GP Flashcards

Question

How is anal cancer managed?

Answer 1

Chemo-radiotherapy for all except T1N0 – can use WLE Surgical management for advanced disease if chemoradiotherapy failed: Mostly abdominoperineal resection – left with colostomy

Answer 2

Caused by plugging of anal ducts which drain anal glands Organisms – E. coli, bacteroides, enterococcus Classified by position as – perianal, ischioanal, pelvirectal intersphincteric

Answer 3

Pain, worse on sitting Pus-like discharge from anus May be systemically unwell – fever On examination – erythematous, fluctuant tender perianal mass which may be discharging pus If deeper may have no external signs but severe tenderness on PR

Answer 4

Antibiotics, analgesia Examination under anaesthesia and incision and drainage – left to heal by secondary intention Intra-operative proctoscopy to check for fistula

Answer 5

Abnormal connection between anal canal and perianal skin Typically occurs as a consequence of perianal abscess Risk factors – IBD (Crohn’s), diabetes, trauma to anal region, previous radiotherapy

Answer 6

Recurrent perianal abscess Intermittent/continuous discharge – blood, mucus, faeces, pus Can see or feel tract on examination Investigation – MRI to visualise anatomy of tract

Answer 7

Fistulotomy (superficial) – laying open tract and allowing to heal by secondary intention Placement of a seton (high tract) – brings together and closes tract, allows for drainage to prevent infection

Answer 8

Can be used to predict trajectory of tract of perianal fistula Opening posterior to transverse anal line – tract will follow curved course to posterior midline Opening anterior to transverse anal line – tract will follow straight radial course to dentate line

Answer 9

Primary adrenal insufficiency – Addison’s disease, autoimmune Secondary adrenal insufficiency – lack of ACTH from pituitary, causes include pituitary tumour, infection, surgery, radiotherapy, Sheehan’s syndrome (blood loss during childbirth leads to pituitary necrosis) Tertiary adrenal insufficiency – lack of CRH from hypothalamus, usually due to withdrawal of long-term steroids

Answer 10

Lethargy, weakness, anorexia, nausea and vomiting, weight loss Bronze skin pigmentation (Addison’s) Hypotension – postural especially Investigation findings: Hyponatraemia Hyperkalaemia Hypoglycaemia Metabolic acidosis Primary – high ACTH Secondary – low ACTH Addison’s – adrenal autoantibodies (adrenal cortex antibodies, 21-hydroxylase antibodies) Short synacthen test Give synthetic ACTH Measure blood cortisol at baseline, after 30 minutes and after 60 minutes Failure of cortisol to rise (less than double baseline) indicates primary adrenal insufficiency

Answer 11

Replacement steroids – hydrocortisone (glucocorticoid replacement), fludrocortisone (mineralocorticoid replacement) Steroid card and emergency ID tag – can’t stop suddenly Hydrocortisone doses doubled during acute illness

Answer 12

Reduced consciousness Hypotension Hypoglycaemia, hyponatraemia, hyperkalaemia Very unwell! Management IV hydrocortisone – must replace first IV fluid resuscitation Correct hypoglycaemia Monitor and correct electrolytes

Answer 13

Sustained reduction in systolic of 20mmHg or more and/or diastolic of 10mmHg within 3 minutes of standing

Answer 14

Neurogenic – autonomic dysfunction e.g. T2DM, Parkinson’s, SCLC, amyloidosis Non-neurogenic – cardiac disease, dehydration/adrenal insufficiency, vasodilation (e.g. fevers), medications (diuretics, alpha-blockers for prostatic hypertrophy, anti-HTN, insulin, levodopa, tricyclics)

Answer 15

Non-pharmacological – avoid standing quickly, prolonged standing, hot environments, large meals, compression stockings, counter-manoeuvres Pharmacological Fludrocortisone – expands plasma volume, contraindicates in heart failure, ascites, CKD, can cause severe hypokalaemia Midodrine – short-acting vasopressor Pyridostigmine – acetylcholinesterase inhibitor, vasoconstrictive effect while standing

Answer 16

Viral – rotavirus, norovirus, adenovirus Bacterial – E. Coli (watch out for 0157, produces Shiga toxin which causes haemolytic uraemic syndrome, worse with Abx), campylobacter jejuni, Shigella, salmonella, bacillus cereus, staph aureus toxin

Answer 17

E. coli – faeces, salads, water Campylobacter – raw/uncooked poultry, untreated water, unpasteurised milk Shigella – drinking water, swimming pools, food Salmonella – raw eggs or poultry Bacillus cereus – food not immediately in fridge after cooking, typically rice left out at room temp

Answer 18

If mild and not systemically unwell – fluid intake, rehydration with oral rehydration salt solution, no antibiotics, advice for reducing transmission Avoid work/social settings for at least 48 hours after last episode of diarrhoea/vomiting Antidiarrhoeals e.g. loperamide not indicates Can take stool sample for microscopy, culture, and sensitivities In hospital: Dehydration – IV fluids Antibiotics for patients with risk of complications when causative organism and sensitivities established

Answer 19

Diverticulum – outpouching of bowel wall, herniation of colonic mucosa through muscular wall of colon, usually in sigmoid colon Usually occur with age, chronic constipation, NSAID use Diverticulosis – presence of diverticula Diverticular disease – symptoms due to diverticula Diverticulitis – acute inflammation of diverticula

Answer 20

Diverticular disease – intermittent lower abdominal pain, colicky, relieved by defection Altered bowel habit, flatulence, nausea Rectal bleeding Diverticulitis Acute pain, sharp, in LIF Localised tenderness Rectal bleeding Systemic upset – anorexia, fever Perforation – peritonism/peritonitis

Answer 21

Diverticulitis – CT abdomen/pelvis Signs – thickening of colonic wall, pericolic fat stranding, abscesses, localised air bubbles, free air (DO NOT PERFORM COLONOSCOPY IN SUSPECTED DIVERTICULITIS DUE TO RISK OF PERFORATION) Diverticular disease – flexible sigmoidoscopy

Answer 22

Simple analgesia Fluid/fibre intake Laxatives – bulk forming (ispagula husk), avoid stimulants Mild diverticulitis – oral antibiotics If recurrent acute diverticulitis may need resection

Answer 23

Uncomplicated – oral co-amoxiclav, analgesia, only take clear liquids for 2-3 days Complicated – NBM, IV antibiotics, analgesia, may require emergency surgery (Hartmann’s procedure – sigmoid colectomy with formation of end colostomy, anastomosis possible later)

Answer 24

Risk factors Age Genetics – hereditary non-polyposis colorectal carcinoma (Lynch syndrome), familial adenomatous polyposis Family history Low fibre diet Obesity Smoking Alcohol IBD Aetiology – mostly progression of normal mucosa to colonic adenoma (polyps) to invasive adenocarcinoma Adenomas can be present for 10 years or more before malignant transformation, occurs in 10%

Answer 25

HNPCC (Lynch syndrome) – autosomal dominant 90% develop cancers, usually of proximal colon, poorly differentiated and highly aggressive Most common gene mutations – MSH2 and MLH1 Risk of other cancers – endometrial cancer (2nd most common), ovary, stomach, small intestine etc. FAP – autosomal dominant Formation of hundreds of polyps by age 30-40, inevitably develop cancer Due to mutation in APC gene Prophylactic total colectomy with ileo-anal pouch in early 20s Also risk duodenal tumours Gardner’s syndrome – FAP + osteomas of skull and mandible, retinal pigmentation, thyroid carcinoma, epidermoid cysts

Answer 26

Red flags – 2ww referral: =>40 with unexplained weight loss and abdominal pain =>50 with unexplained rectal bleeding => 60 with IDA or change in bowel habit Positive occult blood screening test (qFIT) Right-sided – abdominal pain, IDA, palpable mass in RIF, present late Left-sided – rectal bleeding, change in bowel habit, tenesmus, palpable mass in LIF or PR

Answer 27

50-74 get qFIT test every 2 years – occult faecal blood test If positive get colonoscopy If negative no follow-up required Over 74 can request screening Also used in patients with symptoms which don’t meet 2ww criteria

Answer 28

FBC – microcytic anaemia CEA – tumour marker, not used for diagnosis but to monitor disease progression and screen for recurrence Gold-standard is colonoscopy with biopsy (if frail may use CT colongraphy) Staging investigations CT CAP MRI rectum – rectal cancers Endo-anal US for early rectal cancers

Answer 29

TNM mostly used now Also have Duke’s: A – confined to muscularis propria B – extension through muscularis C – involving regional lymph nodes D – distant mets

