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Finals/Misc. > Core Conditions/2 Key things > Flashcards

Core Conditions/2 Key things Flashcards

1
Q

Asthma: adult stepwise management

A

SABA → ICS → add LTRA → switch to LABA + ICS ± LTRA → swap to MART ± LTRA → increase ICS, seek expert advice

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2
Q

Asthma: example of each type of drug

A

SABA: salbutamol
ICS: beclometasone
LTRA: montelukast
LABA: salmetrol
SAMA: ipratropium bromide, tiotropium

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3
Q

Acute asthma: PEFR criteria for a life threatening, severe and moderate asthma attack

A

Life threatening: <33% best/predicted
Severe: 33-50% best/predicted
Moderate: 50-70%

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4
Q

Pulmonary embolism: treatment

A

Oral apixaban for at least 3 months, or give LMWH if unsuitable

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5
Q

Pulmonary embolism: what might you see on an ABG?

A

Respiratory alkalosis as high respiratory rate causes patient to blow off extra CO2

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6
Q

Community acquired pneumonia: what is the CRB-65 score?

A

Confusion = 1
Resp rate ≥ 20 = 1
Systolic BP <90 = 1
65 years or older = 1
Score of 2 or more → consider hospital admission

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7
Q

CAP: antibiotic treatment?

A

500 mg amoxicillin PO TDS for 5 days (low risk)
OR
IV co-amoxiclav for 5 days (high risk)

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8
Q

Hospital acquired pneumonia: definition

A

New infection appearing > 48 hours after admission

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9
Q

HAP: most likley organism

A

s.pneumoniae

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10
Q

COPD: what will spirometry show?

A

Obstructive picture with FEV1/FVC ratio <0.7

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11
Q

COPD: what is the MRC dysponea scale?

A

Graded from 1 to 5:
grade 1 = not troubled except during strenuous exertion
grade 4 = stops for breath after 100 metres
grade 5 = too breathless to leave the house/breathless during dressing/undressing

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12
Q

What is alpha-1 antitrypsin deficiency?

A

ɑ1AT is a glycoprotein mainly produced by the liver , it balances neutrophil-protease enzymes in the lungs, ∴ deficiency can lead to increased elastase, breaking down alveolar walls and causing emphysematous changes

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13
Q

How do you treat a large pleural effusion?

A

Drain large pleural effusions slowly, max. 1.5 L at a time, with 2 hour intervals.
Rapid drainage can lead to re-expansion pulmonary oedema.

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14
Q

Pneumothorax: 3 risk factors

A

Smoking
Marfan’s
Menstruation in women with endometriosis

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15
Q

Treatment of a pneumothorax:

A

Primary:
- <2cm rim on CXR and not SOB = discharge, follow-up in 4 weeks
- >2cm rim or SOB = aspirate (to to twice then consider chest drain)
Secondary:
- <2cm rim, no SOB, <50 years = aspirate
- >2cm rim, or SOB, or >50 = chest drain

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16
Q

What is a tension pneumothorax?

A

Damage to the pleura allows air to continuously enter the pleural space, but it cannot leave.
Trapped air compresses the lungs, heart, blood vessels and other structures in the chest.

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17
Q

How do you treat a tension pneumothorax?

A

If suspected, do a thoracostomsy (needle decompression) before waiting for a CXR.

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18
Q

AKI: define stage 1, 2 and 3 AKI

A

Stage 1: 1.5-1.9 times baseline increase in creatinine OR <0.5 ml/kg/hr urine output for 6 hours

Stage 2: 2-2.9 times baseline increase in urine output OR <0.5 ml/kg/hr urine output for 12 hours

Stage 3: 3 times baseline increase in creatinine OR <0.5 ml/kg/hr urine output for 24 hours OR anuria for 12 hours-

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19
Q

What is the most common type of AKI?

A

Pre-renal AKI, typically secondary to renal hypoperfusion

Renal hypoperfusion can occur due to: hypotension (cardiac failure, sepsis), reduced circulating volume (haemorrhage, dehydration), oedematous state, renal arterty occlusion, drugs (ACEi/NSAID)

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20
Q

Give three types of intrinstic AKI and a cause of each:

A
  1. Vascular: large vessel atherosclerosis, thromboembolic disease, small vessel disease (secondary to vasculitis or malignant HTN)
  2. Glomerular: primary (necrotising glomerulonephritis, malignancy), secondary (systemic disease e.g. SLE, vasculitis)
  3. Tubulointerstitial: acute tubular necrosis, acute intersititial nephritis
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21
Q

What is acute tubular necrosis (ATN)?

A

Anoxia of renal tissue leads to necrosis.
Can be caused by: decreased renal perfusion, nephrotoxic drugs, myoglobin (rhabdomyolysis), multiple myeloma
Can take up to 6 weeks to regenerate, may require haemodialysis in the interim.

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22
Q

What is a post renal AKI?

A

AKI caused by obstruction, can occur anywhere along the urinary tract from the renal pelvis to the urethra. Leads to hydronephrosis. Aim of treatment is to remove or bypass obstruction e.g. nephrostomy, bladder catheter, dilatation of strictures.

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23
Q

Define CKD:

A

Reduced kidney function (eGFR) for >3 months (measured on two separate occaisons) with evidence of kidney damage e.g. structural abnormality of USS, persistent sediment (haematuria/proteinuria), hx of renal transplant.

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24
Q

What investigations might be used to diagnose CKD? (3)

A

First pass morning urine sample to check albumin:creatinine ratio (>3 mg/mmol confirms proteinuria)

Low calcium can also indicate CKD (as kidneys are not activating vit D and ∴ less calcium is absorbed in the gut)

Bilateral small kidneys on USS

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25
Q

CKD is graded in how many stages? what criteria is included in the final/worst stage?

A

Stages 1 to 5
Stage 5: established renal failure, eGFR <15 or on dialysis
(Renal replacement therapy is required once eGFR <10)

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26
Q

Nephrotic syndrome: classic triad

A
  1. Proteinuria >3g in 24 hours
  2. Hypoalbuminemia - serum albumin <25g/L
  3. Peripheral oedema (rapid and severe pitting oedema)
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27
Q

Nephrotic syndrome:
- Give two causes
- How do you manage it?

A

Causes:
Primary = minimial change disease
Secondary = diabetes/SLE/amyloid

Tx: fluid restriction, diuresis (furosemide), tx underlying cause

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28
Q

Nephritic syndrome: 3 signs

A
  1. Haematuria (macro or microscopic)
  2. Oliguria
  3. Proteinuria (much less than in nephrotic though)

(4. Fluid retention/oedema)

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29
Q

Nephritic syndrome:
- Give 2 causes

A

Primary: IgA nephropathy
Secondary: Post-strep, vasculitits

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30
Q

Kidney transplant: what is hyperacute transplant rejection?

A

Type II hypersensitivity reaction, onset immediately (24-48 hours post-op), caused by pre-existing antibodies against donor’s ABO/HLA antigens.

No treatment possible, must remove graft.

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31
Q

Kidney transplant: give 5 possible complications and when they might occur

A
  1. Hyperacute transplant rejection: immediately post-op
  2. Acute tubular necrosis of graft: first few weeks post-op
  3. Acute graft failure: within 6 months post-op
  4. Chronic graft failure/recurrence of original renal disease: >6 months post op
  5. Post-transplant urinary leak: early post-op
  6. Other: UTI, vascular thrombosis
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32
Q

Polycystic kidney disease: what are the two types?

A

Autosomal dominant: presents in adulthood, PKD1 (chromosome 16) mutation

Autosomal recessive: presents antenatally, most won’t live past childhood, causes Potter syndrome, liver cirrhosis, and lung hypoplasia

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33
Q

BPH: what scoring systems are used to help determine management?

A

International Prostate Sx Score: 8-19 = moderately symptomatic, 20-35 = severely

Bother score: impact of LUTS on QoL, score >3 requires treatment

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34
Q

BPH: what are the first and second line drugs used?

A
  1. Alpha blockers e.g. tamsulosin
  2. 5-alpha reductase inhibitors e.g. finasteride (NB: must used condoms, excreted in semen)
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35
Q

Prostate carcinoma: what investigations are needed? (4)

A
  1. PSA level
  2. DRE: hard, craggy, asymmetrical, loss of central sulcus
  3. MRI prostate: reported on Likert scale, if >3 then…
  4. Prostate biopsy - transrectal USS guided or transperineal
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36
Q

Prostate carcinoma: treatment options (4)

A
  1. Watchful waiting
  2. External beam radiotherapy
  3. Hormone therapy e.g. biclutamide (androgen receptor blocker), goserelin (GnRH agonist)
  4. Surgery e.g. radical prostatectomy
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37
Q

Lower UTI: what might a urine dipstick show?

A

Positive nitrates
Positive leukocytes
RBCs

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38
Q

Lower UTI:
Treatment in women, men, pregnant people

A

Nitrofurantoin 100 mg BD PO for 3 days in women, 7 days in men or pregnant women, or…

Trimethoprim 200 mg BD PO for 3 days in women, 7 days in men

NB: trimethoprim is CI in the first trimester of pregnancy, and should never be co-prescribed with methotrexate

NB: avoid nitrofurantoin in patients with eGFR <45, avoid in third trimester of pregnancy (risk of neonatal haemolysis)

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39
Q

How might acute prostatitis present?

A
  • Recent hx of UTI, STI or catheter
  • Low grade pain (sometimes radiating to the back), fever, LUTs progressing to anuria, haematospermia
  • Soggy, boddy prostate on DRE
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40
Q

How do you treat prostatis?

A

Ciprofloxacin, analgesia

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41
Q

What is the most common kidney tumour in adults?

A

Renal cell carcinoma: typically papillary, chromophone or collecting duct carcinoma

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42
Q

What staging system is used for renal cell carcinoma?

A

Roberston staging 1 to 4:
1 = renal capsule only
2 = invades perinephric fat
3 = invades renal vein/IVC/local lymph nodes
4 = invades distal viscera/distant mets (commonly lung [50%] and bone [30%])

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43
Q

What is a Wilm’s tumour?

A

Nephroblastoma: the most common renal tumour in children.

Presents with abdominal mass and haematuria.

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44
Q

Bladder cancer:
What is the most common type?
Give one other type:
What causes both types?

A
  1. Transitional cell carcinoma (90%) - arises from exposure to aromatic amines and smoking
  2. Squamous cell carcinoma - schistosomiasis (parasite), long term catheters
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45
Q

2 week wait criteria for bladder cancer:

A

45+ years and: unexplained visible haematuria without UTI or visible haematuria persisting/recurring after successful tx for UTI

60+ years and: unexplained non-visisble haemturia and dysuria or raised WCC on blood test

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46
Q

Urolithiasis: 3 anatomical areas where stones commonly get stuck

A
  1. Pelvicureteric junction
  2. Pelvic brim
  3. Vesicoureteric junction
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47
Q

Urolithiasis: gold standard diagnostic test

A

non-contrast CT KUB

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48
Q

What is a hydrocele? How does it present?

A

Peritoneal fluid collection between the layers of the tunica vaginalis.
Presents as a painless swelling of the testicle. Transilluminates on examination.
Surrounds the testis, will NOT feel seperate.

