Surg Flashcards
Q: What is Tamoxifen and its mechanism of action?
Selective oEstrogen Receptor Modulator (SERM)
Acts as an oestrogen receptor antagonist and partial agonist
Used for oestrogen receptor-positive breast cancer
Q: What are the adverse effects of Tamoxifen?
Menstrual disturbance: vaginal bleeding, amenorrhoea
Hot flushes (3% stop due to climacteric side effects)
Venous thromboembolism
Endometrial cancer
Q: What are Anastrozole and Letrozole, and how do they work?
Aromatase inhibitors
Reduce peripheral oestrogen synthesis
Important for postmenopausal women as aromatisation is the main source of oestrogen
Used for ER-positive breast cancer in postmenopausal women
Q: What are the adverse effects of aromatase inhibitors?
Osteoporosis
Hot flushes
Arthralgia, myalgia
Insomnia
Q: What does NICE recommend when starting a patient on aromatase inhibitors?
Perform a DEXA scan to assess bone density
Q: What are the features and treatment for Fibroadenoma?
Develops from a whole lobule
Mobile, firm breast lumps
12% of all breast masses
Over 2 years, up to 30% may get smaller
No increase in risk of malignancy
If >3cm, surgical excision is usual
Phyllodes tumours should be widely excised (mastectomy if large)
Q: What are the features and treatment for Breast Cyst?
7% of all Western females present with a breast cyst
Smooth, discrete lump (may be fluctuant)
Small increased risk of breast cancer (especially in younger women)
Cysts should be aspirated
Blood-stained or persistently refilling cysts should be biopsied or excised
Q: What are the features and treatment for Sclerosing Adenosis?
Presents as a breast lump or pain
Causes mammographic changes mimicking carcinoma
Distorts the distal lobular unit without hyperplasia (complex lesions show hyperplasia)
Considered a disorder of involution
No increased risk of malignancy
Biopsy of lesions is recommended; excision not mandatory
Q: What are the features and treatment for Epithelial Hyperplasia?
Variable clinical presentation: from generalized lumpiness to discrete lump
Increased cellularity of the terminal lobular unit; atypical features may be present
Atypical features and family history of breast cancer greatly increase malignancy risk
If no atypical features, conservative management
With atypical features, either close monitoring or surgical resection
Q: What are the features and treatment for Fat Necrosis?
Up to 40% of cases have a traumatic aetiology
Physical features mimic carcinoma
Mass may initially increase in size
Diagnosis by imaging and core biopsy
Q: What are the features and treatment for Duct Papilloma?
Usually presents with nipple discharge
Large papillomas may present with a mass
Discharge originates from a single duct
No increased risk of malignancy
Treatment: Microdochectomy
Q: What is the most common type of breast cancer, and what may it arise from?
Invasive ductal carcinoma
May arise from ductal carcinoma in situ (DCIS)
Q: What factors are involved in the pathological assessment of breast cancer?
Tumour assessment
Lymph node assessment
Sentinel lymph node biopsy to minimize morbidity of axillary dissection
Q: What surgical options are available for breast cancer treatment?
Wide local excision
Mastectomy
Q: What factors influence the choice between mastectomy and wide local excision?
Mastectomy is preferred for multifocal tumours, central tumours, and large lesions in small breasts
Wide local excision is preferred for solitary lesions, peripheral tumours, and small lesions in large breasts
DCIS >4cm tends to require mastectomy, whereas DCIS <4cm may be treated with wide local excision
Patient choice
Q: When is surgery generally offered for breast cancer?
The vast majority of patients diagnosed with breast cancer
Exception: Very frail, elderly patients with metastatic disease (managed with hormonal therapy)
Q: How is axillary lymphadenopathy managed prior to breast cancer surgery?
No palpable axillary lymphadenopathy:
Pre-operative axillary ultrasound
If negative → sentinel node biopsy
Clinically palpable lymphadenopathy:
Axillary node clearance at primary surgery
May lead to arm lymphedema and functional impairment
Q: What are the surgical options for breast cancer and their indications?
Mastectomy:
Multifocal tumour
Central tumour
Large lesion in a small breast
DCIS >4cm
Wide Local Excision:
Solitary lesion
Peripheral tumour
Small lesion in a large breast
DCIS <4cm
Q: When is radiotherapy recommended for breast cancer?
After wide-local excision to reduce recurrence risk (~two-thirds reduction)
After mastectomy for:
T3-T4 tumours
Four or more positive axillary nodes
Q: When is hormonal therapy used in breast cancer treatment?
Offered if tumours are hormone receptor-positive
Tamoxifen:
Used for pre- and peri-menopausal women
Aromatase inhibitors (e.g., Anastrozole):
Used for postmenopausal women
Targets peripheral oestrogen synthesis
Q: What is the most common biological therapy used for breast cancer, and when is it effective?
Trastuzumab (Herceptin)
Effective only in 20-25% of HER2-positive tumours
Q: What are the NICE referral guidelines for suspected breast cancer for a 2-week pathway referral?
Age ≥30 with an unexplained breast lump (with or without pain)
Age ≥50 with any of the following symptoms in one nipple only:
Discharge
Retraction
Other concerning changes
Q: When should a suspected cancer referral be considered for breast cancer?
Skin changes suggesting breast cancer
Age ≥30 with an unexplained lump in the axilla
Q: When is a non-urgent referral recommended for suspected breast cancer?
Age <30 with an unexplained breast lump (with or without pain)
Q: What are the predisposing factors for breast cancer?
BRCA1 and BRCA2 genes (40% lifetime risk of breast/ovarian cancer)
1st-degree relative with premenopausal breast cancer (e.g., mother)
Nulliparity or first pregnancy >30 years (twice the risk compared to women having first child <25 years)
Early menarche and late menopause
Combined hormone replacement therapy (relative risk increases by 1.023 per year of use)
Combined oral contraceptive use
Previous breast cancer
Not breastfeeding
Ionising radiation
p53 gene mutations
Obesity
Previous surgery for benign breast disease (possible more follow-up needed as scar may hide lumps)
Q: What is the NHS Breast Screening Programme and who is it offered to?
Offered to women aged 50-70 years
Mammogram every 3 years
Women >70 years can still have mammograms but must arrange their own appointments
Q: What are the common types of breast cancer?
Invasive ductal carcinoma (No Special Type - NST) (most common)
Invasive lobular carcinoma
Ductal carcinoma-in-situ (DCIS)
Lobular carcinoma-in-situ (LCIS)
Q: What is Paget’s disease of the nipple and its association with breast cancer?
Eczematoid nipple change linked with breast malignancy
Present in 1-2% of breast cancer cases
50% associated with an underlying mass lesion, with 90% being invasive carcinoma
30% without a mass still have underlying carcinoma
Q: What is inflammatory breast cancer?
Cancer cells block lymphatic drainage
Causes inflamed breast appearance
Rare, around 1 in 10,000 cases
Q: What are the features of fibroadenoma?
Common in women under 30 years
Discrete, non-tender, highly mobile lumps (“breast mice”)
Q: What are the features of fibroadenosis (fibrocystic disease)?
Common in middle-aged women
“Lumpy” breasts, possibly painful
Symptoms may worsen before menstruation
Q: What are the typical features of breast cancer?
Hard, irregular lump
Possible nipple inversion
Skin tethering
Q: What is Paget’s disease of the breast?
Intraductal carcinoma
Reddening and thickening of the nipple/areola
May resemble eczematous changes
Q: What is mammary duct ectasia?
Dilatation of large breast ducts
Most common around menopause
Tender lump around the areola
Green nipple discharge
If ruptured, may cause local inflammation (“plasma cell mastitis”)
Q: What is a duct papilloma?
Local epithelial proliferation in large mammary ducts
Hyperplastic, not malignant or premalignant
May present with blood-stained discharge
Q: What are the features of fat necrosis?
More common in obese women with large breasts
Often follows minor or unnoticed trauma
Initial inflammatory response
Firm, round lump that may become hard and irregular
Can mimic breast cancer, requiring investigation
Q: What are the features of a breast abscess?
More common in lactating women
Red, hot, tender swelling
Q: What other benign lesions may develop in the breast?
Lipomas
Sebaceous cysts
Q: What is a fibroadenoma?
Develops from a whole lobule
Mobile, firm, smooth breast lump (“breast mouse”)
Represents 12% of all breast masses
Q: Does fibroadenoma increase the risk of malignancy?
No increase in risk of malignancy
Q: When is surgical excision recommended for a fibroadenoma?
If the fibroadenoma is >3cm
Q: What is cyclical mastalgia?
A common cause of breast pain in younger females
Varies in intensity with the menstrual cycle
Q: What are the clinical features of cyclical mastalgia?
Not usually associated with point tenderness of the chest wall (more likely to be Tietze’s syndrome)
Pain intensity varies according to the menstrual cycle
Examination focuses on identifying focal lesions (e.g., cysts)
Q: What is the management for cyclical mastalgia?
Wear a supportive bra
Conservative treatments: oral and topical analgesia
Flaxseed oil and evening primrose oil are sometimes used but not recommended
If no improvement after 3 months and pain affects quality of life, consider referral
Q: What hormonal agents may be used for cyclical mastalgia?
Bromocriptine
Danazol
However, many women discontinue due to adverse effects
Q: What is duct ectasia?
Dilatation and shortening of the terminal breast ducts within 3cm of the nipple
Common, with incidence increasing with age
Q: What are the typical features of duct ectasia?
Nipple retraction
Occasionally creamy nipple discharge
Q: How can duct ectasia be confused with another condition?
It may be confused with periductal mastitis, which presents in younger women, particularly smokers
Periductal mastitis typically involves periareolar or subareolar infections and may be recurrent
Q: What treatment options are available for patients with troublesome nipple discharge due to duct ectasia?
Microdochectomy (if young)
Total duct excision (if older)
Q: What is mastitis?
Inflammation of the breast tissue
Typically associated with breastfeeding, affecting around 1 in 10 women
Q: What are the features of mastitis?
Painful, tender, red hot breast
Fever and general malaise may be present
Q: What is the first-line management of mastitis?
Continue breastfeeding
Simple measures: analgesia, warm compresses
Q: When should mastitis be treated with antibiotics?
If the patient is systemically unwell
If there is a nipple fissure
If symptoms don’t improve after 12-24 hours of effective milk removal
If culture indicates infection
Q: What is the first-line antibiotic for mastitis?
Oral flucloxacillin for 10-14 days
Q: What is the most common organism causing infective mastitis?
Staphylococcus aureus
Q: What should continue during antibiotic treatment for mastitis?
Breastfeeding or expressing
Q: What can happen if mastitis is left untreated?
It may develop into a breast abscess, which requires incision and drainage
Q: What are the common causes of nipple discharge?
Physiological: During breastfeeding
Galactorrhoea: Commonly caused by emotional events or drugs (e.g. histamine receptor antagonists)
Hyperprolactinaemia: Often caused by pituitary tumours (microadenomas or macroadenomas)
Mammary duct ectasia: Most common in menopausal women, typically results in thick, green discharge, more common in smokers
Carcinoma: Often blood-stained, may present with an underlying mass or axillary lymphadenopathy
Intraductal papilloma: More common in younger patients, may cause blood-stained discharge without a palpable lump
Q: How is nipple discharge assessed?
Examine the breast to determine if there is a mass lesion
All mass lesions should undergo Triple assessment
Q: How are investigations for nipple discharge reported?
M for mammography followed by a numerical code:
1: No abnormality
2: Abnormality with benign features
3: Indeterminate, probably benign
4: Indeterminate, probably malignant
5: Malignant
Q: What is the management of non-malignant nipple discharge?
Exclude endocrine disease
Nipple cytology is unhelpful
Advise smoking cessation for duct ectasia
Total duct excision may be required for severe symptoms of duct ectasia
Q: What is mammary duct ectasia?
A common condition in up to 25% of normal female breasts
Typically presents with nipple discharge, often thick and green
More common in women over 50
Not the same as periductal mastitis
A normal variant of breast involution
Q: What is periductal mastitis?
Occurs at a younger age than duct ectasia
May present with inflammation, abscess, or mammary duct fistula
Strongly associated with smoking
Treatment typically involves antibiotics, with abscesses requiring drainage
Q: What is an intraductal papilloma?
A growth of papilloma in a single duct
Usually presents with clear or blood-stained discharge originating from a single duct
Does not increase the risk of malignancy
Q: How is a breast abscess treated?
Commonly associated with lactational mastitis, usually caused by Staphylococcus aureus
Treatment involves antibiotics and ultrasound-guided aspiration
Overlying skin necrosis may require surgical debridement
A mammary duct fistula may develop as a complication
Q: What is tuberculosis of the breast?
Rare in Western countries, usually secondary to tuberculosis
Affects women later in childbearing years
Chronic breast or axillary sinus may be present in up to 50% of cases
Diagnosis is made by biopsy, culture, and histology
Q: What is Paget’s disease of the nipple?
