenomyosis?

A

NICE recommend the same treatment for adenomyosis as for heavy menstrual bleeding.

When the woman does not want contraception; treatment can be used during menstruation for symptomatic relief, with:

  • Tranexamic acid when there is no associated pain (antifibrinolytic – reduces bleeding)
  • Mefenamic acid when there is associated pain (NSAID – reduces bleeding and pain)

Management when contraception is wanted or acceptable:

Mirena coil (first line)
COCP
Cyclical oral progestogens
Progesterone only medications such as the pill, implant or depot injection may also be helpful.

Other options are that may be considered by a specialist include:

GnRH analogues to induce a menopause-like state
Endometrial ablation
Uterine artery embolisation
Hysterectomy

43
Q

Heavy menstrual bleeding is also called…

A

menorrhagia

44
Q

Causes of menorrhagia?

A

Dysfunctional uterine bleeding (no identifiable cause)
Extremes of reproductive age
Fibroids
Endometriosis and adenomyosis
Pelvic inflammatory disease (infection)
Contraceptives, particularly the copper coil
Anticoagulant medications
Bleeding disorders (e.g. Von Willebrand disease)
Endocrine disorders (diabetes and hypothyroidism)
Connective tissue disorders
Endometrial hyperplasia or cancer
Polycystic ovarian syndrome

45
Q

managment for dysfunctional uterine bleeding - which menorrhagia without a cause?

A

When the woman does not want contraception; treatment can be used during menstruation for symptomatic relief, with:

  • Tranexamic acid when there is no associated pain (antifibrinolytic – reduces bleeding)
  • Mefenamic acid when there is associated pain (NSAID – reduces bleeding and pain)

Management when contraception is wanted or acceptable:

Mirena coil (first line)
COCP
Cyclical oral progestogens
Progesterone only medications such as the pill, implant or depot injection may also be helpful.

Other options are that may be considered by a specialist include:

GnRH analogues to induce a menopause-like state
Endometrial ablation
Uterine artery embolisation
Hysterectomy

46
Q

what are 2 things in a gynae history you sometimes forget to ask?

A

Intermenstrual bleeding and post coital bleeding
pain during sex

47
Q

when should an outpatient hysteroscopy be arranged?

A

Suspected submucosal fibroids
Suspected endometrial pathology, such as endometrial hyperplasia or cancer
Persistent intermenstrual bleeding

48
Q

a patient presents with galactorrhea (excessive or inappropriate production of milk) and amenorrhoea what diagnosis are you thinking and how do you investigate?

A

investigation- Prolactin (hyperprolactinaemia is a cause of anovulation) when symptoms of galactorrhea or amenorrhoea

49
Q

what does high FSH in a women represent? measured on day 2-5 of cycle

A

High FSH suggests poor ovarian reserve (the number of follicles that the woman has left in her ovaries). The pituitary gland is producing extra FSH in an attempt to stimulate follicular development.

50
Q

what might high LH in a women suggest? - measured on day 2-5 of cycle

A

High LH may suggest polycystic ovarian syndrome (PCOS).

51
Q

what is the most accurate marker of ovarian reserve?

A

Anti-Mullerian hormone can be measured at any time during the cycle and is the most accurate marker of ovarian reserve. It is released by the granulosa cells in the follicles and falls as the eggs are depleted. A high level indicates a good ovarian reserve.

52
Q

management for tubal factors affecting female fertility? (3)

A

The options for women with alterations to the fallopian tubes that prevent the ovum from reaching the sperm and uterus include:

Tubal cannulation during a hysterosalpingogram
Laparoscopy to remove adhesions or endometriosis
In vitro fertilisation (IVF)

53
Q

What is the single parameter in semen analysis that if suboptimal is least favourable in achieving a spontaneous pregnancy?

Count
Morphology
Motility
PH
Volume

A
54
Q

Testosterone is necessary for sperm creation. The hypothalamo-pituitary-gonadal axis controls testosterone. Hypogonadotrophic hypogonadism (low LH and FSH resulting in low testosterone), can be due to:

A

Pathology of the pituitary gland or hypothalamus

Suppression due to stress, chronic conditions or hyperprolactinaemia

Kallman syndrome which is a condition characterized by delayed or absent puberty and an impaired sense of smell. (genetic condition)

55
Q

Delayed puberty is caused by two reasons what are they?

