Surgery Flashcards
Define acute cholecystitis
Acute inflammation of the gall bladder, most commonly caused by gall stones
epidemiology of acute cholecystitis
- Develops in 10% of people with symptomatic gall stones
- Gall stones are common - 10% of people over the age of 50y have gall stones
- Females > Males (3:1) before the age of 50 years
- Can occur at any age but most commonly occurs in overweight, middle-aged women
Aetiology of acute cholecystitis
• Calculous Cholecystitis (Gall bladder stones) - 90-95%
⁃ Stone Types:
1. Pure cholesterol stones - 10%
⁃ Often solitary, large and round
⁃ Most common stone in Asia
⁃ Radiolucent
- Pure pigment (bile salts) stones - 10%
⁃ Occasionally associated with haemolytic anaemia due to increased formation of bile
pigment from Hb
⁃ Radiolucent - Mixed stones - 80%
⁃ Combination of calcium salts, cholesterol and pigment stones
⁃ Usually multiple stones
⁃ 10% are radioopaque
• Acalculous Cholecystitis (Others):
⁃ Severe trauma
⁃ Sepsis
⁃ Helminthic infection - common in Asia
⁃ Salmonella associated Typhoid fever –> 2° cholecystitis
⁃ CMV associated with AIDs-related cholecystitis
⁃ Longterm TPN
Risk factor for acute cholecystitis
5Fs of gallbladder disease - fair, forty, female, fat, fertile
- Increasing age
⁃ Female (pregnancy and use of the OCP)
⁃ Obesity or rapid weight loss
⁃ Chronic haemolytic disorders (pigment stones)
⁃ Longterm TPN (alters bile constituents)
⁃ Previous Sx or inflammation (Crohnʼs) affecting the terminal ileum (alters bile constituents as most of
the bile salts are reabsorbed here)
Pathophysiology of acute cholecystitis
Calculous cholecystitis:
1. Obstruction of the GB neck or cystic duct causing a closed-loop obstruction
⁃ Usually by impacted gall stones –> acute inflammation of the GB wall
⁃ Choledocholilithiasis
2. Distention of the GB
⁃ Due to continuing mucus secretion from the cells located at the neck of the GB
⁃ Bacterial multiplication
3. Blood flow and lymphatic drainage compromised
⁃ Due to increased pressure of the closed-loop obstruction
4. Arterial blood flow compromised
⁃ Pressure increases above arterial pressure –> ischaemia, necrosis and perforation
Acalculous cholecystitis:
• Exact mechanism unknown
clinical features of acute cholecystitis
• Hx:
⁃ Severe continuous RUQ abdominal pain lasting >30min
⁃ May begin in the epigastrium and migrate to the RUQ
⁃ Associated nausea, vomiting and anorexia
⁃ Right shoulder tip or scapular pain:
Due to peritoneal irritation involving the diaphragm (phrenic nerve)
⁃ Previous Hx of biliary colic:
Intermittent severe epigastric and RUQ pain that resolves after a few hours
GB tenderness during episodes
• Examination:
⁃ Fever (common)
⁃ Murphyʼs Sign
⁃ Pain on inspiration when two fingers are placed over the RUQ
⁃ RUQ mass - GB may be palpated in 30-40% of cases
⁃ Jaundice (uncommon) - due to obstruction of the common bile duct
investigations for acute cholecystitis
- Bloods:
⁃ FBC - Elevated WBCs (unlike in biliary colic)
⁃ CRP - Elevated (unlike biliary colic)
⁃ LFTs - Elevated GGT, ALP and bilirubin
⁃ Serum amylase - to exclude acute pancreatitis
⁃ Trop T - ECG - rule out MI
- RUQ U/S:
⁃ Distended GB
⁃ Thickened GB wall
⁃ +/- Gall stones
⁃ Positive Murphyʼs Sign
⁃ Pericholecystic fluid (collection of fluid seen around the GB during)
DDx of acute cholecystitis
• Appendicitis - highly situated appendix
• Right basal pneumonia
• Perforated peptic ulcer
• Pancreatitis
• MI
• Biliary colic
• Acute cholangitis - Charcotʼs triad of fever,
jaundice and RUQ pain
Management of acute cholecystitis
Initial management/Supportive care:
⁃ Nill by mouth (NBM)
⁃ IV hydration, correction of electrolyte abnormalities, Analgesia
⁃ Antibiotics (gram negative cover) - 2nd gen cephalosporin + metronidazole
Rx is usually initially conservative unless complicated (e.g. perforation)
⁃ As above
⁃ +/- Cholecystectomy performed after 48 hours (“hot lap chole”)
⁃ or Allow inflammation to settle and GB removal in 2-3 months
Complicated –> Sx
Poor surgical candidates receive a percutaneous cholecystostomy tube
complications and prognosis of acute cholecystitis
Complications:
• Perforation - 10%
⁃ Due to failed conservative management and delayed presentation due to transient symptom relief
from GB decompression
⁃ Leads to generalised biliary peritonitis
⁃ 30% mortality rate with free perforation
• Suppurative cholecystitis
⁃ Thickened GB wall infiltrated with WBCs, intra-wall abscess and necrosis
⁃ May result in perforation
• Gangrenous cholecystitis - 2-30%
⁃ Occurs most commonly at the fundus of the GB due to vascular compromise
Prognosis:
• Gall bladder perforation carries a 30% mortality rate
• Untreated acute acalculous cholecystitis is life-threatening - up to 50% mortality rate
epidemiology and risk factors of gall stones
Epidemiology
⁃ Common - 10% of age>50 years
RF:
⁃ Females, overweight, multiparity, increases with age
clinical features of gall stones
⁃ Often asymptomatic until they obstruct
⁃ “Colicky pain” - Pain that comes and goes in the RUQ due to impaction of the stones into the neck of the GB
⁃ Obstructive jaundice if stones involve the common bile duct
sequelae of gall stones
- Non-obstructive gall stones –> asymptomatic
⁃ Transient obstruction of the cystic duct –> biliary colic
⁃ Recurrent obstruction –> chronic cholecystitis
⁃ Permanent obstruction of the cystic duct –> acute cholecystitis
⁃ Obstructed common bile duct –> obstructive jaundice
⁃ Obstructed ampula –> acute pancreatitis
Ix of gall stones
-LFTs - Obstructive picture
⁃ Increased PTT due to vit K deficiency
⁃ U/S - presence of gall stones
⁃ ERCP - can also be interventional in removing stones near the ampula
⁃ MRCP (magnetic resonance cholangiopancreatography) - visualise the biliary tree but no therapeutic use
⁃ Haemolysis screen if pigmented stones suspected or found
define colorectal cancer
any malignancy arising from the colon or rectum
epidemiology of CRC
- 3rd most common cancer in men and women in the developed world
- Rare before 50 years
- Mortality rates are similar in men and women but increase in men over 50 year
AETIOLOGY of CRC
Risk factors:
Family Hx
Western Diet
Low fibre and high fats –> prolongs colonic transit time
Processed and red meats –> toxic nitrogenous waste fermented in the gut
Risk demonstrated in migrating populations to western countries and adopting western diet
Excess alcohol
T2DM
Ulcerative colitis - Risk increases by 1% per year after 10 years of active disease Smoking
Inherited genetic causes:
FAP (Familial Adenomatous Polyposis)
⁃ Autosomal dominant mutation in the APC gene –> >100 polyps forming by teenage years
⁃ Inevitably 100% will develop colorectal cancer if untreated
HNPCC (Hereditary Non-Polyposis Colorectal Cancer) or Lynch Syndrome
⁃ Defects in mismatch repair genes –> 70% lifetime risk of developing CRC
⁃ Increase risk of other cancers such as endometrial, ovarian, urothelial, small bowel and brain
⁃ Exhibits “incomplete penetration” (not everyone with the defect will develop the disease)
Peutz Jaghers Syndrome
⁃ Causes hamartomatous polyps throughout the GIT
⁃ Typically have freckles around the mouth and on the hands, feet and genitalia
⁃ 50% die by age 50 due to polyp-related complications such as intessusception or cancer
pathophysiology of CRC
• “Adenoma-carcinoma sequence”
• Lesion Characteristics:
⁃ Most lesions are exophytic (protrude into the lumen)
⁃ Later they progressively ulcerate and invade the muscular bowel wall
⁃ Invasion of the serosa and surrounding tissue –> stromal or annular fibrosis –> narrowing & obstruction
metastases of CRC
Direct:
⁃ Tumour directly invades neighbouring tissue and can cause fistulas between adjacent structures such as the stomach, small bowel, bladder,
• Lymphatic:
⁃ Mesenteric LN –> Para-aortic LN
*LN = lymph node
• Haematogenous:
⁃ Liver
⁃ Lungs and brain (uncommon)
Presentation of CRC
• Asymptomatic - in early stages of disease
• Iron-deficiency Anaemia
⁃ Occult bleeding from the tumour surface over time causes iron-deficiency anaemia
⁃ Iron-deficiency anaemia in a patient >50 years is CRC until proven otherwise
⁃ Can be the only presentation of a right-sided CRC
• Rectal bleeding
⁃ Carcinomas distal to the splenic flexure causes visible PR bleeding
⁃ Blood can be mixed into the stool which is a sign of a cancer more proximal
• Change in bowel habit
⁃ Loose stools (in particular) are caused by secretions of blood or mucus into the bowel lumen
⁃ Mucus is secreted by adenomatous lesions and can also cause hypokalaemia if severe
• Bowel Obstruction
⁃ The more distal the tumour, the more likely it is to cause obstruction due to the narrower diameter of the left colon and the formation of harder stools
• Tenesmus
⁃ “The feeling of incomplete evacuation”
⁃ Caused by a tumour in the lower 2/3rds of the rectum causing a sudden urge to defecate
• Bowel Perforation
⁃ Caused by cancer invading completely through the bowel wall –> Acute abdomen with peritonitis
⁃ E.g. Left iliac fossa pain caused by pericolic abscess (collection formed due to perforation)
examination and investigation for CRC
• General: (signs of late disease)
⁃ Cachexia, weight loss, malaise and supraclavicular node enlargement
• Abdo Exam:
⁃ Usually normal
⁃ Mass
⁃ Hepatomegaly (due to liver mets)
• Rectal Exam:
⁃ MUST be performed if CRC is suspected - Most cancers are located in the distal 12cm of the colon
⁃ Assess Pouch of Douglas (through the anterior wall of the rectum)
⁃ Inspect/sample stool/blood/mucus
Ix:
• Bloods
- Anaemia
- Altered liver enzymes - liver mets
• Colonoscopy is gold standard
• Fixed or flexible sigmoidascope can be performed at the time of presentation without bowel prep
- Fixed can reach 50% of CRCs and flexible (75%)
• CXR and CT for analysis of mets
STAGING OF CRC
• Dukes Classification:
⁃ A - Limited to the mucosa
⁃ B - Invaded through the mucosa +/- adjacent tissue but no nodes