An eczematoid change of the nipple associated with an underlying breast malignancy
Present in 1-2% of patients with breast cancer
In half of these patients, it is associated with an underlying mass lesion
90% of patients with a mass lesion will have invasive carcinoma
30% of patients without a mass lesion will have underlying carcinoma
The remainder will have carcinoma in situ
Differs from eczema of the nipple as it primarily involves the nipple before spreading to the areola
Q: How is Paget’s disease of the nipple diagnosed?
Diagnosis is made by punch biopsy
Mammography and ultrasound of the breast are also used
Q: What is the treatment for Paget’s disease of the nipple?
Treatment depends on the underlying lesion (e.g., surgery for carcinoma)
Q: What are the main types of stomas?
Ileostomy:
Location: Right iliac fossa
Appearance: Spouted
Output: Liquid
Colostomy:
Location: Varies, more likely on the left side of the abdomen
Appearance: Flushed
Output: Solid
Q: What is the typical cause of acute mesenteric ischaemia?
An embolism causing occlusion of an artery supplying the small bowel, often the superior mesenteric artery
Commonly associated with atrial fibrillation
Q: What are the clinical features of acute mesenteric ischaemia?
Severe, sudden onset abdominal pain
Pain out of proportion to physical exam findings
Q: How is acute mesenteric ischaemia managed?
Immediate laparotomy, especially if signs of advanced ischemia (e.g., peritonitis or sepsis) are present
Poor prognosis if surgery is delayed
Q: What is the most common type of anal cancer?
Squamous cell carcinoma (SCC) (80% of cases)
Other types include melanomas, lymphomas, and adenocarcinomas
Q: What are the risk factors for anal cancer?
HPV infection (HPV16 or HPV18 subtypes)
Anal intercourse and a high lifetime number of sexual partners
Men who have sex with men
HIV infection and immunosuppressive medications
Women with a history of cervical cancer or cervical intraepithelial neoplasia (CIN)
Smoking
Q: What are the common clinical features of anal cancer?
Perianal pain and bleeding
A palpable lesion
Faecal incontinence
Rectovaginal fistula in neglected female cases
Q: What investigations are used for anal cancer?
Digital rectal examination and anoscopy with biopsy
Imaging (CT, MRI, endo-anal ultrasound, PET)
HIV testing
Q: What is an anal fissure?
A longitudinal or elliptical tear in the squamous lining of the distal anal canal.
Acute if present for less than 6 weeks, chronic if present for more than 6 weeks.
Q: What are the risk factors for anal fissures?
Constipation
Inflammatory bowel disease
Sexually transmitted infections (e.g., HIV, syphilis, herpes)
Q: What are the typical features of an anal fissure?
Painful, bright red rectal bleeding
90% occur on the posterior midline
If located elsewhere, consider underlying causes like Crohn’s disease
Q: What is the management for an acute anal fissure (< 1 week)?
Soften stool with a high-fiber diet and plenty of fluids
First-line: bulk-forming laxatives (lactulose if not tolerated)
Lubricants such as petroleum jelly before defecation
Topical anaesthetics and analgesia
Q: What is the management for a chronic anal fissure?
Continue above techniques
First-line treatment: topical glyceryl trinitrate (GTN)
If ineffective after 8 weeks, consider referral for surgery (sphincterotomy) or botulinum toxin
Q: What are haemorrhoids and their treatment options?
Location: 3, 7, 11 o’clock positions
Internal or external
Treatment:
Conservative
Rubber band ligation
Haemorrhoidectomy
Q: What are the features of an anal fissure?
Presents with painful rectal bleeding
Location: midline (posterior midline 90%) & 12 o’clock position, distal to the dentate line
Chronic fissure (> 6 weeks) presents with:
Ulcer
Sentinel pile
Enlarged anal papillae
Q: What are the causes of proctitis?
Crohn’s disease
Ulcerative colitis
Clostridioides difficile
Q: What are the types of anorectal abscesses and their common organisms?
Common organisms: E. coli, Staph aureus
Positions:
Perianal
Ischiorectal
Pelvirectal
Intersphincteric
Q: What is an anal fistula and its common cause?
Usually results from a previous anorectal abscess
Types:
Intersphincteric
Transsphincteric
Suprasphincteric
Extrasphincteric
Goodsall’s rule helps determine the location
Q: What is rectal prolapse and its association with childbirth?
Associated with childbirth and rectal intussusception
May be internal or external
Q: What is pruritus ani and its causes?
Extremely common
In children: often related to worms
In adults: may be idiopathic or associated with conditions like haemorrhoids
Q: What is an anal neoplasm and its common type?
Squamous cell carcinoma is the most common
Unlike adenocarcinoma in the rectum
Q: What is a solitary rectal ulcer and its association?
Associated with chronic straining and constipation
Histology: mucosal thickening, lamina propria replaced with collagen and smooth muscle (fibromuscular obliteration)
Q: What are the common presenting features of colorectal cancer?
Change in bowel habits (e.g., constipation, diarrhoea, alternating between both, frequent bowel movements)
Rectal bleeding (bright red or melena)
Abdominal pain and discomfort (due to tumour obstruction or inflammation)
Unexplained weight loss (sign of advanced disease)
Anaemia (fatigue, weakness, shortness of breath due to chronic bleeding)
Bowel obstruction (severe abdominal pain, nausea, vomiting in advanced cases)
Q: What are the staging requirements for newly diagnosed colorectal cancer?
Carcinoembryonic antigen (CEA) test
CT of the chest, abdomen, and pelvis
Full colon evaluation with colonoscopy or CT colonography
MRI of the mesorectum for tumours below the peritoneal reflection
Q: What are the general surgical management options for colonic cancer?
Resectional surgery is the primary treatment for colon cancer
Anastomosis following resection (depends on blood supply, mucosal apposition, and no tissue tension)
Obstruction management: stenting or resection (avoiding defunctioning stomas in modern practice)
Q: What are the surgical options for different locations of colon cancer?
Caecal, ascending, or proximal transverse colon: Right hemicolectomy (Ileo-colic anastomosis)
Distal transverse, descending colon: Left hemicolectomy (Colo-colon anastomosis)
Sigmoid colon: High anterior resection (Colo-rectal anastomosis)
Upper rectum: Anterior resection (TME) (Colo-rectal anastomosis)
Low rectum: Anterior resection (Low TME) (Colo-rectal anastomosis with optional defunctioning stoma)
Anal verge: Abdomino-perineal excision of rectum (no anastomosis)
Q: What is the management for emergency colorectal cancer surgery?
Emergency resections often lead to an end colostomy due to high risk of anastomosis failure, especially with perforation
Hartmann’s procedure: sigmoid colon resection with an end colostomy, which may be reversed later
Ileo-colic anastomoses are safer in the emergency setting and typically do not require defunctioning stomas
Q: What are the NICE referral guidelines for colorectal cancer in 2023?
Use of Faecal Immunochemical Test (FIT) for referral in these cases:
Abdominal mass
Change in bowel habit
Iron-deficiency anaemia
Age 40+ with unexplained weight loss and abdominal pain
Age <50 with rectal bleeding and unexplained symptoms (abdominal pain, weight loss)
Age 50+ with unexplained rectal bleeding, abdominal pain, or weight loss
Age 60+ with anaemia, even without iron deficiency
Q: What should be done if the FIT test result is positive?
Referral should be made through the suspected cancer pathway
Q: What should be done if the FIT test result is negative?
Safety netting is recommended
If ongoing concern (e.g., abdominal mass), refer on the suspected cancer pathway
Continued investigation is crucial to reach a definitive diagnosis
Q: Who is eligible for NHS screening for colorectal cancer?
Ages 60-74 (England) or 50-74 (Scotland) are routinely screened every 2 years
Individuals aged over 74 can request screening
Eligible individuals receive FIT tests via post
Q: How does the NHS screening programme work?
The FIT test detects human haemoglobin in stool to check for occult blood
Abnormal results lead to an offer of colonoscopy
Q: When is the FIT test recommended for patients outside the 2-week referral criteria?
Patients ≥ 50 with unexplained abdominal pain or weight loss
Patients < 60 with changes in bowel habit or iron deficiency anaemia
Patients ≥ 60 with anaemia, even without iron deficiency
Q: What is the role of colorectal cancer screening?
Screening for colorectal cancer can reduce mortality by 16%.
Most cancers develop from adenomatous polyps, which can be detected early through screening.
Q: What is diverticular disease?
Diverticular disease involves the herniation of colonic mucosa through the muscular wall of the colon.
The usual site is between the taenia coli, where vessels pierce the muscle to supply the mucosa, sparing the rectum (which lacks taenia).
Q: What are the symptoms of diverticular disease?
Altered bowel habit
Rectal bleeding
Abdominal pain
Q: What are the complications of diverticular disease?
Diverticulitis
Haemorrhage
Fistula development
Perforation and faecal peritonitis
Abscess formation
Diverticular phlegmon
Q: How is diverticular disease diagnosed?
Colonoscopy, CT cologram, or barium enema can identify diverticular disease.
In acutely unwell patients, plain abdominal films and an erect chest x-ray help identify perforation.
Abdominal CT scan with oral and intravenous contrast is used to identify acute inflammation and local complications like abscess formation.
Q: What are the treatment options for diverticular disease?
Increase dietary fibre intake
Mild diverticulitis: Managed conservatively with antibiotics.
Peri-colonic abscesses: Should be drained surgically or radiologically.
Recurrent episodes requiring hospitalization: Segmental resection may be needed.
Hinchey IV perforations (faecal peritonitis): Require resection and stoma, with a high risk of post-operative complications and HDU admission.
Less severe perforations: Managed by laparoscopic washout and drain insertion.
Q: What is diverticulitis?
Diverticulitis is the infection of a diverticulum, an out-pouching of the intestinal mucosa.
The presence of diverticula is referred to as diverticulosis, and when these cause symptoms, it is called diverticular disease.
Diverticula are usually found in the sigmoid colon, though in Asian patients, they may be found in the right colon.
Q: What are the risk factors for diverticulitis?
Age
Lack of dietary fibre
Obesity, especially in younger patients
Sedentary lifestyle
Q: What are the symptoms of diverticular disease?
Intermittent abdominal pain, particularly in the left lower quadrant
Bloating
Change in bowel habit: constipation or diarrhoea
Q: What are the symptoms of acute diverticulitis?
Severe abdominal pain in the left lower quadrant (right lower quadrant in some Asian patients)
Nausea and vomiting (20-60%) due to ileus or complicated diverticulitis
Change in bowel habit: constipation (50%) or diarrhoea (25%)
Urinary frequency, urgency or dysuria (10-15%) due to bladder irritation
PR bleeding
Complications:
Pneumaturia or faecaluria (suggests colovesical fistula)
Vaginal passage of faeces or flatus (suggests colovaginal fistula)
Q: What are the signs of diverticulitis?
Low-grade pyrexia
Tachycardia
Tender left iliac fossa (LIF)
Palpable mass (in 20% of cases, due to inflammation or abscess)
Reduced bowel sounds
Guarding, rigidity, and rebound tenderness (suggests complicated diverticulitis with perforation)
Q: What investigations are used for diverticulitis?
FBC: Raised WCC
CRP: Raised
Erect CXR: May show pneumoperitoneum in cases of perforation
AXR: May show dilated bowel loops, obstruction, or abscesses
CT: Best modality to identify abscesses
Colonoscopy: Should be avoided initially due to the increased risk of perforation in diverticulitis
Q: How is mild acute diverticulitis managed?
Managed with oral antibiotics, a liquid diet, and analgesia.
Q: When should a patient with diverticulitis be admitted to the hospital?
If symptoms do not settle within 72 hours, or if the patient presents with more severe symptoms, hospital admission is required for IV antibiotics.
Q: What is Dukes’ classification?
Dukes’ classification describes the extent of spread of colorectal cancer.
Q: What are the stages in Dukes’ classification and their 5-year survival rates?
Dukes’ A: Tumour confined to the mucosa
5-year survival: 95%
Dukes’ B: Tumour invading the bowel wall
5-year survival: 80%
Dukes’ C: Lymph node metastases
5-year survival: 65%
Dukes’ D: Distant metastases
5-year survival: 5% (20% if resectable)
Q: What are haemorrhoids and where are they located?
Haemorrhoidal tissue is part of the normal anatomy that contributes to anal continence.
These mucosal vascular cushions are found in the left lateral, right posterior, and right anterior portions of the anal canal (at the 3 o’clock, 7 o’clock, and 11 o’clock positions respectively).
Haemorrhoids occur when this tissue becomes enlarged, congested, and symptomatic.
Q: What are the clinical features of haemorrhoids?
Painless rectal bleeding (most common symptom)
Pruritus (itching)
Pain: usually not significant unless thrombosed
Soiling: may occur with third or fourth degree piles
Q: What are the types of haemorrhoids?
External: Originate below the dentate line and are prone to thrombosis, may be painful.
Internal: Originate above the dentate line and generally do not cause pain.
Q: How are internal haemorrhoids graded?
Grade I: Do not prolapse out of the anal canal.
Grade II: Prolapse on defecation but reduce spontaneously.
Grade III: Can be manually reduced.
Grade IV: Cannot be reduced.
Q: What is the management for haemorrhoids?
Soften stools: Increase dietary fibre and fluid intake.
