GP Flashcards
Describe the clinical presentation of irritable bowel syndrome
For >6 months:
Abdominal pain and/or
Bloating and/or
Change in bowel habit
Abdominal pain relieved by defecation or associated with altered bowel habit
Symptoms worse with eating
Mucus in stool
May also have lethargy, nausea, bladder symptoms
How is irritable bowel syndrome managed?
Pharmacological:
Pain - antispasmodics e.g. buscopan
Constipation – laxatives (avoid lactulose, causes bloating)
Diarrhoea – loperamide
Second-line – low-dose tricyclics
Psychological interventions – non-responsive after >12 months, CBT
Dietary advice – regular meals, drink lots of water, reduce alcohol/fizzy drink intake, limit processed foods
Which pathogens most commonly cause cellulitis?
Strep pyogenes (group A strep)
Staph aureus
How does cellulitis present?
Erythema, swelling, pain, discharge
Golden-yellow crust = staph aureus
May have bullae with more severe
Systemically unwell – fever, malaise, nausea
How is cellulitis diagnosed?
Clinical diagnosis for mild
Swabs for culture and sensitivities to guide antibiotic therapy
Bloods – FBC, CRP, LFTs, U+Es, blood cultures
More severe – imaging to look for underlying osteomyelitis/septic arthritis
How is cellulitis classified? What are the implications of the classification in terms of admission?
Eron classification
I – no systemic toxicity, no uncontrolled co-morbidities
II – systemically well or systemically well with co-morbidity (e.g. PVD)
III – significant systemic upset or unstable co-morbidity that may interfere with treatment response
IV – sepsis or severe life-threatening infection e.g. necrotising fasciitis
Admit for IV antibiotics if Eron III or IV, severe or rapidly deteriorating, young or old, immunocompromised, lymphoedema, facial or periorbital cellulitis
What is the empirical antibiotic treatment of choice for cellulitis?
Oral flucloxacillin
Penicillin allergic – oral clarithromycin, erythromycin (pregnancy) or doxycycline
If suspicion of MRSA – oral/IV vancomycin
If requiring IV – IV flucloxacillin, IV vancomycin
List the typical causative organisms of necrotising fasciitis
Type 1 (most common) – mixed aerobes and anaerobes
Type 2 – strep pyogenes
Describe the clinical presentation of necrotising fasciitis
Rapidly spreading wound infection causing skin and deeper soft tissue necrosis – crepitus/gas gangrene, bullae, necrosis are late signs
Acute onset
Pain, swelling, erythema at site
Pain ‘out of keeping’ with physical signs
Hypoaesthesia
Systemic upset, signs of haemodynamic upset – fever, tachycardia
Describe the assessment and management of necrotising fasciitis
ABG – raised lactate +/- metabolic acidosis
Signs of multi-organ dysfunction – renal failure, impaired liver function, raised glucose, coagulopathy
Blood cultures
Management:
A-E assessment
Resuscitation – IV fluids
Broad spectrum empirical IV antibiotics
- Flucloxacillin
- Benzylpenicillin
- Metronidazole
- Clindamycin
- Gentamicin
Urgent surgical debridement – may need later reconstructive surgery
What is the gold-standard investigation for varicose veins?
Duplex US to assess valve incompetence
List treatment options for varicose veins
Compression stockings – check ABPI for PVD
Venous ulceration – compression bandaging
Surgical management options:
Vein ligation, stripping and avulsion
Foam sclerotherapy
Thermal ablation
What are the potential complications for treatment of varicose veins?
Haemorrhage
Thrombophlebitis – foam/ablation
DVT
Disease recurrence
Nerve damage – saphenous or sural
How is lymphoedema managed?
Manual lymphatic drainage
Compression bandages
Exercises to improve drainage
Weight loss if overweight
Good skin care
What are anal fissures? How are they classified by duration? What are the risk factors for developing them?
Tears of the squamous lining of the distal anal canal
<6 weeks – acute
>6 weeks chronic
Risk factors
Constipation
IBD
STIs e.g. HIV, syphilis, herpes
How do anal fissures present?
Painful, bright red, rectal bleeding
90% on posterior midline – if alternative consider underlying pathology e.g. Crohn’s
How are anal fissures managed?