⁃ C - Nodal involvement
⁃ D - Distant mets
• TNM:
⁃ Tumour:
⁃ T1 = Tumour invasion of submucosa
⁃ T2 = Muscularis propria
⁃ T3 = Serosa
⁃ T4 = Other adjacent organs
• Nodes:
⁃ Nx - Nodes not assessed
⁃ N0 = No nodal involvement
⁃ N1= Metastasis to 1-3 nodes
⁃ N2 = > 3 nodes
• Metastasis
⁃ N0 = No distant metastasis
⁃ M1 = Metastasis present
management of CRC
• Surgical Resection + Resection of draining lymph nodes
⁃ Depends on the location of lesion
• Radio and chemotherapy play some role in reducing recurrence rates in Duke C tumours
what is VTE
- Venous Thromboembolism (VTE) manifests as DVTs and PEs
- Preventable cause of death in hospital patients
- Many at-risk patients do not receive adequate DVT/PE prophylaxis
- Hospital-acquired DVT/PE usually clinically silent
RF for VTE
• Patient Factors:
⁃ Age > 40 years
⁃ Obesity
⁃ Immobility
⁃ Varicose veins
⁃ Long haul flights
⁃ Previous DVT/PE
⁃ Thrombophilia
⁃ Antithrombin deficiency
⁃ Protein C + S deficiency
⁃ Factor 5 Leiden variant
⁃ Antiphospholipid syndrome/Lupus
⁃ Oestrogen therapy - OCP, HRT
• Disease/Surgical Factors
⁃ Surgery - Especially pelvis, hip, knee or lower limbs
⁃ Trauma
⁃ Malignancy
⁃ Cardiac failure
⁃ Infection or Inflammatory conditions
⁃ IBD
⁃ Nephrotic syndrome
⁃ Polycythemia
⁃ Sickle-cell anaemia
risk stratification for VTE
VTE pharmacology
non pharmacological Rx for VTE
Definition, epidemiology and RF for bladder cancer
Definition: Malignancy derived from the tissue of the urinary bladder
Epidemiology:
• Rare before 50 years
• Males > Females (3:1)
Risk Factors:
• Aniline dyes - used in rubber and cable industries (20-60x increased risk of TCC)
• Smoking
• Cyclophosphomide
• Urachal remnants –> adenocarcinoma
• Urinary schistosomiasis and other chronic bladder infections –> SCCs
classification of bladder cancer
Classification:
• Benign
⁃ Transitional cell papilloma
⁃ Grow inwards into the bladder wall
⁃ Considered low grade carcinomas since they have a tendency to recur after removal
⁃ Regular cystoscopy is recommended due to malignant potential
• Malignant
⁃ Transitional cell carcinoma - 90%
⁃ Most common form of malignancy of the bladder
⁃ Squamous cell carcinoma
⁃ Arises in areas of metaplasia
⁃ Adenocarcinoma (uncommon)
⁃ Occurs in urachal remnants (embryological remnant)
⁃ 2°
⁃ Direct invasion from adjacent structures - e.g. colonic, renal, ovarian, uterine, prostatic Ca
spread of bladder cancer
• Direct invasion:
⁃ Initially through the muscularis propria of the bladder
⁃ Perivesical tissue where it can enter the colon
⁃ The uterus may be involved in women & the prostate may be involved in men
⁃ The carcinoma does not cross the rectovesical pouch
• Distant spread –> lungs, brain, bones and liver
definition, epidemiology and RF of transitional cell carcinoma (bladder cancer)
Definition:
• Malignancy of the transitional cells that line the urinary tract from the renal pelvis to the urethra
Epidemiology:
• Most common cancer of the bladder (90%)
• Males > females (3:1)
• Lowest incidence in Asian countries
• Occupational exposure accounts for 1/4 of cases
Aetiology:
• Risk factors:
⁃ Cigarette smoke
⁃ Age
⁃ Male
⁃ Exposure to carcinogens:
⁃ Analine (aromatic amines) used in dye and rubber industries
⁃ Due to carcinogens like β-naphthyl amine in the urine
⁃ Polycyclic hydrocarbons - coal, aluminium and roofing-industries
⁃ Pelvic radiation
⁃ Chemotherapy with cyclophosphamides
⁃ Chronic inflammation - Schistosomiasis infection and chronic IDCs
pathology and clinical features of transitional cell carcinoma (bladder cancer)
Pathology:
• Malignancies more common at the base, trigone and at the ureteric orifices
• Commonly multiple that can extend from the renal pelvis to the urethra
Clinical Features:
• Painless Haematuria (microscopic or macroscopic)
• Dysuria (common)
• Frequency/urgency of micturition
investigations of transitional cell carcinoma (bladder cancer)
Investigations:
• Urinalysis - haematuria; pyuria can also be present
• Urine cytology - Positive in high-grade carcinomas (90%) and always signifies TCCs
⁃ Urine typically contains transitional cells that are shed from the urinary tract
⁃ Non-invasive method for diagnosing cancer
⁃ Not good for low-grade cancers (30%)
• Imaging:
⁃ Renal/bladder U/S
⁃ CT abdo/pelvis
⁃ IV pyelogram - visualise the kidneys at varying stages after injection of IV contrast ⁃> May see filling defect, obstruction or hydronephrosis
• Cystoscopy
management and prognosis of transitional cell carcinoma (bladder cancer)
Management:
• TNM staging
• Surgical:
⁃ Low risk superficial cancers - Transurethral resection of Bladder Tumour
⁃ High risk - TURBT + post-op intra-vesicular chemo
• Invasive tumours:
⁃ Pre and Post-op chemo or radiotherapy
⁃ Sx - Radical cystectomy with LN disection
• Metastatic disease
⁃ Systemic chemo + Sx + radiotherapy
Prognosis:
• Low grade lesions - high risk of tumour recurrence but low risk of disease progression and death
• High grade lesions - high risk of recurrence and progression
⁃ Overall survival with cystectomy is ~ 50%
types of kidney stones
Definition and epidemiology of urinary retention
Definition:
Impaired urinary flow due to physical obstruction at any level from renal calyces to external urethral meatus.
Epi:
- Male < 60yrs - Renal Calculi
- Male > 60yrs - Benign Prostatic Hypertrophy (BPH)
- Females - Pregnancy & Renal Calculi
pathophysiology of urinary retention
•Intraluminal
- Calculi (Renal Colic)
- Blood clot
- Rupture - traumatic or iatrogenic
•Luminal
- Stricture/stenosis - native or iatrogenic
- Ischaemia
- Haematoma
- Tumour
•External
- Pregnancy
- BPH (Benign Prostatic Hypertrophy)
- Other neoplastic process or mass
when to inflate the catheter baloon?
•1) Ensure IDC all the way to the hilt
2) Ensure Urine Flowing through IDC
3) Watch patients face when inflating the balloon, feel for significant resistance
4) Pull IDC back and feel balloon tug on bladder neck
Haematuria
- Macroscopic vs microscopic
- Differential causes → 20% underlying malignancy and 80% benign causes, infection, stone, inflammation
worry if you see clots, clot retention, fever
Management:
Wash the bladder continuously
Upper and lower tract imaging + Urine cytology + Referral to urologist for cystoscopy
Epidemiology and presentation of renal colic
- Epidemiology:
- 5-15% prevalence
- 30-40 years common, but any age
- 2:1 M:F but changing
Presentation:
- Severe pain - “Loin to groin”
- Restlessness - “Writhing agony”
- Nausea & vomiting
- Haematuria
Diagnosis of renal colic
Diagnosis:
History
Physical exam
Urinalysis
Dipstick
Formal m/c/s
Blood tests (UEC, FBC)
Imaging studies
Imaging:
CT KUB
X-Ray KUB (85% visible)
Indications of urgent treatment for renal colic
Indications for urgent treatment:
- Septic -
- Temperature > 37.80
- Tachycardic
- Hypotensive
- Renal impairment
- Creatinine raised – everyone is different but >200
- Single kidney
- Uncontrolled pain Despite adequate analgesia
- Urgent treatment options:
1. Ureteric stent
2. Nephrostomy tube
definition of Testicular torsion
•DEF: Rotation of the testis on its spermatic cord causing occlusion of its venous drainage and blood supply.
Epidemiology, presentation and Rx of testicular torsion
- Epidemiology:
- Commonly 12-19yo
- 75% cases < 20yo
Presentation:
- Acute onset pain
- Swollen, tender testicle
- Firm texture
- High riding or horizontal lie
- Absence of cremasteric reflex
- Treatment:
- Surgical exploration
- Do not delay surgery for further investigation
Define Fournier’s Gangrene
Necrotising infection involving the soft tissue of the perineum and external genetalia.
Epidemiology and pathophysiology of Fournier’s Gangrene
- Epidemiology:
- Most commonly 60-70yo
- Overall mortality ~ 40%
- Associated sepsis ~ 80% mortality
- Diabetes mellitus ~ 50% cases
- Medically immunosuppression ~ 10% cases
- Pathophysiology:
- Anaerobic and aerobic organisms – polymicrobial
- Aggressive and frequently fatal
E. coli, Klebsiella, enterococci along with anaerobes (Bacteroides, Fusobacterium, Clostridium, anaerobic or microaerophilic streptococci
presentation of Fournier’s Gangrene
- Necrotic perineal tissue
- Rapidly progressive cellulitis
- Immunocompromised:
- Diabetic
- Alcoholic
- Malnutrition
- Medication (steroids, immunosuppressants)
- Malignancy
Crepitus and foul smelling exudate usually with more advanced infection
treatment for fournier’s gangrene
•Broad spectrum antibiotics – polymicrobial infection
Tazocin/Meropenem + vancomycin + clindamycin
- Debridement of all non-viable tissue as urgent as possible
- Often requires several trips to theatre for repeat debridement and eventual reconstruction
clinda has antitoxin effect for strep toxin
define Paraphimosis
Condition where the foreskin becomes trapped behind the glans penis
Usually due to chronic inflammation under the prepuce and development of a phimosis
presentation, complications and management of paraphimosis
- Presentation:
- Uncircumcised male
- Painful, irreducible foreskin
- Swollen glans penis
- Complications:
- Gangrenous glans penis
- Management:
- Reduce foreskin
- Manually
- Shift the oedema – glucose; ice; pressure
- Surgical release (dorsal slit) with local
Penile Priaprism
persistent erection of the penis that is not associated with sexual stimulation or desire
presentation and aetiology of penile priaprism
- Presentation
- Prolonged erection with failure of detumescence
- Ischaemic vs high-flow
- Ischaemic: fully erect and painful
- Aetiology
- Haematological – sickle cell•
Iatrogenic – penile injections
•Medication/Drugs – cocaine
90% of men with erection >24hrs will lose the ability to have intercourse again. Early return to flaccidity usually carries good outcomes
management of penile priaprism
define penile fracture
Rupture or tear of the tunica albuginea of the corpus cavernosum typically occurs when excessive bending force is applied to the erect penis.