Topical treatments: Local anaesthetics and steroids may be used for symptom relief.
Outpatient treatments: Rubber band ligation is superior to injection sclerotherapy.
Surgery: Reserved for large, symptomatic haemorrhoids that do not respond to outpatient treatments.
Newer treatments: Doppler-guided haemorrhoidal artery ligation and stapled haemorrhoidopexy.
Q: How are acutely thrombosed external haemorrhoids managed?
Typically present with significant pain and a purplish, oedematous, tender subcutaneous perianal mass.
If presenting within 72 hours, referral for excision should be considered.
If after 72 hours, managed with stool softeners, ice packs, and analgesia.
Symptoms typically settle within 10 days.
Q: What is ischaemic colitis?
Ischaemic colitis is an acute but transient compromise in blood flow to the large bowel.
This reduced blood flow can lead to inflammation, ulceration, and haemorrhage.
Q: Where is ischaemic colitis more likely to occur?
It is more likely to occur in ‘watershed’ areas such as the splenic flexure, which are located at the borders of the territories supplied by the superior and inferior mesenteric arteries.
Q: What investigation finding may be seen in ischaemic colitis?
‘Thumbprinting’ on abdominal x-ray, which is due to mucosal oedema and haemorrhage.
Q: What is large bowel obstruction?
Large bowel obstruction occurs when the passage of food, fluids, and gas through the large intestines becomes blocked.
Q: What are the common causes of large bowel obstruction?
Tumour (60% of cases), particularly in distal colonic and rectal tumours.
Volvulus.
Diverticular disease.
Q: What are the clinical features of large bowel obstruction?
Absence of passing flatus or stool.
Abdominal pain.
Abdominal distention.
Nausea and vomiting (late symptom, may suggest more proximal lesion).
Peritonism may be present if associated with bowel perforation.
Q: What are the initial investigations for large bowel obstruction?
Abdominal x-ray: Diagnostic if the diameter is greater than 10-12 cm for the caecum, 8 cm for the ascending colon, or 6.5 cm for the recto-sigmoid.
CT scan: High sensitivity and specificity (over 90%) for identifying obstruction and its aetiology.
Q: What is the initial management of large bowel obstruction?
Nil by mouth (NBM).
IV fluids.
Nasogastric tube with free drainage.
If perforation is suspected, IV antibiotics and emergency surgery may be required.
If no perforation, conservative management can be trialled for up to 72 hours before considering further intervention.
Q: When is surgery required for large bowel obstruction?
Emergency surgery is needed if there is peritonitis or bowel perforation.
Resection of the perforated or ischaemic bowel and addressing the underlying cause of the obstruction may be performed.
Q: What is a perianal abscess?
A perianal abscess is a collection of pus within the subcutaneous tissue around the anus, typically originating from the tissue surrounding the anal sphincter.
Q: What are the symptoms of a perianal abscess?
Pain around the anus, worse on sitting.
Hardened tissue in the anal region.
Pus-like discharge from the anus.
If longstanding, features of systemic infection may be present.
Q: What are the common causes of perianal abscesses?
Typically colonised by gut flora such as E. coli.
Staphylococcus aureus infections are more likely to be skin-related.
Q: How are perianal abscesses investigated?
Inspection and digital rectal examination.
Colonoscopy and blood tests may be used to investigate the underlying cause.
MRI and transperineal ultrasound are used in complex cases or when complications are suspected, with MRI being the gold standard
Q: What are some conditions associated with perianal abscesses?
Inflammatory bowel disease (IBD), especially Crohn’s disease.
Diabetes mellitus, due to its effect on wound healing.
Underlying malignancy, increasing the risk of abscess formation and perforation.
Q: What is the treatment for a perianal abscess?
Incision and drainage under local anaesthetic.
Wound can be packed or left open to heal in 3-4 weeks.
Antibiotics may be used if there is systemic upset but are not helpful for wound healing.
Q: What is the significance of the color of rectal bleeding in diagnosing the source?
Bright red blood is usually from the rectum or anal canal.
Dark red blood suggests a proximal source.
Malaena (black, tarry stools) indicates blood from a gastro-duodenal source.
Q: What is the typical presentation of fissure in ano?
Painful bright red rectal bleeding post-defecation in small volumes.
Associated with constipation.
Muco-epithelial defect, usually midline posteriorly (anterior fissures more likely due to underlying disease).
Q: How are haemorrhoids identified and what is their typical bleeding pattern?
Bright red rectal bleeding post-defecation.
No blood mixed with stool.
Bleeding seen on toilet paper or as drops in the pan.
Proctoscopy may reveal internal haemorrhoids that are often impalpable.
Q: What symptoms are characteristic of Crohn’s disease when associated with rectal bleeding?
Bright red or mixed blood with stool.
Associated with altered bowel habit, malaise, fissures, and abscesses.
Proctoscopy may show indurated mucosa and skip lesions.
Q: What findings are typical in ulcerative colitis related to rectal bleeding?
Bright red blood mixed with stool.
Associated with diarrhoea, weight loss, and nocturnal incontinence.
Colonoscopy reveals continuous mucosal lesions.
Q: What are the signs of rectal cancer associated with rectal bleeding?
Bright red blood mixed with stool.
Associated with altered bowel habits, tenesmus, and possible metastatic symptoms.
Proctoscopy reveals a fixed or mobile mucosal abnormality.
Q: What are the baseline investigations for rectal bleeding?
Digital rectal examination.
Procto-sigmoidoscopy as the minimal test.
In young patients with suspected haemorrhoids, sigmoidoscopy may suffice.
Q: When should colonoscopy be performed in patients with rectal bleeding?
If symptoms suggest inflammatory bowel disease or altered bowel habits.
If sigmoidoscopy does not provide a clear diagnosis or the patient is not young.
Q: What is the standard management for fissure in ano?
First-line: GTN ointment (0.2%) or diltiazem cream applied topically.
If unsuccessful, consider Botulinum toxin injections.
Internal sphincterotomy may be required if treatments fail.
Q: How are haemorrhoids managed?
Lifestyle advice (e.g., increased fiber).
Small internal haemorrhoids: injection sclerotherapy or rubber band ligation.
External haemorrhoids: haemorrhoidectomy.
Modern procedures: HALO procedure and stapled haemorrhoidectomy.
Q: What are the treatment options for rectal cancer?
Anterior resection or abdomino-perineal excision.
Total mesorectal excision (TME) is standard of care.
Most resections below the peritoneal reflection require a defunctioning ileostomy.
Preoperative radiotherapy is often required.
Q: What is the surgical treatment option for ulcerative colitis (UC) in cases of disease requiring maximal therapy or prolonged steroid use?
Proctocolectomy (surgical resection of the colon and rectum).
Subtotal colectomy may be performed in emergency cases of poorly controlled colitis that fail to respond to medical therapy.
Q: When is proctocolectomy indicated in ulcerative colitis?
Malignant transformation or dysplastic transformation of the colonic epithelium.
Longstanding UC with risk of cancer.
Q: What is the typical procedure in an emergency setting for patients with poorly controlled ulcerative colitis?
Subtotal colectomy with creation of an end ileostomy.
Rectum may be stapled off or left in situ if the bowel is very oedematous.
Q: What are restorative surgical options in ulcerative colitis?
Ileoanal pouch procedure, but only if the rectum is still in situ.
This is not typically possible after proctectomy.
Q: What is the role of surgery in Crohn’s disease?
Surgical resection improves symptoms but does not provide a cure.
Surgery may be indicated for complications such as fistulae, abscesses, and strictures.
Q: What are the typical symptoms of thrombosed haemorrhoids?
Significant pain.
A tender lump around the anus.
Q: What does the examination reveal in cases of thrombosed haemorrhoids?
Purplish, oedematous, and tender subcutaneous perianal mass.
Q: What is the management approach if a patient presents with thrombosed haemorrhoids within 72 hours?
Referral for excision may be considered.
Q: How are thrombosed haemorrhoids typically managed if presented after 72 hours?
Use of stool softeners, ice packs, and analgesia.
Symptoms typically settle within 10 days.
Q: What is volvulus?
Torsion of the colon around its mesenteric axis, leading to compromised blood flow and closed-loop obstruction.
Q: What are the two common types of volvulus and their prevalence?
Sigmoid volvulus (80% of cases).
Caecal volvulus (20% of cases).
Q: What are some associations of sigmoid volvulus?
Older patients.
Chronic constipation.
Chagas disease.
Neurological conditions (e.g., Parkinson’s disease, Duchenne muscular dystrophy).
Psychiatric conditions (e.g., schizophrenia).
Q: What are some associations of caecal volvulus?
Adhesions.
Pregnancy
Q: What are the common clinical features of volvulus?
Constipation.
Abdominal bloating.
Abdominal pain.
Nausea/vomiting.
Q: How is sigmoid volvulus diagnosed on abdominal film?
Large bowel obstruction with a dilated loop of colon and often air-fluid levels.
Presence of coffee bean sign.
Q: How is caecal volvulus diagnosed on abdominal film?
Small bowel obstruction.
Q: What is the management for sigmoid volvulus?
Rigid sigmoidoscopy with rectal tube insertion.
Q: What is the management for caecal volvulus?
Operative management, often requiring right hemicolectomy.
Q: What are the characteristic exam features of peptic ulcer disease?
Duodenal ulcers: Epigastric pain relieved by eating.
Gastric ulcers: Epigastric pain worsened by eating.
Features of upper gastrointestinal haemorrhage (e.g., haematemesis, melena).
Q: What are the characteristic exam features of appendicitis?
Initial pain in the central abdomen before localising to the right iliac fossa (RIF).
Anorexia, tachycardia, low-grade pyrexia.
Rovsing’s sign: More pain in RIF than LIF when palpating LIF.
Q: What are the characteristic exam features of acute pancreatitis?
Severe epigastric pain, often due to alcohol or gallstones.
Vomiting common.
Tenderness, ileus, and low-grade fever may be present.
Rare signs include Cullen’s sign (periumbilical discolouration) and Grey-Turner’s sign (flank discolouration).
Q: What are the characteristic exam features of biliary colic?
RUQ pain radiating to the back and interscapular region, often following a fatty meal.
Obstructive jaundice may cause pale stools and dark urine.
Q: What are the characteristic exam features of acute cholecystitis?
Continuous RUQ pain.
Fever, raised inflammatory markers, and white cells.
Murphy’s sign: Arrest of inspiration on palpation of RUQ.
Q: What are the characteristic exam features of diverticulitis?
Colicky pain typically in the LLQ.
Fever, raised inflammatory markers, and white cells.
Q: What are the characteristic exam features of abdominal aortic aneurysm?
Severe central abdominal pain radiating to the back.
May present catastrophically (e.g., sudden collapse) or sub-acutely with persistent severe pain and developing shock.
History of cardiovascular disease may be present.
Q: What are the characteristic exam features of intestinal obstruction?
History of malignancy or previous operations.
Vomiting and no recent bowel movements.
‘Tinkling’ bowel sounds.
Q: What are some unusual and medical causes of abdominal pain to consider?
Acute coronary syndrome.
Diabetic ketoacidosis.
Pneumonia.
Acute intermittent porphyria.
Lead poisoning.
Q: What does Rovsing’s sign indicate?
Appendicitis: More pain in the right iliac fossa (RIF) when palpating the left iliac fossa (LIF).
Q: What does Boas’ sign indicate?
Cholecystitis: Right scapular pain or discomfort due to gallbladder inflammation.
Q: What does Murphy’s sign indicate?
Cholecystitis: Arrest of inspiration upon palpation of the RUQ (right upper quadrant).
Q: What does Cullen’s sign indicate?
Pancreatitis or other intra-abdominal haemorrhage: Periumbilical discolouration (bruising).
Q: What does Grey-Turner’s sign indicate?
Pancreatitis or other retroperitoneal haemorrhage: Flank discolouration (bruising).
Q: What are the characteristic features of abdominal swelling due to intestinal obstruction?
History of malignancy/previous operations
Vomiting
Not opened bowels recently
Tinkling bowel sounds
Q: What are the characteristic features of abdominal swelling due to ascites?
History of alcohol excess
Cardiac failure
Q: What are the characteristic features of abdominal swelling due to urinary retention?
History of prostate problems
Dullness to percussion around the suprapubic area
Q: What are the characteristic features of abdominal swelling due to ovarian cancer?
Older female
Pelvic pain
Urinary symptoms (e.g., urgency)
Raised CA125
Early satiety, bloating
Q: What are the common features of abdominal wall hernias?
Palpable lump
Cough impulse
Pain
Obstruction (more common in femoral hernias)
Strangulation (may compromise bowel blood supply, leading to infarction)
Q: What are the characteristics of an inguinal hernia?
Accounts for 75% of abdominal wall hernias
95% of patients are male
Lifetime risk of 25% in men
Located above and medial to the pubic tubercle
Strangulation is rare
Q: What are the characteristics of a femoral hernia?
Located below and lateral to the pubic tubercle
More common in women, particularly multiparous ones
High risk of obstruction and strangulation
Surgical repair required
Q: What are the characteristics of an umbilical hernia?