Acute
Soften stool – high-fibre diet, high fluid intake, bulk-forming laxatives
Lubricants before defection
Topical anaesthetics
Analgesia
Chronic
Continue as with acute
Topical GTN first-line
If ineffective after >8 weeks referral for sphincterotomy or botox injection
What are haemorrhoids? What are the risk factors for developing haemorrhoids?
Enlarged vascular cushions around the anus – present at 3, 7 and 11 o’clock
Risk factors:
Chronic constipation, straining when defecating
Pregnancy and vaginal birth
Obesity
Raised-intrabdominal pressure – weight-lifting, chronic cough
Low-fibre diet
Describe the clinical presentation of haemorrhoids and types of haemorrhoids.
Lump around anus, particularly when defecating
Painless, bright red bleeding on toilet paper or after opening bowels (not mixed with stool)
Sore/itchy anus
Types:
External – originate below dentate line, more prone to thrombosis
Internal – originate above dentate line
How are haemorrhoids managed?
Soften stool – diet and fluid intake
Topical local treatments – Anusol (astringent to shrink), lidocaine cream (germoloids), steroid-containing creams (short-term only)
Non-surgical treatments:
Rubber band ligation
Injection sclerotherapy
Infra-red coagulation
Bipolar diathermy
Surgical options:
Haemorrhoidal artery ligation
Haemorrhoidectomy – can result in faecal incontinence
How do thrombosed haemorrhoids present? How are they managed?
Acutely painful, purple, swollen lump around anus
If present <72 hours can have surgical management – excision
Otherwise – conservative management with stool softeners, analgesia, ice packs, usually resolve within 10 days
Describe the aetiology of anal cancers
Majority squamous cell carcinomas – below dentate line
Other 10% are adenocarcinomas from upper anal epithelial
Main risk factor is HPV, also HIV, age, smoking, Crohn’s, immunosuppression
Describe the clinical presentation of anal cancer
Pain
Bleeding
Discharge
Pruritus
Palpable mass
Infection/fistula in locally invasive disease
Sphincter involvement – incontinence, tenesmus
On examination – ulceration, wart-like lesions, mass on PR, inguinal lymphadenopathy
How is anal cancer diagnosed?
Proctoscopy to visualise
Examination under anaesthetic + biopsy
Staging:
USS-guided FNA of palpable LNs
CT CAP for mets
MRI pelvis for local invasion
How is anal cancer managed?
Chemo-radiotherapy for all except T1N0 – can use WLE
Surgical management for advanced disease if chemoradiotherapy failed:
Mostly abdominoperineal resection – left with colostomy
Describe the aetiology of ano-rectal abscesses and their classification
Caused by plugging of anal ducts which drain anal glands
Organisms – E. coli, bacteroides, enterococcus
Classified by position as – perianal, ischioanal, pelvirectal intersphincteric
How do ano-rectal abscesses present?
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
How are ano-rectal abscesses managed?
Antibiotics, analgesia
Examination under anaesthesia and incision and drainage – left to heal by secondary intention
Intra-operative proctoscopy to check for fistula
What is a fistula-in-ano? Describe the aetiology and risk factors.
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
How does a fistula-in-ano present? How is it investigated?
Recurrent perianal abscess
Intermittent/continuous discharge – blood, mucus, faeces, pus
Can see or feel tract on examination
Investigation – MRI to visualise anatomy of tract
How are fistulas-in-ano managed?
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
What is Goodsall’s rule?
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
List causes of adrenal insufficiency
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
Describe the clinical presentation of adrenal insufficiency and the investigation findings
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
How is adrenal insufficiency managed?
Replacement steroids – hydrocortisone (glucocorticoid replacement), fludrocortisone (mineralocorticoid replacement)
Steroid card and emergency ID tag – can’t stop suddenly
Hydrocortisone doses doubled during acute illness
How does an adrenal crisis present? How is it managed?
Reduced consciousness
Hypotension
Hypoglycaemia, hyponatraemia, hyperkalaemia
Very unwell!
Management
IV hydrocortisone – must replace first
IV fluid resuscitation
Correct hypoglycaemia
Monitor and correct electrolytes
Define postural hypotension
Sustained reduction in systolic of 20mmHg or more and/or diastolic of 10mmHg within 3 minutes of standing
List causes of postural hypotension
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)
How is postural hypotension managed?