presentation, treatment and complications of penile fracture
- Presentation:
- History of risk-taking behavior
- Pop or cracking sound
- Sudden onset pain
- Tumescence
- Haematoma
- Treatment:
- Urgent urology review
- Surgical intervention
- Complications:
- 50% impotence
- Peyronie’s disease
Distal radius # MOI, epi, RF, clinical features
MOI: FOOSH
Epidemiology:
Accounts for 17.5% of all adult fractures
F>M (2-3:1)
Bimodal age distribution
- Younger patients due to high energy mechanisms
- Older patients due to low energy mechanisms
Risk factors:
Osteoporosis, DR# is predictor for subsequent fractures → DEXA
Clinical features:
wrist pain, swelling, deformity, examine skin for open wounds, NV status (motor, sensory of ulnar, rad and med N), radial pulse for perfusion of hand
Colles’ # vs smith’s #
colles’ → Low-energy, dorsally displaced, extra-articular #
smith’s → low energy, volarly displaced, extra articular #
Monteggia injury
- Proximal 1/3 ulna fracture with associated radial head dislocation
- Epidemiology → Rare in adults, common in children 4-10yo
- Clinical presentation→ Pain & swelling at elbow
- Examination:
1. Inspection: ?obvious dislocation, skin integrity
2. ROM & stability
3. NV exam
PIN neuropathy (Wrist extension & radial deviation, Thumb extension, MCP extension)
- Pain & swelling at elbow
Scaphoid # MOI and epidemiology
MOI: FOOSH, high or low energy mechanism
Epidemiology: Account for 60% of carpal bone fractures, 15% of wrist injuries, M>F (2:1), most common in 30s, Waist (65%), proximal 1/3 (25%), distal 1/3 (10%)
Scaphoid # clinical presentation
- Variable level of wrist pain
- Wrist swelling. Rarely any ecchymosis, haematoma or gross deformity
- Pain with resisted pronation
- Provocative tests: 1. Anatomic snuffbox tenderness (dorsal) 2. Scaphoid tubercle tenderness (volar) 3. Scaphoid compression test (scaphoid loading)
scaphoid # imaging and management
- Imaging
- XR: PA, lat, oblique, scaphoid view (20deg wrist ext, 20deg ulnar deviation)
- If radiographs unremarkable (27%), but high clinical suspicion → CT
- Management
- Stable nondisplaced fracture → thumb spica cast
- If unstable, or displaced >1mm → perc screw
Epidemiology, MOI, examination and imaging of humeral shaft #
Epidemiology & MOI:
- Bimodal age distribution (Young patients with high-energy trauma; Elderly, osteopenic patients with low-energy injuries)
Examination
- NV status: radial nerve!
* Imaging - AP & lateral xray with view of joint of above & below
management of humeral shaft #
- Coaptation splint, then functional brace (90% union rate)
-
ORIF
Absolute indications: - Open fracture
- Vascular injury requiring repair
- Brachial plexus injury
- Floating elbow (ipsilateral forearm #)
- Compartment syndrome
Relative indications:
Bilateral humerus #
Polytrauma patient
Pathological #
both bone forearm #
MOI: fall from height e.g. playground equipment
Epidemiology: ??
Clinical presentation:
- Forearm pain & refusing to move arm
- Exam:
Swelling deformity, ecchymosis
Check for open wounds e.g. puncture
Complete examination of ipsilateral limb
for concomitant injury
NV exam, check compartments
Imaging
AP & lat of forearm, wrist & elbow
Management
CR & above elbow cast +/- tens nail
NOF # immediate management
- NOF pathway:
ECG
CXR
IDC & U/A
Bloods
Analgesia
FI block - withhold anticoagulants
- NBM + chart IVF
- call ortho!
definitive management of NOF #
- Non-op?
- Non-ambulatory, minimal pain, high risk surgical candidate
- Very rare!
- Operative management
- Intracapsular vs extracapsular fractures
- Hemi vs total arthroplasty
- Timing of surgery?
- As soon as medically possible
- Should be within 24-48 hours
intracapsular vs extracapsular NOF #
- Intracapsular
- Subcapital, transcervical, basicervical
- More likely to disrupt blood supply to femoral head → AVN, so are treated with arthroplasty in elderly
- Extracapsular
- Intertrochanteric, subtrochanteric
- Treated with internal fixation device e.g. IMN
- Capsule of hip joint attaches along intertrochanteric line on anterior femur & ~1.5cm above intertroch line posteriorly
blood supply of femur
- Profunda femoris a branches off ext iliac artery
- Medial & lateral femoral circumflex arteries branch off this & encircle the base of the femoral neck, giving off retinacular vessels which supply the femoral head in a retrograde manner
- NOF#s can disrupt this blood supply → AVN of femoral head
complications of NOF #
- AVN (10-45%)
- Risk depends on initial degree of displacement, nonanatomical reduction
- Non-union (5-30%)
- Dislocation
- High with THA (~10%, 7x higher than hemi)
- Loss of independence
- Mortality
- 30% at 1 year
- Pre-injury mobility is the biggest determinant of postoperative survival
- Mortality risk is decreased at 30 days & at 1 year post-op when surgical intervention is performed within 24 hours of admission
Define SSI (surgical site infection)
Infection related to an operative procedure
that occurs at or near the surgical incision
within 30 days of the procedure
or
within 90 days if prosthetic material is
implanted at surgery
How do we know a surgical site infection (SSI) has occurred?
Clinical criteria for defining Surgical Site infecton include one or more of the following: -
- A purulent exudate draining from a surgical site
- A positive fluid culture obtained from a surgical site that was closed primarily
- A surgical site that is reopened in the setting of at least one clinical sign of infection (warmth, pain, erythema and swelling,) and is culture positive or not cultured
- The surgeon’s diagnosis of infection
what is the triad that indicates acute cholangitis?
Sudden onset of a triad of symptoms including jaundice, right upper quadrant pain and rigours (Charcot’s triad) indicates acute cholangitis.
Mirizzi’s syndrome
Mirizzi’s syndrome is where a stone impacted in the neck of the gallbladder causes distension of the gallbladder and jaundice due to extrinsic compression of the common hepatic/common bile duct.
Investigations for jaundice
-
Blood test
a. Full blood count along with red cell indices including reticulocyte counts are useful in identifying the presence and type of anaemia (secondary to haemolysis, haemoglobinopathies) and thrombocytopenia (secondary to portal hypertension).
b. bilirubin, albumin and INR convey information on liver function, with platelets conveying information on the level of fibrosis, unconjugated and conjugated bilirubin fractions. The most common cause of an isolated elevated bilirubin concentration is Gilbert’s syndrome.
c. albumin
d. PT time and INR will be raised, clotting factors 2, 5, 7, 9, 10 will eb reduced
e. ALP - ALP is usually high in childhood (bone growth) and pregnancy (placental production)
f. GGT
f. AST, ALT. AST is good for alcohol related liver injury and autoimmune hep
2. IMAGING
a. U/S (preferred) - cyst, steatosis
b. CT - Computed tomography (CT) with oral
and intravenous contrast agents may demonstrate liver, biliary
and pancreatic tumours, portal lymphadenopathy and tumour
spread beyond the organ of origin. It can show biliary dilatation
and the level of obstruction (Figure 4). It may demonstrate a
cirrhotic liver, with a nodular or fine cobblestone appearance of
the margin, liver lobar asymmetry, caudate hypertrophy and
features of portal hypertension such as varices, splenomegaly
and ascites.
c. MRI
D. PET
e. MRCP - Magnetic resonance cholangiopancreatography (MRCP), using T2 weighted sequences, is a non-invasive, non-contrast method of obtaining an accurate ‘road map’ of the biliary tree and has now superseded diagnostic endoscopic retrograde cholangiopancreatography (ERCP)
f. ERCP - ERCP with a side viewing duodenoscope is widely considered to be the gold standard for investigation of biliary and pancreatic duct pathology. It permits direct examination and biopsy of the ampulla in cases of suspected ampullary carcinoma. Cannulation of the ampulla, injection of water-soluble contrast agents and real-time screening permits diagnostic and therapeutic manoeuvres such as endoscopic sphincterotomy, gallstone extraction, biliary brushing for cytology and insertion of plastic or metal endobiliary or pancreatic duct stents.
g. liver biopsy - It is generally not recommended to biopsy a liver tumour if the patient has resectable disease, due to the risk of disease dissemination and such a biopsy should only be performed after multidisciplinary team discussion.
h. Laparoscopy - Laparoscopy is used selectively in the staging of hepaticopancreatico-biliary malignancies, in particular looking for small-volume peritoneal disease, not seen on cross-sectional imaging, which might preclude a major resection.
i. PET CT - staging of hepato-pancreatico-biliary cancers.
define cholangitis +its causes
- Inflammation and/or infection of the biliary tree
- Often referred to as ‘biliary sepsis’
- rare but can be 1-2% after ERCP
Causes of cholangitis:
- Obstruction of biliary tree secondary to gallstones (including Mirizzi’s syndrome, gallstone-related oedema compressing biliary tree as opposed to gallstones themselves) (Commonest cause)
- Infection post-ERCP
- Invasion by tumour (Pancreatic, cholangiocarcinoma, hepatocellular carcinoma, metastases)
- Roundworm or liver fluke infection (common overseas)
- HIV cholangiopathy
presentation and DDx of cholangitis
Presentations of cholangitis
The following make up the classical ‘Charcot’s triad’
- Jaundice
- Fever
- RUQ pain – severe
- Shock (due to sepsis) and confusion added to Charcot’s triad = Reynold’s pentad
- Jaundice may not always be present, especially if a patient already has a biliary stent in situ
- PMHx
- Gallstones
- Cholecystitis
- HIV
- Peritonism is uncommon and suggests alternative cause, e.g. appendix or ruptured gall bladder
Differential diagnosis of cholangitis
- Cholecystitis
- Other causes of acute jaundice
- CBD gallstone causing obstructive jaundice
management of cholangitis
Initial management of cholangitis
- Blood tests:
- Full blood count
- Urea and electrolytes
- Clotting
- Amylase
- Inflammatory markers
- Blood cultures
- Usually gram-negative: E.coli, Klebsiella, Enterobacter
- Imaging:
- AXR – may show ileus or air in biliary tree (e.g. after ERCP; gas-producing organisms; cholecystenteric-fistula)
- USS – gallstones or dilated ducts
- CT abdomen
- Prompt IV fluid resuscitation
- Prompt IV antibiotics
- Broad spectrum with gram-negative cover
- Often IV Tazocin 4.5g three times daily or IV Meropenem 1g three times daily but check local guidelines or guided by culture sensitivities
- Catheterisation for fluid balance
- These patients are often sick and may need HDU or ITU management
Further management of cholangitis
- MRCP (magnetic retrograde cholangiopancreatography)
- ERCP (endoscopic retrograde cholangiopancreatography)
- This can be diagnostic and therapeutic as stones can be removed and a sphincterotomy performed at the Sphincter of Oddi to prevent future episodes
- There is, however, a significant associated morbidity and mortality
- Pancreatitis (up to 5%)
- Cholangitis (up to 3.5%)
- Perforation (up to 0.6%)
- Death (0.2%)
- Biliary scintography
- Radio-active substance secreted in bile
- Can demonstrate an obstruction if diagnosis unsure
- Cholecystectomy
- All patients with an episode of biliary sepsis secondary to gallstones should be referred to the surgeons for consideration of an elective cholecystectomy once recovered.
complications and prognosis of cholangitis
Complications of cholangitis
- Septic shock and death
- Intra-abdominal collection
Prognosis of cholangitis
- Acute cholangitis has a high mortality (7-40%),
- Higher mortality in patients with co-morbidities, e.g. elderly, renal failure, cirrhosis, metastatic disease, failure to respond to antibiotics
What do you need to discuss with the patient to obtain consent?