A

Hypogonadotrophic hypogonadism: a deficiency of LH and FSH (Leading to a deficiency of the sex hormones testosterone and oestrogen)

Hypergonadotrophic hypogonadism: a lack of response to LH and FSH by the gonads (the testes and ovaries) - so the gonatrophins are being produced (LH and FSH) but the gonads (ovaries and testes) are not responding to it.

56
Q

what are gonads

A

testes and ovaries

57
Q

what are some causes of Hypergonadotropic Hypogonadism?

A

Hypergonadotrophic hypogonadism is the result of abnormal functioning of the gonads. This could be due to:

  • Previous damage to the gonads (e.g. testicular torsion, cancer or infections, such as mumps)
  • Congenital absence of the testes or ovaries

-Kleinfelter’s Syndrome (XXY)

-Turner’s Syndrome (XO)

58
Q

what is the difference betwen HPV results and cytology (dyskaryosis found) on a cervical smear?

A

when a cervical smear test is taken the sample is initially tested for the HPV virus. If the HPV is negative then the cells are not examined and the sample is considered negative. if HPV is positive then the cells are examined for precancerous/cancerous changes.

HPV is a virus that is the most common cause of cervical cancer.

precancerous changes =(dyskaryosis).

Cytology results:

Inadequate
Normal
Borderline changes
Low-grade dyskaryosis
High-grade dyskaryosis (moderate)
High-grade dyskaryosis (severe)
Possible invasive squamous cell carcinoma
Possible glandular neoplasia

59
Q

The most common cause of cervical cancer is infection with human papillomavirus (HPV). HPV is also associated with anal, vulval, vaginal, penis, mouth and throat cancers. what are the risk factors for HPV infection?

A

HPV is primarily a sexually transmitted infection.

Increased risk of catching HPV occurs with:

Early sexual activity
Increased number of sexual partners
Sexual partners who have had more partners
Not using condoms

60
Q

risk factors for cervical cancer?

A

You can think of the risk factors for cervical cancer in terms of:

Increased risk of catching HPV

Later detection of precancerous and cancerous changes (non-engagement with screening)

Other risk factors:
-Smoking
-HIV (patients with HIV are offered yearly smear tests)
-Combined contraceptive pill use for more than five years
-Increased number of full-term pregnancies
-Family history
Exposure to diethylstilbestrol during fetal development (this was previously used to prevent miscarriages before 1971)

61
Q

how often are women offered a cervical smear test?

A

Every three years aged 25 – 49
Every five years aged 50 – 64

There are some notable exceptions to the program:

-Women with HIV are screened annually
-Women over 65 may request a smear if they have not had one since aged 50
-Women with previous CIN may require additional tests (e.g. test of cure after treatment)
-Certain groups of immunocompromised women may have additional screening (e.g. women on dialysis, cytotoxic drugs or undergoing an organ transplant)
-Pregnant women due a routine smear should wait until 12 weeks post-partum

62
Q

What is the management based on these smear results?
-Inadequate sample
-HPV negative
-HPV positive with normal cytology
-HPV positive with abnormal cytology

A

Inadequate sample – repeat the smear after at least three months

HPV negative – continue routine screening

HPV positive with normal cytology – repeat the HPV test after 12 months

HPV positive with abnormal cytology – refer for colposcopy

63
Q

process of colposcopy?

A

It involves inserting a speculum and using equipment (a colposcope) to magnify the cervix. This allows the epithelial lining of the cervix to be examined in detail. During colposcopy, stains such as acetic acid and iodine solution can be used to differentiate abnormal areas.

Acetic acid causes abnormal cells to appear white.

iodine solution to stain the cells of the cervix. Iodine will stain healthy cells a brown colour. Abnormal areas will not stain.

A punch biopsy or large loop excision of the transformational zone can be performed during the colposcopy procedure to get a tissue sample.

64
Q

aims of HPV vaccine and what it protects from?