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
List the most common causes of gastroenteritis
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
Describe the typical causes of gastroenteritis by bacterial pathogen
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
Describe management of gastroenteritis
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
Describe the pathophysiology and manifestations of diverticular disease
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
Describe the clinical presentation of diverticular disease and acute diverticulitis
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
How is diverticular disease/diverticulitis diagnosed?
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
How is diverticular disease managed?
Simple analgesia
Fluid/fibre intake
Laxatives – bulk forming (ispagula husk), avoid stimulants
Mild diverticulitis – oral antibiotics
If recurrent acute diverticulitis may need resection
How is acute diverticulitis managed?
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)
Describe the aetiology and risk factors for colorectal cancer
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%
Describe the genetic syndromes associated with colorectal cancer
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
Describe the presentation of and referral criteria for colorectal cancer
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
Describe the screening programme for colorectal cancer
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
How is colorectal cancer diagnosed?
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
Describe the staging of colorectal cancer
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
How is colorectal cancer managed?
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
Presentation of gastric volvulus
Vomiting
Epigastric pain
Failure to pass NG tube
Describe the cause of bowel obstruction
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
How do bowel obstructions present?
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
How is bowel obstruction investigated?
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
How is acute bowel obstruction managed?
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
What are the potential complications of acute bowel obstruction?
Bowel ischaemia
Bowel perforation – peritonitis – sepsis
Hypovolaemic shock leading to AKI etc.
Describe the clinical features and consequences of malabsorption
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)
What are the most common causes of malabsorption?
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
List the major classes of laxatives, describe their mechanism of action and give examples
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)
List the types of hernias and the epidemiology of each
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
Define hernia and list terms used to describe the characteristics of hernias
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
Describe the anatomy of inguinal hernias and how direct and indirect can be differentiated
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)
Describe the clinical presentation of an inguinal hernia
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
How are inguinal hernias managed?
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
What are the major complications of hernias?
Incarceration
Strangulation – bowel ischaemia and necrosis
Obstruction
Describe the anatomy and presentation of femoral hernias
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)
How are femoral hernias managed?
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
Describe the clinical presentation of obturator hernias and how they are managed
> 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
Describe the anatomy and presentation of a Richter’s hernia
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
Describe the differential diagnosis for abdominal masses by location
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
Describe the differential diagnosis for generalised and localised abdominal pain
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
Describe the differential diagnosis for abdominal distension
Fat – obesity
Flatus – intestinal obstruction
Fetus – pregnancy
Fluid – ascites, distended bladder
Faeces – constipation, faecal impaction
Tumour
Organomegaly
Describe the presentation, investigation, and management of breast cysts
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
Describe the presentation and management of fibrocystic breast changes
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
Describe the aetiology, presentation, and management of mastitis/breast abscesses
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
Describe the aetiology and presentation of breast fibroadenomas
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
How are fibroadenomas managed? Describe their prognosis.
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
Describe the aetiology, presentation, diagnosis and management of traumatic fat necrosis of the breast
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
Describe the differential diagnosis for breast pain
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
Describe the aetiology, presentation, diagnosis, and management of mammary duct ectasia
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
Describe the aetiology, presentation, investigation and management of duct papillomas
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
What is the differential diagnosis for galactorrhoea? How is galactorrhoea diagnosed and managed?
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
Describe the causes of gynaecomastia
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
Describe the histological types and epidemiology of breast cancer and pre-cancerous conditions
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
List the risk factors for breast cancer
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
Describe the investigation, management and prognosis of breast carcinoma in situ
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
Describe the clinical presentation of invasive breast cancer
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
Criteria for 2ww referral for breast cancer
=>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
How are breast lumps assessed?
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
Describe screening for breast cancer
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
Describe the investigation of breast cancer
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
List the options for management of breast cancer and describe when each may be appropriate
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
What are the potential complications of breast cancer and treatment of cancer?
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
Describe the mechanism of action of hormonal therapies used in breast cancer
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
Describe the diagnosis of asthma
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
Describe the management of asthma in adults
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
Describe the aetiology and presentation of COPD
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
How is COPD diagnosed and the severity categorised?
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
Describe the long-term management of COPD
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!!)