For a consent to be valid what condi?ons must be sa?sfied?
If patient does not have capacity to consent it can be given by ‘a person responsible’. explain.
Spouse
- Guardian
- ‘carer’ – not paid
- Close relative, friend
- if no person responsible able to be found only then guardianship tribunal will act
what if say patient unconscious and needs emergency treatment?
In an emergency, where the patient is unable to give consent and the treatment is required immediately: (i) to save the person’s life; (ii) to prevent serious injury to a person’s health; (iii) to prevent the patient from suffering or continuing to suffer signiSicant pain or distress; the procedure/treatment may be carried out in the absence of consent.
definition, epi, RF of breast carcinoma
Definition:
• Breast cancer in situ → Cancer that is confined to the duct (DCIS) or lobule (LCIS) in which it originated from & does not
extend beyond the basement membrane
• Primary invasive breast cancer
• Metastatic breast cancer
Epidemiology:
- 1 in 10 women will develop breast cancer
- 2nd most common cancer killer in women after lung cancer
- Rare below the age of 30 years
- 10% have a genetic predisposition
Risk factors:
- Female (100x) • Increasing Age (> 30 years) • FHx
- Hormonal factors:
⁃ Early menarche (< 11yr) and late menopause (>51 yr)
⁃ Exogenous Oestrogen exposure (OCP or HRT)
⁃ Nulliparity
- Radiation exposure - E.g. ionising radiation exposure in adolescence/early adulthood
- Benign breast conditions ⁃ Atypical lobular or ductal hyperplasia (4-5x)
aetiology of breast cancer
pathology of breast cancer
investigations of breast cancer
management of breast cancer
Staging: (Used to guide treatment and prognosis) ⁃ Estimate tumour size ⁃ Histological type ⁃ Estimate tumour spread (Nodes vs. Distant Mets)
• Sx ⁃ Lumpectomy, LN clearance, Mastectomy ⁃ Reconstructive surgery • Radiotherapy - improves loco-regional control
• Chemotherapy - improves systemic control
• Hormonal therapy - only for oestrogen receptor +ve Ca ⁃ (1) Ovarian ablation, (2) oestrogen receptor modulators (tamoxifen), (3) aromatase inhibitors ⁃ Greatest benefit in post-menopausal women
Complications: • Nausea and vomiting from chemotherapy (short-term high) • Osteopenia and osteoporosis ⁃ Due to continued suppression of oestrogen by aromatase inhibitors (long-term high) ⁃ Encourage weight-bearing exercises and Ca2+ supplements • Vasomotor symptoms ⁃ Including hot-flushes, sleep disturbances, irritability and vaginal dryness ⁃ Occurs due to premature ovarian failure due to cytotoxic therapy • Recurrence ⁃ Variable
Prognosis: • Breast cancer survival is calculated from Nottingham Prognostic Index ⁃ Only useful for 10 year survival • Depends on staging
anatomy of breast cancer
epidemiology of breast lump
Epidemiology: • Breast lumps are a common but only ~15% are cancerous • 1 in 10 women develop breast cancer • 2nd most common cancer killer of women • Incidence of breast cancer increases with age • Incidence increases with prolonged exposure to oestrogen: ⁃ Use of OCP or HRT ⁃ Early menarche or late menopause • Male breast cancers account for < 1% of cases • Most common causes of Breast Lump: 1. Carcinoma of the breast 2. Cyst 3. Fibroadenoma 4. Fibroadenosis
DDx of breast lump
Benign Breast Masses:
- Cysts ⁃ Common in the peri-menopausal age ⁃ Uncommon after menopause –> suspect cancer ⁃ Present with a short history as painful,tender swelling in the breast ⁃ Appear as well-defined rounded opacities on mammography and U/S will distinguish solid from cyst ⁃ Newly diagnosed or symptomatic cysts should be aspirated via FNA ⁃ If blood fluid –> send to pathology and perform Core biopsy
- Fibroadenoma ⁃ Most common benign neoplasia of the breasts ⁃ Presents as a discrete, usually solitary, firm masses that are mobile and not attached to the skin ⁃ Arise from the entire breast lobule and have both stromal and epithelial components ⁃ Occur more commonly during the 3rd decade of life ⁃ Cause unknown but thought to be hormonally driven
- Fibrocystic breasts ⁃ Most commonly found in premenopausal and peri-menopausal women ⁃ Relatively uncommon post-menopausal & should raise suspicion of malignancy ⁃ Pathological features include cysts, epithelial hyperplasia, apocrine metaplasia & cystic dilation/ fibrosis ⁃ Pts sometimes present with a discrete mass, when in actual fact it is fibrocystic changes ⁃ Characteristics of cysts: ⁃ Mobile and have distinct borders on examination ⁃ Sometimes fluctuate with the menstrual cycle ⁃ Anechoic on U/S
- Fat necrosis ⁃ Occurs 2° breast trauma ⁃ May be iatrogenic due to breast augmentation or biopsy or trauma (seatbelt injury) ⁃ Lesions present as hard, fixed masses and acoustic shadowing on U/S –> biopsy
- Breast Abscess ⁃ Typically occur in women that are breastfeeding ⁃ Thought to result from ruptured sub-aeriolar ducts that leak into the periductal space ⁃ Must be differentiated from inflammatory breast cancer (does not present as a mass)
- Intraduct Papilloma ⁃ Benign neoplasm that arises from the subareolar ducts ⁃ Present with watery-clear or blood-stained nipple discharge from a single duct ⁃ If papilloma mass may be palpable
Malignant Breast Masses:
- 1° ⁃ (1) Intraduct carcinoma, (2) Invasive carcinoma, (3) Pagetʼs disease of the nipple, (4) Sarcoma
- 2° ⁃ Direct invasion from tumours of the chest wall ⁃ Metastatic deposits from melanoma or others (rare)
DDx: Discharge From the Nipple
Hx of breast lump
examination of breast lump
investigations of breast lump
breast lump flow chart
Definition, epi, aetiology, pathophys of AAA
clinical presentation and management of AAA
random points on acute abdomen pain
definition and aetiology of acute abdomen pain
focussed history on acute abdo pain
surgical sieve for abdo pain
congenital vs acquired
acute vs chronic
- Vascular = Ischaemic colitis, AAA rupture
- Infection = Gastroenteritis
- Neoplastic = Bowel cancer
- Drugs/Iatrogenic = Paracetamol OD
- Inflammation = Appendicitis
- Congenital = Meckelʼs diverticulitis
- Autoimmune = Food allergy
- Trauma = MVA causing ruptured spleen
- Endocrine/Metabolic = DKA
- Mechanical/Anatomical = Volvulus
causes of hollow organ obstruction (dressed from acute abdo pain)
Important Examples With Abdominal Pain
- Ruptured Aortic Aneurysm
⁃ Pain: Abdo, iliac fossa, genitals
⁃ Distension
⁃ Loss of aortic pulsation
⁃ Hypotension and collapse
⁃ Retroperitoneal bleed
⁃ Warning bleed - may occur prior to a massive rupture
- Practice points: • Renal colic is a suspected ruptured-AAA until proven otherwise*
2. Perforated Peptic Ulcer
⁃ Sudden onset of severe pain, initially epigastric
⁃ Pain spreads as contamination spreads
⁃ Broad-like rigidity on examination (peritonism)
⁃ Absent bowel sounds ⁃ Dehydration
⁃ AXR: Free gas under the diaphragm
- Practice points: • Major fluid shifts is a key feature • Donʼt underestimate dehydration*
3. Bowel Obstruction
⁃ Colicky abdominal pain
⁃ Nausea and vomiting
⁃ Distension
⁃ Constipation/Obstipation (severe constipation)
⁃ Classification: ⁃ Complete vs. Incomplete ⁃ Closed loop vs. Open loop ⁃ Small vs. Large bowel
- Practice Points: • All bowel obstructions are closed loop until proven otherwise = Medical Emergency*
- • All colonic or distal small bowel obstructions are due to cancer until proven otherwise*
- • Think for causes: Bolus, stricture, compression or twist (volvulus)*
4. Pancreatitis
⁃ Central constant abdominal pain
⁃ Radiation through to the back
⁃ Flexed posture
⁃ Hx: ⁃ Gallstones or alcohol (1° causes) ⁃ Drugs or toxins ⁃ Metabolic disease (diabetes or lipid disorder)
⁃ Family Hx ⁃ Evidence of a retroperitoneal bleed: (rare) ⁃ Grey-Turner sign = bruising of the flanks ⁃ Cullenʼs sign = periumbilical bruising
⁃ Diagnostic bloods: ⁃ Amylase and lipase = elevation gives strong evidence but is NOT diagnostic ⁃ WCC/Neutrophilia ⁃ ESR/CRP elevated
- Practice Points: • Hx and enzyme levels give initial diagnosis • Enzymes are strongly suggestive but NOT diagnostic, especially amylase • Enzyme levels do NOT correlate reliably with severity and may be transitory • Normal levels do NOT exclude pancreatitis • Imaging gives definitive diagnosis*
5. Appendicitis
⁃ Closed loop obstruction
⁃ Central colicky abdominal pain + vomiting, nausea and reflex anorexia
⁃ Constant pain localising to the RIF later - McBurneyʼs Point tenderness
⁃ Peritonitis
⁃ Perforation –> Generalised signs ⁃ DDx: ⁃ Viral illness or gastroenteritis ⁃ PID ⁃ IBD Obstructions
- Practice Points: • RIF pain + PV bleeding = Ruptured ectopic until proven otherwise*
6. Ureteric Obstruction (Renal Colic)
⁃ Ureters are hollow, muscular and retroperitoneal
⁃ Lateral/posterio-lateral abdominal pain (flank pain)
⁃ Radiating to the Iliac Fossa or groin
⁃ Calculus on plain AXR
⁃ Haematuria common ⁃ UA, MSU, US and CT
Practice Point: • Renal colic is a ruptured/leaky AAA until proven otherwise
Def, epi, aetiology, pathophysiology of acute appendicitis
presentation of acute appendicitis
Presentation:
• History: ⁃ Central abdominal pain, < 72 hours, that localises to the RIF over time ⁃ Localisation occurs over 12-24 hours
⁃ Localising site can differ depending on the location of the appendix
⁃ Anorexia, nausea and vomiting (1-3x)
⁃ Caused by distension of the appendix
• Other Presentations:
⁃ If the appendix lies near the rectum –> local irritation and diarrhoea
⁃ If it lies near the bladder or ureter –> urinary frequency, dysuria and microscopic pyuria
⁃ Retrocoele appendix –> no localisation but irritation of the psoas muscle causing the psoas sign and obturator sign
⁃ Abdominal rigidity
• Examination:
⁃ Generally: Pt may looked flushed, unwell, and febrile
⁃ McBurneyʼs Point tenderness
⁃ Signs of peritoneal inflammation: ⁃ RIF pain, guarding and rebound tenderness ⁃ Ask the patient to cough or bloat and suck in their stomach - will cause pain if the peritoneum is inflamed ⁃ Rebound tenderness can be elicited by percussion