Symmetrical bulge under the umbilicus
Q: What are the characteristics of a paraumbilical hernia?
Asymmetrical bulge
Half the sac is covered by skin above or below the umbilicus
Q: What are the characteristics of an epigastric hernia?
Lump in the midline between the umbilicus and the xiphisternum
Risk factors include extensive physical training, coughing, and obesity
Q: What are the characteristics of an obturator hernia?
Hernia through the obturator foramen
More common in females, typically presents with bowel obstruction
Q: What are the characteristics of a congenital inguinal hernia in children?
Indirect hernias from a patent processus vaginalis
Occur in around 1% of term babies, more common in premature babies and boys
60% right-sided, 10% bilateral
Should be surgically repaired soon after diagnosis due to the risk of incarceration
Q: What are the characteristics of an infantile umbilical hernia?
Symmetrical bulge under the umbilicus
More common in premature and Afro-Caribbean babies
The majority resolve without intervention before age 4-5 years
Complications are rare
Q: What is acute appendicitis?
Acute appendicitis is the most common acute abdominal condition requiring surgery, particularly in young people aged 10-20 years.
Q: What is the characteristic abdominal pain in acute appendicitis?
Peri-umbilical pain (visceral stretching) radiating to the right iliac fossa (RIF) due to localized parietal peritoneal inflammation.
The migration of pain from the centre to RIF is a strong indicator.
Pain often worsens on coughing or going over speed bumps.
Children often cannot hop on the right leg due to pain.
Q: What are the other features of acute appendicitis?
Vomiting (usually once or twice, marked vomiting is unusual).
Diarrhoea is rare but may occur with pelvic appendicitis or abscess.
Mild pyrexia (37.5–38°C); higher temperature suggests other conditions like mesenteric adenitis.
Anorexia is very common.
Q: What are the key examination findings in acute appendicitis?
Generalized peritonitis or localized peritonism (if perforation has occurred).
Rebound tenderness, percussion tenderness, guarding, and rigidity.
Retrocaecal appendicitis may have fewer signs.
Psoas sign: pain on extending the hip (if retrocaecal appendix).
Digital rectal examination may reveal a boggy sensation in pelvic abscess or right-sided tenderness with a pelvic appendix.
Q: How is acute appendicitis diagnosed?
Raised inflammatory markers (neutrophil-predominant leucocytosis in 80-90%).
Urine analysis: excludes pregnancy in females, renal colic, and UTI. Mild leucocytosis may be seen in appendicitis but no nitrites.
Imaging: Ultrasound in females for pelvic organ pathology; CT scan used in the US but not widely in the UK due to radiation concerns.
Q: What is the management for acute appendicitis?
Appendicectomy via open or laparoscopic approach (laparoscopic is now preferred).
Prophylactic intravenous antibiotics to reduce wound infection.
Perforated appendicitis requires copious abdominal lavage.
Appendix mass: broad-spectrum antibiotics and consideration for interval appendicectomy.
In elderly patients, be cautious of caecal malignancy or perforated sigmoid diverticular disease.
Antibiotics alone: Successful in many cases, but often requires longer hospital stay, and 20% of patients may need appendicectomy within 12 months.
Q: What is the significance of thyroid peroxidase (microsomal) antibodies in blood testing?
Found in autoimmune thyroid diseases
100% of patients with Hashimoto’s thyroiditis
Present in 70% of patients with Graves’ disease
Q: When are antibodies to TSH receptor measured and what do they indicate?
Found in individuals with Graves’ disease
Present in 95% of Graves’ disease patients
Q: What is the role of thyroglobulin antibodies in blood testing?
Not useful for distinguishing between different thyroid diseases
May be used for follow-up in thyroid cancer patients
Q: What is the clinical significance of measuring calcitonin levels?
Released from parafollicular cells of the thyroid
Elevated levels are often found in medullary thyroid carcinoma
Q: What is cryptorchidism and when does it typically resolve?
A congenital undescended testis that fails to descend into the scrotum by 3 months of age
At birth, 5% of boys may have an undescended testis; by 3 months, the incidence drops to 1-2%
Postnatal descent occurs in most cases
Q: What are some congenital defects associated with cryptorchidism?
Patent processus vaginalis
Abnormal epididymis
Cerebral palsy
Mental retardation
Wilms’ tumor
Abdominal wall defects (e.g., gastroschisis, prune belly syndrome)
Q: How does retractile testes differ from cryptorchidism?
A retractile testis can be manually moved into the scrotum and stays there when released
If the testis returns rapidly to the inguinal canal, surgery may be indicated
Q: Why is it important to correct cryptorchidism?
Reduces the risk of infertility
Allows for examination of the testis for testicular cancer
Prevents testicular torsion
Improves cosmetic appearance
Males with undescended testes are 40 times more likely to develop testicular cancer (seminoma)
Intra-abdominal testes have a 50% risk of testicular cancer
Q: What is the recommended treatment for cryptorchidism?
Orchidopexy is recommended between 6 to 18 months of age
Involves inguinal exploration, mobilization of the testis, and implantation into a dartos pouch
Intra-abdominal testis should be evaluated laparoscopically
Late presentation in teenage years may require orchidectomy due to non-functioning testis and increased malignancy risk
Q: What is the first ECG finding in hyperkalaemia?
Peaked or ‘tall-tented’ T waves
Q: What are the ECG findings in hyperkalaemia?
Peaked or ‘tall-tented’ T waves (occurs first)
Loss of P waves
Broad QRS complexes
Sinusoidal wave pattern
Ventricular fibrillation
Q: When should gastric feeding be used over post-pyloric feeding?
Use gastric feeding unless there is upper GI dysfunction (then use duodenal or jejunal tube)
Q: How should NG tube placement be verified?
Check NG placement using aspiration and pH
Check post-pyloric tubes with AXR
Q: How long should a PEG tube remain in place before removal?
PEG can be used 4 hours after insertion, but should not be removed until >2 weeks after insertion
Q: When should enteral feeding be considered in surgical patients?
Consider preoperative enteral feeding if the patient is malnourished, has unsafe swallowing, inadequate oral intake, and a functional GI tract
Q: What is a femoral hernia?
Occurs when part of the bowel or other abdominal viscera passes into the femoral canal
The femoral canal is a potential space in the anterior thigh that can be occupied by herniated contents via the femoral ring
Q: What are the key features of a femoral hernia?
A lump in the groin, usually mildly painful
Inferolateral to the pubic tubercle, distinguishable from inguinal hernias which are supermedial to the pubic tubercle
Typically non-reducible, but can be reducible in some cases
Cough impulse is often absent due to the small femoral ring
Q: What is the management of a femoral hernia?
Surgical repair is necessary due to the risk of strangulation
Can be done laparoscopically or via laparotomy
Hernia support belts/trusses should not be used due to the risk of strangulation
In an emergency, laparotomy may be required
Q: What is the risk of strangulation in a direct inguinal hernia?
Low risk of strangulation
Q: What is the risk of strangulation in an indirect inguinal hernia?
Low risk of strangulation
Q: What is the risk of strangulation in a femoral hernia?
High risk of strangulation
Q: What is a hiatus hernia?
Herniation of part of the stomach above the diaphragm
Q: What are the two types of hiatus hernias?
Sliding hiatus hernia: gastroesophageal junction moves above the diaphragm (95% of cases)
Rolling (paraoesophageal) hiatus hernia: gastroesophageal junction remains below the diaphragm, but a separate part of the stomach herniates through the oesophageal hiatus
Q: What are the risk factors for hiatus hernia?
Obesity
Increased intraabdominal pressure (e.g. ascites, multiparity)
Q: What are the common features of a hiatus hernia?
Heartburn
Dysphagia
Regurgitation
Chest pain
Q: What is the most sensitive investigation for hiatus hernia?
Barium swallow
Q: What is the first-line investigation for suspected hiatus hernia?
Endoscopy (often finds the hiatus hernia incidentally)
Q: What is the management approach for hiatus hernia?
Conservative management: weight loss
Medical management: Proton pump inhibitors (PPI) therapy
Surgical management: indicated mainly for symptomatic paraesophageal hernias
Q: What are the common features of an inguinal hernia?
Groin lump
Located superior and medial to the pubic tubercle
Disappears on pressure or when the patient lies down
Discomfort and ache, often worse with activity; severe pain is uncommon
Strangulation is rare
Q: How should inguinal hernias be managed in medically fit patients, even if asymptomatic?
Surgery is recommended for medically fit patients
Q: What is the preferred method of repair for unilateral inguinal hernias?
Open surgery
Q: What is the preferred method of repair for bilateral and recurrent inguinal hernias?
Laparoscopic surgery
Q: What are the most common primary liver tumors?
Cholangiocarcinoma
Hepatocellular carcinoma
Hepatoblastoma
Sarcomas (rare)
Lymphomas
Carcinoids (most often secondary, but primary can occur)
Q: What accounts for 95% of all liver malignancies?
Metastatic disease
Q: What is the most common primary liver tumor?
Hepatocellular carcinoma (75% of primary liver tumors)
Q: What is the primary risk factor for hepatocellular carcinoma?
Chronic liver disease, especially cirrhosis and chronic hepatitis B infection
Q: What imaging modalities are used to diagnose hepatocellular carcinoma?
CT and MRI (usually both)
Q: What is the role of α-fetoprotein (AFP) in diagnosing hepatocellular carcinoma?
AFP is elevated in almost all cases of hepatocellular carcinoma
Q: What is the mainstay of treatment for operable hepatocellular carcinoma?
Surgical resection
Q: What is the second most common primary liver malignancy?
Cholangiocarcinoma
Q: What is the main risk factor for cholangiocarcinoma?
Primary sclerosing cholangitis
Q: What is the typical presentation of cholangiocarcinoma?
Jaundice (by the time of presentation, most cases are not resectable)
Q: What are the elevated tumor markers in cholangiocarcinoma?
CA 19-9
CEA
CA 125
Q: What is the main imaging modality used for cholangiocarcinoma diagnosis?
CT/MRI and MRCP
Q: What is the best treatment for cholangiocarcinoma?
Surgical resection (though often not possible due to local invasion or lobar atrophy)
Q: What is the typical presentation of a Mallory-Weiss Tear?
History of antecedent vomiting followed by vomiting of a small amount of blood
Little systemic disturbance or prior symptoms
Q: What are the features of a hiatus hernia of the gastric cardia?
Longstanding history of dyspepsia
Often overweight patients
Uncomplicated hiatus hernias should not cause dysphagia or haematemesis
Q: What are the signs that suggest oesophageal rupture?
Severe chest pain without cardiac diagnosis
Signs of pneumonia without convincing history
History of vomiting
Erect chest X-ray shows infiltrate or effusion in 90% of cases
Q: What is the typical presentation of squamous cell carcinoma of the oesophagus?
Progressive dysphagia
Often associated with weight loss
Little to no history of previous GORD symptoms
Q: What is the typical presentation of adenocarcinoma of the oesophagus?
Progressive dysphagia
May have a history of GORD or Barrett’s oesophagus
Q: What are the features of peptic stricture?
Longer history of dysphagia, often non-progressive
Usually associated with GORD symptoms
Lack of systemic features seen with malignancy
Q: What is the typical presentation of a dysmotility disorder of the oesophagus?
Episodic, non-progressive dysphagia
Retrosternal pain may accompany the episodes
Q: What is the main diagnostic tool for oesophageal disease?
Upper GI endoscopy
Q: When should pH and manometry studies be used in oesophageal disease diagnosis?
If upper GI endoscopy fails to demonstrate a mechanical stricture, these tests, along with radiological contrast swallows, help in diagnosis
Q: What are the typical features of appendicitis presenting as right iliac fossa pain?
Pain radiating to right iliac fossa
Anorexia
Typically short history
Diarrhoea and profuse vomiting are rare
Q: What are the features of Crohn’s disease presenting with right iliac fossa pain?
Often long history
Signs of malnutrition
Change in bowel habit, especially diarrhoea
Q: What are the causes of mesenteric adenitis, which may present with right iliac fossa pain?
More common in children
Causes include Adenoviruses, Epstein-Barr virus, beta-haemolytic Streptococcus, Staphylococcus spp., Escherichia coli, Streptococcus viridans, and Yersinia spp.
Higher temperature than appendicitis
Enlarged mesenteric lymph nodes on laparotomy
Q: What are the features of diverticulitis presenting with right iliac fossa pain?
May present with both left and right sided disease
Clinical history may be similar to appendicitis, with some change in bowel habit
A CT scan may help refine diagnosis
Q: What is Meckel’s diverticulitis and its typical presentation with right iliac fossa pain?
A congenital abnormality present in about 2% of the population
Typically 2 feet proximal to the ileocaecal valve
May be lined by ectopic gastric mucosal tissue, causing bleeding
Q: What are the features of a perforated peptic ulcer presenting with right iliac fossa pain?
Usually produces upper quadrant pain but can be lower
Sharp, sudden onset of pain
May present with pain in the right iliac fossa
Q: How does an incarcerated right inguinal or femoral hernia present with right iliac fossa pain?