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49
Q

Tx of primary and secondary hydrocele:

A

Primary hydrocele in a newborn: self-resolves within first few months, treat surgically if not resolved by 1-2 years

Secondary: monitor/surgery depending on severity/impact, aspirate if poor surgical candidate

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50
Q

Which side is a varicocele more common on? Why?

A

Left side because of venous drainage:
left gonadal vein → left renal vein → IVC (longer course than the right gonadal vein which drains directly into the IVC ∴ varicocele is more common on the left side)

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51
Q

What is an epididymal cyst?

A

Benign, non-painful cystic swelling of the epididymis (lies above and behind the testis).
Will transilluminate on examination and feel seperate to the testis.

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52
Q

What is epididymo-orchitis? What causes it?

A

Inflammation of the epididymis and testicle.
2/3rds are infective e.g. STI, UTI, mumps
1/3 are idiopathic

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53
Q

What sign on examination can help you differentiate between epididymo-orchitis and torsion?

A

Phren’s sign: elevation of the scrotum reduces the pain → likely epididymo-orchitis

Reduced/absent cremasteric reflect → torsion

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54
Q

Testicular torsion: how quickly must it be detected and treated?

A

Within 4-6 hours

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55
Q

Testicular torsion: 4 risk factors

A
  1. Youth
  2. Poorly descended testis
  3. Bell clapper deforminity (high attachment of the tunica vaginalis)
  4. Previous torsion
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56
Q

What invesitgation is needed in testicular torsion?

A

USS doppler (will show decreased arterial flow)

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57
Q

What is the most common type of testicular cancer?

A

Germ cell tumour e.g. teratoma and seminoma

(therefore investigations includes urine hCG and AFP)

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58
Q

4 risk factors for testicular cancer:

A
  1. Family hx
  2. Cryptorchidism (undescended testis, even after surgery)
  3. Infertility
  4. Kleinfelter’s syndrome (XXY - tall, gynaecomastia, small testes)
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59
Q

What is the difference between an indirect and direct inguinal hernia?

A

Direct: enters the inguinal canal through Hesselbach’s triangle (bordered by: rectus abominis, epigastric vessels, poupart’s ligament), exits at the superficial ring

Inirect: enters the inguinal canal at the deep/internal ring, exits at the superficial ring

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60
Q

3 possible complications of an inguinal hernia:

A
  1. Incarceration: hernia cannot be reduced, may lead to obstruction and strangulation
  2. Obstruction: passage of faecal matter is blocker, presents with vomiting, abdo pain, absolute constipation
  3. Strangulation: base of hernia becomes tight and blocks off blood supply → surgical emergency
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61
Q

Pyelonephritis: management including oral, IV and options if pregnant

A
  1. Send MSU first!
  2. Oral first line: cefalexin
  3. IV first line: ceftrixaone
    Pregnant: oral cefalexin, IV cefuroxime
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62
Q

Give three medications that can be used to treat urge incontinence:

A
  1. Tolterodine - antimuscarinic
  2. Oxybutinin - antimuscarinic
  3. Mirabegron - B3 receptor agonist
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63
Q

Give one medication that can be used to treat stress incontinence:

A

Duloxetine - causes stronger urethral contractions to increase sphincter tone

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64
Q

Which type of incontinence is more common in men? What are some underlying causes?

A

Urge
BPH, stones, neuropathic (MS, Parkinson’s)

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65
Q

Which type of incontinence is more common in women?

A

Stress

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66
Q

How will prolonged vomiting affect serum Cl-, K+ and pH?

A

Hypochloraemia - due to vomiting HCl
Metabolic alkalosis - due to loss of acid (HCl)
Hypokalaemia:
Dehydration and sodium loss stimulates aldosterone via RAAS,
Aldosterone triggers sodium to be reabsorbed from the collecting duct in exchange for potassium,
Potassium is lost in the urine -> hypokalaemia

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67
Q

How will prolonged diarrhoea affect blood pH?

A

Normal anion gap metabolic acidosis: due to loss of HCO3- in diarrhoea

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68
Q

Both IgA nephropathy and post-strep glomerulonephritis can present with a recent URTI and haematuria, what other presenting symptoms might help you differentiate between the two?

A

IgA:
- Develops 1-2 days post-URTI
- Young males
- Macroscopic haematuria
Post-strep:
- Develops 1-2 weeks post-URTI
- proteinuria
- Low complement

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69
Q

What is nephrogenic diabetes insipidus?

A

Kidneys are resistant to ADH resulting in inadequate reabsorption of water in the collecting ducts

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70
Q

Which genetic mutations are associated with coeliac disease?

A

HLA-D2Q and HLA-DQ8

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71
Q

What investigations are needed for coeliac disease? What might they show? (6)

A
  1. FBC - low Hb
  2. Low B12
  3. Low ferritin
  4. LFTs - raised ALT
  5. IgA TTG: if positive then do a duodenal biopsy via upper endoscopy whilst on a gluten containing diet, should show: increased intraepithelial WBCs, villous atrophy, crypt hyperplasia
  6. Other: bone profile, vit D, stool sample
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72
Q

Upper GI malignancy 2 week wait referral criteria:

A

Dysphagia at any age
>55 years old with weight loss and any of the following: upper abdo pain, dyspepsia, reflux

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73
Q

What is Barrett’s oesophagus?

A

Metaplasia of normal stratified squamous epithelium of the distal oesophagus to columnar epithelium, as a result of GORD

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74
Q

How do you treat a peptic ulcer caused by H.Pylori?

A

Triple therapy: PPI, clarithromycin, amoxicillin

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75
Q

Give three types of peptic ulcer - which is more common?

A

Gastric: mainly in elderly people on the lesser curve of the stomach
Duodenal: four times more common than gastric
Jejunal: associated with zollinger-ellison syndrome

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76
Q

Give two types of oesophageal cancer:

A

Squamous cell: often proximal oesophagus, associated with smoking, alcohol and chronic achlasia

Adenocarcinoma: often distal oesophagus, associated with GORD/Barrett’s, obesity, high fat diet, incidence is rising

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77
Q

What is a Krukenberg tumour?

A

An ovarian tumour normally resulting from metstatic gastric cancer spreading via the lymphatic vessels

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78
Q

What is ulcerative collitis?

A

Inflammatory bowel disease limited to the colon and rectum.
Continuous inflammation, affecting the superficial mucosa only.
Smoking is protective.

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79
Q

Ulcerative colitis is classified as mild, moderate and severe using which index?

A

Truelove and Witt’s severity index

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80
Q

Investigations for ulcerative collitis:

A

Faecal calprotectin (>150 = IBD likely)
FBC - anaemia
U&E
LFTs
ESR & CRP - raised
Gold standard diagnostic test: colonoscopy with at least 2 biopsies from 5 different sites

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81
Q

Treating a severe acute UC flare:

A

IV steroid
Consider adding IV clicospoinr or infliximab
Consider surgery, likelihood increased if: stool freq >8/day, pyrexia, tachycardia, dilatation, low albumin or Hb, high platelets or CRP

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82
Q

Treating a mild-moderate UC flare:

A
  1. Topical ASA (mesalazine, sulfasalazine)
  2. Still not better after 4 weeks? Oral ASA
  3. Still not better? Short course of oral steroid
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83
Q

Maintaining remission in UC:

A
  1. Topical or oral lose dose ASA (mesalazine, sulfasalazine)
  2. Consider adding azathioprine or mercaptopurine if: had two or more flares in previous 12 months or remission is not maintained by ASA
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84
Q

6 complications of ulcerative colitis:

A
  1. toxic megacolon
  2. haemorrhage (long standing anaemia)
  3. VTE - acute flare causes high risk of DVT, give LMWH
  4. hypokalaemia
  5. colonic cancer
  6. osteoporosis
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85
Q

What is Crohn’s?

A

Transmural granulomatous inflammation affecting any part of the gut from the mouth to the anus

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86
Q

Investigations for Crohn’s:

A
  1. Gold standard: endoscopy
  2. Colonoscopy IF not septic/risk of perforation
  3. May have barium studies to show strictures, fistulae, rose thorn ulceration
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87
Q

Inducing remission in Crohn’s:

A
  1. first line = prednisolone
  2. may be given 5-ASA if very mild disease only in the colon
  3. May be given budesonide if mild/moderate ileocaecal disease only
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88
Q

Maintaining remission in Crohn’s:

A
  1. mild-moderate disease: azathioprine or mercaptopurine first line, methotrexate second line
  2. severe disease: inflixima, adalimumab (can only be used for 12 mo at a time)
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89
Q

How do you treat a perianal fistula?

A

Examination only ever done under anaesthetic
MRI
Treat with oral metroniadazole & surgical ‘seton’ - a threat to keep the tract open, preventing premature skin closure leading to an abscess

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90
Q

How do you treat c.diff? What about a life-threatening episode?

A

First episode: oral vancomycin
Life threatening: oral vancomycin and IV metronidazole

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91
Q

How do you treat an upper GI bleed? (8)
What else must you do if it is caused by oesophageal varices? (3)

A
  1. ABCDE - determine stability
  2. Cannulas (2xs large bore)
  3. Crystalloid fluids - IV saline 500 ml over 15 mins
  4. Cross match 2 units and coagulation screen
  5. Correct clotting abnormalities - give platelets if <50 x 10⁹/L, give FFP if PT more than 1.5 xs normal
  6. Catheter - monitor fluid balance, aim for >30 mls/hr urine output
  7. Call for help! And keep nil by mouth
  8. Camera - urgent endoscopy immediately after resus, within 24 hours, then IV PPI infusion for 72 hours, oral PPI for 4-8 weeks

Varices:
- Terlipressin (ADH analogue)
- Prophylactic co-amoxiclav to reduce risk of rebleeding
- Variceal banding via OGD

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92
Q

Your patient has just had an OGD to treat an upper GI bleed, what medication do they need?

A

IV PPI for 72 hours, then oral for 4-8 weeks

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93
Q

What medication can you give to prevent oesophageal varices bleeding?

A

beta-blocker

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94
Q

What is Charcot’s triad? What is it a sign of?

A

Fever
RUQ pain
Jaundice
= ascending cholangitis

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95
Q

What is Reynold’s pentad?

A

Charcot’s triad (fever, RUQ pain, jaundice) AND hypotension and confusion

= severe ascending cholangitis, increased mortality

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96
Q

What investigations are needed for acute cholecystitis? What would they show?

A
  1. Normal LFTs
  2. Raised infection markers (ESR, CRP)
  3. USS is first line diagnostic test, if still uncertain then HIDA scan
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97
Q

How does acute cholecystitis present? (4)

A

RUQ pain - may radiate to the right shoulder
Fever
Murphy’s sign
Nausea & vomiting

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97
Q

How does acute cholecystitis present? (4)

A

RUQ pain - may radiate to the right shoulder
Fever
Murphy’s sign
Nausea & vomiting

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98
Q

Signs on examination of a patient with appendicitis: (3)

A
  1. Tender RIF
  2. Low grade pyrexia
  3. Positive Rosving’s sign (RIF pain elicited by pressing on LIF)
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99
Q

What investigations are needed for suspected appendicitis?

A

Urine hCG
USS abdo/pelvis if ?gynae
Bloods: raised CRP, ESR, etc.