Describe the aetiology and clinical presentation of acute exacerbations of COPD
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
How are acute exacerbations of COPD managed?
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
Describe the clinical presentation and diagnosis of idiopathic pulmonary fibrosis
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
Describe the causes of pulmonary fibrosis
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
Describe the causes of bronchiectasis
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
Describe the clinical presentation of bronchiectasis
Chronic cough with large volume sputum production
Haemoptysis
Dyspnoea
Course creps
Rhonchi
High-pitched inspiratory squeaks and pops
How is bronchiectasis managed?
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
Describe the clinical presentation of tuberculosis infection
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
How is tuberculosis diagnosed?
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
Describe treatment of tuberculosis
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
Describe the mechanism of action and side effects of drugs used for management of tuberculosis
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
Describe the aetiology and clinical presentation of pneumonia
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
How is hospital acquired pneumonia defined?
Develops >48 hours since admission
How is pneumonia assessed?
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)
List atypical causes of pneumonia and their defining features
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)
How is pneumonia managed?
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
List causes of anaemia
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
Describe the presentation of anaemia
Dyspnoea
Tiredness
Headaches
Dizziness
Pallor
Tachycardia
Koilonychia
Angular chelitis
Atrophic glossitis
Brittle hair and nails
How is iron deficiency anaemia managed?
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)
List causes of thrombocytopaenia
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
Describe the pathophysiology and consequences of heparin-induced thrombocytopaenia
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
List causes of haemolytic anaemia
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
Describe the clinical consequences of thalassaemias
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)
How does hereditary spherocytosis present? How is it managed?
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)
Describe the aetiology and presentation of urinary tract infections
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
How are UTIs managed?
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
Describe aetiology and presentation of bladder cancer
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
2ww referral for bladder cancer
Over 45 with unexplained visible haematuria, without UTI or persisting after treatment for UTI
Over 60 with microscopic haematuria plus dysuria or raised WCC
How is bladder cancer diagnosed and managed?
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
List the types of renal stones and their aetiology and features
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
Describe the presentation of renal stones
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
How are renal stones investigated and managed?
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
What causes non-gonococcal urethritis? How is it managed?
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
Describe the aetiology and presentation of post-streptococcal glomerulonephritis
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
Describe the histological features of membraneous glomerulonephritis.
How is membraneous glomerulonephritis managed? Describe the prognosis.
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
Describe the aetiology and presentation of Goodpasture’s syndrome
Anti-GBM antibodies attack glomerulus and pulmonary basement membranes
Causes glomerulonephritis and pulmonary haemorrhage – AKI and haemoptysis classically
Describe the aetiology and histological appearance of rapidly progressive glomerulonephritis
Rapid loss of renal function
Cause – secondary to Goodpasture’s syndrome, Wegner’s granulomatosis, SLE
Red cell casts in urine
Histology - crescenteric glomerulonephritis
Describe the causes of oliguria
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)
Describe the aetiology and presentation of epididymo-orchitis
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
How is epididymo-orchitis diagnosed and managed?
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
Describe diagnosis of HIV
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
Describe the prophylaxis available to reduce risk of HIV infection
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
List the most common causes of erectile dysfunction
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)
Describe the assessment and management of erectile dysfunction and contraindications to management
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
Describe the aetiology, presentation and management of a hydrocoele
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
Describe the types of testicular tumours and their epidemiology
Pre-pubertal – yolk-sac, teratoma
Older – lymphoma, seminomas
Risk factors – cryptorchidism, infertility, Klinefelter’s, mumps orchitis, FHx
Describe the presentation, assessment, and management of testicular tumours
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
Describe the aetiology and presentation of benign prostatic hyperplasia
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
How is benign prostatic hypertrophy assessed and managed?
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)
How is acute urinary retention managed?
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
Describe the aetiology and presentation of prostate cancer
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
Describe diagnosis and management of prostate cancer
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
Describe the aetiology, presentation and clinical consequences of polycystic kidney disease
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
Describe diagnosis and management of polycystic kidney disease
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
List options for renal replacement therapy
Haemodialysis – via AV fistula or central venous catheter (tunnelled or non-tunnelled)
Peritoneal dialysis – continuous ambulatory or automated
Renal transplant
List potential complications of renal replacement therapy
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
Describe the aetiology and presentation of gastro-oesophageal reflux disease
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
How is gastro-oesophageal reflux disease assessed and managed?