Answer 30

Surgery curative Radiotherapy and chemotherapy used as adjuvant/neoadjuvant or palliative treatments Surgery – usually regional colectomy with primary anastomosis or stoma formation Right hemicolectomy or extended right hemicolectomy Caecal or ascending colon tumours, extended for transverse Ileocolic, right colic and right branch of middle colic (branches of SMA/V) divided and removed with mesenteries Left hemicolectomy Descending colon tumours Left branch of middle colic (branches of SMA/V), inferior mesenteric vein and left colic vessels (branches of IMA/V) divided and removed with mesenteries Sigmoidcolectomy Sigmoid colon tumours IMA fully dissected out with tumour Anterior resection High rectal tumours, >5cm from anus Leaves rectal sphincter intact if anastomosis performed Often initially defunctioning loop ileostomy, reversed 4-6 months later Abdominoperineal resection Low rectal tumours, <5cm from anus Excision of distal colon, rectum, and anal sphincters, left with permanent colostomy Hartmann’s procedure Used in emergency bowel surgery, such as obstruction or perforation Complete resection of recto-sigmoid colon with formation of end colostomy and closure of rectal stump

Answer 31

Vomiting Epigastric pain Failure to pass NG tube

Answer 32

Most common: Small bowel – adhesions, hernia Large bowel – malignancy, diverticular disease, volvulus Others Strictures – secondary to Crohn’s Intussusception – paediatric Gallstone ileus Ingested foreign body Faecal impaction Meckel’s diverticulum – paediatric

Answer 33

Abdominal pain and distension – colicky, cramping pain due to peristalsis Vomiting – earlier in proximal, later in distal Absolute constipation – early in distal, later in proximal Dehydration – significant third spacing Focal tenderness Tinkling bowel sounds Tympanic to percussion

Answer 34

Bloods including G&S Monitor renal function and electrolytes – 3rd spacing VBG – metabolic derangement (dehydration, vomiting) CT scan with contrast – imaging of choice in suspected bowel obstruction AXR sometimes used first line – SBO – dilated bowel (>3cm), central abdominal, valvulae conniventes visible LBO – dilated bowel (>6cm or >9cm at caecum), peripheral, haustral lines visible

Answer 35

NBM NG tube Strict fluid balance and IV fluids for resuscitation Surgery – suspicion of intestinal ischaemia or closed loop obstruction, cause requiring surgical correction (strangulated hernia, obstructing tumour), failure to improve with conservative measures Generally laparotomy, may need resection of bowel with defunctioning stoma

Answer 36

Bowel ischaemia Bowel perforation – peritonitis – sepsis Hypovolaemic shock leading to AKI etc.

Answer 37

GI – diarrhoea, weight loss, bloating, abdominal pain, steatorrhoea, flatulence Extra-intestinal – anaemia, osteopaenia, secondary hyperparathyroidism, peripheral neuropathy, amenorrhoea, infertility, impotence, oedema/ascites (protein loss), faltering growth/delayed puberty in children Deficiencies – iron, B12, folic acid, vitamin D, calcium, vitamin K and other coagulation factors (bleeding)

Answer 38

Pancreatic dysfunction – chronic pancreatitis, cystic fibrosis, pancreatic cancer, Zollinger-Ellison syndrome Obstructive jaundice Coeliac disease, cow’s milk intolerance Crohn’s/ulcerative colitis Short bowel syndrome Hypo/hyperthyroidism Diabetes mellitus

Answer 39

Osmotic laxatives – increase amount of fluid in bowel to soften stool, e.g. lactulose, movicol Stimulant – stimulate bowel to contract expelling faeces e.g. senna, picosulphate Bulk forming laxatives – help stool to retain water therefore soften stool e.g. ispaghula husk Rectal medications – glycerin suppository (stimulant), phosphate enema (stimulant)

Answer 40

Direct inguinal – older men, raised intra-abdominal pressure Indirect inguinal – baby boys, congenital Femoral – older women, raised intra-abdominal pressure Umbilical – babies, associated with Afro-Caribbean ethnicity, Down’s syndrome, mucopolysaccharide storage disorders Epigastric – middle-aged men, chronic raised-intra-abdominal pressure Paraumbilical – chronic raised intra-abdominal pressure Obturator – elderly women

Answer 41

Hernia = protrusion of a viscus into an abnormal space Reducible – contents of hernia can be manipulated back into original position Incarcerated or irreducible – contents of hernia cannot be pushed back to their original position, usually painful Obstructed – contents of hernia are so compressed that bowel lumen is no longer patent, causing obstruction Strangulated – compression of hernia contents by fascial defect prevents blood flow leading to ischaemia, which can lead to infarction and necrosis, present with severe pain

Answer 42

Inguinal hernia = protrusion of abdominopelvic contents through superficial inguinal ring into groin Normal descent of testes in men or round ligament in women through inguinal canal (+ ilioinguinal nerve and genital branch of genitofemoral nerve), enter at deep inguinal ring and exit at superficial inguinal ring Deep ring is just above mid-point of inguinal ligament, superficial is just above and lateral to the pubic tubercle Direct – caused by defect in posterior wall of inguinal canal (in Hesselbach’s triangle) If reduce and put finger over deep inguinal ring, still protrudes (emerging through posterior defect still) Indirect – enters deep ring, passes through inguinal canal and exits superficial ring If reduce and put finger over deep inguinal ring, stays reduced (abdominal contents can’t enter canal)

Answer 43

Groin lump – superior and medial to pubic tubercle Usually disappears on pressure or when patient lies down Mainly asymptomatic, may have groin pain/discomfort with activity, rarely becomes strangulated

Answer 44

If symptomatic – surgical repair Options for surgical repair: Open repair – most commonly Lichtenstein technique, preferred for large hernias Laparoscopy repair – total extra-peritoneal or transabdominal pre-peritoneal, quicker recovery and less complications, better for recurrent or bilateral Risk of strangulation about 2% per year, if asymptomatic can discuss need for surgical intervention in future, risk of strangulation and symptoms to look out for

Answer 45

Incarceration Strangulation – bowel ischaemia and necrosis Obstruction

Answer 46

Abdominal viscera pass into femoral canal via the femoral ring Groin lump – inferior and lateral to pubic tubercle Usually quite small Typically non-reducible (small size of femoral ring)

Answer 47

All femoral hernias need surgical repair, ideally within 2 weeks, due to high risk of strangulation Two surgical approaches: Low approach – incision below inguinal ligament High approach – incision above inguinal ligament, preferred for emergency as can easily access compromised bowel

Answer 48

>90% present as emergency with obstruction/strangulation Deep position so often not a lump on examination Often have pain/paraesthesia in inner thigh due to compression of obturator nerve by hernia, worse with internal rotation of hip and better with hip flexion (Howship-Romberg sign) Management – usually emergency surgery to relieve obstruction and resect compromised bowel

Answer 49

Partial herniation of bowel involving only one edge – usually anti-mesenteric border Presents with pain from strangulation without features of obstruction, can then develop peritonitis with bowel perforation

Answer 50

Epigastric: AAA Gastric cancer Pancreatic pseudocyst or tumour Pyloric stenosis – babies Transverse colon cancer Left lobe of liver Right hypochondrium: Hepatomegaly Enlarged gallbladder – empyema, CBD obstruction Kidney mass Colon cancer Left hypochondrium: Splenomegaly Kidney mass Pancreatic cancer Colon cancer Right iliac fossa: Colon cancer Ovarian cyst/tumour Appendiceal abscess Psoas abscess Lymphadenopathy Crohn’s disease Ileocaecal TB Transplanted kidney Left iliac fossa: Colon cancer Faeces – loaded sigmoid, constipation Diverticular disease Ovarian tumour or cyst Psoas abscess Crohn’s Transplanted kidney Lymphadenopathy Suprapubic: Endometrial cancer Bladder cancer Enlarged bladder – retention Fibroids Pregnancy Ovarian mass e.g. cyst Inguinal: Herniae – inguinal, femoral Lymphadenopathy Vascular – saphena varix, aneurysm, pseudoaneurysm Psoas abscess Ectopic/undescended testes Hydrocoele of spermatic cord

Answer 51

Generalised: Peritonism – perforated peptic ulcer, bowel, AAA, ectopic pregnancy Early appendicitis Pancreatitis Ischaemic bowel Central/peri-umbilical: Small bowel ischaemia Acute appendicitis Small bowel obstruction Pancreatitis Testicular torsion Medical e.g. DKA Epigastric: Pancreatitis Gastritis Peptic ulcer Cancer – gastric, pancreatis Boerhaave syndrome IBS Pulmonary – pneumonia, pleurisy Cardiac – MI, pericarditis Left hypochondrium: Pancreatitis Ruptured spleen Acute pyelonephritis Right hypochondrium: Biliary colic Acute cholangitis Cholecystitis Hepatitis Hepatomegaly Fitz-Hugh-Curtis syndrome Perforated duodenal ulcer Acute pyelonephritis RIF: Appendicitis Crohn’s Meckel’s diverticulum Colon cancer IBS Ectopic pregnancy Acute ovarian event – torsion, rupture, haemorrhage PID Endometriosis Renal colic UTI Hip pathology LIF: Diverticulitis Colitis Colon cancer Constipation IBS Ectopic pregnancy Acute ovarian event PID Endometriosis Renal colic UTI Hip pathology Suprapubic: Urinary retention Cystitis Uterine – PID, fibroid, menstruation Groin: Renal calculi Scrotal – testicular torsion, Epididymo-orchitis Inguinal hernia Hip pathology

Answer 52

Fat – obesity Flatus – intestinal obstruction Fetus – pregnancy Fluid – ascites, distended bladder Faeces – constipation, faecal impaction Tumour Organomegaly