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100
Q

Causes of acute pancreatitis: (10)

A

I GET SMASHED
Idiopathic
Gallstones
Ethanol
Trauma
Steroid use
Mumps
Autoimmune
Scorpion sting
Hypercalcaemia & hypertriglycerideamia
ERCP
Drugs/medications e.g. sitagliptin, sodium valproate

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101
Q

What are the dvla rules about driving if you have diabetes?

A

If you have more than one severe hypoglycaemic episode in the previous 12 months you must surrender your licence while the DVLA review the situation. You can re-apply in 3 months.

Severe = symptomatic hypoglycaemic episode requiring help.

If you are a group 2 driver (HGV/lorry) you must notify the dval after only one severe episode.

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102
Q

What happens to urine osmolality after water deprivation and after synthetic ADH in cranial DI, nephrogenic DI and primary polydipsia?

A

Cranial:
- Low after deprivation
- High after ADH
(because the kidneys can respond to the ADH)
Nephrogenic:
- Low after deprivation
- Still low after ADH
(kidneys can’t respond to ADH)
Primary polydipsia:
- High after deprivation
- High after ADH

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103
Q

What is primary polydipsia?

A

Patient drinking excessive quantities of water. Their ADH is functionally normally.

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104
Q

Vitamin C deficiency:

A

Loose teeth
Poor wound healing
Bleeding gums, epistaxis, haematuria
Malaise

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105
Q

Tx of an acute migraine

A

900 mg dispersable aspirin
Triptan (injection>nasal spray>tablet)

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106
Q

How long do migraines usually last?

A

4 to 72 hours

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107
Q

1st and 2nd line prophylactic tx of migraines:

A

1st line: propranolol 80-160 mg daily + avoid triggers

2nd line: topiramate

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108
Q

How does a cluster headache present? (3)

A
  1. Severe unilateral pain behind the eye
  2. Duration 15 mins - 3 hours
  3. Sudden ‘clockwork’ onset
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109
Q

Acute & prophylactic tx of cluster headaches:

A

Acute: oxygen & triptan
Prophylactic: verapamil

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110
Q

Trigeminal neuralgia presentation:

A

~2 seconds of stabbing pain unilaterally in trigeminal nerve distribution, face screws up with pain

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111
Q

Tx of trigeminal neuralgia:

A

Carbamazepine, ?surgical decompression of nerve

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112
Q

Presentation of GCA/Temporal arteritis: (8)

A
  1. Age >50
  2. New headache
  3. Tender scalp
  4. Tender temporal artery
  5. Jaw claudication
  6. Amaurosis fugax
  7. Raised ESR
  8. Often associated with polymyalgia rheumatica
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113
Q

Tx of GCA/temporal arteritis:

A

Prednisolone immediately PO or IV methylprednisolone if visual loss present

Urgent biopsy within two weeks

Continue steroids for 2 years

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114
Q

Two risk factors for a subdural haemorrhage:

A
  1. Elderly
  2. Alcoholics

Trauma shears bridging veins which are more stretched and vulnerable in an atrophied brain (due to age or chronic alcohol use)

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115
Q

How does a subdural haemorrhage affect consciousness levels?

A

Fluctuating consciousness levels.
Symptoms of headache and drowsiness can be present for weeks as ICP increases slowly.
NB: crescent shape on CT head

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116
Q

How does an extradural haemorrhage present?

A

Deteriorating consciousness level, sometimes with a lucid interval then another sudden deterioration.
Associated with focal neurological signs
Lemon shape on CT head

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117
Q

Common pathophysiology of an extradural haematoma:

A

Trauma to the temporal bone damages the middle meningeal artery or vein

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118
Q

Rheumatoid arthritis:
1. Symmetrical or asymmetrical arthritis?
2. Worse or better with activity?
3. Morning stiffness?
4. Other associated symptoms (5):

A
  1. Symmetrical distal polyarthritis
  2. Better with activity, worse with rest
  3. Morning stiffness often present
  4. Flu-like illness, muscle aches, weight loss, weakness, fatigue
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119
Q

What is the pathophysiology of rheumatoid arthritis?
How would you explain this to a patient?

A

Autoimmune condition where chronic inflammation of the synovial lining of joints, tendon sheaths and bursa causes pain, swelling and deformity.

“The body’s immune system normally protects you by fighting infection and other illness. RA is an autoimmune condition, where the immune system gets confused and starts attacking your own healthy joints. This causes persistent inflammation of the lining of joints and tendons, which results in pain and swelling. It normally affects small joints in your hands and feet. RA can also cause flu-like symptoms of fatigue, weight loss and muscle aches”

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120
Q

Rheumatoid arthritis:
1st, 2nd and 3rd line maintenance treatment:
Tx for a flare:

A

Maintenance:
First line = monotherapy with methotrexate, leflunomide or sulfasalzine
Second line = combine any 2 of the above drugs
Third line = add a biologic (e.g. TNF-inhibitor)

Flare:
Short-term glucocorticoid e.g. IM methylprednisolone and short term NSAIDs e.g. ibuprofen (plus PPI cover)

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121
Q

Give 6 risk factors for osteoarthritis:

A

Obesity
Increasing age
Occupation
Trauma
Female sex
Family history

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122
Q

XR changes from osteoarthritis:

A

Loss of joint space
Osteophytes
Subarticular sclerosis (increased density of bone along the joint line)
Subchondral cysts

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123
Q

What is ankylosing spondylitis?

A

A seronegative spondyloarthritis (and therefore associated with the HLA-B27 gene) that causes inflammation vertebral column and sacroiliac joints, leading to progressive fusion of the spine (“bamboo spine”).

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124
Q

How does ankylosing spondylitis typically present?

A

Commonly affects young men (late teens/early 20s)
Gradual onset over >3 months
Low back pain
Sacroiliac/buttock pain
Pain worse at rest, improves with movement
Morning stiffness lasts >30 mins

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125
Q

Name three seronegative spondyloarthritis conditions:
What gene are these related to?

A

Psoriatic arthritis
Reactive arthritis
Ankylosing spondylitis

HLA-B27

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126
Q

Which STI most commonly causes septic arthritis?

A

Gonorrhoea

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127
Q

Name two conditions that are associated with the HLA-DR4 gene:

A

Type 1 diabetes
Rheumatoid arthritis

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128
Q

Give an important possible side effect of TNF-alpha inhibitors:

A

reactivation of TB - get a chest XR before starting!

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129
Q

What would the aspirate fluid show in gout?

A

No bacterial growth
Needle shaped monosodium urate crystals
Negatively bifringent of polarised light

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130
Q

What would the aspirate fluid show in pseudogout?

A

No bacterial growth
Rhomboid shaped calcium pyrophosphate crystals
Positively bifringent of polarised light

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131
Q

1st, 2nd and 3rd line acute tx of gout:

A
  1. NSAIDs
  2. Colchicine (NB: diarrhoea is a common SE)
  3. Steroids
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132
Q

What T score from a DEXA scan qualifies as osteopenia and osteoporosis?

A

osteopenia = -1 to -2.5
osteoporosis = less than -2.5

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133
Q

What is FRAX?

A

A tool to predict the risk of a fragility fracture over the next 10 years

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134
Q

What is polymyalgia rheumatica?

A

Inflammatory condition causing pain and stiffness in the shoulders, pelvic girdle and neck. Strongly associated with GCA/temporal arteritis.

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135
Q

Presentation of polymyaglia rheumatica:

A

Typically affects white women aged >50, symptoms should be persistent for at least 2 weeks:
1. Bilateral shoulder pain (may radiate to elbows)
2. Bilateral pelvic girdle pain
3. Pain is worse with movement
4. Pain interferes with sleep
5. Morning stiffness lasting at least 45 minutes

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136
Q

How do you treat polymyalgia rheumatica?

A

Start with prednisolone 15 mg OD, if no response after 1 week consider an alternative diagnosis.

Should see a 70% improvement in symptoms after 3-4 weeks, then can start a reducing regimen.

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137
Q

What is myasthenia gravis?

A

Autoimmune destruction/damage of nicotinic ACh receptors on the post-synaptic side of neuromuscular junctions - involves both T and B cells

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138
Q

Presentation of myasthenia gravis: (5)

A
  1. Increasing and relapsing muscle fatigue
  2. Ptosis (often bilateral)
  3. Myasthenic snarl (can be elicited by asking patient to count up to 50 then smile)
  4. Diplopia
  5. Normal tendon reflexes
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139
Q

Tx of myasthenia gravis: (4)

A
  1. Reversible ACh inhibitors e.g. pyridostigmine
  2. Immunosuppression with prednisolone
  3. Thymectomy
  4. +/- monoclonal antibodies e.g. rituximab
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140
Q

How does idiopathic pulmonary fibrosis affect FEV1, FVC, and FEV1/FVC? Is this a restrictive or obstructive pattern?

A

FEV1 - variable
FVC - decreased
FEV1/FVC - increased
= restrictive

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141
Q

5 symptoms/signs of idiopathic pulmonary fibrosis:

A
  1. > 50 years old
  2. Insidious onset of SOB
  3. Dry cough
  4. Bibasal fine end-inspiratory crackles
  5. Finger clubbing
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142
Q

CXR findings for idiopathic pulmonary fibrosis:

A

Bilateral interstitial shadowing = typically small, irregular, peripheral opacities that initially have a ground glass appearance and will progress to a honeycomb appearance

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143
Q

Two medications that slow the progression of idiopathic pulmonary fibrosis:

A
  1. Pirfenidone
  2. Nintendabin
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144
Q

Summarise the lower limb dermatomes:

A

Anterior:
Outer thigh = L2
Inner thigh = L3
Inner calf = L4
Outer calf & foot = L5

Posterior:
Bum = S5, S4, S3
Hamstrings to mid calf = S2
Lower calf, ankle, sole of foot & pinky toe = S1

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145
Q

Which patients should have a target INR of 3.5?

A

Those with recurrent DVT or PE currently receiving anticoagulation

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146
Q

What is the target INR for most conditions?

A

2.5

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147
Q

If a patient on warfarin is NOT bleeding, and has an INR of 5.0-8.0, what should you do?

A

Withold 1 or 2 doses of warfarin
Reduce subsequent maintenance dose

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148
Q

If a patient on warfarin has MINOR bleeding and has an INR of 5-8, what should you do?

A

Stop warfarin
Give IV vitK
Restart when INR <5

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149
Q

If a patient on warfarin has an INR of >8, what should you do?

A

Stop warfarin
Give vit K (IV if bleeding, oral if not)
Restart when INR <5

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150
Q

If a patient on warfarin has major bleeding - what should you do?

A

Stop warfarin
Give IV vit K
Give dried prothrombin complex
(or FFP if unavailable)

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151
Q

How is acute pancreatitis diagnosed?