A

The HPV vaccine is ideally given to girls and boys before they become sexually active. The intention is to prevent them contracting and spreading HPV once they become sexually active. The current NHS vaccine protects against strains 6, 11, 16 and 18:

Strains 6 and 11 cause genital warts
Strains 16 and 18 cause cervical cancer

TOM TIP: A common exam task is to counsel parents about their child receiving the HPV vaccine. They are upset because they believe this implies their daughter or son is sexually promiscuous. Focus on the fact it needs to be given before they become sexually active and that it protects them from cervical cancer and genital warts. HPV is very common and infection is the number one risk factor for cervical cancer.

65
Q

what are the risk factors for endometrial cancer?

A

it is an oestrogen-dependent cancer, meaning that oestrogen stimulates the growth of endometrial cancer cells.

You can think of the risk factors for endometrial cancer in relation to the patient’s exposure to unopposed oestrogen. Unopposed oestrogen refers to oestrogen without progesterone (progesterone provides endometrial protection). Unopposed oestrogen stimulates the endometrial cells and increases the risk of endometrial hyperplasia and cancer.

Situations where there is increased exposure of unopposed oestrogen are:

  • Increased age
    -Earlier onset of menstruation
    -Late menopause
    -Oestrogen only hormone replacement therapy
    -No or fewer pregnancies
    -Obesity (adipose tissue is a source of oestrogen)
    -Polycystic ovarian syndrome (due to a lack of ovulation and it is the corpus luteum that produces progesterone. For endo protection pcos women should be on cocp, ius or cyclical progesterones).
    -Tamoxifen (has an anti-oestrogenic effect on breast tissue, but an oestrogenic effect on the endometrium).
  • t2dm

intrestingly smoking is protective

66
Q

COCP is a risk factor in which cancers and protective in which cancers

A

Risk factor for breast and cervical
protective for ovarian and endometrial.

67
Q

what are protective factors for ovarian cancer?

A

Having a higher number of lifetime ovulations increases the risk of ovarian cancer. Factors that stop ovulation or reduce the number of lifetime ovulations, reduce the risk:

Combined contraceptive pill
Breastfeeding
Pregnancy

68
Q

what genes increase the risk of ovarian cancer?

A

BRACA 1 AND 2

69
Q
A
70
Q

difference between lichen sclerosus and lichen planus

A

Lichen sclerosus is a chronic inflammatory skin condition that presents with patches of shiny, “porcelain-white” skin. It commonly affects the labia, perineum and perianal skin in women. It can affect other areas, such as the axilla and thighs. It can also affect men, typically on the foreskin and glans of the penis.

Lichen sclerosis may be confused with other conditions that include “lichen” in the name. Lichen refers to a flat eruption that spreads. It is important not to get lichen sclerosus confused with lichen simplex or lichen planus.

Lichen simplex is chronic inflammation and irritation caused by repeated scratching and rubbing of an area of skin. This presents with excoriations, plaques, scaling and thickened skin.

Lichen planus is an autoimmune condition that causes localised chronic inflammation with shiny, purplish, flat-topped raised areas with white lines across the surface called Wickham’s striae.

71
Q

what is pelvic inflammatory disease? and difference to pyelonephritis

A

Pelvic inflammatory disease (PID) is inflammation and infection of the organs of the pelvis, caused by infection spreading up through the cervix. It is a significant cause of tubular infertility and chronic pelvic pain.

pyenlo is going up your wee hole, this is going up your vag hole

72
Q

what are the risk factors for Pelvic inflammatory disease?

A

Most cases of pelvic inflammatory disease are caused by one of the sexually transmitted pelvic infections.

There risk factors for pelvic inflammatory disease are the same as any other sexually transmitted infection:

Not using barrier contraception
Multiple sexual partners
Younger age
Existing sexually transmitted infections
Previous pelvic inflammatory disease
Intrauterine device (e.g. copper coil)

73
Q

what are the typical examination findings for someone with pelvic inflammatory disease?

A

Examination findings may reveal:

Pelvic tenderness
Cervical motion tenderness (cervical excitation)
Inflamed cervix (cervicitis)
Purulent discharge
Patients may have a fever and other signs of sepsis.

74
Q

what is peritonitis?

A

inflammation of the peritoneal lining

75
Q

what are the signs of peritonitis

A

rebound and percussion tenderness, guarding and rigidity

76
Q

what is Rovsing’s sign?