Answer 53

Benign, fluid-filled lumps Very common in women 30-50, especially perimenopausal Can cause pain, often cyclical related to menses On examination feel smooth, well-circumscribed, fluctuant, mobile lump Investigation – aspiration If blood-stained fluid or persistently refill should be excised, otherwise resolve with aspiration Small increased risk of breast cancer, especially in younger women

Answer 54

Most common in middle-aged menstruating women Fluctuating breast size and lumpiness, breast pain/tenderness, typically occur before menstruation and resolve when menstruation begins Improve or resolve after menopause Management: NSAIDs Avoid caffeine Apply heat Hormonal treatments e.g. tamoxifen under specialist guidance

Answer 55

Infection of the mammary ducts causes mastitis, which can lead to formation of breast abscess Often associated with lactation Most common organism is staph aureus Mastitis – purulent nipple discharge, localised pain, warmth, erythema, swelling Breast abscess: Present as painful, immobile, subcutaneous lumps, tethered to skin, with erythema and warmth of skin Tender on palpation May have fever, malaise, signs of sepsis Management: Lactational mastitis – conservative management, continue breastfeeding, breast massage, heat, simple analgesia Antibiotics (flucloxacillin or erythromycin/clarithromycin) if symptoms don’t improve Breast abscess – antibiotics, drainage (aspiration or incision and drainage), send fluid for C+S

Answer 56

Benign tumours of stromal/epithelial breast tissue More common in women 20-40, respond to oestrogen and progesterone so usually regress after menopause Presentation: Firm, smooth, mobile Painless Well-circumscribed Up to 3cm diameter

Answer 57

Generally – 1/3 regress, 1/3 enlarge, 1/3 stay same size If diagnostic uncertainty – US +/- FNA Management – observation and reassurance Can excise if large

Answer 58

Occurs after traumatic injury to breast tissue, leads to fibrosis and calcification Presents as immobile, firm lump at area of injury, may be bruising Diagnosis – triple assessment – US/mammogram, FNA Management – exclude breast cancer, treat conservatively or surgically excise if required

Answer 59

Cyclical – related to menstruation, typically during 2 weeks before menstruation with other premenstrual symptoms Breast cancer Infection – mastitis or breast abscess Pregnancy Trauma Extra-mammary causes – MSK conditions (e.g. costochondritis), soft tissue injury, rib fracture Referred pain from cardiac (IHD) or GI (reflux, peptic ulcer) conditions

Answer 60

Usually in perimenopausal women, smoking is major risk factor Terminal mammary ducts become dilated, shortened and inflamed Presentation – nipple discharge (creamy, green, brown, bloody), tenderness, nipple retraction/inversion, lump below/around areolar complex Can be confirmed with US Usually no treatment required, smoking cessation advice, can have surgical excision of the duct (microdochectomy) if older and problematic

Answer 61

Warty lesion, proliferation of epithelial cells in ducts Benign Mostly occur between 35-55 Presentation: Often asymptomatic, picked up incidentally Nipple discharge – clear or blood-stained Tenderness/pain Palpable lump Diagnosis – triple assessment, ductography (inject contrast into duct and perform mammogram) Management – complete surgical excision, histology examination after to check for abnormalities missed on biopsy

Answer 62

Hyperprolactinaemia: Idiopathic Prolactinomas – prolactin-secreting pituitary adenomas Endocrine disorders – hypothyroidism, PCOS Medications – dopamine antagonists Diagnosis: Pregnancy test for all women of childbearing age Serum prolactin TFTs MRI to diagnose pituitary tumours Management: Dependent on underlying cause Dopamine agonists e.g. bromocriptine or cabergoline Prolactinoma – trans-sphenoidal removal of tumour

Answer 63

Idiopathic Hyperprolactinaemia – prolactinoma, dopamine antagonists Physiological in adolescents High oestrogen – obesity, testicular cancer (Leydig cell tumour), liver cirrhosis/failure, hyperthyroidism, hCG secreting tumour (SCLC) Low testosterone – hypothalamus/pituitary conditions, Klinefelter’s, orchitis, testicular trauma/torsion Medications – anabolic steroids, dopamine antagonists, digoxin, spironolactone, GnRH agonists, opiates, alcohol

Answer 64

Invasive ductal carcinoma and ductal carcinoma in-situ: Most common Four subtypes of DCIS – papillary, cribiform, solid and comedo, mostly mixed Invasive lobular carcinoma and lobular carcinoma in-situ: LCIS predominantly in pre-menopausal women, most commonly bilateral compared to DCIS Invasive lobular more common in older women, more difficult to detect Others (rarer): Medullary breast cancer Mucinous (mucoid or colloid) breast cancer Metaplastic breast cancer Lymphoma of the breast Inflammatory breast cancer Phyllodes tumour 50% benign, 25% borderline, 25% malignant

Answer 65

Female sex Increasing age – risk doubles every 10 years until menopause Family history Genetic – 10%, BRCA1/2 Exposure to unopposed oestrogen – early menarche, late menopause, nulliparity, long-term use of HRT, OCP Previous benign breast disease, obesity, alcohol consumption, smoking Breastfeeding is protective

Answer 66

DCIS often detected during screening due to presence of microcalcifications, confirmed with biopsy LCIS does not have microcalcifications, difficult to detect on imaging, usually only picked up incidentally on biopsy Prognosis DCIS – 2x risk of invasive breast cancer LCIS – greater risk of malignant transformation (7-12x increased risk of invasive breast cancer) Any DCIS should be surgically excised – breast-conserving with WLE or mastectomy if widespread/multifocal LCIS management dependent on extent of disease – low-grade usually monitored, if have BRCA1/2 may need bilateral prophylactic mastectomy

Answer 67

Often asymptomatic, picked up on screening Breast or axillary lump – hard, irregular, ill-defined, tethered or fixed Asymmetry or swelling Abnormal nipple discharge – unilateral, bloody Nipple retraction Skin changes – dimpling, peau d’orange, Paget’s) Mastalgia (rarely) Late signs associated with metastases – weight loss, bone pain, fatigue

Answer 68

=>30 with unexplained breast lump with or without pain =>50 with unilateral nipple discharge, retraction Consider for skin changes suggestive of breast cancer or => with unexplained lump in axilla

Answer 69

Triple assessment – History and examination by breast surgeon Radiological imaging Core biopsy or FNA Imaging – US for younger women (<40), mammogram for older Biopsy – FNA for smaller cystic lumps, core biopsy better for diagnosis

Answer 70

Women 50-70 every 3 years, mammogram Increased risk – screening from younger age First degree female relative diagnosed with breast cancer <40 First degree male relative diagnosed with breast cancer at any age First degree relative with bilateral breast cancer, primary diagnosed <50 Two first degree relatives, or one first-degree and one second-degree diagnosed with breast cancer at any age One first-degree or one-second degree with breast cancer at any age AND one first-degree or second-degree diagnosed with ovarian cancer at any age Three first-degree or second-degree relatives diagnosed with breast cancer at any age

Answer 71

Initially triple assessment – examination, imaging (US/mammogram), FNA/core biopsy MRI assess size/features of tumour LN assessment – US then biopsy of abnormal nodes Sentinel LN biopsy during surgery – isotope contrast and blue die injected into tumour area, first node which goes blue/shows up on scan gets biopsied to look for spread Test for receptors – ER, PR and HER2 Gene profiling – gives probability of recurrence as distant metastasis, guides treatment Staging – CT CAP, isotope bone scan

Answer 72

Surgery – most offered surgery unless old and frail with metastatic disease Breast-conserving (wide local excision) or mastectomy depending on extent of tumour Axillary clearance if nodal disease Offered breast reconstruction to give cosmetically suitable result – immediate or delayed, implant or flap Radiotherapy – in breast-conserving surgery to reduce recurrence Chemotherapy – neoadjuvant (shrink before surgery), adjuvant (reduce recurrence after surgery) or treatment (metastatic or recurrent) Hormone treatment – for oestrogen-receptor positive Premenopausal – tamoxifen Postmenopausal – aromatase inhibitors (letrozole, anastrozole) Other options – fulvestrant (selective oestrogen receptor downregulator), GnRH agonists (goserelin), ovarian surgery (usually in BRCA1/2 mutations) Targeted treatment: Trastuzumab (Herceptin) or pertuzumab – HER2 positive

Answer 73

Metastases: Liver Lung Bone Brain Surgery – lymphoedema Radiotherapy – local skin and tissue irritation/swelling, fibrosis and shrinking of breast tissue, skin colour changes Tamoxifen – prevents osteoporosis but increases risk of endometrial cancer, VTE Trastuzumab (Herceptin) – heart failure, arrhythmia, hypertension

Answer 74

Tamoxifen – selective oestrogen receptor modulator, acts to block oestrogen receptors in breast but stimulate those in uterus and bones Aromatase inhibitors – inhibits aromatase which converts androgens to oestrogens, decreasing oestrogen production