A

Primarily clinical diagnosis without imaging. Useful supporting blood tests include: ↑amylase, ↑lipase, ↑WCC, ↑LDH

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152
Q

What blood tests can help establish the severity of acute pancreatitis? (3)

A

↑WCC > 16 = severe disease
↑LDH >350 = severe disease
Low calcium = severe disease

Amylase does NOT correlate with severity of disease

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153
Q

Features of rhabdomyolysis:

A

AKI with disproportionately raised creatinine
Raised creatinine kinase - at least 5 times the upper limit of normal (>10,000)
Myoglobinuria
Hypocalcaemia
raised phosphate

Typically following a prolonged epileptic seizure or a fall with a long lie

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154
Q

3 important steps in managing HIV, other than antiretroviral therapy:

A
  1. close monitoring of CVS risk factors
  2. annual cervical smear (increased risk of HPV and cervical cancer)
  3. Up to date vaccinations (avoid live vaccines)
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155
Q

Give 5 neurological complications that can arise in HIV/AIDS:

A
  1. Toxoplasmosis infection → mutliple lesions on head CT, with ring/nodular enhancement, Thalium SPECT negative
  2. Primary CNS lymphoma → single lesion, solid/homongenous enhancement, Thalium SPECT positive, associated with EBV
  3. Progressive mutlifocal leukoencephalopathy (PML) → widespread demylination due to infection of oligodendrocytes by JC virus
  4. Encephalitis → due to CMV or HIV itself, oedematous brain on CT
  5. Cryptococcus → fungal infection stains with india ink, CT shows meningeal enhancement and cerebral oedema
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156
Q

HIV diarrhoea - name two causative organisms:

A
  1. cryptosporidium - an intracellular protozoa, most common
  2. mycobacterium avium intracellulare - atypical, only in individuals with CD4 <50
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157
Q

What CD4 count constitutes AIDS?

A

CD4 <200 cells/mm³

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158
Q

What viral load constitutes undectable HIV?

A

50-100 copies/ml

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159
Q

How does HIV present?

A

Initial seroconversion flu-like illness in the first few weeks of infection
Asymptomatic period
Progression to immunodeficiency presenting with opportunistic infections and AIDS defining illnesses

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160
Q

Give 6 AIDS defining illnesses:

A
  1. Kaposi’s sarcoma - tumours appear as purple patches/nodules on the skin, associated with human herpes virus 8
  2. Pneumocystis jirovecii pneumonia - stains with silver
  3. Cytomegalovirus infecition
  4. Candidiasis
  5. Lymphomas
  6. TB
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161
Q

Draw a diagram to show the extra-ocular muscles, the movements they make and their innervation:

A
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162
Q

A CN III palsy will have what affect on the eyes?

A

Ptosis, down and out gaze, fixed dilated pupil

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163
Q

A CN IV palsy will have what affect on the eyes?

A

Impaired downwards gaze, vertical diplopia

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164
Q

A CN VI palsy will have what affect on the eyes?

A

Impaired abduction, horizotal diplopia

165
Q

If there is a lesion affecting the hypoglossal nerve, which direction will the tongue deviate?

A

Towards the lesion

166
Q

What is acute angle closure glaucoma?

A

When the iris bulges forwards, sealing off the trabecular meshwork from the anterior chamber and preventing the drainage of aqueous humour. Leads to increasing intra-ocular pressure, particularly in the posterior chamber. Will cause optic nerve damage and permanent vision loss if not urgently treated.

167
Q

How does acute angle closure glaucoma present? (5)

A
  1. Severely painful and red eye
  2. Blurred vision
  3. Halos around light
  4. Headache
  5. N&V
168
Q

What would you find when examining an eye with acute angle closure glaucoma? (5)

A

Red eye
Hazy cornea
Fixed and dilated pupil
Firm eyeball on palpation
Decreased acuity

169
Q

Name 4 drugs that can be used to help treat acute angle closure glaucoma:

A

Pilocarpine
Acetazolamide
Glycerol/mannitol
Timolol
Dorzolamide
Brimonidine

170
Q

How is open angle glaucoma different to angle-closure glaucoma?

A

In open angle glaucoma resistance in the trabecular meshwork increases slowly, slowly making it more difficult for aqueous humour to leave the eye and increasing intraocular pressure.

171
Q

How does open angle glaucoma present?

A

Gradual closing in of peripheral vision leading to tunnel vision.
Gradual onset of fluctuating pain, headaches, blurred vision and halos appearing around lights (particularly at night time).

172
Q

Diagnosis of open angle glaucoma: (3)

A
  1. goldmann applanation tonometry to check intraocular pressure
  2. fundoscopy to check for optic disc cupping and optic nerve health
  3. visual field assessment to check for peripheral vision loss
173
Q

1st line treatment of open angle glaucoma

A

Prostaglandin analogue eye drops e.g. latanoprost

SE: eyelash growth, eyelid pigmentation, iris browning

174
Q

What is optic disc cupping?

A

A normal optic disc has a small indent in the center, usually less than half the size of the disc.

Optic cupping occurs when increased pressure (e.g. in glaucoma) in the eye causes this indent to become wider and deeper. An optic cup >0.5 times the size of the disc is abnormal.

175
Q

How do you treat a relapse/flare in multiple sclerosis?

A

IV or PO methylprednisolone 500 mg/day over 4 hours
PPI cover

176
Q

What is multiple sclerosis?

A

Autoimmune mediated inflammation of the nervous tissue of the brain and spinal cord, causing loss of the myelin sheath

177
Q

Signs/symptoms of multiple sclerosis:

A
  1. Optic neuritis
  2. Internuclear ophthalmoplegia (lesion in the medial longitudinal fasciculus causing impaired adduction in one eye, and horizontal nystagmus in the other)
  3. Lhermitte’s sign (electric shock)
  4. Uhthoff’s sign (symptoms worsen with rise in body temp)
  5. Sensory or cerebellar ataxia (positive Rhomberg’s test)
  6. Numbness and paraesthesia
  7. Trigeminal neuralgia
  8. Incontinence
  9. Limb paralysis, foot drop
  10. Bell’s palsy (drooping of one side of the face)
  11. Horner’s syndrome (ptosis, miosis, anhidrosis)
178
Q

Name a non-drowsy antihisatmine

A

Loratadine

179
Q

What is optic neuritis and how does it present?

A

Inflammation of the optic nerve leading to subacute vision loss occuring over hours to days, mainly affects younger people (<30), usually unilateral and often recurrent.

180
Q

Signs and symptoms of optic neuritis: (4)

A
  1. Decreased visual acuity and colour vision (unilateral)
  2. Pain on eye movement (→ retrobulbar optic neuritis)
  3. RAPD
  4. Optic disc may look normal (→retrobulbar optic neuritis), or swollen
181
Q

6 signs of hypertensive retinopathy:

A
  1. Silver wiring/copper wiring (thickened walls of arterioles)
  2. Arteriovenous nipping (thickened arterioles compress veins where they cross)
  3. Cotton wool spots (ischeamia and infarction damages nerve fibres)
  4. Hard exudates (damaged vessels leak lipids)
  5. Retinal haemorrhages
  6. Papilloedema
182
Q

A positive scarf test indicates what pathology?

A

Acromioclavicular joint arthritis

183
Q

A positive empty can test indicates what pathology?

A

Supraspinatus tendinopathy

184
Q

3 differentials for shoulder pain following a trauma:

A

Rotator cuff tear
Fracture
Shoulder dislocation

185
Q

Rotator cuff muscles and their movements:

A

Supraspinatus - arm abduction
Infraspinatus - arm external rotation
Teres minor - arm external rotation
Subscapularis - arm internal rotation

186
Q

3 differentials for shoulder pain with no history of trauma:

A

Supraspinatus tendinopathy
Glenohumeral arthritis
Acromioclavicular arthritis

187
Q

What is frozen shoulder?

A

Adhesive capsulitis: inflammation and fibrosis of the shoulder joint capsule leading to adhesions that limit the ROM

Can be primary (spontaneous) or secondary (following trauma, surgery or immobilisation)

Has three phases: painful (worse at night), stiff, thaw - can last up to 3 years

188
Q

How do you differentiate between an arterial and a venous leg ulcer?

A

Arterial:
- Deep
- Smaller
- Less likely to bleed
- More painful
- Painful on raising, less painful on lowering
Venous:
- More superficial
- Larger with sloping/irregular borders
- More likely to bleed
- Less painful
- Painful on lowering, less painful on raising

189
Q

How do you treat a venous ulcer?

A

Refer to tissue viability and pain specialists
Tx can involve debridement, compression, dressing, abx if indicated, analgesia
Pentoxifylline can aide healing

190
Q

What is Bowen’s disease?

A

A squamous cell carcinoma in situ, arising from the outer layers of the epidermis and has a low risk of progressing to an invasive SCC

Commonly presents in older women with a fixed, well-defined, non-itchy patch

191
Q

What is the second most common type of skin tumour? Give 3 risk factors

A

Squamous cell carcinoma
RF: sun exposure, immunosuppression, chronic inflammation (leg ulcers)

192
Q

What is the most common type of skin tumour in fair skin?

A

Basal cell carcinoma

193
Q

What does a basal cell carcinoma look like? (4)

A

Shiny, pearly nodule with rolled edge
Telangiectasia (irregular blood vessels across surface)
Transluscent (minimal keratin)
Slow growing

194
Q

Name 4 types of malignant melanoma:
Which is the most common? Which is the rarest?

A
  1. Superficial spreading - most common, 70% of cases
  2. Nodular - second most common
  3. Lentigo maligna - less common
  4. Acral lentiginous - rarest
195
Q

Which type of malignant melanoma commonly affects the following groups:
- Younger people
- Middle aged people
- Older people
- People with darker skin pigmentation

A
  1. Superficial spreading - affects the arms, legs, back and chest of younger people
  2. Nodular - middle aged people, affects sun exposred areas
  3. Lentigo maligna - older people with chronic sun exposure
  4. Acral lentiginous - nails, palms or soles of feet in people with darker skin pigmentation
196
Q

Give 3 major diagnostic criteria for malignant melanoma and 4 secondary/minor features:

A

Major
1. Change in size
2. Change in shape
3. Change in colour
Minor
1. Diameter ≥ 7mm
2. Inflammation
3. Oozing or bleeding
4. Altered sensation

197
Q

How do you calculate serum osmolality?

A

2 x serum sodium + serum glucose + serum urea

(all in mmol/L)

198
Q

Which antibiotics is MRSA resistant to?

A

Meticillin resistance = resistance to beta-lactam antibiotics which includes penecillins, cephalosporins and carbapenems

199
Q

What type of antibiotic is vancomycin?

A

A glycopeptide antibiotic - works by inhibiting cell wall synthesis

200
Q

How should a GTN spray be used in angina?

A

Stop and rest
Use spray as prescribed, wait 5 mins
Still in pain? Readminister, wait 5 mins
Still in pain? Readminister, wait 5 mins
Still in pain? Call an abulance (don’t wait more than 15 mins to call)

201
Q

What is acute coronary sydrome?

A

A thrombus from an atherosclerotic plaque blocks a coronary artery resulting in: unstable angina, a STEMI or an NSTEMI

202
Q

After an acute coronary syndrome, what secondary prevention is given? (6)

A

Aspirin 75 mg
Another antiplatelet e.g. clopidogrel for up to 12 months
ACEi
Atenolol or another beta-blocker
Atorvastatin (or another statin)
(Aldosterone antagonist for those which clinical HF, initiated within 3-4 days of MI, preferable after ACEi is started)

203
Q

What investigations are needed in unstable angina?

A

Trop (normal)
ECG (no pathological changes)
Further investigations such as echo, cxr, CT coronary angiogram

204
Q

How do you treat a STEMI?

A

ABC
High flow O2 if hypoxic and not CI
Morphine 5-10mg IV and cyclizine 50mg IV
GTN spray/tablet
Aspirin 300 mg
Ticargrelor
PCI if available within 2 hours of presentation, thrombolysis if not
Transfer to CCU

205
Q

Where on an ECG would you see an anterior STEMI? Which artery is involved?