⁃Decreased bowel sounds
Other Signs: (usually uncommon or unreliable)
⁃ Obturator sign - internal rotation of the flexed hip –> abdominal pain. Associated with a pelvic appendix
⁃ Psoas sign - Extension of the R hip –> RLQ pain. Associated with retrocecal appendix
⁃ Rovsingʼs sign - palpation of LIF causes RIF pain. Indicates right sided parietal peritoneal irritation
Cardinal Features: • Abdo pain lasting < 72 hours • Vomiting 1-3x • Facial flush • RIF tenderness • Anterior tenderness on rectal exam • Fever to 38.5°C • No evidence of UTI on microscopy
Risk Factors: • < 40 years • Male • Low dietary fibre • Smoking
investigations of acute appendicitis
- Bloods:
⁃ FBC → Leukocytosis and neutrophilia (70%)
⁃ LFTs
⁃ UECs
⁃ Pregnancy test
- Urinalysis - may rule out UTI but microscopic haematuria and pyuria are found in 30% of patients with acute appendicitis due to inflammation around the bladder and ureters
- Imaging: NOT routinely done in patients with acute appendicits unless diagnosis is unclear ⁃ Abdominal and Pelvic CT: Thick wall (>2cm), appendicolith, abscess, free fluid, fat stranding etc. ⁃ U/S abdomen: Investigate inflammation and exclude gynae causes
diagnosis and ddx of acute appendicitis
treatment for acute appendicitis
• Uncomplicated: ⁃ 1st line = Appendicectomy with Sx antibiotic prophylaxis
⁃ Open or via laparoscopy
• Complicated: (perforation or abscess) ⁃ Fluid resuscitation before surgery
⁃ Severe appendicitis, especially if perforated, will require a full course of broad-spectrum antibiotics
⁃ Appendicectomy (usually open)
• Prognosis: o Pts treated in a timely fashion have good outcomes o Wound infection and intraabdominal abscess are potential complications o Laparoscopy has been shown to reduce complications
Complications: • Infection (most common post-surgical complication) ⁃ Wound infection or intra-abdominal abscess ⁃ Both occur in perforated appendicitis and not common in simple appendicitis
structure and function of the appendix and surface anatomy
define acute pancreatitis
Pancreatitis:
An inflammatory process in which the pancreas auto-digests itself
- Acute: Occurs on the back of a normal pancreas and can return to normal on resolution
- Chronic: Continuing inflammation causing irreversible structural changes
- Sx emergency! - Acute Pancreatitis can be a KILLER!! - 20% are severe = multi-organ failure - Mortality in 20-40%
aetiology of acute pancreatitis
Aetiology: (I GET SMASHED)
- Ideopathic
- Gallstones (60%) - temporarily lodging at the sphincter of Oddi
- Ethanol (30%) - leads to intracellular accumulation and premature activation of pancreatic enzymes
- Tumours
- Surgeries - ERCP
- Microbiological - Mumps, CMV, Hep B
- Autoimmune - SLE, Crohnʼs disease
- Scorpion venom
- Hyperlipidaemia/hypothermia/hypercalcaemia
- Embolic/ischaemia
- Drugs and toxins - diuretics, sulfonamides, oestrogens, corticosteroids
pathophysiology of acute pancreatitis
Pathophysiology:
- Initiating step: ⁃ Injury or trigger causes exocrine pancreatic dysfunction ⁃ Acinar cell damage
- Destructive step: ⁃ Release of lytic enzymes & intracellular lysosomes
⁃ Intracellular trypsin triggers the entire zymogen activation cascade
⁃ Inflammatory cells release superoxides and proteolytic enzymes
- Results in: ⁃ Pancreatic cell digestion + inflammation ⁃ Lipase action causes peripancreatic fat necrosis
⁃ Fee FAs then bind Ca2+ –> Hypokalaemia
⁃ Causes oedematous pancreatitis
⁃ Protease action destroys blood vessel walls –> haemorrhage
⁃ Causes haemorrhagic pancreatitis ⁃ –> SIRS (systemic inflammatory response syndrome) –> SHOCK!
classification of acute pancreatitis
Classification:
- Oedematous - 70% ⁃ Pancreatic parenchyma and surrounding retroperitoneal structures are engorged with interstitial fluid and infiltration of inflammatory cells
- Severe/necrotising - 25% ⁃ Necrosis may be sterile or infective
- Haemorrhagic - 5% ⁃ Bleeding into the parenchyma and surrounding retroperitoneal structures with extensive necrosis
clinical features of acute pancreatitis
Clinical Features:
- Hx : ⁃ Severe epigastric pain radiating to the back ⁃ Severe nausea and vomiting - very common (70-80%) ⁃ Fever, dehydration, hypotension, tachycardic or SHOCKED ⁃ May follow alcoholic binge or previous Hx of gallstones
- Examination: ⁃ Epigastric tenderness + guarding, and rigidity in severe cases ⁃ Relieved by sitting forward
⁃ Grey-Turnerʼs Sign = Left flank ecchymosis (haemorrhagic pancreatitis) - (uncommon) ⁃ Due to retroperitoneal bleed
⁃ Cullenʼs Sign = Periumbilical ecchymosis (haemorrhagic pancreatitis)- (uncommon) ⁃ Due to blood tracking from the retroperitoneum along lig Terres
⁃ Foxʼs sign = Ecchymosis over the inguinal ligament area ⁃ Signs of hypercalcaemia (uncommon)
investigations of acute pancreatitis
- Bloods: ⁃ FBC, UECs, LFTs (obstructive picture for gallstones), CRP ⁃ Serum Amylase or Lipase ⁃ Lipase more sensitive; amylase elevated 3x above normal ⁃ Amylase > 1000 is diagnostic BUT can may be normal even in severe cases ⁃ Other causes of elevated amylase = cholecystitis, aneurysm leak, perforated peptic ulcer, intestinal ischaemia
- Imaging: ⁃ CXR: ⁃ Atelectasis or pleural effusion (especially on left side) - due to ARDS ⁃ AXR: ⁃ Sentinal loop sign = isolated dilatation of a the prox jejunum due to inflammation around the pancreas ⁃ Cut-off sign = gas distending the right colon but abruptly stops in the mid or left transverse colon
⁃ U/S: ⁃ May show pancreatic inflammation and stranding, calcifications or fluid collection
⁃ CT (contrast) Abdo - consider ⁃ Most sensitive and specific ⁃ Used when biochemical findings are equivocal ⁃ Segmental enlargement of pancreas, irreguluar contour and obliteration of peri-pancreatic fat, necrosis or pseudocyst
DDx of acute pancreatitis
DDx:
- Peptic ulcer disease - Longstanding epigastric pain, does not often radiate to back, reflux, heartburn, NSAID use
- Perforated viscous - Acute abdomen with peritoneal signs, normal lipase, CXR shows sub-diaphragmatic air
- Intestinal obstruction - Hx of abdo Sx, obstipation, emesis, decreased bowel sounds
- Choledocholithiasis - Severe RUQ pain of sudden onset, jaundice, hx of gall stones, may occlude common bile duct and cause acute pancreatitis
management, complications and prognosis of acute pancreatitis
acute pancreatitis pathophys flowchart
chronic pancreatitis
- Commonly caused by alcohol (long-term excess)
- Fibrosis replaces pancreatic parenchyma
- Exocrine atrophy
- May result in malabsorption due to loss of pancreatic enzymes
pancreatitis CT
more CT
more CT 2
Def, epi, RF, classification, spread of bladder cancer
bladder cancer (transitional cell carcinoma/TCC) → def, epi
Definition: • Malignancy of the transitional cells that line the urinary tract from the renal pelvis to the urethra
Epidemiology: • Most common cancer of the bladder (90%) • Males > females (3:1) • Lowest incidence in Asian countries • Occupational exposure accounts for 1/4 of cases
bladder cancer (transitional cell carcinoma/TCC) → aetiology
⁃ Cigarette smoke
⁃ Age
⁃ Male
⁃ Exposure to carcinogens:
⁃ Analine (aromatic amines) used in dye and rubber industries (Due to carcinogens like β-naphthyl amine in the urine)
⁃ Polycyclic hydrocarbons - coal, aluminium and roofing-industries
⁃ Pelvic radiation
⁃ Chemotherapy with cyclophosphamides
⁃ Chronic inflammation - Schistosomiasis infection and chronic IDCs
pathology and clinical features of TCC bladder cancer
Pathology: • Malignancies more common at the base, trigone and at the ureteric orifices • Commonly multiple that can extend from the renal pelvis to the urethra
Clinical Features: • Painless Haematuria (microscopic or macroscopic) • Dysuria (common) • Frequency/urgency of micturition
investigations of TCC
- Urinalysis - haematuria; pyuria can also be present
- Urine cytology - Positive in high-grade carcinomas (90%) and always signifies TCCs ⁃ Urine typically contains transitional cells that are shed from the urinary tract ⁃ Non-invasive method for diagnosing cancer ⁃ Not good for low-grade cancers (30%)
- Imaging: ⁃ Renal/bladder U/S ⁃ CT abdo/pelvis ⁃ IV pyelogram - visualise the kidneys at varying stages after injection of IV contrast ⁃ May see filling defect, obstruction or hydronephrosis
- Cystoscopy
management and prognosis for TCC
Management:
- TNM staging
- Surgical:
⁃ Low risk superficial cancers - Transurethral resection of Bladder Tumour
⁃ High risk - TURBT + post-op intra-vesicular chemo
• Invasive tumours:
⁃ Pre and Post-op chemo or radiotherapy
⁃ Sx - Radical cystectomy with LN disection
• Metastatic disease
⁃ Systemic chemo + Sx + radiotherapy
Prognosis: • Low grade lesions - high risk of tumour recurrence but low risk of disease progression and death • High grade lesions - high risk of recurrence and progression ⁃ Overall survival with cystectomy is ~ 50%
anatomy of skull
traumatic brain injuries
primary brain injuries
secondary brain injuries
secondary brain trauma - subdural haematoma
secondary brain trauma - intracranial and infection
skull #
cerebral herniation
cerebral perfusion pressure
Diverticulitis - def and epi
Definitions: • Diverticulum (pleural = diverticula) = ⁃ Out-pouching or herniation of the wall of a hollow organ
- Diverticulosis = The presence of diverticula
- Diverticulitis = Inflammation of the diverticula
Epidemiology: • Incidence increases with age: ⁃ <10% at 40 years ⁃ 50% at 50 years • Western-region problem and associated with poor fibre diets • Vegetarians have a lower incidence of diverticular disease • Right-sided diverticula are more common in Asian populations • Left-sided diverticula are more common in western countries and are found in left side (mainly sigmoid) • Female predominance in older age
diverticulitis - aetiology and RF
Aetiology:
- Multifactorial. Genetic and environmental factors.
