General Surgical Topics Flashcards

HPB Urology

1
Q

What are the risk factors for cholelithiasis?

A
Female
Obesity (>30 BMI)
Family history of gallstones
drugs (exogenous estrogen, ceftriaxone) 
Pregnancy 
Diabetes
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2
Q

What is the classic presentation of gallstones (cholelithiasis)

How is best to investigate gallstones?

What is a differential?

Management if asymptomatic?

Management if symptomatic?

Follow up?

A
  1. Pain in the upper abdomen or right upper quadrant, lasting for more than 30 minutes, but less than 8 hours. Biliary colic steady, severe >5/10 - simple should resolve within 5 hours
  2. May be associated with nausea and vomiting
  3. Postprandial
  4. No fever
  5. No Jaundice

Investigate with

  1. Abdominal ultrasound
  2. Liver function test

Though both can be normal

Differential includes:

  1. peptic ulcer disease
  2. gastritis
  3. IBS
  4. GORD
  5. Tumour
  6. Bile duct stricture
  7. Acute hepatitis

Management:
Asymptomatic
if found in a normal biliary tree - explain very common and no treatment required.

Symptomatic:
Surgical referral

Pain relief - diclofenac 75mg IM
IM opioid if above contraindicated
Paracetamol
Avoid trigger foods - until after surgery

FOLLOW UP:

  • follow up 2 weeks after (clinic?)
  • symptom check
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3
Q

How does cholelithiasis, cholecystitis, choledocholithasis, cholangits, and acute pancreatitis compare in their presentation?

A
  1. Cholelithiasis (gallstones in the gallbladder) RUQ or upper abdominal pain which resolves within 5 - 8 hours. No fever, No Jaundice, no leukocytosis
  2. Cholecystitis (inflammation of the gallbladder due to stones)- biliary pain lasting more than 5 hours accompanied by fever, marked RUQ pain (Murphy’s sign positive)
    Leukocytosis, no jaundice
  3. Choledocholithasis, stone obstructing the bile ducts: biliary pain and jaundice.
  4. Cholangitis - inflammation of common bile duct and gallbladder: CHARCOT’s triad - biliary pain, jaundice and fever - medical emergency
  5. Acute pancreatitis - epigastric pain radiating to the back due to bile duct stones obstructing the pancreatitic duct - can be peritonitic.
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4
Q

What is the classic presentation of renal stone disease?

What are the first line investigations?

A
  • Acute, severe flank pain that radiates to the ipsilateral groin, may be asymptomatic
  • Previous episodes of renal stones
  • Nausea and vomiting
  • Urinary frequency/urgency - as stones pass and lodge in the ureter or intramural tunnel, irritating the bladder
  • Haematuria - microscopic common and rarely macroscopic
  • Testicular pain: due to radiating pain
  • Obesity (increased BMI is a risk factor)
  • Always consider AAA in those >55
  1. Urinalysis - microhaematuria. infection
  2. FBC and differential ? Infection
  3. U & E - kidney function - high calcium may indicate hyperparathyroidism, or hyperuricaemia: gout
  4. Urine pregnancy test in women before scans
  5. non-contract helical CT scan - Always check if they have had a recent scan - if so contact the urology Registrar
  6. Stone analysis
  7. Consider a plain film X-ray KUB
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5
Q

What are the risk factors for getting renal stones?

A
  • High protein intake
  • High salt diet
  • White
  • Male (10% lifetime risk for men - 7% for women)
  • Dehydration ( 2 - 3 litres a day at least)
  • Crystalluria (increased calcium oxalate in the urine, increased cystine, struvite and uric acid.
  • Obesity
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6
Q

What is the management of renal stones?

What follow up do patients need?

A
  1. Main goal is symptomatic relief and hydration
    - Analgesia and anti-emetics
    - No infection: opioids (tramadol PO or IV) and NSAIDs (Diclofenac PO or PR):
    If they require morphine (give after above trial) they are likely to require admission.
  2. Assess for infection (IV ABX/ sepsis 6 which will require immediate urological review for decompression (ureteric stent, percutaneous nephrostomy, but interventional radiology) to reduce risk of life threatening septic shock.
  3. ? Medical expulsive therapy - alpha blockers and calcium channel blockers for stones < 10 mm.

Follow up:
Follow in the stone clinic:
? CT KUB or Plain film KUB

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7
Q

What are the symptoms of acute prostatitis

What are the risk factors for prostatitis?

What investigations do you need to do?