Answer 75

First-line investigations: Spirometry – restrictive picture FEV1 and FVC reduced, FEV1:FVC <70% Bronchodilator reversibility - >12% and 200ml or 400ml increase in FEV1 ?Bronchial challenge with histamine/methacholine FeNO testing (fractional exhaled nitric oxide) Adults >= 40 ppb positive Children >= 35 ppb positive If diagnosis uncertain: PEFR testing – asthma diary, 2-4 weeks, look for diurnal variation (>20% variability) Skin prick testing for allergy Bloods – eosinophil count, total IgE

Answer 76

General: Avoid triggers – allergens Smoking cessation Influenza and pneumococcal vaccination Personalised asthma action plan Step 1 – SABA (salbutamol) Step 2 – add low dose ICS Step 3 – add trial leukotriene receptor antagonist (montelukast) Step 4 – add LABA (salmeterol), continue LTRA depending on dose Step 5 – switch ICS/LABA for MART that includes low-dose ICS Step 6 – moderate dose ICS MART, or switch to separate moderate dose ICS and LABA Step 7 – increase ICS to high-dose (not part of MART) or add additional drug (LAMA, theophylline) +/- specialist referral

Answer 77

Smoking – main risk factor Occupational exposure Air pollution Alpha-1 anti-trypsin deficiency Shortness of breath – exertional and progresses to rest Wheeze Productive cough Recurrent LRTIs Headache – CO2 retention Pursed lip breathing Peripheral cyanosis Finger clubbing Barrel chest CO2 retention flap Cor pulmonale – signs of right heart failure, peripheral oedema, hepatomegaly

Answer 78

Spirometry – FEV1/FVC <70% Little response to bronchodilators Severity based on FEV1 Stage 1 – FEV1 >80% predicted Stage 2 – FEV1 50-79% predicted Stage 3 – FEV1 30-49% predicted Stage 4 FEV1 <30% predicted Other investigations: CXR – rule out cancer, hyperinflation, flattened diaphragm FBC – polycythaemia (response to chronic hypoxia) Sputum culture for chronic infections e.g. pseudomonas Serum alpha-1 antitrypsin

Answer 79

General: Smoking cessation Influenza and pneumococcal vaccination Step 1 – SABA or SAMA Step 2 – no asthmatic features give LABA and LAMA, asthmatic features give LABA and ICS Step 3 – triple therapy with LABA, LAMA and ICS In more severe cases can use nebulisers (salbutamol and/or ipratropium), oral theophylline, oral mucolytics (carbocysteine), long-term prophylactic antibiotics (azithromycin), long-term home oxygen therapy Long term oxygen therapy indications: pO2 <7.3 or pO2 7.3-8 and secondary polycythaemia, peripheral oedema or pulmonary hypertension (Can’t give to current smokers!!)

Answer 80

Most common organisms – Haemophilus influenzae Strep pneumoniae Moraxella catarrhalis Presentation Increased sputum production Purulent sputum Increased dyspnoea, cough, wheeze Type 2 respiratory failure – raised CO2 with low O2

Answer 81

Oxygen therapy – maintain sats 88-92% Nebulisers – salbutamol (SABA) and ipratropium (SAMA) Oral steroids (IV if severe) Antibiotics if symptoms suggestive of an infective cause – fever, purulent sputum, focal creps Oral doxycycline, oral amoxicillin or oral clarithromycin If severe – IV aminophylline, NIV (BiPaP), intubation and ventilation

Answer 82

Men 50-70 Progressive exertional dyspnoea Bibasal fine end-inspiratory creps Dry cough Clubbing Spirometry – restrictive picture (FEV1 normal/decreased, FVC decrease, FEV1/FVC increased) CT is investigation of choice for diagnosis – ground glass opacities peripherally which progress to honeycombing

Answer 83

Upper zone Hypersensitivity pneumonitis (extrinsic allergic alveolitis) Coal worker’s pneumoconiosis Silicosis Sarcoidosis Ankylosing spondylitis TB Radiation-induced pulmonary fibrosis – radiation for breast/lung cancer Lower zone (more common) Idiopathic pulmonary fibrosis Connective tissue disorders e.g. SLE Drug-induced – amiodarone, bleomycin, methotrexate Asbestosis

Answer 84

Post-infectious – most common: Recurrent childhood LRTIs TB Pulmonary disease: COPD Asthma Congenital: CF Primary ciliary dyskinesia Alpha-1 antitrypsin deficiency Connective tissue disease: RA SLE Sarcoidosis

Answer 85

Chronic cough with large volume sputum production Haemoptysis Dyspnoea Course creps Rhonchi High-pitched inspiratory squeaks and pops

Answer 86

Chest physio Smoking cessation Mucolytics Antibiotics for infections (most commonly haemophilus, pseudomonas, klebsiella, strep pneumoniae), potentially long-term prophylactic antibiotics Bronchodilators for severe Surgery – resection or transplant

Answer 87

Often asymptomatic Fever, lethargy, anorexia, weight loss, night sweats, lymphadenopathy Pulmonary – cough, purulent sputum or haemoptysis, dyspnoea, pleuritic chest pain Symptoms of extra-pulmonary disease – urinary symptoms, back pain, headache, chest pain, abdominal pain/bloating

Answer 88

To diagnose latent TB – Mantoux test – inject tuberculin and measure skin response, can be falsely negative in immunosuppressed/young Interferon-gamma release assay – used where Mantoux may be falsely negative or to confirm after Mantoux is positive If positive, to diagnose active TB – CXR – signs suggestive of pulmonary TB, upper lobe consolidation/cavitation/granuloma formation, hilar lymphadenopathy Sputum sample for Ziehl-Nielsen staining for acid-fast bacilli, culture and sensitivities (drug-resistance is common) Sputum culture is gold standard but can take weeks NAAT – allows rapid diagnosis, less sensitive than culture

Answer 89

Active 2 months of: Ethambutol Pyrazinamide Rifampicin Isoniazid Another 4 months of: Rifampicin Isoniazid Latent: 6 months of isoniazid only OR 3 months of rifampicin and isoniazid

Answer 90

Rifampicin – inhibits bacterial DNA dependent RNA polymerase preventing transcription of DNA to mRNA Potent liver enzyme inducer Hepatitis Orange secretions Flu-like symptoms Isoniazid – inhibits mycolic acid synthesis Peripheral neuropathy – must be given with pyridoxine (Vit B6) Hepatitis Agranulocytosis Live enzyme inhibitor Pyrazinamide – inhibits fatty acid synthase Hyperuricaemia causing gout Arthralgia, myalgia Hepatitis Ethambutol – inhibits arabinosyl transferase which polymerises arabinose to arabinan Optic neuritis – check visual acuity before and during treatment Adjust dose in renal impairment

Answer 91

Most common organisms – Viral – rhinovirus, adenovirus, coronavirus Bacterial - strep pneumoniae, staph aureus, haemophilus, atypical (myoplasma), pneumococcal, klebsiella (alcoholics) Fungal – pneumocystis jiroveci Presentation Cough with purulent sputum Dyspnoea Pleuritic chest pain Fever Malaise Signs of infection – temp, tachycardia, hypotension, confusion, low sats, creps, bronchial breathing, dullness to percussion

Answer 92

Develops >48 hours since admission

Answer 93

CRB-65 (community) Confusion – AMT <8/10 Respiratory rate >30 Blood pressure – SBP <=90 and/or diastolic <=60 Age >65 Hospital assessment if score more than 0, especially if score 2 or more CURB-65 (hospital) Confusion Urea >=7 Respiratory rate >30 Blood pressure – SBP <=90 and/or diastolic <=60 Age >65 Home care if 0 or 1, hospital admission for 2 or more, consider ICU for 3 or more Investigations CXR – consolidation Bloods – FBC, U+Es, CRP, blood cultures Sputum sample Legionella antibodies if at risk (recent holiday, infected water exposure)

Answer 94

Legionella – exposure to infected water/air conditioning, causes hyponatraemia which leads to SIADH Mycoplasma – erythema multiforme rash (target lesions), neurological symptoms in young patients Chlamydophila – school aged children with mild-moderate chronic pneumonia Coxiella burnetti (Q fever) – exposure to animals and bodily fluids (typically farmer) Chlamydia psittaci – contact with infected birds (typically farmer)

Answer 95

Oxygen – sats 94-98% unless risk of type 2 respiratory failure, then 88-92% IV fluids Analgesia for pleuritic pain DVT prophylaxis Low-severity CAP – amoxicillin, 5 days Moderate and high-severity (CURB-65 >3) – IV clarithromycin + IV amoxicillin (or co-amoxiclav if in HDU/ICU) All need CXR in 6 weeks to check for resolution

Answer 96

Microcytic – TAILS Thalassaemia Anaemia of chronic disease (more commonly normocytic) Iron deficiency anaemia Lead poisoning Sideroblastic anaemia Normocytic – 3As, 2Hs Acute blood loss Anaemia of chronic disease – including CKD Aplastic anaemia Haemolytic anaemia Hypothyroidism Macrocytic: Megaloblastic Vitamin B12 deficiency Folate deficiency Normoblastic Alcohol Reticulocytosis (haemolytic anaemia or blood loss) Drugs e.g. azathioprine, methotrexate Liver disease Hypothyroidism Pregnancy Myelodysplasia