A

Primarily in the anterior leads: V3 and V4
Can also affect septal leads (V1, V2) and lateral leads (V5, V6, I, aVL), making it an extensive anterior STEMI

May also be seen with classic tombstone shape formed by elevated J point and T wave with significant ST elevation

= Left anterior descending artery

206
Q

What is the GRACE score?

A

Used to assess for the need for PCI in an NSTEMI

Gives a 6 month risk of death or repeat MI after an NSTEMI

5-10% → consider PCI within 4 days of admission

207
Q

Tx of an NSTEMI: (6)

A

Beta blocker
Aspirin
Ticagrelor 180 mg stat (or clopidogrel 300mg)
Morphine and cyclizine
Anticoagulant - LMWH or fonaparinux
Nitrates

O2 if hypoxic
Prepare to transfer to CCU

208
Q

What is Dressler’s syndrome?

A

A localised immune response 2-3 weeks after an MI, causing pericarditis

209
Q

Px of dressler’s syndrome: (3)

A

Pleuritic chest pain
Low grade fever
Pericardial rub on auscultation

210
Q

Complications of Dressler’s syndrome:

A

Pericardial effusion
Pleural effusions - transudative (watery)
Cardiac tamponade

211
Q

Ix and Tx of dressler’s syndrome:

A

Ix: ECG (global ST elevation, T wave inversion), echo (pericardial effusion), raised inflammatory markers

Tx: NSAIDs, steroids, pericardiocentesis

212
Q

Sx of right sided heart failure: (3)

A

Raised JVP
Ankle oedema
Hepatomegaly (smooth, tender, firm, pulsatile liver edge)

213
Q

What blood marker can be used to determine the severity of heart failure?

A

NT-pro-BNP
>2000 = urgent referral to be seen within 2 weeks
400-2000 = referral to be seen within 6 weeks

214
Q

Mx of HF with reduced EF (≤40%):
Which of these drugs reduces mortality?

A

ACEi - improves ventricular function, reduces mortality (switch to ARB if not tolerated)
BB - decreases HR, myocardial oxygen demand and RAAS activation

Add a loop diuretic if fluid overloaded
Add of low dose aldosterone antagonist if sx are continuing despire ACEi, BB and diuretic

Still sx? get specialist advice

215
Q

Explain your system for interpreting x-rays:

A
  1. Details - age, name, DOB
  2. RIPE:
    - Rotation
    - Inspiration = 5-6 anterior ribs, 8-10 posterior ribs
    - Projection = AP or PA?
    - Exposure = left hemidiaphragm visible, vertebrae visible behind heart
  3. Airway: trachea (central, deviated?), carina, right and left main bronchi, hilum
  4. Breathing: lung markings, pleura
  5. Cardiac: heart size, major vessels (aortic knob)
  6. Diaphragm: right side higher than left, costophrenic angles
  7. Extras: NG, PICC, ECG electrodes, chest drain, sternotomy clips
216
Q

What is the most common bacterial cause of an infective COPD exacerbation?

A

H.influenzae

217
Q

What are ‘cannonball’ metastases?

A

Large round well-circumscribed masses seen on chest xray, indicative of metastases from renal cell carcinoma (and choriocarcinoma or endometrial cancer)

218
Q

Which are the lateral leads of an ECG? Which arteries supply the lateral aspect of the heart?

A

Leads I, aVL, V5, V6

Circumflex artery and left coronary artery (i.e. the left atrium and the posterior aspect of the left ventricle)

219
Q

Which leads are the anterior leads of ECG?
Which arteries supply the anterior aspect of the heart?

A

V3 and V4

Left anterior descending and left coronary artery (i.e. the anterior aspect of the left ventricle and septum)

220
Q

Which are the inferior leads of an ECG? Which arteries supply the inferior aspect of the heart?

A

I, III, aVF
Right coronary artery (supplies the right atrium and right ventricle)

221
Q

How do you calculate rate on an ECG?

A

300 / n of large squares in an r-r interval

222
Q

What does 1 large and 1 small sq represent on an ECG?

A

1 small square = 0.04 seconds
1 large square = 0.2 seconds

223
Q

Normal values for:
PR interval
QRS complex
QT interval

A

PR = 3-5 small squares
QRS < 3 small squares
QT ~0.42 seconds

224
Q

2 conditions that cause a prolonged PR interval:

A

Rheumatic fever heart disease
Digoxin toxicity

225
Q

What criteria are used to diagnose PCOS?

A

Rotterdam criteria
2 out of 3 of:
1) Polycystic ovaries (12 or more peripheral follicles or increased ovarian volume >10cm3
2) Oligo-ovulation or anovulation
3) Clinical/biochemical signs of hyperandrogenism

226
Q

PCOS increases your risk of….(4)

A
  1. Endometrial cancer
  2. Diabetes
  3. Stroke/TIA
  4. Obstructive sleep apnoea
227
Q

What is primary dysmenorrhoea?

A

Painful peroids with no underlying pelvic pathology

228
Q

Pelvic inflammatory disease: give 6 symptoms and 4 findings on examination

A

Symptoms:
1. Pelvic or low abdo pain
2. Abnormal vaginal discharge
3. Abnormal bleeding (intermenstrual, post-coital)
4. Pain during sex (dyspareunia)
5. Fever
6. Dysuria
Examination:
1. Pelvic tenderness
2. Cervical motion tenderness (cervical excitation)
3. Inflamed cervix (cervicitis)
4. Purulent discharge

229
Q

What is the most common cause of PID? Which causative organism causes more severe cases of PID?

A

Most common: chlamydia
Most severe: gonorrhoea

230
Q

Tx of PID:

A

IM ceftriaxone 1g STAT and doxycycline 100mg PO for 14 days and metronidazole 400 mg BD PO for 14 days

231
Q

Management of ovarian cysts:

A

Small cyst = should resolve in three cycles
50-70 mm = require yearly monitoring
50-100 mm and persistent or haemorrhagic = require surgical removal

232
Q

What is a corpus luteal cyst? Give one factor that increases the risk of this type of cyst forming

A

Ordinarily the corpus luteum should breakdown when pregnancy doesn’t occur, however it can fill with fluid/blood forming a cyst

Clomifene use

233
Q

What is endometriosis?

A

Ectopic endometrial tissue outside the uterus, possibly caused by retrograde menstruation

A lump of endometrial tissue = endometrioma
Endometrioma in the ovaries = chocolate cyst
Adenomyosis = endometrial tissue within the myometrium (muscular layer of the uterus) (NB: causes a raised CA125)

234
Q

Presentation of endometriosis: (5)

A

Dyspareunia
Dysmenorrhoea
Cyclical pelvic pain (or continuous for >6 months)
Subfertility
Cyclical associated symptoms e.g. urinary and bowel symptoms

235
Q

What are fibroids?

A

Benign tumours of the smooth muscle of the uterus, sensitive to oestrogen

236
Q

Presentation of fibroids:

A
  1. Heavy/prolonged menstruation
  2. Pain (worse during menstruation)
  3. Bloating
  4. Urinary/bowel symptoms
  5. Deep dyspareunia
  6. Reduced fertility
  7. +/- palaable pelvic mass on bimanual examination
237
Q

7 complications of fibroids:

A
  1. Heavy menstrual bleeding → IDA
  2. Red degeneration → ischaemia, infarction and necrosis of the fibroid causing severe abdo pain, low-grade fever, tachycardia and vomiting (occurs most frequently with larger fibroids during the second or thrid trimester of pregnancy)
  3. Torsion of the fibroid → usually affects pedunculated fibroids
  4. Malignant change → leiomyosarcoma (very rare <1%)
  5. Urinary outflow obstruction and UTIs
  6. Pregnancy complications e.g. miscarrigae, premature labour, obstructive delivery
  7. Reduced fertility
238
Q

Define: menopause, premature menopause and early menopause

A

Menopause: amenorrhea for >1 year, occurs on average at 51 years old

Premature menopause = <40 years (results from premature ovarian insufficiency)

Early menopause = <45 years

239
Q

HRT increases your risk of…(4)

A
  1. VTE (particularly with oral HRT) (2-3xs increased risk)
  2. Ischaemic stroke and coronary artery disease (with long term use in older women)
  3. Breast cancer (combined HRT)
  4. Endometrial cancer (risk reduced by adding progesterone)
240
Q

Benefits of HRT: (3)

A
  1. Reduced vasomotor symptoms (hot flushes, night sweats)
  2. Improved symptoms such as: low mood, decreased libido, poor sleep
  3. Decreased risk of osteoporosis
241
Q

When do you use cyclical vs continuous HRT?

A

Cyclical: early or pre-menopause/still having periods
Continuous: menopause (>12 months without periods)

242
Q

When is oestrogen only HRT used?

A

ONLY if a patient has had a hysterectomy (with uterus removal!)

243
Q

Types of hysterectomy:

A

Total: womb and cervix removed
Subtotal: cervix left in place
Total with bilateral salpino-oopherectomy: womb, cervic, fallopian tubes and ovaria removed
Radical: womb and surrounding tissues are all removed including fallopian tubes, part of the vagina, ovaria, lymph glands and fatty tissue

THINK: subtotal hysterectomy = must carry on having cervical smears

244
Q

Explain the physiology of menopause:

A
  1. The development of follicle declines
  2. Oestrogen production decreases, progesterone levels are low
  3. LH and FSH increase
  4. Ovulation doesn’t occur
  5. Endometrium doesn’t develop
  6. Menstruation stops
245
Q

Perimenopausal symptoms:

A

Hot flushes
Emotional lability
Vaginal dryness and atrophy
Reduced libido
Irregular periods
Premenstrual syndrome
Joint pains

246
Q

What advice should you give about contraception to people going through menopause?

A

You need effective contraception for:
- 2 years after the last menstrual period if <50 years olds
- 1 year after the last menstrual period if >50

247
Q

When should you investigate for primary amenorrhea?

A

If >13 years old with no features of secondary sexual development OR some features but no progression for over 2 years

248
Q

What is secondary amenorrhea?

A

No menstruation for more than 3 months after previous regular menstruation OR previous infrequent/irregular periods and no periods for 6-12 months

249
Q

What investigations are needed to diagnose premature ovarian insufficiency?

A

Raised FSH (>40), two samples taken >4 weeks apart
Low oestradiol

250
Q

What is premenstrual syndrome? How is it investigated?

A

Symptoms during the luteal phase, should resolve once menstruation begins.

Ask them to keep a symptom diary. Give a GnRH analogue to halt the cycle and see if symptoms resolve.

251
Q

What is Meig’s triad?

A
  1. Ovarian fibroma (benign ovarian tumour)
  2. Pleural effusion
  3. Ascites
    Typically occurs in older women, requires surgical removal of the fibroma
252
Q

4 contraindications for HRT:

A

Current or previous breast cancer
Any oestrogen-sensitive cancer
Undiagnosed vaginal bleeding
Untreated endometrial hyperplasia

253
Q

What is hypogonadotropic hypogonadism?

A

Deficiency of LH and FSH leading to a deficiency of testosterone and oestrogen

254
Q

What is hypergonadotropic hypogonadism?

