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 types of testicular tumours and their epidemiology
Pre-pubertal – yolk-sac, teratoma
Older – lymphoma, seminomas
Risk factors – cryptorchidism, infertility, Klinefelter’s, mumps orchitis, FHx