Answer 97

Dyspnoea Tiredness Headaches Dizziness Pallor Tachycardia Koilonychia Angular chelitis Atrophic glossitis Brittle hair and nails

Answer 98

Address underlying cause e.g. menorrhagia, dietary deficiency Oral iron first-line (ferrous sulfate, ferrous fumarate) for 3 months Consider IV iron if oral contraindicated, ineffective or not tolerated – check compliance and manage side effects (e.g. constipation, take after meals, reduce dose frequency)

Answer 99

Problems with platelet production: Sepsis B12 or folic acid deficiency Liver failure – reduced thrombopoietin production Leukaemia Myelodysplastic syndrome Problems with destruction: Medications – sodium valproate, methotrexate, isotretinoin, antihistamines, PPIs Alcohol ITP Heparin-induced thrombocytopaenia Haemolytic uraemic syndrome

Answer 100

Development of antibodies against platelets in response to exposure to heparin – against platelet factor 4 Activate clotting mechanisms and destroy platelets so have thrombocytopaenia and clots

Answer 101

Hereditary Membrane – hereditary spherocytosis/elliptocytosis Metabolism – G6PD deficiency Haemoglobinopathies – sickle cell, thalassaemia Acquired Immune (Coombs-positive) Autoimmune – warm/cold antibody type Alloimmune – transfusion reaction, haemolytic disease of the newborn Drugs – methyldopa, penicillin Non-immune (Coombs-negative) Microangiopathic haemolytic anaemia – TTP, HUS, DIC, malignancy, pre-eclampsia Prosthetic heart valves Paroxysmal nocturnal haemoglobinuria Malaria Dapsone Zieve syndrome

Answer 102

Alpha-thalassaemia 1 or 2 alleles abnormal – hypochromic, microcytic but typically normal Hb 3 abnormal – HbH disease, hypochromic, microcytic anaemia with splenomegaly 4 abnormal – death in utero due to hydrops fetalis Beta-thalassaemia Minor – hypochromic, microcytic anaemia Major – failure to thrive, hepatosplenomegaly, microcytic anaemia (requires repeated transfusion which leads to iron overload, so need iron chelation)

Answer 103

Presentation – failure to thrive, jaundice, gallstones, splenomegaly, aplastic crisis precipitated by parvovirus infection, spherocytes on blood film Management – Acute haemolytic crisis – supportive management, transfusion if needed Long term – folate replacement, splenectomy (stops spherocytes from being destroyed)

Answer 104

Common organisms: E. Coli Klebsiella Enterococcus Risk factors: Women Pregnancy Catheter Sexually active BPH Diabetes Children – vesicoureteral reflux Presentation: Urinary frequency, urgency Incomplete voiding Dysuria Haematuria New incontinence Confusion in elderly Lower abdominal/flank pain Upper – fever and chills, nausea and vomiting, renal angle tenderness

Answer 105

Uncomplicated lower UTI in adult, non-pregnant women: Can try supportive care with analgesia, fluids If prescribing antibiotic – oral nitrofurantoin (eGFR >45) or trimethoprim for 3 days, can give delayed and advise to start if symptoms do not improve within 48 hours or worsen at any time Pregnant, no haematuria, including asymptomatic bacteriuria: Nitrofurantoin (avoid at term), or amoxicillin (if susceptible) or cefalexin for 7 days Catheter-associated UTI (not pregnant), men: Don’t treat catheter-associated asymptomatic bacteriuria Nitrofurantoin, trimethoprim or amoxicillin (if sensitive) for 7 days Upper UTI: Non-severe no sepsis – oral ciprofloxacin or oral trimethoprim, 7 days Urosepsis/pyelonephritis – IV gentamicin, if eGFR <2 oral ciprofloxacin, for 7 days Always send MSSU for culture and sensitivities to guide antibiotic therapy

Answer 106

Risk factors for urothelial (transitional cell) >90%: Smoking Occupational – rubber, dyes Cyclophosphamide Risk factors for squamous cell carcinoma: Schistosomiasis Smoking Presentation: Haematuria – usually painless, macroscopic

Answer 107

Over 45 with unexplained visible haematuria, without UTI or persisting after treatment for UTI Over 60 with microscopic haematuria plus dysuria or raised WCC

Answer 108

Investigation – cystoscopy and biopsy or TURBT Spread – pelvic MRI, distant disease CT scanning Management – superficial may be managed with TURBT, may need intravesical chemotherapy, surgery (radical cystectomy and ileal conduit) or radical radiotherapy

Answer 109

Calcium oxalate – hypercalcaemia, high dietary oxalate, radio-opaque Cysteine – associated with homocysteinuria, radio-opaque Uric acid – hyperuricaemia due to diet, haematological disease, associated with gout, ileostomy, radioluscent Calcium phosphate – hypercalcaemia, renal tubular acidosis, high urinary pH, radio-opaque Struvite – formed of magnesium, ammonium, phosphate, associated with chronic infections, slightly radio-opaque

Answer 110

Renal colic – intermittent, severe, pain radiating from loin to groin, associated with nausea and vomiting Haematuria Flank tenderness Reduced urine output Symptoms of infection if present

Answer 111

Diagnosis – CT KUB is gold-standard Management Analgesia - NSAID IV fluids <5mm – likely to pass spontaneously, within 4 weeks of symptom onset If >5mm or conservative management failed can use shockwave lithotripsy, uteroscopy, percutaneous nephrolithotomy to pass stone If obstruction due to stones + infection this I a surgical emergency – nephrostomy tube, ureteric catheter or stent Prevention: Calcium stones – increase fluid intake, low salt diet, thiazide diuretics Oxalate stones – cholestyramine, pyridoxine Uric acid – allopurinol, urinary alkalinisation e.g. oral bicarbonate

Answer 112

Urethritis where gonococcal bacteria not identified from swab Causes – Cause not found in 50% Chlamydia Mycoplasma genitalium E. Coli Trichomonas vaginalis Management – oral azithromycin or doxycycline

Answer 113

Occurs following infection with group A strep (strep pyogenes), usually tonsillitis Caused by immune complex deposition in glomeruli Usually young children Visible haematuria Proteinuria, leading to oedema Hypertension Oliguria Raised anti-streptolysin O titre Low C3

Answer 114

Histology – IgG and complement deposits on basement membrane ACEi or ARB – reduce proteinuria and improve prognosis Immunosuppression – only in severe or progressive disease, most spontaneously resolve 1/3 – spontaneous remission 1/3 – remain proteinuric 1/3 – develop ESRF

Answer 115

Anti-GBM antibodies attack glomerulus and pulmonary basement membranes Causes glomerulonephritis and pulmonary haemorrhage – AKI and haemoptysis classically

Answer 116

Rapid loss of renal function Cause – secondary to Goodpasture’s syndrome, Wegner’s granulomatosis, SLE Red cell casts in urine Histology - crescenteric glomerulonephritis

Answer 117

Pre-renal: Hypovolaemia Cardiac disease – MI, PE, cardiac tamponade, congestive heart failure Vascular – renal artery stenosis, thrombosis Renal: Vasculitis, glomerulonephritis, acute tubular necrosis Post-renal: Obstruction – upper or lower tract obstruction (ureteral stricture, stone, BPH, tumours)

Answer 118

Young men – STIs e.g. gonorrhoea, chlamydia Older men – E. Coli, enterococcus, klebsiella Mumps Presentation: Dysuria Urethral discharge - purulent Unilateral testicular swelling, erythema, pain Prehn’s sign – testicular pain better on elevating scrotum Tenderness especially over epididymis Systemically unwell – fever

Answer 119

Urine C+S NAAT for chlamydia/gonorrhoea Charcoal swab of urethra discharge for gonorrhoea C+S If suspect mumps – saliva swab for PCR, serum antibodies US to rule out torsion/tumours Management If STI most likely – one off ceftriaxone IM plus doxycycline for 10-14 days If enteric most likely – send MSU, empirically treat with quinolone (ofloxacin or levofloxacin) or co-amoxiclav if quinolone contraindicated

Answer 120

Screen those with risk factors (based on sexual history, travel history, IV drug use etc.) or presenting with other STI Test those with symptoms suggestive of seroconversion or AIDS-defining illnesses Verbal consent only needed for testing HIV antibodies and p24 antigen combined test Antibodies will develop at 4-6 weeks post-infection, 99% do by 3 months P24 antigen usually positive from 1-4 weeks after infection (earlier than antibody) If asymptomatic potentially exposed test at 4 weeks post-exposure Repeat testing at 3 months post-exposure if initially negative If symptomatic test now Can then test HIV RNA levels for viral load, CD4 count

Answer 121

PreP – pre-exposure prophylaxis For those at high risk (including MSM, transgender people who have sex with men, HIV-negative partners of HIV-postivie people with detectable/unknown viral load), combination of emtricitabine and tenofovir taken daily Post-exposure prophylaxis – given dependent on risk Combination of antiretrovirals (e.g. Tenofovir, emtricitabine) as soon as possible, up to 72 hours post-exposure, for 4 weeks Reduced risk of transmission by 80% Taken up to 72 hours post-exposure