A

Gonads fail to respond to stimulation from gonadotrophins (LH and FSH) leading to a deficiency of testosterone and oestrogen.
The lack of negative feedback causes the anterior pituitary to produce increasing amounts of LH and FSH

255
Q

Causes of hypogonadotropic hypogonadism: (5)

A

Abnormal functioning of the hypothalamus or pituitary, this could be caused by:
- Previous damage/surgery
- Growth hormone insufficiency
- Hypothyroidism
- Kallman syndrome
- Excessive dieting or exercise

256
Q

2 week wait criteria for suspected endometrial cancer:

A

post-menopausal bleeding OR >55 with unexplained discharge or visible haematuria and raised platelets, anaemia or raised glucose levels

257
Q

What USS finding would increase your suspicision of endometrial cancer?

A

endometrial thickness >4mm in a post-menopausal woman

258
Q

Key risk factors for endometrial cancer:

A

Anything that increases exposure to unopposed oestrogen:
- obesity (adipose tissue releases oestrogen)
- PCOS (anovulation)
- Tamoxifen
- No or fewer pregnancies
- Earlier onset of menstruation

259
Q

Why does PCOS increase your risk of endometrial cancer? How is this risk reduced?

A

Normally, when ovulation occurs, a corpus luteum is formed in the ovaries from the ruputred follicle that released the egg.
It is the corpus luteum that produces progesterone, providing endometrial protection during the luteal phase of the cycle.
PCOS can cause anovulation and therefore the corpus luteum doesn’t develop, and progesterone isn’t produced → exposure to unopposed oestrogen
To reduce this risk people with PCOS should be given the COCP or the mirena coil or cyclical progestogens.

260
Q

2 risk factors for endomentrial cancer that are NOT related to unopposed oestrogen:

A
  1. DM2
  2. hereditary nonpolyposis colorectal cancer or Lynch syndrome
261
Q

What is a pipelle biopsy? Give an alternative/similar investigation:

A

A biopsy done as outpatient using a speculum and a thin tube (pipelle). It is highly sensitive for endometrial cancer.

Other investigations for endometrial cancer:
TVUSS for endometrial thickness (>4mm post-menopause is abnormal)
Hysteroscopy with endometrial biopsy

262
Q

5 risk factors for ovarian cancer:

A
  1. BRCA1, BRCA2
  2. obesity
  3. recurrent clomifene
  4. smoking
  5. increased number of ovulations: early menarche, late menopause, no pregnancies (∴ anything that reduces lifetime number of ovulations reduces risk e.g. COCP, breastfeeding, pregnancy)
    Peak incidence is as 60 years old
263
Q

What is the risk of malignancy index? Which gynae cancer is it used for?

A

Used to estimate risk of an ovarian mass being malignant, includes:
- Menopausal status
- USS findings
- CA125 level

264
Q

What are ovarian teratomas? What investigations can help diagnose these?

A

Benign ovarian tumours arising from the germ cells.
Contain various tissue types: skin, teeth, hair, bone.
Particularly associated with ovarian torsion.
Ix:
- Raised alpha-fetoprotein
- Raised hCG

265
Q

What would you see on histology when looking at a Krukenberg tumour?

A

Signet ring cells
(Krukenberg = ovarian tumour metstasied to somewhere else)

266
Q

How does ovarian cancer present?

A

Very non-specific ∴ often found very late, more than 70% have spread beyond the pelvis at diagnosis.
- Abdo bloating
- Early satiety
- Pelvic pain
- Urinary symptoms (freq, urge)
- Weight loss
- Abdo/pelvic mass
- Ascites

267
Q

2 week wait criteria for suspected ovarian cancer:

A

Immediate 2ww if you find any one of:
- Ascites
- Pelvic mass (unless clearly fibroids)
- Abdominal mass
Get a CA125 first then 2ww if >50 and presenting with:
- New change in bowel habit/IBS
- Abdominal bloating
- Weight loss
- Early satiety
- Pelvic pain
- Urinary freq or urgency

268
Q

What cancer is CA125 a marker for? What else can cause a raised CA125?

A

Epithelial cell ovarian cancer

Endometriosis
Fibroids
Adenomyosis
Pelvic infection
Liver disease
Pregnancy

269
Q

What is the most common type of cervical cancer?

A

Squamous cell carcinoma

270
Q

Cervical smears: at what age and how frequently?

A

Every 3 years for 25-49 year olds
Every 5 years for 50-64 year olds

271
Q

Which strains of HPV cause warts? Which cause cervical cancer?

A

HPV 6 and 11 = warts
HPV 16 and 18 = cancer (cervical and 80% of anal cancer)

272
Q

RF for cervical cancer: (6)

A

Anything that increases your risk of catching HPV:
- Early sexual activity
- Increased n of sexual partners
- Sexual partners who have had more partners
- Not using condoms
Non-engagement with cervical screening
HIV (need yearly smears)
COCP use for >5 years
Family hx
Smoking

273
Q

How does cervical cancer present?

A

usually asymptomatic, may have non-specific symptoms e.g. post-coital bleeding, red-brown discharge, purulent discharge

274
Q

What might you see on a speculum examination that would cause you to suspect cervical cancer? What would you do next?

A

Cervical ulceration, inflammation, bleeding or a visible tumour.
Urgent cancer referral for colposcopy.

275
Q

What is cervical intraepithelial neoplasia (CIN)?

A

The grading system for the level of dysplasia (pre-malignant change) in the cells of the cervix. Diagnosed on colposcopy:
CIN I = mild
CIN II = moderate, likely to progress if untreated
CIN III = severe, very likely to progress if untreated

276
Q

What results can you get from a cervical smear? What do you do next?

A

Smear results = cytology & HPV status:
- Inadequate sample → repeat in 3 months
- HPV neg. → continue normal screening
- HPV pos. with normal cytology → repeat HPV test in 12 months
- HPV pos. with abnormal cytology (dyskaryosis) → refer for colposcopy

277
Q

What type of vulval cancer is most common?

A

squamous cell carcinoma

278
Q

4 risk factors for vulval cancer

A

> 75 years old
Immunosuppression
HPV infection
Lichen sclerosis

279
Q

Px of vulval cancer: (4)

A

Irregular mass
Fungating lesion
Ulceration
Bleeding

280
Q

Can you have a cerivcal smear if pregnant?

A

No, you must be at least 12 weeks post-partum

281
Q

What is the most common identifiable cause of post-coital bleeding?

A

Cervical ectropion

282
Q

What is the most common cause of post-menopausal bleeding?

A

Vaginal atrophy

283
Q

Described the menstrual cycle:

A

Follicular phase: days 1 to 14
- LH and FSH stimulate follicles to develop
- Follicles produce oestrogen
- Oestrogen causes a drop in LH and FSH
- Drop in LH and FSH causes follicles to die, except for one dominant follicle
- Dominant follicle secretes lots of oestrogen
- High oestrogen causes a surge of LH and FSH
- Surge of LH and FSH causes follicle to rupture and release the oocyte
= OVULATION

Luteal phase: days 14 to 28
- Remainder of the empty dominant follicle forms the corpus luteum
- Corpus luteum produces lots of progesterone (and some inhibin)
- Progesterone and inhibin suppress LH and FSH release, oestrogen continues to fall

Meanwhile…days 0 to 5 in the cervix, the old endometrium is shed = menses
Days 5 onwards = proliferation of the endometrium, growth of spiral arteries, consistency of the cervical mucus changes

284
Q

What is androgen insensitivity syndrome?

A

An X-linked recessive condition where a genetically male child (46XY) has end-organ resistance to testosterone causing them to have a female phenotype.

Features:
- Primary amenohorrea
- Undescended testes causing groin swellings

285
Q

6 causes of primary amenorrhoea:

A
  1. Gonadal dysgenesis (e.g. Turner’s syndrome) = most common
  2. Testicular feminisation
  3. Congenital malformation of the genital tract
  4. Functional hypothalamic amenorrhoea e.g. secondary to anorexia
  5. Congenital adrenal hyperplasia
  6. Imperforate hymen
286
Q

7 causes of secondary amenorrhea:

A
  1. Hypothalamic amenorrhea (secondary to stress, excessive exercise)
  2. PCOS
  3. Hyperprolactinaemia
  4. Premature ovarian failure
  5. thyrotoxicosis* (*hypothyroidism can also cause amenorrhea)
  6. Sheehan’s syndrome
  7. Asherman’s syndrome
287
Q

What sign would you see on USS that indicates PCOS?

A

TVUSS shows ‘string of pearl’ appearance

288
Q

PCOS blood results:

A

High testosterone
High LH
Normal FSH
Low progesterone
Low SHBG (sex hormone binding globulin)

289
Q

What is Fitz-Hugh-Curtis Syndrome?

A

A complication of PID; inflammation of the liver capsule leads to adhesions between the liver and peritoneum.

Px: Right upper quadrant pain, shoulder tip pain.

290
Q

What is a leiomyoma?

A

Ovarian fibroid

291
Q

Which class of antibiotics are safe to use at any stage during pregnancy?

A

cephalosporins

292
Q

How can tetracyclines affect pregnancy?

A

Can stain the baby’s teeth and cause skeletal developement problems

293
Q

Treatment of urge incontinence: (4)

A

Start with least invasive and work up:
- Bladder training
- Anticholinergic = oxybutinin
- Mirabegron
- botox injection

294
Q

What can cause urinary overflow incontinence in women?

A

Chronic urinary retention due to obstruction, results in incontinence without the urge to pass urine.

Causes include: fibroids, pelvic tumours, anticholinergics, neuro conditions (MS)

295
Q

How does a retrocele present?

A

Constipation, urinary retention, palpable lumb in the vagina

296
Q

Who qualifies for fertility investigations in primary care?

A

Anyone who has been trying to conceive for 1 year with frequent UPSI (every 2-3 days)

Anyone who has been trying to conceive for 6 months with frequent UPSI, if: the woman is ≥36 or there is a known cause of infertility or there is a hx of predisposing factors

297
Q

What infertility investigations are available in primary care?

A

Male:
- Semen analysi (sperm count, motility, morphology, vitality, concentration, volume)
- Chlamydia screening
Female:
- Mid-luteal progesterone (~day 21) to assess if ovulation is occuring
- FSH and LH levels to assess ovarian function (poor ovarian function → high FSH and LH)
- Chlamydia screening

298
Q

Risk factors for ectopic pregnancy: (9)

A

Anything that slows the passage of the ovum!
1. Smoking
2. PID
3. Prior fallopian tube surgery
4. IVF
5. Early first sexual intercourse (<18)
6. Age >35 at presentation
7. Black ethnicity
8. Endometriosis
9. Progesterone-only pill

299
Q

How do you investigate for an ectopic pregnancy? What will results show?

A

TVUSS: blob/bagel/tubal ring sign i.e. a mass in the fallopian tube containing an empty gestational sac

300
Q

What is an ectopic pregnancy?

A

A pregnancy implanted outside the uterus, most commonly in the fallopian tube

301
Q

Mx of an ectopic pregnancy:

A

Offer surgical tx if: in significant pain, adenxal mass>35mm, fetal heartbeat present, hCG>1500

Medical tx: single dose methotrexate

Make sure to advise avoiding getting pregnant for the next 3 months! And that there may be no bleeding as the tissue can be resorbed by the body

Surgical tx is laparoscopic salpingectomy, unless there is high risl of infertility in which case you can consider laproscopic salpingotomy

302
Q

In pregnancy of unknown location bHCG is used to determine if there is an intrauterine pregnancy, ectopic pregnancy or miscarriage - how?