Right iliac fossa pain if right-sided
Can cause bowel obstruction
Q: What are the features of bowel perforation secondary to caecal or colon carcinoma presenting with right iliac fossa pain?
Seldom localised to right iliac fossa
Complete large bowel obstruction with caecal distension may cause pain before perforation
Q: What is the most common cause of small bowel obstruction?
Adhesions, often following previous surgery
Hernias are the next most common cause
Q: What are the typical features of small bowel obstruction?
Diffuse, central abdominal pain
Nausea and vomiting
Typically bilious vomiting
‘Constipation’ with complete obstruction and lack of flatulence
Abdominal distension, especially with lower levels of obstruction
‘Tinkling’ bowel sounds (more common in early obstruction)
Q: What is the first-line imaging for suspected small bowel obstruction?
Abdominal x-ray
Distended small bowel loops with fluid levels
Small bowel is considered dilated if >3cm in diameter
Q: What is the definitive investigation for small bowel obstruction?
CT scan
More sensitive, particularly in early obstruction
Q: What are the initial management steps for small bowel obstruction?
NBM (Nil by mouth)
IV fluids
Nasogastric tube with free drainage
Some patients may settle with conservative management
Surgery may be required if conservative management fails
Q: What is an inguinal hernia?
Protrusion of viscera or abdominal contents through the superficial inguinal ring
Typically consists of small bowel, though not always
Can enter the inguinal canal either directly or indirectly
Q: What is the difference between reducible and incarcerated inguinal hernias?
Reducible hernia: The herniated tissue can be pushed back into the abdomen
Incarcerated hernia: The hernia cannot be reduced, and there is a risk of strangulation
Q: What is strangulation in the context of inguinal hernia?
A surgical emergency where the blood supply to the herniated tissue is compromised
Can cause ischemia or necrosis of the bowel, potentially leading to permanent tissue loss or perforation
Occurs in about 1 in 500 inguinal hernia cases
Q: What are the indications that an inguinal hernia is at risk of strangulation?
Episodes of pain in a hernia previously asymptomatic
Irreducible hernias
Q: What are the symptoms of strangulated hernias?
Pain
Fever
Increase in the size of the hernia or erythema of overlying skin
Peritonitic features (guarding, localized tenderness)
Bowel obstruction (distension, nausea, vomiting)
Bowel ischemia (bloody stools)
Q: What are the key diagnostic steps for suspected strangulated inguinal hernias?
Imaging is not necessary but can be useful to exclude other pathologies
Abdominal X-ray or CT may be used to assess for obstruction
Erect chest X-ray is recommended for suspected perforation
Full blood count and arterial blood gas analysis may show:
Leukocytosis
Raised lactate
Q: What is the management for a strangulated inguinal hernia?
Immediate surgery (open or laparoscopic) with mesh repair
Any dead bowel must be removed
Avoid manual reduction of strangulated hernias, as it may lead to peritonitis
Q: What are the criteria for brain stem death testing?
Deep coma of known aetiology
Reversible causes excluded
No sedation
Normal electrolytes
Q: What are the key tests for brain death?
Fixed pupils unresponsive to light
No corneal reflex
Absent oculo-vestibular reflexes (no eye movements after ice-cold water injection into ears)
No response to supraorbital pressure
No cough reflex to bronchial stimulation or gagging to pharyngeal stimulation
No respiratory effort after ventilator disconnection for 5 minutes (or longer, ensuring CO2 levels rise to at least 6.0 kPa)
Q: What is the requirement for testing brain death?
Test performed by two doctors with at least 5 years of post-graduate experience
One of the doctors must be a consultant
Neither doctor can be a member of the transplant team if organ donation is being considered
The test should be done on two separate occasions
Q: What are the indications for a CT head within 1 hour of a head injury according to NICE?
GCS < 13 on initial assessment
GCS < 15 at 2 hours post-injury
Suspected open or depressed skull fracture
Any sign of basal skull fracture (e.g., haemotympanum, ‘panda’ eyes, CSF leakage from ear or nose, Battle’s sign)
Post-traumatic seizure
Focal neurological deficit
More than 1 episode of vomiting
Q: What are the indications for a CT head within 8 hours of a head injury according to NICE?
Age 65 or older
History of bleeding or clotting disorders (including anticoagulants)
Dangerous mechanism of injury (e.g., pedestrian/cyclist struck by motor vehicle, occupant ejected from vehicle, fall >1 metre or 5 stairs)
More than 30 minutes’ retrograde amnesia before the injury
Q: What is the specific guideline for patients on warfarin who sustain a head injury?
Perform a CT head scan within 8 hours of the injury if no other indications for immediate CT head scan
Q: What are the two main types of primary brain injury?
Focal (e.g., contusion, haematoma)
Diffuse (e.g., diffuse axonal injury)
Q: What is diffuse axonal injury and how does it occur?
Occurs due to mechanical shearing following deceleration, causing disruption and tearing of axons
Q: What is secondary brain injury and how does it develop?
Caused by factors like cerebral oedema, ischaemia, infection, tonsillar or tentorial herniation
It exacerbates the original injury by disrupting cerebral autoregulation, making the brain more susceptible to blood flow changes and hypoxia
Q: What is the Cushings reflex and when does it occur?
Hypertension and bradycardia
Often a pre-terminal event in the context of raised intracranial pressure
Q: What is an extradural (epidural) haematoma and what causes it?
Bleeding between the dura mater and the skull, often from acceleration-deceleration trauma or a blow to the side of the head
Typically caused by rupture of the middle meningeal artery, especially in the temporal region
Q: What are the features of an extradural haematoma?
Features of raised intracranial pressure
Possible lucid interval
Q: What is a subdural haematoma and its risk factors?
Bleeding between the dura mater and the outermost meningeal layer, commonly around the frontal and parietal lobes
Risk factors include old age, alcoholism, and anticoagulation
Q: What are the symptoms of a subdural haematoma?
Slower onset of symptoms compared to epidural haematomas
Fluctuating confusion and consciousness
Q: What is a subarachnoid haemorrhage and its common cause?
Sudden occipital headache, often due to a ruptured cerebral aneurysm
Can also occur in traumatic brain injury
Q: What is an intracerebral haematoma and its causes/risk factors?
A collection of blood within the substance of the brain
Causes include hypertension, vascular lesions, cerebral amyloid angiopathy, trauma, brain tumour, or infarct
Patients present similarly to ischaemic stroke
Q: How is an intracerebral haematoma treated?
Often managed conservatively by stroke physicians
Large clots in patients with impaired consciousness may require surgical evacuation
Q: What is hydrocephalus and what causes it?
Hydrocephalus is the accumulation of cerebrospinal fluid (CSF) in the ventricular system of the brain, caused by an imbalance between CSF production and absorption
Q: What are the common symptoms of hydrocephalus?
Headache (worse in the morning, lying down, and during valsalva)
Nausea and vomiting
Papilloedema
Coma (in severe cases)
Q: How does hydrocephalus present in infants?
Increase in head circumference due to unclosed skull sutures
Bulging and tense anterior fontanelle
‘Sunsetting’ eyes (failure of upward gaze) due to compression of the superior colliculus of the midbrain
Q: What are the two main types of hydrocephalus?
Obstructive (‘non-communicating’) hydrocephalus
Non-obstructive (‘communicating’) hydrocephalus
Q: What causes obstructive (non-communicating) hydrocephalus?
Structural pathology blocking CSF flow
Causes include tumours, acute haemorrhage (e.g., subarachnoid or intraventricular haemorrhage), and developmental abnormalities (e.g., aqueduct stenosis)
Q: What causes non-obstructive (communicating) hydrocephalus?
Imbalance in CSF production and absorption
Can be due to increased CSF production (e.g., choroid plexus tumour) or failure of reabsorption at the arachnoid granulations (e.g., meningitis or post-haemorrhagic)
Q: What is normal pressure hydrocephalus?
A form of non-obstructive hydrocephalus with large ventricles but normal intracranial pressure
Classic triad: dementia, incontinence, and disturbed gait
Q: What is the first-line imaging investigation for hydrocephalus?
CT head (fast and shows adequate resolution of the brain and ventricles)
Q: When is MRI used in the investigation of hydrocephalus?
MRI is used for more detailed investigation, particularly when an underlying lesion is suspected
Q: What is the role of lumbar puncture in hydrocephalus?
Diagnostic and therapeutic: allows for CSF sampling, opening pressure measurement, and CSF drainage to reduce pressure
Q: What is the treatment for acute, severe hydrocephalus?
External ventricular drain (EVD), typically inserted into the right lateral ventricle, draining into a bag at the bedside
Q: What is the treatment for long-term hydrocephalus?
Ventriculoperitoneal shunt (VPS), which diverts CSF from the ventricles to the peritoneum
Q: Why is lumbar puncture contraindicated in obstructive hydrocephalus?
It may cause brain herniation due to differences in cranial and spinal pressures
Q: What is a subarachnoid haemorrhage (SAH)?
An intracranial haemorrhage where blood accumulates within the subarachnoid space, deep to the subarachnoid layer of the meninges
Q: What is the most common cause of spontaneous SAH?
Intracranial aneurysm (saccular ‘berry’ aneurysms), accounting for around 85% of cases
Q: What conditions are associated with berry aneurysms?
Hypertension
Adult polycystic kidney disease
Ehlers-Danlos syndrome
Coarctation of the aorta
Q: What are the classical presenting features of SAH?
Sudden-onset severe headache (‘thunderclap’)
Occipital headache, peaking within 1-5 minutes
Nausea and vomiting
Meningism (photophobia, neck stiffness)
Coma and seizures
ECG changes including ST elevation
Q: What is the first-line investigation for suspected SAH?
Non-contrast CT head
Q: How does a CT head present in SAH?
Acute blood appears hyperdense (bright) on CT, often in the basal cisterns, sulci, and sometimes the ventricular system
Q: What is the role of lumbar puncture (LP) in SAH diagnosis?
If CT head is normal within 6 hours of symptom onset, no LP is needed
If CT is done >6 hours after onset and is normal, perform an LP at least 12 hours after symptom onset to check for xanthochromia (red blood cell breakdown)
Xanthochromia and normal or raised opening pressure in CSF suggest SAH
Q: What is the management of confirmed aneurysmal SAH?
Supportive care (bed rest, analgesia)
Venous thromboembolism prophylaxis
Discontinuation of antithrombotics (reversal of anticoagulation if present)
Nimodipine to prevent vasospasm
Surgical intervention within 24 hours (coiling by interventional neuroradiologists or craniotomy and clipping by neurosurgeons)
Q: What are the complications of aneurysmal SAH?
Re-bleeding (most common in the first 12 hours)
Hydrocephalus (treated with external ventricular drain or ventriculoperitoneal shunt)
Vasospasm (delayed cerebral ischaemia, typically 7-14 days after onset)
Hyponatraemia (due to SIADH)
Seizures
Q: What is a subdural haemorrhage (SDH)?
A collection of blood deep to the dural layer of the meninges, an extra-axial (extrinsic) lesion
Can be unilateral or bilateral
Q: How can subdural haematomas be classified?
Acute: Symptoms develop within 48 hours, rapid neurological deterioration
Subacute: Symptoms develop within days to weeks, gradual progression
Chronic: Develop over weeks to months, common in the elderly, may not recall specific injury
Q: What are the typical symptoms of a subdural haematoma?
Neurological symptoms: Altered mental status (confusion to coma), focal deficits (weakness, aphasia), headache, seizures
Physical findings: Papilloedema, pupil changes (unilateral dilated pupil), gait abnormalities, hemiparesis/hemiplegia
Behavioral/cognitive changes: Memory loss, personality changes, cognitive impairment
Other: Nausea, vomiting, drowsiness, signs of increased ICP (Cushing’s triad)
Q: What is the difference in presentation between acute and chronic subdural haematoma?
Acute: Rapid neurological deterioration, often after high-impact trauma
Chronic: Gradual onset of confusion, reduced consciousness, or neurological deficits over weeks to months
Q: What is the primary cause of acute subdural haematomas?
High-impact trauma, often associated with other brain injuries
Q: What does a CT scan show in acute subdural haematomas?
Crescentic collection, hyperdense (bright) compared to the brain
May show mass effect (midline shift, herniation)
Q: What is the management of small or incidental acute subdural haematomas?
Conservative observation
Surgical options include monitoring intracranial pressure or decompressive craniectomy
Q: What causes chronic subdural haematomas?
Rupture of small bridging veins due to brain atrophy, commonly in elderly and alcoholic patients
Can also occur in infants (e.g., shaken baby syndrome)
Q: What does a CT scan show in chronic subdural haematomas?
Crescentic collection, hypodense (dark) compared to brain
Mass effect without restriction by suture lines
Q: What is the management of large or symptomatic chronic subdural haematomas?
Surgical decompression with burr holes if there is confusion, neurological deficit, or severe imaging findings
Q: At what age does duodenal atresia typically present, and how is it diagnosed?
Age at presentation: Few hours after birth
Diagnosis: AXR shows double bubble sign, contrast study may confirm
Q: What is the treatment for duodenal atresia?
Treatment: Duodenoduodenostomy
Q: At what age does malrotation with volvulus typically present, and how is it diagnosed?