Answer 122

Psychogenic – most common, especially in younger men (still have morning erections/spontaneous erections, history mental illness e.g. anxiety, new partner etc.) Vascular disease – hypertension, atherosclerosis, hyperlipidaemia, smoking Neurological disease - Parkinson’s, MS, stroke, spinal cord injury, peripheral neuropathy Hormonal – hypogonadism, hyperprolactinaemia, thyroid disease, Cushing’s Systemic disease – diabetes, renal failure Structural – Peyronie’s, penile/pelvic trauma Drugs – anti-psychotics, anti-depressants, anti-convulsants, antihypertensives, beta-blockers, diuretics, recreational drugs (Frequently multi-factorial)

Answer 123

Tests to rule out organic causes – FBC, LFTs, U&Es, lipids, HbA1c, TFTs, serum total testosterone, serum prolactin Modify risk factors – diet, smoking, diabetic control, alcohol intake Psychosexual counselling PDE-5 inhibitors (sildenafil, vardenafil) – take on an empty stomach 30 minutes before intercourse, can last 4 hours (if lasts longer seek medical attention) Contraindications – concurrent nitrate use, cardiovascular or cerebrovascular disease in previous 6 months (including hypo/hypertension) Side effects – headache, flushing, dizziness Penile prosthesis – inflatable implants, semirigid rods

Answer 124

Communicating – usually in newborns, patency of processus vaginalis which allows peritoneal fluid to leak into scrotum Non-communicating – excessive fluid production within tunica vaginalis Presentation – unilateral scrotal swelling, fluctuant, painless, transilluminates Confined to scrotum, can ‘get above’ it Can develop secondary to epididymo-orchitis, testicular torsion, testicular tumours Usually conservative management, should US to exclude underlying cause e.g. tumour

Answer 125

Pre-pubertal – yolk-sac, teratoma Older – lymphoma, seminomas Risk factors – cryptorchidism, infertility, Klinefelter’s, mumps orchitis, FHx

Answer 126

Presentation: Testicular lump – hard, irregular, usually painless, does not transilluminate Testicular pain Hydrocele Torsion Gynaecomastia – Sertoli cell (oestrogen producing) Assessment: Testicular US Tumour markers AFP – non-seminoma BhCG – germ cell tumours (seminoma and non-seminoma) LDH – general malignancy marker Staging - CT Royal Marsden staging – local spread, LN above and below diaphragm, distant mets (LN, lungs, liver, brain) Management: Radical orchidectomy Chemotherapy Radiotherapy Fertility management – sperm banking

Answer 127

Older men Hyperplasia of stromal and epithelial cells of prostate Presentation: Hesitancy Urgency Frequency Straining to pass urine Dribbling Incomplete voiding Poor stream Nocturia UTIs Urinary retention – oliguria/anuria, painful then painless, suprapubic distension

Answer 128

Investigations – PR exam, urine dip for infection PSA – if there is obstructive symptoms or if patient preference (unreliable) Management: 1st line - alpha-1 agonists (tamsulosin, alfuzosin) Decrease smooth muscle tone of bladder and prostate Adverse effects – dizziness, postural hypotension, dry mouth, depression 2nd line – 5 alpha-reductase inhibitors e.g. finasteride Block conversion of testosterone to dihydrotestosterone If patient has significantly enlarged prostate, high risk of progression May take 6 months to work, reduce volume of prostate Adverse effects – erectile dysfunction, reduced libido, ejaculation problems, gynaecomastia Combination therapy (alpha-1 agonist and 5-alpha reductase inhibitor) if moderate/severe symptoms Can add antimuscarinic e.g. tolterodine if storage + voiding symptoms Surgery – transurethral resection of prostate (TURP), transurethral electrovaporisation of prostate (TEVAP), holmium laser enucleation of the prostate (HoLEP)

Answer 129

Confirm with bladder US - >300cc Insert urinary catheter, measure volume drained in 15 minutes (>400 confirms acute retention) Post-obstructive diuresis – IVF and correct electrolytes

Answer 130

Most are adenocarcinoma, in peripheral zone, testosterone dependent Often asymptomatic Lower urinary symptoms of obstruction: Frequency Urgency Hesitancy Dribbling Poor stream Nocturia Other symptoms Haematuria, haematospermia Erectile dysfunction Back, perineal or testicular pain PR exam – asymmetrical, hard, nodular enlargement, loss of median sulcus

Answer 131

Diagnosis: PSA – unreliable marker Can also be raised in BPH, UTIs, prostatitis, exercise (cycling), recent ejaculation or prostate stimulation PR exam First-line examination – multiparametric MRI of the prostate Prostate biopsy to diagnose – transrectal or transperineal Isotope bone scan to check for bony mets Use Gleason grading system and TNM for staging Management: Surveillance or watchful waiting if early/low grade External beam radiotherapy Brachytherapy Hormone therapy – androgen receptor blockers, GnRH agonists (goserelin), bilateral orchidectomy (rare) Chemotherapy - docetaxel Surgery – radical prostatectomy

Answer 132

Genetic – autosomal dominant (more common) and autosomal recessive ADPKD – mostly chromosome 16, 15% chromosome 4 ARPKD – chromosome 6 Causes formation of multiple cysts on the kidneys, also associated with cerebral berry aneurysms, hepatic/splenic/pancreatic/ovarian and prostatic cysts, mitral regurgitation, colonic diverticula, aortic root dilatation Presentation: Family history Bulky kidneys on examination Incidental finding on imaging Cyst rupture – haematuria Hypertension/cardiovascular disease Renal impairment – ESRF by 40s/50s in ADPKD, childhood in ARPKD Loin pain Renal stones more common

Answer 133

Diagnosis ARPKD – often antenatal due to oligohydramnios US – cysts on kidneys Genetic testing Management ADPKD – tolvaptan (vasopressin receptor 2 antagonist), slows cyst development and renal failure RRT

Answer 134

Haemodialysis – via AV fistula or central venous catheter (tunnelled or non-tunnelled) Peritoneal dialysis – continuous ambulatory or automated Renal transplant

Answer 135

Haemodialysis: Thrombophlebitis Steal syndrome Thrombosis Line infection, sepsis Hypertension Peritoneal dialysis: Spontaneous bacterial peritonitis Peritoneal fibrosis – failure Fluid retention Hyperglycaemia Renal transplant: Acute rejection Chronic rejection Complications of immunosuppression – opportunistic infections, cancers (lymphoma, skin cancer) Recurrence of original disease DVT/PE

Answer 136

Risk factors: H. Pylori infection Excess alcohol consumption Smoking Obesity Pregnancy NSAIDs Presentation – burning pain in chest/epigastrum, worse lying down or after meals, waterbrash, chronic dry cough, acidic taste in mouth, bloating

Answer 137

Endoscopy if: >55 Symptoms >4 or persistent despite treatment Dysphagia Weight loss Gold-standard for diagnosis – 24-hour oesophageal pH monitoring Testing for H Pylori – carbon-13 urea breath test, stool antigen test, rapid urease test during endoscopy Management: Lifestyle advice Antacids e.g. gaviscon Proton pump inhibitor – omeprazole, lansoprazole H2 receptor antagonists – ranitidine H. Pylori eradication – PPI plus amoxicillin + clarithromycin or metronidazole, for 7 days

Answer 138

Uncomplicated: PPI +/- H. Pylori eradication if test positive Acute bleeding: A-E assessment IV PPI Endoscopic intervention – adrenaline injection, cauterisation If endoscopic intervention fails – IR with arterial embolisation, surgery Perforation: A-E assessment Erect CXR to look for pneumoperitoneum Emergency surgery

Answer 139

Liver disease (cirrhosis) causes increased vascular resistance through liver, leading to portal vein hypertension, causes enlargement of veins including oesophageal Combined with liver disease-associated coagulopathy Presentation: Asymptomatic until bleed Cause melaena and/or haematemesis

Answer 140

Prophylaxis: Propranolol Endoscopic variceal band ligation Transjugular intrahepatic portosystemic shunt (TIPSS) Acute bleed: A-E assessment Fluid resuscitation, blood transfusion Correct clotting Terlipressin (or octreotide 2nd line) Prophylactic IV antibiotics - co-amoxiclav Stop anticoagulants Then endoscopy – variceal band ligation or sclerotherapy Sengstaken-Blakemore tube if uncontrolled haemorrhage TIPSS if recurrent/problematic bleeding