A

Measure bHCG at baseline
Repeat after 48 hour
Doubly = intrauterine
Rising but not doubling = ectopic
Falling by half or more = miscarriage

303
Q

How do you carry out an abortion?

A

Medical abortion: mifepristone, then misoprostol 1-2 days later

Surgical up to 14 weeks: mifepristone, misoprostol, osmotic dilatations and suction

Surgical at 14-21 weeks: cervical dilation and evacuation with forceps

Don’t forget to give anti-D if rhesus neg and over 10 weeks

304
Q

Criteria of viable pregnancy: (2)

A

Fetal pole present when gestation sac reaches 25mm
Fetal heartbeat present what CR length reaches 7mm

305
Q

How do you manage a miscarriage? (conservative, medical, surgical)

A

<6 weeks = expectant management, await miscarriage (as long as there is no pain, RF or Cx) and repeat pregnancy test in 7-10 days

Medical: vaginal or oral misoprostol
Surgical: misoprostol and vacuum aspiration

306
Q

What classifies recurrent miscarriages?

A

3+ consecutive miscarriages

307
Q

What is an incomplete and complete molar pregnancy?

A

Complete: empty oocyte lacking maternal genes is fertilised (karyotype 46) - requires surgical evacuation

Incomplete: oocyte is fertilised by two sperm, three sets of chromosomes (karyotype 69) - requires medical termination

308
Q

Presentaiton of a molar pregnancy: (6)

A
  1. Passing grape liek vesicles
  2. Hyperemesis gravidarum
  3. Hyperthyroidism
  4. Vaginal bleeding
  5. Large for gestation uterus
  6. VERY high bHCG
309
Q

USS finding for a molar pregnancy:

A

snow storm appearance

310
Q

3 risk factors for molar pregnancy:

A
  1. Asian ethnicity
  2. Blood group A
  3. Low protein, low carotene, low folic acid diet
  4. Prev molar pregnancy
  5. Extreme maternal age
311
Q

When is the combined test done?

A

11 to 14 weeks

312
Q

What is the combined test? What does it look for?

A

First line and most accurate screening test, involves USS and bloods.

Looks for high risk of Down’s, Edward’s, or Patau’s.

High risk is shown by: nuchal translucency >6mm, high beta-hcg, low PAPPA (pregnancy associated plasma protein)

If risk if >1 in 150, offer further testing (CVS or amniocentesis).

313
Q

What is the triple test? When is it done?

A

Maternal blood test performed between 14 and 20 weeks.
Includes bHCG, AFP and serum oestriol.
High risk of Down’s = high beta-HCG, low AFP, low oestriol

314
Q

What is chorionic villus sampling? Who is offered it?

A

Any pregnancy with a risk of Down’s >1 in 150.
USS guided biopsy of placental tissue for karyotyping, must be done before 15 weeks.
Risk of miscarriage is thought to be ~1 in 200.

315
Q

What is amniocentesis?

A

Aspiration of amniotic fluid to sample fetal cells for karyotypic. Done at 15-20 weeks. 1 in 100 miscarry.

316
Q

What is non-invasive prenatal testing?

A

Fetal DNA fragments are checked from a maternal blood test. Not a definitive test but does give a good indication of whether a fetus is affected by Down’s .

317
Q

How long after a termination might a pregnacy test still be positive?

A

Up to 4 weeks

318
Q

4 causes of an antepartum haemorrhage:

A
  1. Placental abruption
  2. Placenta praevia
  3. Vasa praevia
  4. Local anteparum haemorrhagee.g. varicose veins, vaginal lacerations, cervical ectropian
319
Q

Categorise a minor, major and massive antepartum haemorrhage:

A

Minor = <500ml
Major = 500-1000ml
Massive = >1000ml or signs of shock

320
Q

Mx of an antepartum haemorrhage: (6)

A
  1. 2 large grey cannulas
  2. Cross match 4 units of blood
  3. Blood tests - FBC, U&E, coag screen, LFTs
  4. CTG monitoring
  5. Fluids
  6. Escalate quickly!
321
Q

How does placental abruption present? (5)

A
  1. Woody abdomen
  2. Sudden onset severe continuous abdo pain
  3. Dark vaginal bleeding
  4. Shock (inconsistent with external loss)
  5. CTG abnormalities
322
Q

5 risk factors for placental abruption

A
  1. Pre-eclampsia
  2. Multiple pregnancy
  3. Fetal growth restriction
  4. Mutligravida
  5. Trauma
  6. Increased maternal age
  7. Smoking
  8. Cocaine or amphetamine use
  9. Bleeding early in pregnancy
  10. Previous placental abruption
323
Q

How do you manage placental abruption?

A

ANY sign of fetal distress → CAT1 c-section
>36 weeks → deliver baby ASAP
<36 weeks → monitor, give corticosteroids, plan delivery

AND address blood loss, do they need fluids/resus etc.

324
Q

What are normal hb values during pregnancy?

A

Booking clinic: Hb >110
28 weeks: Hb >105
Post partum: Hb>100

325
Q

Anaemia during pregnancy:
- Low MCV →?
- High MCV→?
- Normal MCV→?

A

Low MCV = IDA
High = B12 or folate deficiency
Normal = physiological anaemia due to increased plasma volume in pregnancy

326
Q

What is placenta accreta? When is it found/diagnosed?

A

When the placenta implants deeper, through/past the endometrium, making it difficult to separate and deliver in the third stage of labour.

Found antenatally on USS or during a PPH

327
Q

RF for placenta accreta: (4)

A
  1. prev c-section
  2. prev uterine surgery
  3. increased maternal age
  4. IVF
328
Q

Mx of placenta accreta:

A

Hysterectomy, uterus preserving surgery or expectant management (leave to resorb - very risky)

329
Q

What is vasa praevia?

A

Fetal vessels are exposed, outside the protection of the umbilical cord or placental. Instead they travel through the chorioamniotic membranes and across the internal cervical os.

330
Q

Mx. ofvasa praevia:

A

plan for c-section at 34-36 weeks, give corticosteroids. at32+ weeks

remember digital vaginal exam is CI!

331
Q

What is placenta praevia? How is it diagnosed?

A

Placenta lying wholly or partially in the lower uterine segment.
Seen on routine USS in week 20, confirmed with TVUSS

332
Q

How might placenta praevia present?

A

No pain
Abnormal lie/high head
Profuse red bleeding

333
Q

Mx of placenta praevia:

A

TVUSS at 32 and 36 weeks
Corticosteroidsat 34-35+6 weeks
Planned c-section at 36-37 weeks

334
Q

When is the booking scan?

What is checked at this point? (6)

A

8-12 weeks

Hep B
Syphillis
Chlamydia
BP
BMI
Urine dip (asymptomatic bacteuria? culture, confirm sensitivities, give abx)

335
Q

When is the dating scan? What is checked. at this point?

A

10-14 weeks
Accurate gestational age is calculated from the crown rump length
Multiple pregnancies are identified

336
Q

When is the anomaly scan?

A

18 to 20 weeks
USS identifies any anomalies such as heart conditions

337
Q

Diagnostic criteria for gestational diabetes:

A

OGTT done at booking clinic for women with previous gestational diabetes, done at 24-28 weeks for those with risk factors or suggestive features (e.g. large for dates, polyhydramnios, glucosuria):

Fasting glucose >5.6,
Then asked to drink a 75g glucose drink,
2 hour glucose >7.8

338
Q

Mx of gestational diabetes:

A

Education on monitoring blood sugars (four times a day).

Serial growth scans every 4 weeks from week 28 to 36

Fasting glucose less than 7: start with 2 weeks of exercise/lifestyle changes

Fasting glucose more than 7: start insulin +/- metformin

339
Q

Gestational diabetes, sugar targets:

A

Fasting: 5.3
1 hour post-meal: 7.8
2 hours post meal: 6.4

340
Q

Risk factors for gestational diabetes: (4)

A
  1. BMI > 30
  2. Prev macrosomic baby weighing 4.5kg or more
  3. Prev gestational diabetes
  4. Family origin with high prevalance of diabetes (south Asian, black Caribbean, Middle Eastern)
341
Q

Which diabetic medications can be continues during pregnancy?

A

Metformin can be continued.
Oral hypoglycaemics must be stopped e.g. glicazide
Glibenclamdide (sulfonylurea) can be continued.

342
Q

Diagnostic criteria for pre-eclampsia:

A

Hypertension and one of:
- Proteinuria (P:C>30, A:C>8)
-Placental dysfunction
- End organ dysfunction

343
Q

Definition of pre-eclampsia:

Px of pre-eclampsia: (8)

A

Pre-eclampsia is defined by systolic BP >140 mm Hg or diastolic BP >90 mm Hg in the second half of pregnancy, with ≥1+ proteinuria on reagent stick testing.

  1. Headache
  2. Visual disturbance
  3. N&V
  4. Abdo pain
  5. Oedema
  6. Reduced urine output
  7. Brisk reflexes
  8. Raised AST and ALT
  9. HELLP syndrome
344
Q

Complications of pre-eclampsia: (6)

A
  1. Intrauterine growth restriction
  2. placental abruption
  3. Pre-term labour
  4. Seizures
  5. HELLP (haemolysis, elevated liver enzymes, low platelets)
  6. Renal failure
345
Q

Target BP for pre-eclampsia:

A

135/85

346
Q

Mx of pre-eclampsia:

A
  1. High risk women given 75mg OD aspirin from 12 weeks
  2. Antihypertensive medication:
    1st line = labetalol
    2nd line = nifedipine
    3rd line = methyldopa
  3. IV magnesium sulphate during labour and for 24 hours after to prevent seizures
  4. Deliver by 37 weeks, stay for observation after birth in case of seizures
347
Q

What is HELLP syndrome?

A

Haemolysis, Elevated Liver enzymes, Low Platelets - a combination of features that occurs as a complication from pre-eclampsia

348
Q

How. doyou manage eclamspia?

A

first line = IV magnesium sulphate
2nd line = diazepam

349
Q

What is obstetric cholestasis? Why does it happen?

A

Reduced outflow of bile acids from the liver.
Caused by increased oestrogen and progesterone in later pregnancy (28 weeks+)

350
Q

What will investigations show in obstetric cholestasis? What is the treatment?

A

Raised ALT, AST, GGT and bile acids
Ursodeoxycholic acid

351
Q

Diagnostic criteria for hyperemesis gravidarum:

A
  1. > 5% weight loss
  2. Dehydration
  3. Electrolyte imbalance
352
Q

What scoring system is used to monitor vomiting during pregnancy?

A

PUQE score: <7 mild, 7-12 moderate, >12 severe
(pregnancy unique quantification of emesis)

353
Q

Give 4 anti-emetics used in pregnancy in order of preference/safety:

A
  1. Prochlorperazine
  2. Cyclizine
  3. Ondansetron
  4. Metoclopramide
354
Q

Mx of hyperemesis gravidarum

A

Panbrinex (vit c and b)
fluid resus
anti-emetic
don’t forget to r/o other causes of vomiting e.g. gastritis, apendicitis

355
Q

How do you treat group B strep?