Age at presentation: Usually 3-7 days after birth, may present with peritoneal signs and haemodynamic instability in cases of volvulus with compromised circulation
Diagnosis: Upper GI contrast study (DJ flexure more medially placed), USS may show abnormal orientation of SMA and SMV
Q: What is the treatment for malrotation with volvulus?
Treatment: Ladd’s procedure
Q: At what age does jejunal/ileal atresia present, and how is it diagnosed?
Age at presentation: Usually within 24 hours of birth
Diagnosis: AXR shows air-fluid levels
Q: What is the treatment for jejunal/ileal atresia?
Treatment: Laparotomy with primary resection and anastomosis
Q: At what age does meconium ileus present, and how is it diagnosed?
Age at presentation: Typically in the first 24-48 hours of life with abdominal distension and bilious vomiting
Diagnosis: AXR shows air-fluid levels, sweat test to confirm cystic fibrosis
Q: What is the treatment for meconium ileus?
Treatment: Surgical decompression, segmental resection if there is serosal damage
Q: At what age does necrotising enterocolitis typically present, and how is it diagnosed?
Age at presentation: Usually second week of life
Diagnosis: Dilated bowel loops on AXR, pneumatosis, and portal venous air
Q: What is the treatment for necrotising enterocolitis?
Treatment: Conservative and supportive for non-perforated cases, laparotomy and resection for perforated or deteriorating cases
Q: What are the clinical features of acute cholecystitis?
Right upper quadrant pain, may radiate to the right shoulder
Fever and signs of systemic upset
Murphy’s sign: inspiratory arrest upon palpation of the right upper quadrant
Liver function tests are typically normal, but deranged LFTs may indicate Mirizzi syndrome
Q: What is Mirizzi syndrome?
Gallstone impacted in the distal cystic duct, causing extrinsic compression of the common bile duct
Q: What is the first-line investigation for acute cholecystitis?
Ultrasound
Q: What is the treatment for acute cholecystitis?
Intravenous antibiotics
Cholecystectomy, preferably early laparoscopic cholecystectomy within 1 week of diagnosis (as per NICE guidelines)
Q: What are the main causes of acute pancreatitis?
Alcohol
Gallstones
Q: What is the pathophysiology of acute pancreatitis?
Autodigestion of pancreatic tissue by pancreatic enzymes, leading to necrosis
Q: What are the common clinical features of acute pancreatitis?
Severe epigastric pain, may radiate to the back
Vomiting
Epigastric tenderness, ileus, and low-grade fever on examination
Rare periumbilical discolouration (Cullen’s sign) and flank discolouration (Grey-Turner’s sign)
Q: What is the most commonly used initial investigation for acute pancreatitis?
Serum amylase, raised in 75% of patients (typically > 3 times the upper limit of normal)
Serum lipase, more sensitive and specific than amylase
Causes of acute pancreatitis
Gallstones
Ethanol
Trauma
Steroids
Mumps (other viruses include Coxsackie B)
Autoimmune (e.g. polyarteritis nodosa), Ascaris infection
Scorpion venom
Hypertriglyceridaemia, Hyperchylomicronaemia, Hypercalcaemia, Hypothermia
ERCP
Drugs (azathioprine, mesalazine*, didanosine, bendroflumethiazide, furosemide, pentamidine, steroids, sodium valproate)
Q: What is the most common local complication of acute pancreatitis?
Peripancreatic fluid collections
Occur in 25% of cases
Q: What are peripancreatic fluid collections?
Located in or near the pancreas and lack a wall of granulation or fibrous tissue
May resolve or develop into pseudocysts or abscesses
Aspiration and drainage are best avoided as they may precipitate infection
Q: What are pseudocysts in the context of acute pancreatitis?
Result from organisation of peripancreatic fluid collections
Walled by fibrous or granulation tissue
Typically occur 4 weeks or more after an attack of acute pancreatitis
Most are retrogastric
75% associated with persistent mild elevation of amylase
Q: What is the management of pseudocysts in acute pancreatitis?
Most resolve on their own, can be observed for 12 weeks
If symptomatic, treatment options include endoscopic or surgical cystogastrostomy or aspiration
Q: What is pancreatic necrosis?
Involves both the pancreatic parenchyma and surrounding fat
Severity linked to the extent of parenchymal necrosis and overall necrosis
Sterile necrosis is managed conservatively initially
Q: What is a pancreatic abscess?
Intraabdominal collection of pus associated with the pancreas, but without necrosis
Typically occurs as a result of infected pseudocyst
Treatment options include transgastric drainage or endoscopic drainage
Q: What is the key management for fluid resuscitation in acute pancreatitis?
Aggressive early hydration with crystalloids
In severe cases, 3-6 litres of third-space fluid loss may occur
Aim for a urine output of > 0.5mls/kg/hr
Helps relieve pain by reducing lactic acidosis
Q: How should pain be managed in acute pancreatitis?
Pain is often severe and is a key priority of care
Intravenous opioids are typically required for adequate pain control
Q: What is the role of nutrition in the management of acute pancreatitis?
Patients should not routinely be made nil-by-mouth unless there is a clear reason (e.g. vomiting)
Enteral nutrition should be offered within 72 hours for moderately severe or severe cases
Parenteral nutrition should be used only if enteral nutrition fails or is contraindicated
Q: When is surgery indicated in the management of acute pancreatitis?
Gallstones-induced pancreatitis: Early cholecystectomy
Obstructed biliary system due to stones: Early ERCP
Necrosis with worsening organ dysfunction: Debridement, sometimes with fine needle aspiration
Infected necrosis: Either radiological drainage or surgical necrosectomy, depending on local expertise
Q: What is the most common predisposing factor for ascending cholangitis?
Gallstones
Q: What is Charcot’s triad in ascending cholangitis?
Right upper quadrant (RUQ) pain
Fever
Jaundice
Seen in about 20-50% of patients
Q: What additional features are present in Reynolds’ pentad?
Hypotension
Confusion
In addition to the three features of Charcot’s triad
Q: What are the initial investigations for suspected ascending cholangitis?
Ultrasound to assess bile duct dilation and bile duct stones
Q: What is the treatment for ascending cholangitis?
Intravenous antibiotics
Endoscopic retrograde cholangiopancreatography (ERCP) after 24-48 hours to relieve obstruction
Q: What are the traditional risk factors for biliary colic, referred to as the ‘4 F’s’?
Fat (obesity due to enhanced cholesterol synthesis and secretion)
Female (2-3 times more common in women due to estrogen affecting HMG-CoA reductase)
Fertile (pregnancy)
Forty (age)
Q: What are the common features of biliary colic?
Colicky right upper quadrant abdominal pain
Worse postprandially, especially after fatty foods
Pain radiating to the right shoulder/interscapular region
Nausea and vomiting
No fever
Normal liver function tests and inflammatory markers
Q: What is the first-line investigation for biliary colic?
Ultrasound
Q: What is the management for biliary colic?
Elective laparoscopic cholecystectomy
Q: What is the first-line diagnostic test for Boerhaave’s syndrome?
CT contrast swallow
Q: What is the treatment for Boerhaave’s syndrome if surgery is performed within 12 hours of onset?
Thoracotomy and lavage
Primary repair is usually feasible
Q: What is the management for Boerhaave’s syndrome if surgery is delayed beyond 12 hours?
Insertion of a T tube to create a controlled fistula between the oesophagus and skin
Q: What is the main risk factor for cholangiocarcinoma?
Primary sclerosing cholangitis
Q: What are the typical features of cholangiocarcinoma?
Persistent biliary colic symptoms
Anorexia, jaundice, and weight loss
Palpable mass in the right upper quadrant (Courvoisier sign)
Periumbilical lymphadenopathy (Sister Mary Joseph nodes)
Left supraclavicular adenopathy (Virchow node)
Q: What is a key marker for detecting cholangiocarcinoma in patients with primary sclerosing cholangitis?
Raised CA 19-9 levels
Q: What functional test can be used to assess exocrine function in chronic pancreatitis?
Faecal elastase test
Q: What is the response to H. pylori eradication in low-grade gastric MALT lymphoma?
80% respond to H. pylori eradication if low-grade
Q: What are the absolute contraindications for laparoscopic surgery?
Haemodynamic instability/shock
Raised intracranial pressure
Acute intestinal obstruction with dilated bowel loops (e.g., > 4 cm)
Uncorrected coagulopathy
Q: What are the typical patterns of liver function tests (LFTs) in different types of jaundice?
Pre-hepatic:
Bilirubin: Normal or high
ALT/AST: Normal
Alkaline phosphatase: Normal
Hepatic:
Bilirubin: High
ALT/AST: Elevated (often very high)
Alkaline phosphatase: Elevated but seldom very high
Post-hepatic:
Bilirubin: High to very high
ALT/AST: Moderate elevation
Alkaline phosphatase: High to very high
Q: What is the most common cause of acute bacterial prostatitis?
Escherichia coli (E. coli) is the most commonly isolated pathogen.
Q: What are the risk factors for acute bacterial prostatitis?
Recent urinary tract infection
Urogenital instrumentation
Intermittent bladder catheterisation
Recent prostate biopsy
Q: What are the typical features of acute bacterial prostatitis?
Pain referred to the perineum, penis, rectum, or back
Obstructive voiding symptoms
Fever and rigors
Digital rectal examination: Tender, boggy prostate gland
Q: What is the recommended management for acute bacterial prostatitis?
14-day course of a quinolone (as per the BNF)
Consider screening for sexually transmitted infections
Q: How is acute urinary retention diagnosed?
Bladder ultrasound with a volume of >300 cc confirms the diagnosis.
If the history and examination are consistent, the diagnosis may still be confirmed despite an inconsistent bladder scan.
Q: What is the management of acute urinary retention?
Decompress the bladder via catheterisation.
Measure urine drained in the first 15 minutes:
<200 cc: No acute urinary retention.
400 cc: Leave the catheter in place.
Between 200 and 400 cc: Further case-specific management.
Investigate the underlying cause based on the likely cause (e.g. UTI, BPH, neurological, or gynaecological causes).
Q: What are the common symptoms of BPH?
Voiding (obstructive) symptoms:
Weak or intermittent urinary flow
Straining
Hesitancy
Terminal dribbling
Incomplete emptying
Storage (irritative) symptoms:
Urgency
Frequency
Urgency incontinence
Nocturia
Post-micturition dribbling
Q: What assessments are recommended for BPH?
Dipstick urine: To assess for infection or hematuria.
U&Es: Particularly if chronic retention is suspected.
PSA: Should be done if there are obstructive symptoms or concerns about prostate cancer.
Urinary frequency-volume chart: Should be maintained for at least 3 days.
International Prostate Symptom Score (IPSS):
20-35: Severely symptomatic
8-19: Moderately symptomatic
0-7: Mildly symptomatic
Q: What are the main management options for BPH?
Watchful waiting: For mild symptoms.
Alpha-1 antagonists (e.g., tamsulosin, alfuzosin):
First-line treatment for moderate-to-severe voiding symptoms (IPSS ≥ 8).
Improve symptoms in ~70% of men.
Adverse effects: Dizziness, postural hypotension, dry mouth, depression.
5 alpha-reductase inhibitors (e.g., finasteride):
Indicated for significantly enlarged prostates at high risk of progression.
Reduces prostate volume and may slow disease progression, though symptom improvement may take up to 6 months.
Adverse effects: Erectile dysfunction, reduced libido, ejaculation problems, gynaecomastia.
Combination therapy: Alpha-1 antagonist + 5 alpha-reductase inhibitor, recommended for bothersome moderate-to-severe symptoms with prostatic enlargement.
Antimuscarinics (anticholinergic drugs) (e.g., tolterodine, darifenacin):
May be used if storage and voiding symptoms persist after treatment with alpha-blockers alone.
Q: What is the surgical treatment for BPH?
Transurethral resection of the prostate (TURP): A common surgical option for BPH.
Q: What are the medical indications for circumcision?
Phimosis (tight foreskin that cannot be retracted).
Recurrent balanitis (inflammation of the glans penis).
Balanitis xerotica obliterans (chronic inflammation leading to scarring).
Paraphimosis (inability to return a retracted foreskin to its normal position).
Q: What are epididymal cysts and where are they located?
Epididymal cysts are the most common cause of scrotal swellings seen in primary care.
They are separate from the body of the testicle.
Typically located above and posterior to the testicle.
Q: How is the diagnosis of epididymal cysts confirmed?
Diagnosis may be confirmed with an ultrasound.
Q: What is epididymo-orchitis and what causes it?
Epididymo-orchitis is an infection of the epididymis and/or testes, resulting in pain and swelling.
Most commonly caused by local spread of infections from the genital tract (e.g., Chlamydia trachomatis, Neisseria gonorrhoeae) in sexually active younger adults or from the bladder (E. coli) in older adults with a low-risk sexual history.
Q: What are the key features of epididymo-orchitis?
Unilateral testicular pain and swelling.
Urethral discharge may be present, but urethritis is often asymptomatic.
Factors suggesting testicular torsion:
Patients under 20 years old,
Severe pain and acute onset.