Answer 141

Hepatitis A – Transmitted via faecal oral route – infected water or food Presentation – nausea, vomiting, anorexia, jaundice, cholestasis Resolves without treatment in 1-3 months, complications rare Vaccination available – 2 doses, 6-12 months apart, give to high risk and before travel to high prevalence areas Hepatitis E – Transmitted via faecal oral route – infected water or food Causes mild illness, cleared in 1 month Rarely can cause liver failure, more in immunocompromised and pregnant No vaccine Hepatitis D – Transmitted via blood/bodily fluids, only infects those with hepatitis B If superinfection (hepatitis B positive then becomes infected with hepatitis D) high risk fulminant hepatitis, chronic hepatitis, cirrhosis No vaccine Hepatitis B – Transmitted via blood/bodily fluids, can be vertical transmission during birth Causes fever, jaundice, transaminitis Complications – chronic hepatitis, fulminant liver failure, HCC Vaccination – children, at risk (healthcare, IVDU, sex workers), 10-15% don’t respond Management – pegylated interferon-alpha is only treatment, reduces viral replication (may also use anti-virals e.g. tenofovir) In pregnancy – babies of mothers who are hepatitis B positive receive vaccination and immunoglobulin after birth, no risk of transmission with breastfeeding Hepatitis C – Transmitted via blood/bodily fluids, can have vertical transmission Clinical features – transient transaminitis/jaundice, fatigue, arthralgia Majority develop chronic hepatitis C, associated with arthritis, Sjogren’s, cirrhosis, HCC, glomerulonephritis Anti-viral treatments can cure in >90%

Answer 142

Signs: Jaundice Hepatomegaly (can shrink later) Splenomegaly Spider naevi Palmar erythema Gynaecomastia and testicular atrophy Bruising Ascites Caput medusae Asterixis Investigation results: Decompensated – ALT, AST, ALP, bilirubin deranged Low albumin PT increased Hyponatraemia due to fluid retention Hepatorenal syndrome – U&Es deranged AFP monitor HCC Complications: Malnutrition Portal hypertension, varices, variceal bleeding Ascites and spontaneous bacterial peritonitis Hepato-renal syndrome Hepatic encephalopathy

Answer 143

Monitor for HCC – US and AFP every 6 months High protein, low sodium diet MELD score every 6 months Consider liver transplant Malnutrition – regular meals, low sodium, high protein/calorie, avoid alcohol Portal hypertension/varices – propranolol, elastic band ligation, TIPS, acute management if bleeding Ascites – fluid/sodium restriction, prophylactic antibiotics for SBP (if <15g/L protein in ascitic fluid), spironolactone, paracentesis (tap or drain), TIPS SBP – ascitic culture, IV antibiotics (co-trimoxazole) Hepatorenal syndrome – terlipressin, HAS, TIPS, liver transplant Hepatic encephalopathy – laxatives (lactulose), antibiotics, nutritional support

Answer 144

Childs-Pugh score – grade severity and give prognosis Uses bilirubin, albumin, INR, ascites, encephalopathy MELD (model for end-stage liver disease) – predicts 3-month mortality Uses bilirubin, creatinine, INR, sodium, whether they need dialysis or not

Answer 145

Autosomal dominant, displays genetic anticipation (successive generations have earlier age of onset and more severe disease) Trinucleotide repeat of HTT gene on chromosome 4

Answer 146

Assess risk – Glasgow modified alcohol withdrawal scale Assess for risk of Wernicke’s encephalopathy Benzodiazepines (oral diazepam if able to tolerate, severe may need IV) – fixed dose or treatment triggered depending on risk Wernicke’s or high risk for Wernicke’s – initially IV Pabrinex then oral thiamine, measure and replace magnesium as required

Answer 147

Presentation: Crohn’s – usually non-bloody diarrhoea, weight loss, perianal disease, oral ulcers, palpable abdominal mass in RIF, stricture formation leading to bowel obstruction, fistulae Ulcerative colitis – bloody diarrhoea, LIF pain, tenesmus, strongly associated with PSC and uveitis, higher risk toxic megacolon and colorectal cancer Histological features Crohn’s – terminal ileum most commonly affected, transmural inflammation, skip lesions, cobblestone mucosa, goblet cells, granulomas, strictures, fistulae UC – only colon and rectum affected, mucosal inflammation only, continuous inflammation, inflammatory infiltrate in lamina propria, crypt abscesses

Answer 148

FBC – anaemia Inflammatory markers – CRP, ESR U&Es – dehydration, electrolyte disturbance LFTs – albumin may be low in protein losing enteropathy Serum ferritin, B12, folate and vitamin D – deficiencies due to malabsorption Coeliac serology to exclude coeliac Stool C+S to exclude infective gastroenteritis Faecal calprotectin – if high suggests active inflammation Diagnosis – endoscopy (OGD, colonoscopy, flexible sigmoidoscopy) AVOID COLONOSCOPY IF RISK OF PERFORATION Imaging – CT, MRI, barium enema

Answer 149

Erythema nodosum – tender, red bumps Arthritis Episcleritis – more common in Crohn’s Uveitis – more common in UC Pyoderma gangrenosum – ulcers Primary sclerosing cholangitis – more common in UC

Answer 150

Important to stop smoking – makes Crohn’s worse! Inducing remission: 1st line = Steroids (oral, topical or IV) +/- immunosuppressants e.g., azathioprine (or methotrexate), mercaptopurine 2nd line = 5-ASA drugs e.g. mesalazine Isolated peri-anal disease – metronidazole Refractory/fistulating disease – infliximab (+ azathioprine or methotrexate) Maintaining remission: 1st line – azathioprine or mercaptopurine (check TPMT activity before starting) Others – methotrexate, infliximab, adalimumab Surgery – very commonly needed Stricturing terminal ileal disease – ileocaecal resection Stricturoplasty Perianal disease – laying open fistulae or seton placement, abscess incision and drainage

Answer 151

Inducing remission (mild to moderate): 1st line – topical/oral salicylates e.g., mesalazine 2nd line – steroids Inducing remission (severe): 1st line – IV steroids 2nd line – IV ciclosporin Maintaining remission: Aminosalicylates e.g., mesalazine oral or rectal Azathioprine Mercaptopurine Surgery – panproctocolectomy is curative, create ileostomy or ileo-anal anastomosis (J-pouch)

Answer 152

Truelove and Witt Mild - less than 4 stools daily, no/little blood, apyrexial, normal ESR/CRP, HR less than 70, Hb more than 110 Moderate – 4-6 stools per day, moderate blood, low-grade fever, mildly elevated ESR/CRP, HR 70-90, Hb 105-110 Severe - more than 6 stools per day, high fever, lots of blood, high ESR/CRP, Hb less than 105, HR over 90

Answer 153

Most common – alcohol excess, biliary obstruction e.g., gallstones Others: Autoimmune pancreatitis – SLE, Sjogren’s Hyperlipidaemia Hypercalcaemia Drugs – 5-ASAs, steroids, NSAIDs, diuretics Mumps ERCP

Answer 154

Presentation: Epigastric pain, radiating to back Worse after eating Nausea and vomiting Systemically unwell Epigastric tenderness Grey-Turner’s sign and Cullen’s sign – haemorrhagic pancreatitis (rare) Investigations: Raised amylase, >3x upper limit Lipase – more sensitive than specific, longer half-life so good for delayed presentations US to determine aetiology (look for biliary obstruction) CT for complications – necrosis. Pseudocysts Scoring systems e.g. Glasgow Score

Answer 155

Supportive management: IVF Analgesia Anti-emetics NBM Treat cause e.g., gallstones (ERCP) Treat complications – drainage of collections etc.

Answer 156

Aetiology – mostly alcohol, also genetic (CF, haemochromatosis), ductal obstruction (tumours, stones) Pain – worse following meal Exocrine dysfunction – steatorrhoea Endocrine dysfunction – diabetes mellitus

Answer 157

CT shows calcification Faecal elastase to assess exocrine function Alcohol abstinence Analgesia – difficult to manage pain Creon Insulin ERCP with stenting for strictures, stones Surgical intervention

Answer 158

Pre-hepatic – excess RBC breakdown Unconjugated hyperbilirubinaemia Haemolytic anaemia Gilbert’s syndrome Intra-hepatic – hepatic cell dysfunction Unconjugated and conjugated hyperbilirubinaemia Alcoholic liver disease Viral/autoimmune hepatitis Haemochromatosis PBC or PSC HCC Post-hepatic – obstruction of biliary drainage Conjugated hyperbilirubinaemia Gallstones Cholangiocarcinoma, strictures, drug-induced cholestasis Pancreatic cancer Abdominal masses

Answer 159

AST:ALT >2 – acute alcoholic hepatitis, cirrhosis AST:ALT around 1 – viral hepatitis ALT>AST – chronic liver disease Isolated raised bilirubin with jaundice – suggests pre-hepatic cause e.g. Gilbert’s, haemolysis Albumin – measure of liver synthetic function, can be low in liver disease, acute phase response, enteropathy or nephrotic syndrome AST and ALT – markers of hepatocellular injury ALP – raised in biliary obstruction (also in bone disease, pregnancy, malignancy) GGT – biliary obstruction, alcohol, drugs e.g., phenytoin

Answer 160

Risk factors – female, middle aged, obese, hyperlipidaemia, haemolysis Presentation: Asymptomatic if uncomplicated Biliary colic – Sudden onset severe RUQ/epigastric pain, lasting 30 minutes – hours then subsiding Associated nausea, vomiting, sweating Associated with eating Acute cholecystitis – Persistent RUQ pain which is sharper and more localised, exacerbated by movement, radiating to right shoulder Systemically unwell with vomiting and fever Positive Murphy’s sign (painful inspiratory catch during RUQ palpation – pain on inspiration when palpating gallbladder) May have palpable RUQ mass Ascending cholangitis – Charcot’s triad – RUQ pain, fever and jaundice Hypotension Confusion Raised inflammatory markers