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
Describe management of peptic ulcer disease
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
Describe the aetiology and presentation oesophageal varices
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
Describe the management of oesophageal varices
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
Describe the aetiology, presentation, clinical consequences, prevention and treatment of viral hepatitis
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%
List signs, investigation findings and potential complications of cirrhosis
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
Describe management of cirrhosis and its complications
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
Describe the scoring systems used in liver cirrhosis
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
Describe the genetic basis of Huntington’s disease
Autosomal dominant, displays genetic anticipation (successive generations have earlier age of onset and more severe disease)
Trinucleotide repeat of HTT gene on chromosome 4
Describe the management of alcohol withdrawal
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
Describe presentation of inflammatory bowel disease and compare histological features in Crohn’s and UC
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
How is inflammatory bowel disease diagnosed?
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
List common extra-intestinal features of IBD
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
Describe management of Crohn’s disease
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
Describe management of ulcerative colitis
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)
How are UC flares graded in terms of severity?
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
Describe the aetiology of acute pancreatitis
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
Describe the clinical presentation and diagnosis of acute pancreatitis
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
How is acute pancreatitis managed?
Supportive management:
IVF
Analgesia
Anti-emetics
NBM
Treat cause e.g., gallstones (ERCP)
Treat complications – drainage of collections etc.
Describe the aetiology and clinical presentation of chronic pancreatitis
Aetiology – mostly alcohol, also genetic (CF, haemochromatosis), ductal obstruction (tumours, stones)
Pain – worse following meal
Exocrine dysfunction – steatorrhoea
Endocrine dysfunction – diabetes mellitus
Describe diagnosis and management of chronic pancreatitis
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
What is the differential diagnosis for jaundice?
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
How to interpret LFTs
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
Describe the aetiology and presentation of gallstones and the complications of gallstones
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
Describe the diagnosis and management of biliary disease
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
Describe the presentation of peripheral arterial disease
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
How is peripheral vascular disease diagnosed and managed?
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
Describe the presentation of acute limb ischaemia
Pain
Pallor
Pulselessness
Paraesthesia
Perishingly cold
Paralysis
What are the potential complications of acute limb ischaemia?
Irreversible limb ischaemia requiring amputation
20% mortality rate
Reperfusion injury – compartment syndrome, AKI (due to hyperkalaemia, acidosis, myoglobinaemia)
Describe the aetiology, presentation, diagnosis and management of melanoma
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
List common drugs which cause skin reactions and describe these reactions
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
Describe the presentation and types of psoriasis
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
How is psoriasis managed?
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
How is acne vulgaris managed?
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
Describe the presentation and management of rosacea
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
Describe the presentation of skin squamous cell carcinomas and their precancerous forms
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
How is SCC diagnosed and managed?
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
How are precancerous skin lesions managed?
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
Describe the presentation, diagnosis, and management of basal cell carcinomas
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
Describe the criteria for diagnosis of type 2 diabetes
HbA1c >48
Fasting glucose >7
Random glucose >11
OGTT 2 hour >11
Describe the strategy for management of type 2 diabetes
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
Describe the mechanism of action, side effects and contraindications of metformin
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
Describe the mechanism of action and side effects of SGLT2 inhibitors and give examples
-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
Describe the mechanism of action and side effects of pioglitazone
Thiazolidinedione
MOA – increases insulin sensitivity, decreases gluconeogenesis
Side effects – fluid retention, anaemia, heart failure, increase risk bladder cancer
Weight gain
Low risk hypoglycaemia
Describe the mechanism of action and side effects of DPP-4 inhibitors and give examples
-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
Describe the mechanism of action and side effects of GLP-1 mimetics and give examples
-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
Describe the mechanism of action and side effects of sulfonylureas and give examples
Gliclazide
Increase insulin secretion
Side effects – increased risk CVD
Weight gain
Hypoglycaemia risk
Describe the advantages and disadvantages of insulin-therapy in management of type 2 diabetes
Risk of hypoglycaemia
Causes weight gain
Subcutaneous administration
What is Zieve syndrome?
Coombs negative haemolysis, cholestatic jaundice, transient hyperlipidaemia associated with heavy alcohol use, typically following a binge