Q: What is the most important differential diagnosis for epididymo-orchitis?
The most important differential is testicular torsion, which needs to be excluded urgently to prevent ischaemia of the testicle.
Q: What investigations are done for epididymo-orchitis?
In younger adults, assess for sexually transmitted infections (STIs).
In older adults with a low-risk sexual history, send a mid-stream urine (MSU) for microscopy and culture.
Q: How is epididymo-orchitis managed?
If an STI is suspected, advise urgent referral to a local specialist sexual health clinic.
If the organism is unknown, the BASHH recommends:
Ceftriaxone 500mg intramuscularly (single dose),
Plus doxycycline 100mg orally twice daily for 10-14 days.
If enteric organisms are suspected, send an MSU as above, and empirically treat with an oral quinolone (e.g., ofloxacin) for 2 weeks.
Further investigations may be recommended to exclude any underlying structural abnormalities.
Q: How can you differentiate between organic and psychogenic causes of erectile dysfunction?
Organic causes are favoured by:
Gradual onset of symptoms,
Lack of tumescence,
Normal libido.
Psychogenic causes are favoured by:
Sudden onset of symptoms,
Decreased libido,
Good quality spontaneous or self-stimulated erections,
Major life events,
Relationship problems,
Previous psychological issues,
History of premature ejaculation
Q: What investigations should be done for erectile dysfunction?
10-year cardiovascular risk calculation by measuring lipid and fasting glucose serum levels.
Free testosterone measurement (morning, 9–11am).
If low or borderline, repeat with FSH, LH, and prolactin levels.
If abnormal, refer to endocrinology for further assessment.
Testosterone measurement: universal testing is recommended by the British Society for Sexual Medicine and the European Association of Urology.
Q: What is the first-line management for erectile dysfunction?
PDE-5 inhibitors (e.g., sildenafil/’Viagra’) are first-line treatment for all patients (unless contraindicated).
Sildenafil can be purchased over-the-counter without a prescription.
Q: What is the management for patients who cannot or will not take PDE-5 inhibitors?
Vacuum erection devices are recommended as first-line treatment.
Q: What is a hydrocele and what are the two types?
A hydrocele is the accumulation of fluid within the tunica vaginalis.
Two types:
Communicating hydrocele: Caused by patency of the processus vaginalis, allowing peritoneal fluid to drain into the scrotum. Common in newborn males (5-10%) and usually resolves in the first few months.
Non-communicating hydrocele: Caused by excessive fluid production within the tunica vaginalis.
Q: What are the typical features of a hydrocele?
Soft, non-tender swelling of the hemi-scrotum.
Typically anterior to and below the testicle.
The swelling is confined to the scrotum.
You can get “above” the mass on examination.
It transilluminates with a pen torch.
The testis may be difficult to palpate if the hydrocele is large.
Q: How is the diagnosis of a hydrocele made?
Diagnosis is usually clinical, but an ultrasound is required if there’s any doubt about the diagnosis or if the underlying testis cannot be palpated.
Q: How is a hydrocele managed in infants and adults?
Infantile hydroceles: Usually repaired if not resolved by 1-2 years of age.
In adults, a conservative approach may be taken, depending on the severity of the presentation. Further investigation (e.g., ultrasound) is warranted to exclude any underlying cause such as a tumour.
Q: What are the causes of unilateral and bilateral hydronephrosis?
Unilateral:
Pelvic-ureteric obstruction (congenital or acquired)
Aberrant renal vessels
Calculi
Tumours of the renal pelvis
Bilateral:
Stenosis of the urethra
Urethral valve
Prostatic enlargement
Extensive bladder tumour
Retro-peritoneal fibrosis
Q: What are the first-line investigations for hydronephrosis?
Ultrasound: Identifies the presence of hydronephrosis and can assess the kidneys.
IVU (Intravenous Urography): Assesses the position of the obstruction.
Antegrade or retrograde pyelography: Allows treatment.
If renal colic is suspected, CT scan is used (majority of stones detected this way).
Q: What is the management for hydronephrosis?
Remove the obstruction and drainage of urine.
Acute upper urinary tract obstruction: Nephrostomy tube.
Chronic upper urinary tract obstruction: Ureteric stent or pyeloplasty.
Q: What is priapism and how is it classified?
Priapism is a persistent penile erection lasting longer than 4 hours, not associated with sexual stimulation.
It can be classified into two types:
Ischaemic: Due to impaired vasorelaxation and reduced vascular outflow, leading to congestion and trapping of de-oxygenated blood in the corpus cavernosa.
Non-ischaemic: Due to high arterial inflow, typically caused by fistula formation (congenital or traumatic).
Q: What are the clinical features of priapism?
Persistent erection lasting over 4 hours.
Pain localized to the penis.
History of known haemoglobinopathy or use of relevant medications.
Non-painful erection or not fully rigid erection suggestive of non-ischaemic priapism.
History of trauma to the genital or perineal region suggests non-ischaemic priapism.
Q: What are the investigations for priapism?
Cavernosal blood gas analysis: Differentiates ischaemic (reduced pO2 and pH, increased pCO2) from non-ischaemic priapism.
Doppler/duplex ultrasonography: Assesses blood flow in the penis as an alternative to blood gas analysis.
Full blood count and toxicology screen: Assess for underlying causes.
Q: What is the management for priapism?
Ischaemic priapism:
Medical emergency, aspiration of blood from cavernosa after 4 hours, often combined with saline flush.
If unsuccessful, intracavernosal injection of phenylephrine (vasoconstrictor), repeated at 5-minute intervals.
Surgical options if medical therapy fails.
Non-ischaemic priapism:
Not a medical emergency, usually managed with observation.
Q: What are the features of prostate cancer presentation?
Early prostate cancers: Few symptoms.
Metastatic disease: May present as bone pain.
Locally advanced disease: May present as pelvic pain or urinary symptoms.
Q: What diagnostic tests are used for prostate cancer?
Prostate Specific Antigen (PSA) Test
Digital Rectal Examination (DRE)
Transrectal Ultrasound (USS) (+/- biopsy)
MRI/CT and bone scan for staging.
Q: What is the significance of the PSA test in prostate cancer diagnosis?
Normal upper limit for PSA: 4 ng/ml.
False positives may be caused by: prostatitis, UTI, BPH, vigorous DRE.
Free:Total PSA ratio: If <20%, it is suggestive of cancer, and a biopsy is advised.
Q: What is the pathology of prostate cancer?
95% adenocarcinoma.
In situ malignancy may be found adjacent to cancer, requiring multiple biopsies to confirm.
Often multifocal, with 70% in the peripheral zone.
Graded using the Gleason grading system:
Two grades (1 for dominant, 2 for second most dominant).
Gleason score: 2 (best prognosis) to 10 (worst prognosis).
Lymphatic spread: First to obturator nodes, then to seminal vesicles and distant sites.
Q: What are the treatment options for prostate cancer?
Watch and Wait: Suitable for elderly, multiple co-morbidities, low Gleason score.
Radiotherapy: Curative and palliative options. Similar survival to surgery. Risk of radiation proctitis and rectal malignancy.
Surgery: Radical prostatectomy (surgical removal of the prostate). Common side effect: erectile dysfunction. Robotic surgery is increasingly used.
Hormonal Therapy: Testosterone stimulates prostate tissue. Options include bilateral orchidectomy, LHRH analogues, and anti-androgens.
Active Surveillance: Preferred for low-risk men (clinical stage T1c, Gleason score 3+3, PSA density <0.15 ng/ml/ml). Requires multiple biopsies and re-biopsy. Radical treatment if disease progression occurs.
Q: What are the features of localized prostate cancer?
Often asymptomatic in early stages due to cancers developing in the periphery of the prostate.
Possible symptoms include:
Bladder outlet obstruction: hesitancy, urinary retention.
Haematuria (blood in urine) and haematospermia (blood in semen).
Pain: back, perineal, or testicular.
Digital rectal examination (DRE): asymmetrical, hard, nodular enlargement with loss of median sulcus.
Q: What is the traditional investigation for suspected prostate cancer?
Transrectal ultrasound-guided (TRUS) biopsy.
Q: What is the current first-line investigation for suspected clinically localised prostate cancer according to NICE guidelines?
Multiparametric MRI.
Q: When should PSA testing be considered or offered?
Considered in men with suspected prostate cancer.
Offered to men older than 50 years who request a PSA test.
Q: What is the classical triad of renal cell cancer?
Haematuria.
Loin pain.
Abdominal mass.
Q: What is the management for confined renal cell cancer?
Partial or total nephrectomy depending on tumour size.
T1 tumors (≤ 7 cm) typically treated with partial nephrectomy.
Q: What is the initial management for renal colic?
Pain management and medical therapy:
NSAIDs are recommended as the analgesia of choice (e.g., diclofenac), but risks of cardiovascular events should be considered.
If NSAIDs are contraindicated or insufficient, IV paracetamol is recommended.
For severe pain in patients requiring admission, intramuscular diclofenac is suggested for rapid relief.
Alpha blockers:
Promote smooth muscle relaxation and dilation of the ureter to ease stone passage, recommended for distal ureteric stones <10 mm.
Q: What initial investigations should be done for renal stones?
Urine dipstick and culture.
Serum creatinine and electrolytes (check renal function).
FBC/CRP (to assess infection).
Calcium/urate levels (look for underlying causes).
Stone analysis should be done after stone passage.
Clotting if percutaneous intervention is planned and blood cultures if signs of sepsis.
Q: What imaging is recommended for renal stones?
Non-contrast CT KUB is the preferred imaging, to be performed within 24 hours of admission.
If a patient has a fever, a solitary kidney, or if the diagnosis is uncertain, an immediate CT KUB should be done.
CT KUB has a sensitivity of 97% and specificity of 95% for ureteric stones.
Ultrasound is used for pregnant women and children, though its sensitivity is around 45% and specificity is 90%.
Q: What is the management for renal stones according to NICE guidelines?
Stones < 5mm: Watchful waiting (most pass spontaneously).
5-10mm: Shockwave lithotripsy.
10-20mm: Shockwave lithotripsy or ureteroscopy.
> 20mm: Percutaneous nephrolithotomy.
Ureteric stones:
<10mm: Shockwave lithotripsy + alpha blockers.
10-20mm: Ureteroscopy.
Q: What are the management options for severe renal stones?
Stones < 5mm usually pass within 4 weeks.
More intensive treatment is needed for ureteric obstruction, renal developmental abnormalities (e.g., horseshoe kidney), or previous renal transplant.
Ureteric obstruction with infection is a surgical emergency and requires system decompression via nephrostomy tube, ureteric catheters, or ureteric stent placement.
Q: What are the prevention strategies for renal stones?
Calcium stones:
High fluid intake.
Add lemon juice to water.
Avoid carbonated drinks and limit salt intake.
Potassium citrate may be beneficial.
Thiazide diuretics (increase distal tubular calcium resorption).
Oxalate stones:
Cholestyramine reduces urinary oxalate secretion.
Pyridoxine reduces urinary oxalate secretion.
Uric acid stones:
Allopurinol.
Urinary alkalinization (e.g., oral bicarbonate).
Q: What is an epididymal cyst and its features?
Most common cause of scrotal swellings in primary care.
Separate from the body of the testicle.
Located posterior to the testicle.
Associated conditions:
Polycystic kidney disease.
Cystic fibrosis.
Von Hippel-Lindau syndrome.
Diagnosis is confirmed by ultrasound.
Management:
Usually supportive.
Surgical removal or sclerotherapy may be attempted for larger or symptomatic cysts.
Q: What is a varicocele and its features?
Abnormal enlargement of the testicular veins.
Often asymptomatic, but associated with infertility.
More common on the left side (over 80%).
Classically described as a ‘bag of worms’.
Associated with subfertility.
Q: How is a varicocele diagnosed?
Diagnosis is confirmed with ultrasound with Doppler studies.
Q: What is the management for a varicocele?
Usually conservative.
Surgery may be required if the patient experiences pain.
Debate exists on the effectiveness of surgery for treating infertility.
Q: What are the common features of testicular cancer?
Painless lump (most common presenting symptom).
Pain (in a minority of men).
Hydrocele.
Gynaecomastia (due to increased oestrogen:androgen ratio).
Germ-cell tumours → hCG → Leydig cell dysfunction → increases both oestradiol and testosterone production, but oestradiol rise is relatively greater.
Leydig cell tumours → directly secrete oestradiol and convert androgen precursors to oestradiols.
Q: What are the tumour markers for testicular cancer?
Seminomas: hCG may be elevated in around 20%.
Non-seminomas: AFP and/or beta-hCG elevated in 80-85%.
LDH is elevated in 40% of germ-cell tumours.
Q: What is the first-line investigation for testicular cancer?
Ultrasound.
Q: What is the management for testicular cancer?
Orchidectomy (surgical removal of the testicle).
Chemotherapy and radiotherapy may be given depending on staging and tumour type.
Q: What is testicular torsion?
Twist of the spermatic cord leading to testicular ischaemia and necrosis.
Most common in males aged between 10 and 30 years, with peak incidence between 13-15 years.