- Congenital vs. Acquired ⁃ Meckelʼs diverticulum, Most are acquired due to poor diet and increased intraluminal pressure
- True vs. False ⁃ True diverticula: ⁃ Contain all layers of the mucosal wall - more commonly congenital. False (or pseudo-diverticula) ⁃ Herniated wall does only contains mucosa and muscularis mucosa ⁃
- Traction vs. Pulsion ⁃ Traction - diverticula form due to increased intraluminal pressure that herniates the bowel wall ⁃ Pulsion - diverticula form due to external structures dragging the wall (e.g. inflamed LN)
RF: • Low dietary fibre • Age > 50 • Obesity (weak) • NSAID use (weak)
diverticulitis - pathophys
- Diverticulosis: ⁃ Low fibre diet increases the intestinal transit time and decreases stool volume ⁃ Increased intraluminal pressure due to hard stools and other RF -> herniation between the tinea coli ⁃ Circular muscles thicken and tinea coli shorten-> segmentation of the colonic wall
- Diverticulitis: ⁃ Obstruction of diverticula caused by food or faecal matter ⁃ Bacterial multiplication and increased intraluminal pressure causes distension of the diverticuia ⁃ Impaired venous return –> ischaemia, necrosis and perforation –> peritonitis ⁃ Microperforations can lead to abscess formation
Clinical Features of Diverticulitis
Hx: ⁃ Rapid onset of LIF pain - 70% of diverticular disease; Right sided pain may mimic appendicitis
⁃ Nausea, fever, bloating
⁃ Constipation or change in bowel habit
⁃ PR bleeding (uncommon) - Usually abrupt, painless and profuse bleeding
• Examination: ⁃ LLQ tenderness and voluntary guarding ⁃ Fever, tachycardic ⁃ Diffuse tenderness and rebound tenderness ⁃ Palpable abdominal mass (uncommon) - in cases of abscess formation
diverticulitis - investigations and ddx
Investigations:
• Bloods: ⁃ FBC - leukocytosis (Neutrophilia)
⁃ CRP - elevated
⁃ UECs, LFTs
- CXR - normal unless perforated (pneumoperitoneum)
- CT abdomen ⁃ Thickening of bowel wall, mass, abscess, streaky mesenteric fat ⁃ If CT unavailable consider barium enema or U/S
DDx: • Intestinal obstruction • Ischaemic colitis - must be ruled in with PR bleeding • Colorectal cancer • Ulcerative colitis/Crohnʼs disease
diverticulitis - management
- General advice for diverticulosis ⁃ High-fibre diet, high fluid intake, and stool softeners ⁃ Reduces intracolonic pressure
- Medical Management: ⁃ 1st = IV antibiotics and analgesia ⁃ Amoxycillin, metronidazole ⁃ Paracolic abscess can be drained under radiological guidance
- Sx Management: (resection - segmental colectomy) ⁃ Indications: ⁃ Failed medical management ⁃ Undrainable paracolic sepsis ⁃ Free perforation
- Acute rectal bleeding ⁃ 1st = Endoscopic haemostasis or ⁃ angiographic embolisation ⁃ Supportive + antibiotics ⁃ 2nd = Sx to control bleeding
diverticulitis complications
• Stricture formation/Obstruction (med)
⁃ Inflammation –> fibrosis and constriction of the lumen
⁃ Can lead to partial or complete obstruction
• Perforation
⁃ Microperforation - usually self-contained and conservative management with antibiotics and IVFs
⁃ Free-air perforation - Surgical Emergency
⁃ Abscess perforation –> purulent peritonitis
• Pericolic/paracolic Abscess formation
⁃ Acute diverticulitis with swinging fevers, fluctuating tachy, unresolved abdo pain and tender LIF mass
• Fistula (low)
⁃ Formed when a diverticular abscess ruptures into an adjacent organ such as the bladder or vagina
⁃ Sx repair required
diverticulitis prognosis
- Most pts with uncomplicated diverticulitis recover following medical Rx and donʼt require Sx
- Recurrent disease: ⁃ Occurs in 1/3rd of patients post-successful medical management ⁃ Recurrent disease associated with high mortality
- Post Sx: ⁃ 1/4th will continue to have symptoms
NOF #
classification of burns
burn first aid
estimating % burn
causes of burns
total body water and fluid compartments
water balance
factors that affect h2o requirement
control of water balance
Control of Water Balance:
• Sensors:
- Osmoreceptors ⁃ Specialised cells in the hypothalamus which respond to changes in extracellular tonicity (rather than osmolality) ⁃ Tonicity refers to the osmotic pressure gradient between 2 fluids separated by a semi-permeable membrane ⁃ A hypertonic solution is one that has a higher conc. of solutes outside the cell ⁃ These receptors are very sensitive to changes in [Na+] - respond to 1-2% change in tonicity ⁃ In general, [Na+] can be used as a measure of ECF tonicity ⁃ Note: Cl-, HCO3- & proteins also count towards ECF tonicity
- Baroreceptors ⁃ Baroreceptors are less sensitive (but more potent) than osmoreceptors ⁃ When stimulated the cause a much higher release of ADH than with osmoreceptor stimulation ⁃ Hypovolaemia is a more potent stimulus for ADH release than hyperosmolarity ⁃ Hyovolaemic stimulation will override hypotonic inhibition of ADH release ⁃ Types: ⁃ Volume receptors (low pressure baroreceptors) ⁃ Located in the right atrium and great veins ⁃ Input to the hypothalamus ⁃ High pressure baroreceptors ⁃ Located in the aortic arch and carotid sinus and respond to a change in MAP
- Central controller = Hypothalamus • No anatomically defined centre that is solely responsible for responding to changes in water balance • Key components: ⁃ Osmoreceptors ⁃ Thirst centre ⁃ OVLT (organum vasculosum of the lamina terminalis) & SFO (subfornical organ) ⁃ Respond to Ang-II ⁃ Supraoptic and paraventricular nuclei - ADH synthesis
- Effectors
- Thirst ⁃ Stimuli: ⁃ Hypertonicity: Cellular dehydration acts on osmoreceptors in hypothalamus ⁃ Hypovolaemia: Low volume sensed by low pressure baroreceptors ⁃ Hypotension: Sensed by high pressure baroreceptors ⁃ Ang-II: Released in response to hypotension
- ADH release ⁃ Synthesised in the hypothalamus and transported to the Post. Pituitary ⁃ Actions: ⁃ Increases water reabsorption in the CD of the renal tubules ⁃ Acts on V2 receptors in the cortical and medullary collecting ducts –> synthesis of Aquaporin 2 that increase water reabsorption ⁃ Vasocontrsiction ⁃ Acts on V1, 2 and 3 receptors in blood vessels ⁃ Negative-feedback: ⁃ Reabsorption of water reduces plasma [Na+] and this is detected by the osmoreceptors –> negative-feedback on the hypothalamus
Calculating Daily Fluid Requirements:
Basic IV Fluids:
different IV fluids
MORE IV FLUIDS
groin swelling - epi
Epidemiology: • Swelling/lumps in the groin make up 10% of clinical presentation in general Sx outpatient clinics • Lesser cause of acute surgical problem • Most common are newly formed inguinal hernias
DDx of groin swelling
• Inguinal/Femoral Hernia
⁃ Inguinal hernias: (test ⁃ Have a cough impulse and are not translumminant)
⁃ Indirect hernias
⁃ Emerge from the superficial inguinal ring (above and medial to the pubic tubercle)
⁃ More common in males (8x)
⁃ Potential for incarceration and strangulation
⁃ Direct hernias
⁃ Occurs through the posterior wall of the inguinal canal
⁃ Usually disappears on lying down
⁃ Risk of incarceration if large; low risk of strangulation
⁃ Femoral hernias:
⁃ Occur below and lateral to the pubic tubercle - often abdominal contents, like bowel, migrate into the femoral canal
⁃ More common in females
⁃ Rarely has a cough impulse
⁃ High rate of strangulation (40%)
• Inguinal lymphadenopathy
⁃ Inguinal nodes lie below the inguinal ligament and drains:
- Lower limb, abdo wall below the umbilicus, anal canal, penis & scrotal skin
- BUT not the testes –> Para-aortic nodes
⁃ Enlarged LNs suggest infection, lymphoma or metastases from a 1° lesion
⁃ Lower limb and perineum should be inspected for infections & malignancies
• Femoral artery aneurysm
⁃ Dilation of the common femoral artery just below the inguinal ligament
⁃ Expansile/pulsatile swelling in the groin
⁃ Found in patients > 65years, mostly male
• Saphena varix
⁃ Dilation of the long saphenous vein at its junction with the femoral vein (sapheno-femoral junction) in the groin
⁃ Frequently associated with vericose veins
⁃ Disappears on lying supine
• Psoas Abscess (rare)
- ⁃ Psoas abscess may track down beneath the inguinal ligament and present in the groin
⁃ Causes: ⁃ Classically caused by TB of lumbar vertebra tracking down inside the sheath of the psoas muscle –> “Cold abscess” ⁃ Caused by infection tracking down from a perforation in the left colon –> “Hot/pyogenic Abscess”
Hx, examination and Ix for groin swelling
hiatus hernia - def, epi, aetiology, classification
hiatus hernia: pathophys and clinical features
hiatus hernia: investigation, complications, management, prognosis
hiatus hernia - more on dressed
ulcerative colitis (UC) - epi and aetiology
Ulcerative Colitis: • UC = An acute and chronic relapsing inflammatory disorder of the colon, limited to the mucosa
Epidemiology: • Age: Bimodal, 20s-40s & second peak in 60s • Males > Females • Prevalence is 1 in 1000 • Low incidence in Asia
Aetiology: • Unclear - Associated with genetic predisposition and environmental triggers • Most likely an autoimmune-type process and is initiated by an inflammatory response against normal colonic bacteria • Diet plays a 2° role to disease evolution
UC - rf, pathology, classfiication
Risk Factors: • Family Hx of IBD - 10-20% have at least 1 family member with UC or Crohnʼs • HLA-B27 - Identified in most patients with UC • Ex-smoker or non-smoker
Pathology: • Granular, hypervascular and mildly oedematous mucosa with loss of vascular pattern (seen at colonoscopy) • Acute neutrophil infiltration of the colonic mucosa and submucosa • Mucosal crypt abscesses with goblet cell mucin depletion • Chronic ʻburn-outʼ disease leads to a pale, featureless, ahaustral pattern to the colon