A

IV benzylpenicillin before labour

356
Q

Who should be treated for group B strep?

A

Pregnant women with GBS on vaginal swab or bacteruria AND anyone who previously had a baby with GBS

357
Q

How should twins. bedelivered?

A

Monoamniotic: elective c-section at 32-33+6 weeks
Diamniotic: first baby might be able to deliver vaginally, second needs c-section

358
Q

What is twin-twin syndrome?

Characteristics of both twins (3 each)

A

Twins sharing a placenta, recipient twin receives. the majority of the blood supply whilst donor twin is starved.

Donor: anaemia, oligohydramnios, growth restriction
Recipient: fluid overload, heart failure, polyhydramnios

359
Q

Why do you test pregnant women’s urine at every appointment?

A

Because a UTI increases the risk of pre-term delivery

360
Q

How do you treat a UTI in pregnancy?

A

7 days of antibiotics:
- Nitrofurantoin (not in the third trimester though!)
- Amoxicillin (if sensitivites are known)
- Cefalexin (safe in all stages of pregnancy)

361
Q

Define ‘small for dates/gestational age’:

A

Fetus below the 10th centile for their gestational age, USS is used to measure estimated fetal weight (EFW) and fetal abdominal circumference.

362
Q

Define large for dates/gestational age’:

A

Estimated fetal weight > 90th centile

363
Q

How much does a macrosomic baby weight at birth?

A

> 4.5kg

364
Q

Large for dates babies have increased risks of: (5)

A
  1. Birth injury
  2. Neonatal hypoglycaemia
  3. Obesity
  4. DM2
  5. Shoulder dystocia at birth
365
Q

Large for dates pregnancies pose what risks to the mother? (3)

A
  1. PPH
  2. Perineal tear
  3. Instrumental or c-section delivery
366
Q

5 signs of intrauterine growth restriction:

A
  1. small for gestational age
  2. oligohydramnios
  3. abnormal doppler
  4. reduced fetal movement
  5. abnormal CTG
367
Q

What score is used to predict whether to induce labour?

A

Bishop score
> 8 predicts successful induction

368
Q

4 ways of inducing labour:

A
  1. Membrane sweep - used from 40 weeks
  2. Vaginal prostaglandin E2 - done in hospital
  3. Cervical ripening balloon - used when prostaglandins are not preferred e.g. in a woman with a previous c-section or multiparous
  4. Artificial rupture of membranes with IV oxytocin - used if prostaglandins haven’t worked or are CI
369
Q

What is Prolonged Rupture of Membranes? (PROM)

A

When the amniotic sac ruptures more than 18 hours before delivery

370
Q

What is Preterm Prelabour Rupture of Membranes? (PPROM)

A

When the amniotic sac ruptures before the onset of labour and before 37 weeks gestation

371
Q

What can you measure to check if a pregnant woman’s water has broken?

A

Check vaginal fluid*, high IGFB-1 and high PAMG-1 indicate waters have broken

*pooling of amniotic fluid in the posterior vaginal vault indicates rupture of membranes

372
Q

How do you manage PPROM?

A

Erythromycin 250mg QDS for 10 days/until delivery, induction from 34 weeks

373
Q

What is the biggest risk factor for a prolapsed cord?

A

Abnormal lie after 37 weeks

374
Q

Factors that reduce the risk of a prolapsed cord: (3)

A

Nulliparity
Prolonged pregnancy
Cephalic position

375
Q

Management of a prolapsed cord:

A

Definitive treatment is an emergency c-section!
In the interim you can:
- Position Mum in on all fours (draws the baby away from the cord)
- Physically push the baby off the cord
- Give a tocolytic to minimise contractions

376
Q

4 risk factors for breech delivery:

A

Premature labour
Multiple pregnancy
Placenta praevia
Pelvic deformities

377
Q

Mx of a breech baby before labour:

A

Offer ECV at 36 weeks (27 weeks if multiparous)
ECV:
- Give tocolytic
- Do ECV under doppler USS
- Check CTG
- Give anti-D if rhesus negative

378
Q

What defines a pre-term baby?

A

Baby born before 37 weeks

379
Q

What can you measure to check if a woman is in pre-term labour with intact membranes?

A

<30 weeks = clinical assessment
>30 weeks = check TVUSS to assess cervical length, if <15 mm treat as preterm labour

380
Q

What is fetal fibronectin?

A

The “glue” between the chorion and uterus, found in the vagina during labour.

Can be checked to establish if patient is in preterm labour. FF < 50 ng/ml = preterm labour is unlikely

381
Q

How can you prevent preterm labour? Who should have this prevention?

A

Vaginal progesterone via gel or pessary.
Offered to women with a cervical length less than 25 mm on TVUSS between 16 and 24 weeks.

Cervical cerclage: a stitch in the cervix to support and keep it closed. Offered to women with a cervical length less than 25 mm on TVUSS between 16 and 24 weeks AND who have had a previous premature birth or cervical trauma (colposcopy or cone biopsy)

382
Q

When and why is magnesium sulphate given during pregnancy?

A

Given IV to the mother to protect the baby’s brain during premature delivery.
Given within 24 hours of delivery in preterm babies of less than 34 weeks gestation.
Given IV to the mother to treat/prevent seizures in pre-eclampsia.

383
Q

What is shoulder dystocia?

A

When the baby’s anterior shoulder gets stuck behind the pubic symphysis during labour

384
Q

What is Erb’s palsy?

A

Damage to the brachial plexus resulting. in ‘waiter’s tip’ = adducted, internally rotate arm, pronated forearm

Complication of shoulder dystocia

385
Q

Different techniques to manage shoulder dystocia:

A

Episiotomy
McRoberts manoeuvre
Pressure to the anterior shoulder by pressing on the suprapubic region of the abdomen
Rubins manoeuvre
Wood’s screw manoeuvre
Zavanelli manoever

386
Q

Px of shoulder dystocia:

A

Difficulty delivering the face and head, unable to deliver the shoulders.
Failure of restitution: the head remains face down and doesn’t turn sideways as expected.
Turtle-neck sign - head delivers then retracts back in again.

387
Q

Define a 1st, 2nd, 3rd and 4th degree perineal tear:

A

1st: superficial injury
2nd: includes perineal muscles but does not affect anal sphincter
3rd:
- A = includes <50% of the external anal sphincer
- B = includes >50%
- C = includes both sphincters
4th: includes rectal mucosa & sphincters

388
Q

What degree of perineal tear warrants a c-section for future babies?

A

3rd or 4th

389
Q

4 causes of post partum haemorrhage

A
  1. Tone - uterine atony is the most common cause
  2. Tissue - retained placenta
  3. Trauma - e.g. perineal tear
  4. Thrombin - bleeding disorder
390
Q

Medical management of a PPH:

A

Oxytocin
Ergometrine
Carboprost IM (caution in asthmatics)
Misoprostol
Tranexamic acid

391
Q

Mechanical interventions for PPH:

A

Rub the uterus
Catheterise to empty the bladder

392
Q

Surgical interventions for PPH: (4)

A

Intrauterine balloon tamponade = first line for uterine atony
B lynch suture
Uterine artery ligation
Hysterectomy

393
Q

requirements for a instrumental delivery: (7)

A

FORCEPS:
Fully dialted
OA/OP
Ruptured membranes
Cephalic
Engaged
Pain relief given
Sphincter (bladder empty and catheteristed)

394
Q

6 risks to the baby in an instrumental delivery:

A

Cephalohematoma (ventouse)
Facial nerve palsy (forceps)
Subgaleal haemorrhage
Intracrainal haemorrhage
Skull fracture
Spinal cord injury

395
Q

What drug can you give to treat uterine hyperstimulation?

A

Terbutaline

396
Q

3 reasons for failure to progress in labour:

A

Power (strength of contractions)
Passenger (size, attitude, lie, presentation)
Passage

397
Q

Define first stage delay in labour:

A

less than 2cm dilation in 4 hours, or slowing of progress in a multiparous woman

398
Q

Define second stage delay in labour:

A

Active pushing lasting over 2 hours (nuliparous) or 1 hour (multiparous)

399
Q

Third stage delay in labour:

A

> 30 mins with active management, >60 mins with physiological management

400
Q

What are the 4 categories of c-section:

A

1: threat to life, deliver within 30 minutes
2: urgent, deliver within 75 minutes
3: required but stable
4: elective

401
Q

Anatomical layers resected during a c-section: (8)

A
  1. skin
  2. subcutaneous tissue
  3. rectus sheath
  4. rectus abdominismuscle (separated vertically along the linea alba)
  5. parietal peritoneum
  6. vesicouterine peritoneum
  7. uterus
  8. amniotic sac
402
Q

What is puerpal pyrexia? How do you treat it?

A

Temp >38 in the first 14 days post-partum, caused by endometriosis (most common), UTI, wound infection, mastitis or VTE.

If suspected, immediately refer to hospital for abx.

403
Q

what scoring system is used to screen for post nantal depression?

A

Edinburgh scale

404
Q

What antidepressants are used in breastfeeding women?

A

Sertraline or paroextine

405
Q

What is puerperal psychosis?

A

Post labour psychosis, develops within the first 2 weeks, affects 1 in 1000 deliveries

406
Q

What are the three phases of the first stage of labour?

A
  1. Latent phase: 0 to 3cm dilation, progressing 0.5cm/hour, irregular contractions
  2. Active phase: 4 to 7 cm dilation, progressing 1 cm/hr (0.5 if 1st baby), regular contractions
  3. Transition phase: dilation 7 to 10 cm, 1cm progress/hr, strong and regular contractions
407
Q

What happens in the second stage of labour?

A

1 hour of passive descent (don’t push, helps baby to settle further down)

Active pushing: 2 hours max if 1st labour, 1 hour max if 2nd+ labour

408
Q

What happens in the third stage of labour?

A

Delivery of the cord
Cord traction if delayed
Manual removal in theatre if traction doesn’t work

409
Q

What are Mcrobert’s, Rubin’s, Wood’s screw and Zanelli’s manoeuvre?

A

McRobert’s: pull knees into chest
Rubin’s: reach into vagina, press on anterior shoulder
Wood screw’s: reach introvagina, press on posterior shoulder
Zanelli: push head back in, do emergency c-section

410
Q

What do the following words mean?

  1. Lie
  2. Presentation
  3. Position
  4. Attitude
  5. Augmentation
A
  1. Direction of the baby: transverse, oblique, longitudinal
  2. Which part is closest to the pelvic inlet? e.g. cephalic, breech
  3. Orientation of the head, determined by the occiput, OA is ideal
  4. Degree of flexion of the head
411
Q

Explain the difference between primary, secondary and tertiary hyperparathyroidism:

A

Primary = High PTH, High Calcium
Caused by a parathyroid tumour. Excessive PTH secretion, excessive resorption from calcium from the bones, kidneys and gut.

Secondary = High PTH, Low/normal Calcium
Vitamin D deficiency or CKD means that the kidneys and gut cannot absorb enough calcium. Persistent low calcium detected by the parathyroid gland causes more and more PTH to be secreted. Eventually causes parathyroid gland hyperplasia.

Tertiary = High PTH, High Calcium
Once you fix the underlying cause of secondary hyperparathyroidism, the hyperplased glands continue to secrete too much PTH.

Finals/Misc. (8 decks)

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