Answer 161

First-line investigation – US of the biliary tree MRCP then used for further investigation or if US is negative but high clinical suspicion ERCP – used for imaging, sphincterotomy of sphincter of Oddi, clear stones, insert stents, take biopsies if tumour suspected Complications – bleeding, cholangitis, pancreatitis Asymptomatic gallstones – may be used conservatively, lifestyle advice Biliary colic – analgesia, elective laparoscopic cholecystectomy (emergency if severe pain or multiple attacks) Acute cholecystitis – antibiotics, emergency laparoscopic cholecystectomy Ascending cholangitis – IV fluids, IV antibiotics, urgent decompression of biliary system with ERCP, cholecystectomy when well enough CBD stone causing obstructive jaundice – IV fluids, anti-itch medications, ERCP or emergency laparoscopic cholecystectomy with CBD exploration

Answer 162

Intermittent claudication – cramping pain in legs/buttocks due to ischaemia, initially with exertion (predictable walking distance) then rest pain in critical limb ischaemia Pain at night, relieved by standing/putting feet on floor Cold extremities Sensation loss Ulcers – arterial (punched out, deep, painful, on sites of trauma such as heels) or venous (sloughy, irregular edges, shallow, around gaiter areas, usually medial malleolus, painless) Prolonged CRT Positive Buerger’s test

Answer 163

Ankle-Brachial pressure index: 0.9-1.3 normal 0.6-0.9 mild disease 0.3-0.6 moderate to severe Less than 0.3 severe to critical ischaemia >1.3 suggests calcification Doppler US scan then CT angiography Management Chronic – lifestyle advice, statin, anticoagulation (clopidogrel), diabetic control Surgery – angioplasty, bypass grafting Acute limb ischaemia – Conservative – prolonged course of heparin Surgical – embolectomy, intra-arterial thrombolysis, bypass surgery, angioplasty Irreversible limb ischaemia – urgent amputation

Answer 164

Pain Pallor Pulselessness Paraesthesia Perishingly cold Paralysis

Answer 165

Irreversible limb ischaemia requiring amputation 20% mortality rate Reperfusion injury – compartment syndrome, AKI (due to hyperkalaemia, acidosis, myoglobinaemia)

Answer 166

Main risk factor is UVB exposure Genetic mutations e.g. BRAF Presentation – new naevus or change to existing Asymmetry, irregular, uneven colour, diameter >6mm, evolving Advanced – bleeding, ulceration, lymph node involvement Diagnosis – excision biopsy, sentinel LN biopsy or FNA if clinically suspicious LNs Staging – CT CAP TNM staging Breslow thickness Management Wide local excision +/- lymphadenectomy Metastatic disease common, options for management: Ipilimumab – CTLA4 inhibitor Pembrolizumab and nivolumab – PD1 inhibitors

Answer 167

Amoxicillin – rash with infectious mononucleosis Doxycycline – photosensitivity Trimethoprim – rashes, photosensitivity, pruritus CCB – flushing Steroids – acne Any drug – allergic rash Stevens-Johnson syndrome – penicillins, sulphonamides, anti-epileptics, allopurinol, NSAIDs, OCP

Answer 168

Types: Plaque psoriasis – most common, extensor surfaces and scalp Flexural psoriasis – smooth, on flexural surfaces Guttate psoriasis – triggered by strep infection, multiple red, teardrop lesions Pustular psoriasis – on palms and soles, can be systemically unwell Erythrodermic psoriasis – extensive erythematous inflamed areas, medical emergency Salmon-pink, raised, scaly, itchy, well-demarcated lesions Usually on extensor surfaces, scalp, symmetrical distrubition Auspitz phenomenon – pin-prick bleeding with trauma Koebner phenomenon – development of plaque on areas of trauma Nail changes – pitting, onycholysis, subungal hyperkeratosis

Answer 169

Emollients + 1st line – potent corticosteroid applied once daily plus vitamin D analogue once daily 2nd line – vitamin D twice daily 3rd line – potent corticosteroid applied twice daily or a coal tar preparation once or twice daily Can also use short-acting dithranol Phototherapy – narrowband UVB Systemic therapy 1st line - oral methotrexate Ciclosporin Biologic agents – infliximab, etanercept, adalimumab

Answer 170

Step-up regimen 1. Single topical therapy – topical retinoids, benzoyl peroxide 2. Topical combination therapy – topical antibiotic, benzoyl peroxide, topical retinoid 3. Oral antibiotics – tetracyclines (e.g., doxycycline) + topical retinoid or benzoyl peroxide 4. COCP alternative to oral antibiotics in women 5. Oral isotretinoin Side effects of isotretinoin – Teratogenicity – two forms of contraception in women of childbearing age Dry skin, eyes, mouth, lips – most common Low mood Raised triglycerides Intracranial hypertension Photosensitivity

Answer 171

Presentation: Nose, cheeks, forehead Flushing Telangiectasia Papules and pustules Blepharitis Sunlight exacerbates Management Suncream Erythema/flushing – topical brimonidine (alpha-adrenergic agonist) Papules and/or pustules – topical ivermectin +/- doxycycline

Answer 172

Can be nodular, indurated or keratinised with associated ulceration or bleeding On sun-exposed areas Precancerous lesions: Bowen's disease or actinic keratosis - slow-growing, small, red, scaly lesion

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Diagnosis – biopsy If suspicion of LN involvement – imaging +/- FNA of suspicious nodes Management Surgical – excision biopsy If close margins – wide local excision, Mohs micrographic surgery, adjuvant radiotherapy If small, low risk – curettage and cautery only

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Avoid further damage – sunscreen etc. Fluorouracil cream – causes skin irritation, may need topical steroid Topical diclofenac – fewer side effects, moderate efficacy Topical imiquimod Cryotherapy Curettage and cautery

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Presentation – on sun-exposed areas, small slow-growing lesions, raised pearly edges, telangiectasia, pain, bleeding, ulceration Subtypes – nodular (most common), superficial, Morphoeic, basosquamous Diagnosis – excision biopsy Management Cryotherapy Curretage and electrodissection (small lesions) Immune response modulator – topical imiquimod (superficial) Topical chemotherapy – 5-fluorouracil (superficial) Radiotherapy – older patients Surgical – excision biopsy +/- free flap or skin graft Mohs’ micrographic

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HbA1c >48 Fasting glucose >7 Random glucose >11 OGTT 2 hour >11

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Diagnosis of T2DM – give lifestyle advice, start metformin (give modified release if don’t tolerate), assess CV risk (QRISK), if high risk (QRISK >10%) or established CV disease start SGLT2 inhibitor when stable on metformin, if low risk don’t start SGLT2 inhibitor (At any time if CV risk changes, become high risk start SGLT2) Initial HbA1c target is <48 If >48 start second drug from sulfonylurea, DPP-4 inhibitor, or pioglitazone After second drug added HbA1c target is <53 If >53 add another drug from above or start insulin If >53 swap one drug for GLP-1 inhibitor if BMI >35 or occupational contraindication to insulin (only continue if reduction in HbA1c of at least 11 and 3% weight reduction in 6 months) Measure HbA1c every 3-6 months

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Biguanide MOA – increases sensitivity to insulin and decreases gluconeogenesis Side effects – GI upset, lactic acidosis Contraindications – renal failure (review use if eGFR less than 45, discontinue if eGFR less than 30), conditions predisposing to lactic acidosis (recent MI, sepsis, AKI, severe dehydration) Titrate dose slowly to minimise GI upset Weight neutral Low risk hypoglycaemia

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-gliflozins e.g., dapagliflozin, empagliflozin, canagliflozin Inhibit SGLT2 which reabsorbs glucose in PCT, leads to increased glucose secretion in urine Side effects – UTIs, normoglycaemic acidosis, canagliflozin has been shown to increase risk of lower-limb amputation Weight loss Low risk hypoglycaemia

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Thiazolidinedione MOA – increases insulin sensitivity, decreases gluconeogenesis Side effects – fluid retention, anaemia, heart failure, increase risk bladder cancer Weight gain Low risk hypoglycaemia

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-gliptins e.g., sitagliptin, linagliptin, saxaglitpin Inhibit DPP-4 to increase GLP-1 – increases insulin secretion, inhibits glucagon production, slows GI absorption Side effects – GI upset, URTI symptoms, pancreatitis Weight neutral Low risk hypoglycaemia

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-tide e.g. liraglutide, exenatide Increase insulin secretion, inhibit glucagon production, slow GI absorption Side effects – GI upset, dizziness Weight loss Low risk hypoglycaemia Subcutaneous administration

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Gliclazide Increase insulin secretion Side effects – increased risk CVD Weight gain Hypoglycaemia risk

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Risk of hypoglycaemia Causes weight gain Subcutaneous administration

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Coombs negative haemolysis, cholestatic jaundice, transient hyperlipidaemia associated with heavy alcohol use, typically following a binge