Classification: • Montreal Classification: based on inflammatory extent
⁃ E1 (Ulcerative proctitis) - Limited to the rectum
⁃ E2 (Left-sided UC) - Involves the colorectum distal to the splenic flexure
⁃ E3 (Pancolitis) - Extends proximally to the splenic flexure ⁃ May involve the terminal ileum (ʻbackwash ileitisʼ), 2° to an incompetent ileocecal valve
UC - clinical features
• Hx:
⁃ Diarrhoea or loose stools with passage of blood and mucus
⁃ Frank blood - rare
⁃ Abdominal pain (Ranges from mild crampy to severe pain, Associated with tenesmus to severe pain)
⁃ Systemic symptoms - low-grade fever, anorexia and weight loss (uncommon)
⁃ Acute-on-chronic Toxic Megacolon: ( Profuse diarrhoea and rectal bleeding, Rapid development of hypovolaemia, Distended and tender abdomen with absent bowel sounds)
⁃ Extra-intestinal manifestations: ⁃ Iritis ⁃ Arthritis and spondylitis (common presenting problem) ⁃ Sacroiliitis ⁃ Erythema nodosum
UC - investigations and DDx
UC - management
- All patients must be vaccinated if immunosuppressive therapy is to be given ⁃> Influenza, pneumococcal, Hep B, HPV, varicella zoster
- Fulminant disease:
⁃ 1st = IV corticosteroids + admission
⁃ IV fluids
⁃ Adjunct - Ciclosporin or infliximab (immuno-suppresive Rx)
⁃ Last line = Colectomy
- Mild-Mod disease:
⁃ 1st = Topical or oral corticosteroid (mesalazine)
- Refractory disease:
⁃ Azathioprine (purine analogue) or Infliximab (monoclonal Ab against TNF-α)
UC - complications and prognosis
Complications:
- Toxic megacolon (low) ⁃ Up to 20% of severe colitis progresses to toxic megacolon -> acute form of colonic distension ⁃ Carries a risk of perforation and death
- Colonic adenocarcinoma (long-term medium) ⁃ Develops in 3-5% of patients ⁃ Risk increases 10x if active disease is > 10 years
- Inflammatory pseudo-polyps ⁃ Irregularly shaped islands of colonic mucosa that result from inflammation of the GIT ⁃ Not dysplastic and do not carry a risk of colon cancer
- Primary Sclerosing Cholangitis ⁃ Occurs between 3-7% of UC patients; 70% who have PSC have underlying UC ⁃ Chronic progressive disease characterised by inflammation, fibrosis and stricturing of the intra and extrahepatic biliary tree
Prognosis:
- Overall mortality not increased compared to normal population
- Most common cause of death is toxic megacolon
- Increased mortality seen in older patients that develop complications (shock, malnourished or anaemia)
- 3-5% develop adenocarcinoma
Crohn’s - def, epi, aetiology, pathophys, micro path
Crohn’s - clinical features + Ix
Crohn’s - DDx, prognosis, management, complications
IBD common presentation
crohn’s vc UC
crohn’s vc uc colonoscopy
UC summary
crohn’s summary
Cellulitis and Erysipelas:
Necrotising Fasciitis
SIRS - def, criteria, pathophys
SIRS - sequelae, complications, prognosis
Inguinal/femoral hernia - def and epi
Definition: • Hernias = Abdominal contents protruding through a defect in the abdominal wall
Epidemiology:
- Common Sx out-patient complaint
- Males > Females (8x) - due to anatomical descent of the testes
- Inguinal hernias occur more commonly than femoral hernias in both males and females
- Femoral hernias are more common in females than males
- Can occur at any age but increases in risk as age advances: ⁃ Direct hernias are more common in < 50s
⁃ Indirect hernias are more common in > 50s
• Bilateral hernias can occur up to 20% of the time
inguinal/femoral hernia - aetiology and RF
Aetiology:
- Congenital - due to the processus vaginalis failing to regress
- Acquired - due to degenerative and fatty changes that occur to the abdominal wall over time
- RF:
⁃ Male (8x)
⁃ Age - increases with age
⁃ Familial Hx or hereditary predisposition
⁃ Connective tissue disorders - Marfanʼs syndrome
⁃ COPD - chronic coughing and increased intra-abdominal pressure
⁃ Prematurity
⁃ Smoking
⁃ Obesity, pregnancy, heavy lifting (weak links)
inguinal/femoral hernia - direct vs indirect
Classification:
• Direct vs. Indirect
⁃ Direct: ⁃ Hernial sac comes directly through the abdominal wall (Hesselbachʼs Triangle) due to a weakness in the transversalis fascia ⁃ Occurs medially to the inferior epigastric artery and deep inguinal ring ⁃ Usually always acquired and caused by degeneration + fatty changes in the external oblique aponeurosis
⁃ Indirect: ⁃ Hernial sac comes through the inguinal canal, traversing the deep and superficial inguinal rings ⁃ Follows the course of the spermatic cord in males and can travel into the scrotal sac due to a persistent processes vaginalis ⁃ High risk of incarceration or strangulation ⁃ When the bowel is fused to the peritoneum and herniates = sliding hernia
inguinal/femoral hernia - reducible vs irreducible vs strangulated
⁃ Reducible ⁃ Refers to when the contents of the hernia can be pushed back into place
⁃ Irreducible or Incarcerated ⁃ Refers to when the contents cannot be reduced, but the blood supply is not compromised
⁃ Strangulated ⁃ Refers to an incarcerated hernia where the blood supply has been compromised ⁃ Sx emergency ⁃ Will lead to ischaemia, necrosis and perforation of the bowel
inguinal/femoral hernia - investigations, clinical features, management, DDx, prognosis
inguinal vs femoral hernia
liver neoplasms - classification
HCC (hepatoma)- Def, epi, aetiology
Definition: • 1° cancer of the liver arising from the hepatocytes, predominantly cirrhotic livers • Some patients may not have cirrhosis e.g. Chronic Hep B
Epidemiology: • Distribution largely follows that of Hep B and C in western countries • Incidence on the rise, reflecting increasing prevalence of viral hepatitis • Geographical: ⁃ Uncommon in the West ⁃ Common in central Africa and South-East Asia
Aetiology/Risk Factors: • Liver Cirrhosis (80%) • Chronic Hep B infection • Chronic Hep C cirrhosis • Chronic heavy alcohol use • Haemachromatosis • Diabetes • Obesity • FHx of liver cancer
HCC - pathology, spread, clinical features
Pathology:
• Associated with cirrhosis and is related to chronic inflammation of the liver • Macropath: Tumour either forms a large solitary mass or multiple foci throughout the liver • Dysplastic nodules can be low or high-grade –> HCC ⁃ 1/3rd of high-grade lesions turn cancerous within 2 years and 80% by 5 years
Spread:
- Direct - through the liver substance and into vessels like the portal vein –> portal vein thrombosis (common)
- Lymphatic
- Haematogenous - Late stage
Clinical Features:
- General features: Weight loss, anorexia, malaise, cachexia
- RUQ pain - due to capsular stretching
- Jaundice - late feature
- Signs (common): ⁃ Abdo distention or ascites - associated with cirrhosis ⁃ Asterixis - Hepatic encephalopathy ⁃ Early satiety ⁃ Leg oedema ⁃ Oesophageal or gastric variceal bleeding (more common in decompensated cirrhosis) ⁃ Splenomegaly ⁃ Palmar erythema, spider nevi, periumbilical colateral circulation
HCC - Ix, prognosis, management
Investigations:
• Bloods: ⁃ FBC - ↓Hb (microcytic anaemia from possible variceal bleed) and Thrombocytopenia (as a result of portal HTN)
⁃ LFTs - ↑AST, ALT, ALP and bilirubin; low albumin ⁃ Coags INR/PT - normal or elevated
⁃ Hepatitis serology - may be positive
⁃ Alpha-feto protein (elevated in 70% of HCCs)
- U/S of liver
- CT contrast or MRI
- Tissue biopsy
Management:
- Staging of tumour
- Rx depends on the cause and extent of disease
- Sx resection if solitary and < 3cm
- Liver transplant
- Percutaneous ablation & chemotherapy have an increasing role in HCC management
Prognosis:
- HCC is a very aggressive tumour
- Survival depends on the functional capacity of the liver:
⁃ Untreated or non-Sx approach have 2-4 months
⁃ 5 year survival with symptomatic hepatoma is 0-10%
⁃ Liver transplant has been associated with 75% disease-free survival
⁃ 5 year survival for patients with hepatic resection is 30-70%
Biology of Human Parasitic Fungi - structure and morphology
Biology of Human Parasitic Fungi - reproduction
Reproduction:
• Asexual reproduction
⁃ Occurs when the spores undergo mitotic division
⁃ E.g. Candida only reproduce asexually - Known as Fungi Imperfecti as sexual reproduction is not known to occur in this spp
• Sexual reproduction
⁃ Occurs when the two haploid spores fuse forming a diploid
⁃ Then divide by meiosis
Human disease caused by fungi
Antifungal Drugs and Treatment:
Groups of Mycoses:
group of mycoses part 2
neck lump epidemiology
- Common presentation in primary care
- Often no associated symptoms
- Age differences are important
⁃ Paediatric neck lumps - 75% are benign (infective or inflammatory)
⁃ Adult (> 40yrs) neck lumps - 75% are malignant with 80% of these being 2° metastases
neck lump history
• How long has the lump been there?
⁃ Sudden appearance of a mid-line lump is suggestive of acute haemorrhage into a thyroid cyst
⁃ Rarely sudden lumps are fast-growing carcinoma
⁃ Thyroglossal cysts are always present but may only become noticed after a recent infection
⁃ < few weeks –> likely to be infective
• Growth pattern:
⁃ Masses present for years with little change are likely to be benign neoplasms (salivary gland tumours, paragangliomas or schwannomas)
⁃ Rapidly growing masses are usually infective LNs or rapidly growing lymphomas
⁃ Progressively increasing in size –> neoplastic
• Is the lump painful?
⁃ Most mid-line neck lumps are non-painful, including cancerous growths
⁃ Pain associated with heat, swelling and erythema of a LN suggests infection
• Associated symptoms:
⁃ Symptoms suggestive of hyper or hypothyroidism
⁃ Symptoms of infection: ⁃ Fevers, night sweats, cough or coryza etc.