Q: What are the features of testicular torsion?
Severe pain of sudden onset.
Referred pain to the lower abdomen.
Nausea and vomiting may occur.
On examination:
Swollen, tender testis retracted upwards.
Skin may be reddened.
Cremasteric reflex is lost.
Prehn’s sign (elevation of the testis does not ease the pain).
Q: What is the management for testicular torsion?
Urgent surgical exploration.
If a torted testis is identified, both testes should be fixed, as the bell clapper testis condition is often bilateral.
Bilateral orchidopexy
Q: What are the features of urethral stricture?
Decreased urinary stream.
Incomplete bladder emptying.
Less common symptoms include:
Spraying of urinary stream.
Dysuria.
Q: What are the investigations for urethral stricture?
Uroflowmetry.
Ultrasound postvoid residual (PVR) measurement.
Q: What is the management for urethral stricture?
Dilation.
Endoscopic urethrotomy.
Q: What is the procedure for vasectomy?
A simple operation, usually performed under local anaesthesia (some cases with general anaesthesia).
The patient can go home after a couple of hours.
Q: How long does it take for a vasectomy to be effective?
Doesn’t work immediately.
Semen analysis needs to be performed twice (usually at 12 weeks) before unprotected sex can be resumed.
Q: What is the screening method for abdominal aortic aneurysm (AAA)?
A single abdominal ultrasound is recommended for males aged 65.
Q: What are the screening outcomes for abdominal aortic aneurysms based on aorta width?
< 3 cm: Normal, no further action.
3 - 4.4 cm: Small aneurysm, rescan every 12 months.
4.5 - 5.4 cm: Medium aneurysm, rescan every 3 months.
≥ 5.5 cm: Large aneurysm, refer within 2 weeks to vascular surgery for probable intervention.
Q: What is the management for low rupture risk AAA (aortic diameter < 5.5 cm)?
Abdominal ultrasound surveillance (timed based on aneurysm size).
Optimize cardiovascular risk factors (e.g. stop smoking).
Q: What is the management for high rupture risk AAA (aortic diameter ≥ 5.5 cm or rapidly enlarging > 1 cm/year)?
Refer within 2 weeks to vascular surgery for probable intervention.
Elective endovascular repair (EVAR) or open repair if unsuitable.
EVAR: A stent is placed via the femoral artery to prevent blood collection in the aneurysm. A complication of EVAR is an endo-leak, where the stent fails to exclude blood from the aneurysm, often presenting without symptoms on follow-up.
Q: What is the normal diameter of the infrarenal aorta?
1.5 cm in females.
1.7 cm in males after the age of 50 years.
Q: What is the most common cause of venous leg ulcers?
Venous hypertension secondary to chronic venous insufficiency.
Other causes include calf pump dysfunction or neuromuscular disorders.
Q: What is the location and pain characteristic of venous leg ulcers?
Located above the ankle.
Typically painless.
Q: What is the difference between deep venous insufficiency and superficial venous insufficiency?
Deep venous insufficiency is related to previous DVT.
Superficial venous insufficiency is associated with varicose veins.
Q: What imaging studies are used to assess venous leg ulcers?
Doppler ultrasound to look for reflux.
Duplex ultrasound to examine anatomy and flow of veins.
Q: What is the initial management for venous leg ulcers?
4-layer compression banding after exclusion of arterial disease or surgery.
If ulcers fail to heal after 12 weeks or are >10 cm², skin grafting may be needed.
Q: Where do arterial ulcers typically occur and what is their appearance?
Toes and heel.
They have a deep, punched-out appearance.
Typically painful with possible gangrene.
Q: What is the characteristics of arterial ulcers?
Cold with no palpable pulses.
Low ABPI measurements.
Q: What are the three main patterns of presentation in patients with peripheral arterial disease?
Intermittent claudication.
Critical limb ischaemia.
Acute limb-threatening ischaemia.
Q: What are the 6 P’s of acute limb-threatening ischaemia?
Pale.
Pulseless.
Painful.
Paralysed.
Paraesthetic.
‘Perishing with cold’.
Q: What are the initial investigations for acute limb-threatening ischaemia?
Handheld arterial Doppler examination.
If Doppler signals are present, ankle-brachial pressure index (ABI) should be obtained.
Q: How can acute limb-threatening ischaemia be differentiated between a thrombus and an embolus?
Thrombus:
Pre-existing claudication with sudden deterioration.
No obvious source for emboli.
Reduced or absent pulses in contralateral limb.
Evidence of widespread vascular disease (e.g., MI, stroke, TIA, previous surgery).
Embolus:
Sudden onset of painful leg (< 24 hours).
No history of claudication.
Clinically obvious source of embolus (e.g., atrial fibrillation, recent MI).
Normal pulses in contralateral limb.
Evidence of proximal aneurysm (e.g., abdominal or popliteal).
Q: What is the initial management for acute limb-threatening ischaemia?
ABC approach.
Analgesia: IV opioids are often used.
IV unfractionated heparin to prevent thrombus propagation, especially if the patient is not suitable for immediate surgery.
Vascular review.
Q: What are the definitive management options for acute limb-threatening ischaemia?
Intra-arterial thrombolysis.
Surgical embolectomy.
Angioplasty.
Bypass surgery.
Amputation: for patients with irreversible ischaemia.
Q: What are the features of critical limb ischaemia?
Rest pain in the foot for more than 2 weeks.
Ulceration.
Gangrene.
Patients often report hanging their legs out of bed at night to ease the pain.
Q: What is the ankle-brachial pressure index (ABPI) finding suggestive of critical limb ischaemia?
ABPI < 0.5.
Q: How is the ankle-brachial pressure index (ABPI) interpreted?
1: Normal.
0.6-0.9: Claudication.
0.3-0.6: Rest pain.
<0.3: Impending (severe ischaemia).
Q: What are the features of intermittent claudication?
Aching or burning in the leg muscles following walking.
Patients can typically walk for a predictable distance before the symptoms start.
Symptoms are usually relieved within minutes of stopping.
Not present at rest.
Q: What is the recommended assessment for intermittent claudication?
Check the femoral, popliteal, posterior tibialis, and dorsalis pedis pulses.
Check ankle-brachial pressure index (ABPI).
Duplex ultrasound is the first-line investigation.
Magnetic resonance angiography (MRA) should be performed prior to any intervention.
Q: What medication should all patients with established cardiovascular disease, including PAD, be taking?
A statin, with atorvastatin 80 mg recommended.
Q: What is the first-line medication for PAD recommended by NICE (2010)?
Clopidogrel (preferred over aspirin).
Q: What is the typical presentation of a ruptured abdominal aortic aneurysm (AAA)?
Severe, central abdominal pain radiating to the back.
Pulsatile, expansile mass in the abdomen.
Patients may be shocked (hypotension, tachycardia) or may have collapsed.
Q: What is the management approach for a ruptured AAA?
Surgical emergency: Immediate vascular review for emergency surgical repair.
If haemodynamically unstable, diagnosis is clinical—go straight to theatre.
If haemodynamically stable, a CT angiogram may be used to confirm the diagnosis and assess suitability for endovascular repair.
Q: What are varicose veins?
Dilated, tortuous, superficial veins due to incompetent venous valves.
Most commonly occur in the legs due to reflux in the great saphenous vein and small saphenous vein.
Q: What are common symptoms associated with varicose veins?
Aching, throbbing.
Itching.
Q: What is the first-line investigation for varicose veins?
Venous duplex ultrasound to demonstrate retrograde venous flow.
Q: What are the conservative management options for varicose veins?
Leg elevation.
Weight loss.
Regular exercise.
Graduated compression stockings.
Q: When should a patient with varicose veins be referred to secondary care?
Significant symptoms (pain, discomfort, swelling).
Previous bleeding from varicose veins.
Skin changes due to chronic venous insufficiency.
Superficial thrombophlebitis.
Active or healed venous leg ulcer.
Q: What are the treatment options for varicose veins in secondary care?
Endothermal ablation (radiofrequency or endovenous laser treatment).
Foam sclerotherapy (irritant foam induces vein closure).
Surgical treatments (ligation or stripping).
Acute management for pain in renal colic
IM diclofenac
Most likely causative agent of ascending cholangitis
e coli
What factors indicate severe pancreatitis
age > 55 years
hypocalcaemia
hyperglycaemia
hypoxia
neutrophilia
elevated LDH and AST
How should you manage a diverticulitis flare
oral antibiotics at home for a few days, if that doesnt work then you give Intravenous ceftriaxone and metronidazole
How should you manage congenital inguinal hernia
surgical repair asap
Difference in use between tamoxifen and aromatase inhibitor
tamoxifen - pre+peri menopausal
aromatase inhibitor - post menopausal
What should be given in cases of subarachnoid haemorrhage to avoid vasospasm
nimodipine
What testicular cancer type presents with normal HCG and AFP levels
seminoma
What electrolyte abnormality does SAH cause
SIADH -> hyponatraemia
Sigmoid and Caecal volvulus on AXR
Sigmoid volvulus = coffee bean
Caecal volvulus = looks like a foetus
When is bariatric surgery recommended
BMI >40
Which renal stones are opaque
calcium oxalate
calcium phosphate
triple phosphate
Which renal stones are semi opaque/ground glass appearance
cystine stones
Which renal stones are radio lucent
urate
xanthine
What is the most common cause of large bowel obstruction
tumour (colon cancer)
most common cause of epididymo-orchitis
chlamydia
What hormonal therapy can you give for prostate cancer
GnRH agonists
What do you have to be aware of when using GnRH agonists for prostate cancer and how do you deal with it
‘tumour flare’ - causes a paradoxical increase in LH initially before falling, leading to bone pain, bladder obstruction etc
Anti androgen can help reduce this
Haemodynamic changes seen in cardiogenic shock
increased SVR (vasoconstriction in response to low BP)
increased HR (sympathetic response)
decreased cardiac output
decreased blood pressure
Haemodynamic changes seen in hypovolaemic shock
increased SVR
increased HR
decreased cardiac output
decreased blood pressure
Haemodynamic changes seen in septic shock
occurs when the peripheral vascular dilatation causes a fall in SVR
similar response may occur in anaphylactic shock, neurogenic shock
reduced SVR
increased HR
normal/increased cardiac output
decreased blood pressure
What other condition can ruptured AAA present like
renal colic - loin to groin pain
When you cant resect a pancreatic cancer, what do you do
biliary stenting
How should you treat an inguinal hernia
treat even if asymptomatic
with mesh repair
How should you treat bilateral/recurrent inguinal hernia
laparoscopic mesh repair
How should you treat unilateral inguinal hernia
open mesh repair
Management for symptomatic chronic subdural haemorrhage
burr holes
Management for symptomatic acute subdural haemorrhage
decompressive craniectomy
Ileostomy vs colostomy
Spout + Permanent = End Ileostomy
Spout + Temporarary = Loop Ileostomy
No Spout (flush) = Colostomy
Spout + urine in bag = Ileal conduit
Urine and faeces are irritant to the skin (so create spout). Colostomy contents are hard faeces so less likely to cause irritation to the skin (so can be flush to skin).
What nerve causes the cremasteric reflex
Genitofemoral nerve
What fluid do you give during resuscitation
saline or hartmanns
How should you manage hydronephrosis
nephrostomy - urgently relieve the obstruction causing kidney pressure
Brown pigmentation (haemosiderin), lipodermatosclerosis (champagne bottle legs), and eczema are signs of what
venous insufficiency -> venous ulcer formation
What can total parenteral nutrition (TPN) do to liver function
produced cholestatic picture ie ALP super high
If you have prostatitis, when can you measure PSA
1 month after
What factors mean you have to wait for 48 hours before measuring PSA
Vigorous exercise, ejaculation, and digital rectal examination
What should you do if someone has a hydrocoele
Urgent US to exclude other things
If its a pregnant woman, how should you manage renal stones
ureteroscopy
Relation of Mumps to testicular swelling
mumps causes orchitis
if they have previously had mumps when they were a child, orchitis doesnt happen so it has to be epididymo orchitis
How do you calculate surface area for a burn
Wallace’s Rule of Nine: Each of the following is 9% of the body when calculating surface area % if a burn:
Head + neck, each arm, each anterior part of leg, each posterior part of leg, anterior chest, posterior chest, anterior abdomen, posterior abdomen
In anal cancer, what imaging modality would you use for T staging and M staging
T - CT
M - MRI
Which arteries supply the sigmoid colon
The sigmoid colon is directly supplied by the sigmoid arteries, which branch directly from the inferior mesenteric artery.
What artery supplies the caecum, ascending colon and transverse colon
Superior mesenteric artery
Most common area for prostate cancer
The peripheral zone
What do you give preoperatively in orthopaedic surgeries
LMWH and compression stockings to prevent DVT
‘Snowstorm’ appearance on US of axillary lymph nodes
implant rupture
What is the treatment go FAP if found early
panproctocolectomy - get rid of it all
what is the hallmark sign of tumour lysis syndrome
elevated uric acid
how do you treat an anal fissure that doesnt respond to conservative measures
spincterotomy
blood gas result after giving fluids
hyperchloraemic metabolic acidosis