A

palpation of the left iliac fossa causes pain in the RIF

77
Q

what is psoas sign?

A

pain on extending hip if retrocaecal appendix

Psoas sign is elicited by having the patient lie on his or her left side while the right thigh is flexed backward. Pain may indicate an inflamed appendix overlying the psoas muscle.

78
Q

what forms to make the common bile duct?

A

The cystic duct (connected to gallbladder) and the common hepatic duct.

79
Q

where is the ampulla of vater and The sphincter of Oddi?

A

The ampulla of Vater is located where the bile duct and pancreatic duct join and empty into the small intestine.

The sphincter of Oddi is a ring of muscle surrounding the ampulla of Vater that controls the flow of bile and pancreatic secretions into thde duodenum.

80
Q

where is bile made?

A

liver

81
Q

difference betweem Cholecystitis and Cholangitis

A

Cholecystitis: inflammation of the gallbladder

Cholangitis: inflammation of the bile ducts

82
Q

what is the mechanism of gallbladder contaction?

A

Fat entering the digestive system causes cholecystokinin (CCK) secretion from the duodenum. CCK triggers contraction of the gallbladder, which leads to biliary colic. Patients with gallstones and biliary colic are advised to avoid fatty foods to prevent CCK release and gallbladder contraction.

83
Q

bilary colic vs cholecsytitis vs colangitis

A

Biliary colic is caused by stones temporarily obstructing drainage of the gallbladder. when it falls back into the gallbladder the symptoms resolve. Lasting between 30 minutes and 8 hours

cholecystitis is inflammation of the gallbladder , which is caused by a blockage of the cystic duct preventing the gallbladder from draining. usually caused by stones

cholangitis- surgical emergency - blockage/inflammation in the common bile duct

84
Q

what are the 2 main causes of acute cholangitis?

A

Obstruction in the bile ducts stopping bile flow (i.e. gallstones in the common bile duct)

Infection introduced during an ERCP procedure

85
Q

What is charcot’s triad

A

Acute cholangitis presents with Charcot’s triad:

Right upper quadrant pain
Fever
Jaundice (raised bilirubin)

86
Q

what does percutaneous mean?

A

Through the skin

87
Q

what is Murphy’s sign?

A

Murphy’s sign is elicited in patients with acute cholecystitis by asking the patient to take in and hold a deep breath while palpating the right subcostal area. If pain occurs when the inflamed gallbladder comes into contact with the examiner’s hand, Murphy’s sign is positive

88
Q

where is bilirubin conjugated and what will happen if it cant be?

A

it is conjugated in the liver.

as unconjugated bilirubin is not water soulable it cannot be excretted in the urine (hence you DONT get that dark urine)

89
Q

why is there dark urine and pale stools in jaundice?

A

Dark urine: Urine becomes dark because of the excessive bilirubin is excreted through the kidneys.

Pale stool: The presence of pale stools suggests an obstructive or post-hepatic/liver cause as normal feces get their color from bile pigments.

90
Q

how does bacterial vaginosis change the pH of the vagina?

A

increases pH
Above 4.5

91
Q

what is the most common bacteria causing BV?

Mycoplasma hominis

Prevotella species

Prevotella

Peptostreptococcus

Bacteroides spp.

Gardnerella vaginalis

A

Gardnerella vaginalis

92
Q

Risk factors for bv?

A

Multiple sexual partners (although it is not sexually transmitted)

Excessive vaginal cleaning (douching, use of cleaning products and vaginal washes)

Recent antibiotics

Smoking

Copper coil

93
Q

what age does menopause become purely a clinical diagnosis and for those under this age which blood test is used to make a diagnosis?

A

over 45 and FSH

94
Q

what age do women need to use contraception until?

A

Two years after the last menstrual period in women under 50
One year after the last menstrual period in women over 50

95
Q

what are the two main side effects of the pogesterone depot injection and who is it unsuitable for?

A

weight gain and reduced bone mineral density (osteoporosis).- only in depot

Reduced bone mineral density makes the depot unsuitable for women over 45 years.

96
Q

what is the cut off age for the COCP?

A

50

Consider combined oral contraceptive pills containing norethisterone or levonorgestrel in women over 40, due to the relatively lower risk of venous thromboembolism compared with other options.

97
Q
A