⁃ Symptoms of malignancy - weight loss, fever, night sweats, anorexia or cachexia
⁃ Symptoms suggestive of compression or invasion:
- Mid-line mass may compress the adjacent structures and cause: ⁃ Stridor, dyspnoea, dysphagia
- Changes in the quality of voice or hoarseness (invasion of recurrent laryngeal nerve)
- Otalgia (pain in the ear)
- Multiple lymphadenopathy - infection or lymphoma
• Past Medical Hx:
⁃ Autoimmune disease (Graveʼs disease or Hashimotoʼs thyroiditis), T1DM, pernicious anaemia
⁃ Known risk factors for thyroid malignancy - Radiation therapy or previous thyroid lumps
• Family Hx:
⁃ Autoimmune diseases
⁃ Thyroid dysfunction or cancers
- Smoking and alcohol Hx - Independent risk factors for cancer
- Travel - infection/HIV
neck lump examination - anatomy of the neck
⁃ Divided into central vs. lateral compartments
⁃ Central neck: ⁃ Hyoid bone, thyroid and cricoid cartilages, thyroid isthmus and the trachea
⁃ Lateral neck: ⁃ Divided into the anterior and posterior triangles via the SCM muscle (post. border)
neck lump examination location
- Pre-auricular and angle of the jaw = Parotid gland or lymphoid tissue in the parotid system ⁃ Examine the Facial Nerve (CN 7)
- Central neck = Thyroid goitre, thyroglossal cyst or thyroid cancer ⁃ Examine the thyroid by assessing swallowing
⁃ Thyroglossal cyst will move if patient pokes out tongue
- Anterior triangle
⁃ Lymphadenopathy common here in adults (potentially malignant)
⁃ Congenital masses (paeds) - 2nd branchial cleft cyst (remnant of the 2nd pharyngeal arch)
- Posterior triangle
⁃ Masses here should have a high index of suspicion for malignancy ⁃ E.g. Nasopharyngeal carcinomas
- Supraclavicular ⁃ Especially Left sided suggests metastases of the lungs, GIT or gynaecological
characteristics of neck lump
⁃ Size
⁃ Shape - well defined lesions are less likely to be malignant
⁃ Consistency - hard masses are more suggestive of malignancy
⁃ Tenderness
⁃ Mobility - fixed, firm lesions are suggestive of malignancy
⁃ Pulsatile - carotid artery aneurysm or SC aneurysm
⁃ Concealed by muscle contraction - suggests that the mass is deeper to the muscle
⁃ Infective nodes - isolated, asymmetric, tender, warm and erythematous
neck lump general exam
• ENT examination
⁃ Examine oral cavity and oropharynx
⁃ Bimanual palpation of the floor of the mouth
⁃ Palpate the tongue
⁃ Palpate parotid gland - enlargement (mumps)
⁃ Examine the ears for unilateral serous effusion (nasopharyngeal carcinoma)
⁃ Nasopharyngeal/oropharyngeal examination - requires a mirror or flexible fiberoptic endoscope
- Rule out hyper/hypothyroidism
- Skin & LNs of head and neck ⁃ Look for SCCs or melanomas ⁃ Lymphadenopathy
- Assess cranial nerves - especially CN 7 for facial weakness
- Thyroid gland - If mass moves with swallowing it is associated with the thyroid
- Abdominal examination ⁃ Enlarged liver, spleen or masses
neck lump investigations
DDx neck lump
painful red eye
warning features that require specialist referral for eye
DDx for unilateral red eye
def, epi, RF for pancreatic cancer
Definition: Carcinoma of the pancreas
Epidemiology: • Incidence 12 in 100 000 people & is on the rise
- Men = Women
- Age = 65-75 years
- 4th most common cause of cancer-related deaths
Risk Factors: • Age • Family Hx: Genetic predispositions (5-10%) • Smoking • Chronic pancreatitis • Other hereditary cancer syndromes: ⁃ Hereditary pancreatitis - mutation in PRSS1 gene and is associated with 35% lifetime risk ⁃ Peutz-Jaghers syndrome (hereditary intestinal polyposis syndrome) ⁃ HNPCC - risk of 5%
pathology of pancreatic cancer
• Location:
⁃ Head of pancreas - 65%
⁃ Body - 25%
⁃ Tail - 15%
- Lymph node metastasis is common
- Macropath: Growth is infiltrating, hard and irregular
- Micropath/Classification:
⁃ Exocrine pancreas (Adenocarcinoma - mucous secreting) – most common
⁃ Endocrine pancreas (Acinar cell carcinoma - non-mucous secreting)
⁃ Undifferentiated
⁃ Cystadenocarcinoma - rare and mostly occurs in middle-aged women
spread of pancreatic cancer
• Direct:
⁃ Common bile duct = obstructive jaundice
⁃ Duodenum = occult or overt GIT bleeding; duodenal obstruction
⁃ Portal vein = portal vein thrombosis, portal HTN and ascites
⁃ IVC = bilateral leg oedema
- Lymphatic ⁃ Adjacent + porta hepatic nodes
- Haematogenous ⁃ Liver, lungs, brain, skin
- Trans-coelomic ⁃ Peritoneal seeding and ascites
clinical features of pancreatic cancer
- Jaundice (common) - suggests biliary obstruction or rarely hepatic or hilar nodal mets ⁃ Painless progressive jaundice - classical presentation but uncommon
- Non-specific upper abdo pain (dull or aching)
⁃ Often overlooked by patients and doctors but is one of the 1st symptoms
⁃ Persistent back pain suggests retroperitoneal masses
- General = anorexia, weight loss and lethargy
- Others:
⁃ Steatorrheoa - if pancreatic duct is affected
⁃ Diabetes - glycosuria, polyuria/dypsia of recent onset in the elderly is suspicious if no diabetic RF are present
⁃ Migratory thrombophlebitis (10%) - occurs with malignancy-associated hypercoaguable states - Occurs when mucin is produced in excess by tumour –> activates platelets
• Courvoisierʼs Sign = Painless palpable gall bladder + jaundice
investigations of pancreatic cancer
• Bloods
⁃ FBC - anaemia
⁃ LFTs - obstructive jaundice (↑↑ ALP, GGT and bilirubin)
⁃ Coags / PT = Prolonged if Vit K is malabsorbed
⁃ Ca19-9 - pancreatic cancer marker (consider)
- U/S of abdo - May identify mass or dilated bile ducts
- CT - Assessing tumour size and extent of LN spread
- ERCP - may confirm diagnosis and allow for biopsy (not required before resection
- Staging laparoscopy
management and prognosis of pancreatic cancer
Management:
• Surgical resection - minority of patients are suitable for Sx because pancreatic cancer presents late
⁃ Patients with ampullary carcinoma often present early with jaundice and may be better candidates for Sx ⁃ “Whippleʼs procedure”
- No role for adjuvant chemotherapy
- Palliative procedures may include bypass or stenting procedures for obstructive jaundice
Prognosis: • Without treatment - survival is only a few weeks to months after diagnosis • Post Sx - prognosis is still poor with 5 year survival = 10%
preoperative prep
Bowel Cleansing Technique Prior to Surgery:
• Roles: ⁃ Pre-op bowel preparation decreases the risk of anastomotic leakage
⁃ Reduces the risk of post-op infection
⁃ Easier for the surgeon to operate
• Procedure:
⁃ Withdrawal of solid foods ⁃ Patient is limited to fluids or low-fibre diets a few days prior to surgery
⁃ Purgation ⁃ Refers to the evacuation of the bowel via oral laxatives such as sodium picosulfate ⁃ Diarrhoea caused by this method can cause dehydration in the elderly ⁃ This method cannot be employed if a partial bowel obstruction is suspected
⁃ Enemas and distal bowel washouts ⁃ When there is bowel obstruction, distant bowel washouts and enemas can safely by given pre-op ⁃ “On-table” washouts can also be performed
preoperative antibiotic prophylaxis
- Definition: ⁃ The use of antibiotics to prevent infections at the surgical site
- Rational: ⁃ The majority of post-op infections are caused by the patientʼs own bacterial flora ⁃ The antibiotic given should only cover the likely pathogens, NOT all potential organisms ⁃ Important to use a narrow spectrum antibiotic appropriate to the site of surgery ⁃ It is important to achieve high circulating blood levels by the time of operation
⁃ IV - give at the time of anaesthetic induction
⁃ IM - give at pre-op medications ⁃ A single bolus dose is usually sufficient if the duration of the surgery is 4 hours or less ⁃ Inappropriate use of surgical prophylaxis increases both cost and selective pressures on resistant bacteria ⁃ Persistant antibiotics post surgery does not improve efficacy and increases toxicity and cost
- Indications: ⁃ When the surgery is considered “contaminated” or “clean-contaminated” ⁃ When there is insertion of an artificial device or prosthetic material
- Choice of antibiotic: ⁃ Based on: Patient allergy, site of surgery, duration of surgery and narrow spectrum ⁃ 3rd generation cephalosporins should be avoided due their broad cover
commonly used regimen - antibiotic prophylaxis
prostate cancer - def, epi, aetiology
pathophysiology of prostate cancer
pathology of prostate cancer
clinical features of prostate cancer
investigations of prostate cancer
DDx of prostate cancer
- Benign prostatic hyperplasia - common symptoms but BPH prostates feel “rubbery”; confirm on biopsy
- Chronic prostatitis - manifests > 3months to years with urinary frequency, dysuria and male dyspareunia
management of prostate cancer
prognosis of prostate cancer
renal tumour - def, epi
renal tumour - classification
renal cell carcinoma - def, epi RF, characteristics
renal cell carcinoma - clinical features, Ix, management, prognosis
small bowel obstruction - def, epi, aetiology
pathophys and classification of small bowel obstruction
small bowel obstruction - clinical features and Ix
small bowel obstruction - DDx, management, prognosis
oesophageal cancer - def, epi, aetiology, pathophys
oesophageal cancer - Ix, DDx, Rx, prognosis
oesophageal cancer clinical features and prognosis
clinical features
- Dysphagia – 1st symptom but only presents when ~ 2/3rds of the lumen is obstructed
- Odynophagia
- Weight loss
- Hoarseness of voice (recurrent laryngeal nerve involvement)
- Hiccups, post-prandial cough
prognosis
- Remains one of the most lethal malignancies – 5 year survival = 5%
- Local progression can lead to oesophageal obstruction and severe dysphagia • Metastasises widely to the liver, lungs and bone
stomach cancer - def, epi, aetiology, pathology, clin features
stomach cancer - Ix, DDx, Rx, prognosis
thoracic trauma
tension pneumothorax
simple vs open pneumothorax
haemothorax
cardiac tamponade
trauma - part 1
trauma part 2
Triple assessment for a breast lump
The “Triple Assessment” refers to recommended approach for the investigation of breast symptoms that could be breast cancer
Triple test is more accurate at detecting breast cancer than any of the individual components alone.
When performed accurately, will detect over 99.6% of breast cancers.
A negative on all 3 components is strong evidence that cancer is not present
The Triple Test comprises
1. History + Examination
2. Imaging of the breast (mammogram and/or ultrasound)
3. Biopsy of the mass
breast cancer types
surgical options for breast cancer
- Breast Conserving Surgery – Wide Local Excision, or “lumpectomy”
- Mastectomy
- Axillary Surgery
- Sentinel Node Biopsy
- Axillary Clearance
- Oncoplastic or Reconstructive Surgery
group + hold vs crossmatch
give the pt O negative while we try to identify the pt’s blood group
therapies/products used for clotting
§Fresh Frozen Plasma
§Platelets
§Cryoprecipitate
§Vitamin K
§Prothrombinex
§Factor VII concentrate
§Tranexamic Acid
FFP
platelets
cryoprecipitate
fibrinogen
Massive transfusion protocol (MTP)