A

Lower Urinary Tract Symptoms (LUTS)

  • Dysuria
  • Frequency
  • Perineal discomfort
  • Voiding symptoms - diminished calibre of stream, slowing stream.
  • Variable systemic signs - fever, chills & malaise.
  • Referred pain to the genitalia, perineum and lower back or suprapubic area which are be extreme.
  • Ejaculatory pain
  • Intensely tender prostate gland which may also be soft, boggy and warm to the touch on DRE (also rules out an anorectal cause)

2/3 <50 1/3 >50
The greatest risk factor is UTI -
Benign Prostatic Hyperplasia

Investigations:

  1. urinalysis and culture. [MC&S]
  2. PSA may be elevated
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8
Q

How do you management Acute Prostatitis?

A
  1. ABX - quinolones (ciprofloxacin, ofloxacin, levofloxacin)
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9
Q

What is the most common renal cell carcinoma?

What is the most common symptom?

What are the risk factors?

A

Clear cell renal cell carcinoma (80%)

most commonly asymptomatic and it occurs sporadically - though +ve family history increases risk 4x
R

Risk factors include:
Smoker, 
Male 
55+
black 
obesity 
HTN
FMHx
high parity 
radiation

Diagnostic factors include:
haematuria, palpable abdominal mass
- though it is commonly asymptomatic.

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10
Q

What is an aneurysm?

A

A focal, permanent dilation of an artery or vessel to more than 50% of its normal diameter.

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11
Q

What is the natural history of aneurysms?

A

Asymptomatic growth followed by symptomatic rupture which is often fatal

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12
Q

How is an abdominal aortic aneurysm classified?

A

A dilation of the infra-renal abdominal aorta greater than 3cm.

Patients with AAA < 5.5 cm are under surveillance. Those at or over 5.5 cm should be considered for surgical repair to prevent rupture.

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13
Q

What are the treatments for AAA?

A
  1. Open surgical repair

2. Endovascular Aneurysm Repair (EVAR)

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14
Q

Who is affected more by AAA, men or women?

A

Men (5%)

Women 0.74%

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15
Q

What is the major risk factor for AAA?

What are other risk factors?

A

Smoking - which far surpasses genetics and all other modifiable risk factors. (x8 risk compared to never smokers for development and also smoking is related to faster AAA growth)

Hypercholesterolaemia

Hypertension (considered though not proven with randomised evidence)

Diabetes is protective against the development and progression of AAA?

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16
Q

How does AAA classically present?

What about rupture?

A

Classically asymptomatic found incidentally on investigation for another reason - may be an expansible abdominal mass.

Rupture has a triad of abdominal pain, radiating to the back, haemorrhagic shock and a palpable, expansile pusatile abdominal mass.

17
Q

At what age are people invited to be screened for AAA?

A

Men at screen at aged 65, though actually rupture occurs more frequently in women.

18
Q

why does incisional hernia occur?

How can they present?

What is the gold standard investigation?

A

Incisional hernia occurs after wound healing that is insufficient at the level of the fascia.

The majority are small and asymptomatic. However, small hernia’s can be complicated by incarceration and strangulation presenting with extreme pain, necessitating emergency surgery.

CT - providing information about the musuclofascial quality and viscera outside the abdominal cavity (loss of domain)
DASH - dynamic abdominal sonography for hernia.

19
Q

What are the stages of normal wound healing?

A

1 - inflammatory stage (4 days) - vasodilation and angiogenesis take place and proteinglycans from mast cells cause formation of a gel matrix prepared for deposition of collagen. Macrophages are attracted and recruit fibroblasts for the later sages, and further clear the environment of bacteria and debris. The PMN leukocytes cause phagocytosis of debris by proteinases which weaken the tensile strength of the tissue. Normally 5 mm each side of the wound.

2 - the regenerative stage (proliferative stage)
Movement of fibroblasts into the wound area, synthesis of collage and contraction of the wound, lasts for about 3 weeks. At the end of this stage almost all new collagen has been formed in the wound. Tensile strength is still not sufficient due to lack of cross-linking of collagen.

3 - the remodelling stage. This final stage may continue for years, the newly laid collagen matrix undergoes qualitative changes brought on by mechanical environmental forces, resulting in optimal alignment of fibres to withstand these pressure. Crosslinking occurs (covalent bonding)

Importantly optimising the patient preoperatively with vitamin A, B, C and Cu, Zn and Fe and essential amino acids is important to successful wound healing.