What underlying aetiological factors have been associated with peptic ulcer disease?

Helicobacter pylori infection

Colonizes the entire gastric epithelium and causes increased gastric acid secretion by producing ammonia, which locally suppresses somatostatin inhibition of gastrin release by antral D cells. H. pylori also disrupts mucosal integrity by release of proteases and phospholipases.

Non-steroidal anti-inflammatory drugs (NSAIDs)

Inhibit cyclo-oxygenase and decrease prostoglandin production. Prostaglandins (E type) act to increase both mucosal blood flow and the production of mucus and bicarbonate, which form a protective layer and act as a buffer for gastric acid, respectively. There is a dose-dependent relationship. Selective Cox-2 inhibitors have been shown to lower the risk of gastric ulceration but do not eliminate this risk.

Gallstones

Briefly explain the processes involved in the formation and excretion of bilirubin

Bilirubin is produced in the spleen and reticuloendothelial system as the terminal product of haem catabolism. Unconjugated bilirubin is transported from the spleen in the blood bound to plasma albumin. In the liver, bilirubin is released from albumin and taken up by hepatocytes where conjugation (glucuronidation) occurs by the action of UDP glucuronyl transferase. Bilirubin is then released into the gut where deconjugation and conversion to urobilinogen occurs by the action of gut bacteria. Urobilinogen (water-soluble) is partially reabsorbed by the gut into the portal system (enterohepatic circulation), whilst the remainder is oxidized in the colon to produce stercobilinogen, the brown faecal pigment. Traces of urobilinogen reach the systemic circulation and are excreted in the urine.

List the commonest types of gallstones

Cholesterol stones (~80%) - These are often formed as large, solitary gallstones and are made up of cholesterol monohydrate crystals. These form when the cholesterol concentration of bile exceeds the ability of bile salts to dissolve cholesterol and lectin. This may occur either as a result of supersaturation of the bile with cholesterol or as a result of bile salt deficiency.

What is the commonest site of aneurysm formation?

Prior to the discovery of penicillin, the most common type of aortic aneurysm was of the aortic arch secondary to syphilis. However, in modern practice the infrarenal abdominal aorta (see Figure 10.1) is the most commonly affected. The most common peripheral aneurysmal artery is the popliteal artery.

How may aneurysmal dilatation of the aorta be classified?

By convention, aortic aneurysms are divided into:

1. Ascending and descending thoracic aortic aneurysms (TAA),

2. Thoraco-abdominal aortic aneurysms,

3. Suprarenal aortic aneurysms (involving the renal arteries, coeliac axis and the superior mesenteric artery – the visceral segment),

4. Juxtarenal aortic aneurysms (the aneurysm starts below the renal arteries, but necessitates clamping above them),

5. Infrarenal aortic aneurysms.

Radical mastectomy (Halsted procedure)

Now rarely performed, radical mastectomy entails removal of the whole breast, the pectoralis major and minor muscles and the entire axillary contents en bloc, including the apical (level III) axillary lymph nodes.

Modified radical mastectomy

This procedure is now also uncommon but may be indicated for some very large tumors with palpable axillary nodes or inflammatory breast cancers. The whole breast is removed together with the underlying pectoral fascia. This preserves pectoral muscles and some skin, but the NAC and surrounding skin is excised, together with lymph nodes at least from the lower axilla (level I and II nodes) in an en bloc dissection.

A number of useful statistics can be derived from a matrix table which shows the performance of a diagnostic test compared to a defined reference or “gold” standard.

1. Total subjects tested = TP + FN + FP + TN

2. Number of subjects with disease = TP + FN

3. Number of subjects without disease = TN + FP

4. Sensitivity = percentage correctly identified by the test = TP / (TP + FN)

5. Specificity = TN / (TN + FP)

6. PPV = TP / (TP + FP)

7. NPV = TN / (TN + FN)

8. Accuracy = percentage of correct results in all tests = (TP + TN) / TOTAL

Note that the prevalence of the target disease in the study population (or pre-test probability) has a significant effect on both PPV and NPV. For example, the PPV of an abnormal MRI finding is greater in a high-risk population than it is in the general population at average risk [5].

Chapter outline

• Historical background

• Implant types and terminology

• Fibrous capsule formation and contracture

• The evolution of silicone implants

• Normal MRI features of silicone implants

• MRI appearances of implant complications

• Cancer incidence and detection in women with implants

• Tissue breast reconstructive surgery

• Augmentation by direct injection procedures

Historical background

Over the last hundred or so years, attempts at breast augmentation have been documented using an astonishing variety of materials including ivory, glass beads, ground rubber, gutta percha and ox cartilage [1]. The range of injectable substances used includes paraffin oil, petroleum jelly, glazier’s putty, beeswax, shellac and epoxy resin [1]. Not surprisingly, complications were frequent, often relating to foreign body reactions with tissue necrosis, fistula formation and infection. With the advent of synthetic polymers, new concepts were trialled in the form of polythene chips, polythene tape or strips wound into a ball-shape, polymer sponges, Terylene wool, silastic rubber and polypropylene string, but none of these materials gave a particularly natural cosmetic effect.

Radiation therapy after breast conservation

Following breast-conserving surgery, whole breast irradiation aims to reduce the risk of local recurrence by dealing with any possible residual DCIS, and it may also deal effectively with additional small invasive foci. However, the use of RT is not considered to be any substitute for obtaining pathologically clear margins. Frequently a “boost” is given to the tumor bed during whole breast irradiation.

RT for invasive cancer after BCT

While surgery followed by RT is currently standard treatment for most cases of invasive cancer, RT may be omitted for some favorable lesions (small grade 1, ER-positive, node-negative tumors with complete excision) particularly when these arise in older women (age > 70 years). In such selected cases, the risk of recurrence is probably not more than ~5% at 10 years even without RT. Tamoxifen and/or an aromatase inhibitor are usually then employed.

Chapter outline

• Introduction

• The evolution of MRI-guided biopsy techniques

• Principles of MRI-guided interventions

• MRI-guided hookwire localization

• MRI-guided vacuum-assisted biopsy

• Choosing a vacuum-assisted biopsy system

• Radiologic–pathologic correlation

• Histopathologic lesions which mimic malignancy on MRI

Introduction

The sensitivity of MRI for invasive cancer and DCIS far exceeds that of XRM, and a substantial proportion of these malignant lesions either cannot be seen at all on TUS or cannot be identified with sufficient confidence to allow biopsy. Accordingly, a means of performing MRI-guided tissue sampling is an essential part of any breast MRI service. Frequently, MRI-only lesions (not seen on TUS or XRM) are foci (< 5 mm), small masses (< 10 mm) or focal areas of ductal non-mass enhancement, which can be challenging targets for the relatively small tissue volumes yielded by 14-gauge CNB. Accordingly, the more robust biopsy options of MRI-guided hookwire localization or VAB are preferred.