Abdo conditions Part I Flashcards

1
Q

AAA definition and epidemiology

What are the 2 types?

A

Permanent and irreversibly localised dilation of the AA by 50%. So 3cm or more

5% of population over 60

True aneurysm: ; dilation involves all 3 layers
Pseudoaneurysm: collection of blood in the adventitia

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2
Q

Pathophys of AAA

What is the most common site

A

Results from failure of major structural proteins of aorta – elastin + collagen.

Elimination of elastin from tunica media = aortic wall ↑susceptible to force of blood pressure.

Most commonly found in the infrarenal portion of the AA

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3
Q

Risk factors/ causes of AAA

A

Atherosclerosis RFs: smoking, age, HTN, hyperlipidaemia
Trauma
Infection e.g. endocarditis, tertiary syphillis
Inflammatory causes: Takayasu’s aortitis , Behcet’s disease
CTDs, marfans and ehlers-Danlos
Older caucasian males
FamHx

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4
Q

Symptoms of an unruptured AAA

Symptoms of a ruptured AAA

A

Unruptured: most are asymptomatic
Possible pain in back, abdo, loin or gron

Ruptured: Central abdo pain + lower back pain in pt with unknown aneurysm
SUDDEN +SEVERE. Shock/ collapse/ syncopy
Ruptured AAA should be considered in any pt with hypotension +atypical abdominal symptoms

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5
Q

Signs of a AAA OE

A

Pallor + sweating.
Hypotension (50%).
Mottled skin of the lower body (livedo reticularis)
Grey Turner’s sign (flank brusing)- ONLY IN RETROPERITONEAL HAEMORRHAGE

Pulsatile expansile mass: Felt using bimanual palpation either side of the midline
Decreased ABPI
One or both femoral pulses may be absent

Abdominal bruit
Tachycardia (50%)

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6
Q

Investigations for AAA

A

ECG (if TAA- rule out MI), CXR + possibly lung function tests.

Blood tests:
FBC (may reveal ↑WCC), clotting screen, renal + liver function.
ESR +/or CRP (if inflammatory cause suspected)
Cross-match if surgery planned.

Imaging:
Ultrasound: can detect aorta expansion from as little as 3mm
CT: Visceral arteries, Mural thrombus and Crescent sign’ (blood within thrombus- may predict imminent rupture), para-aortic inflammation, ct with contrast can show rupture of aneurysm.
MRI angiography may be used: safer as nephrotoxic contrast not used

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7
Q

Regarding AAA what should we encourage men >66/ women >70 to do

A
Self- refer to NHS AAA screening programme if they have not been screened and have the following RFs (same applies to women aged 70+): 
COPD
CVD
PVD
FamHx AAA Hyperlipidaemia
HTN
current or ex smoker.
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8
Q

Conservative, medical and surgical management of unruptured AAA

A

Conservative: 3-4.4cm = Annual US
4.5-5.5cm = 3 monthly US
>5.5cm =consider surgery + 3 monthly US
DVLA must be notified of aneurysms >6cm. >6.5cm disqualifies person from driving. Reduce CV risks

Medical: Blood pressure control
Consider Statins (Atrovastatin 80mg), Aspirin 75mg + Antiplatelet therapy- AAA pts have ↑ cardiovascular disease risk.
Surgical: indicated for aneurysms >5.5cm can be open repair or EVAR (stent graft put in through femoral arteries)

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9
Q

Management of ruptured AAA

A

A-E IT! High flow O2.
Two large bore cannulas.
Send blood for FBC, U&E, glucose, clotting screen, LFTs and group & save bloods.
Consider activating major haemorrhage protocol or using O negative blood stored in A&E.
IV analgesia – morphine titrated to response.
IV anti-emetic – cyclizine 50mg.
Give IV fluids if needed but not excessively.
Alert vascular surgeon and anaesthetist at an early stage – aortic cross clamping often required to resuscitate severely hypovolaemic patient

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10
Q

Appendicitis definition

Etymology

Pathophysiology

A

Acute inflammation of the appendix

Most common surgical emergency, lifetime incidence 6%. Can occur at any age but peaks at 10-20 yo

Appendix normally acts as a reservoir for gut associated lymphoid tissue
Luminal obstruction leads to distention of appendix due to increased mucus production, bacterial overgrowth and suppurative inflammation
This causes impaired lymphatic and venous drainage
Resulting in ischaemia, necrosis and potential perf

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11
Q

Risk factors for appendicitis

A
Pos FamHx 
Infection e.g. e.coli and bacteroides 
Malignancy
Children breastfed for <6 months 
Recent viral illness or lymphadenopathy
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12
Q

Appendicitis symptoms

A

Periumbilical/ epigastric crampy abdo pain that moves to the RIF in 24-48 hours
Pain worsened by movement or driving over uneven roads
Constipation though diarrhoea may occur
Sudden relief of pain indicates perforation
Murphy’s triad: Nausea and vomiting, low-grade fever and RIF pain
McBurney’s point: Deep tenderness here is a sign of acute appendicitis. The point is 2/3rds the distance between the navel and the R- ASIS

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13
Q

Appendicitis signs

A
Tachycardia 
Fever (low grade: Between 37.5 and 38.5^C)
Facial Flushing
Dry Tongue 
Halitosis: Chronic bad breath
Peritonism

Rebound or percussion tenderness in RIF
Pain on right during PR exam suggests inflamed low-lying pelvis appendix
Anorexia
Bowel sounds may be reduced particularly on the right side compared to left

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14
Q

Define:

Rovsing’s sign
Psoas sign
Obturator sign
Hop test

A

Rovsing: Positive when pressure over the patient’s left lower quadrant causes pain in the right lower quadrant
Psoas sign: Passive extension of the right thigh with the person in the left lateral position elicits pain in the right lower quadrant
Obturator sign/ cope pain: Passive internal rotation of the flexed right thigh elicits pain in the lower right quadrant. Shows if appendix is close to obturator
Hop test: hopping or jumping causes abdo pain

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15
Q

Appendicitis investigations

A

Bedside:
Urinalysis: To exclude UTI: pts may have leukocytes
Pregnancy test: to exclude ectopic pregnancy
Cap blood glucose: Nausea, vomiting, anorexia may cause hypoglycaemia

Labs
FBC: Will show neutrophil leucocytosis present
U&Es: Anorexia, nausea, vomiting may cause deranged renal function
CRP: May be elevated with acute inflammation
G&S= appendicitis management typically operative

US: Appendix not always visualised but may show non compressible appendix, wall thickening with associated hyperaemia. Should be used in children, pregnant or breastfeeding women
CT: High diagnostic accuracy and reduces negative appendectomy rate. Not routinely indicated: only if diagnosis is uncertain

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16
Q

Appendicitis management?

Name 3 scoring systems that can be used for appendicitis

A

Keep pt NBM and consider referring to surgeons

  • Piperacillin/ tazobactam 4.5g/8hrs- 1-3 doses starting 1hr preop reduces wound infections
  • Cefoxitin: 1-2g ivly as a single dose before surgery followed by 1-2g every 8 hours for 2 doses post-surgery ( can also be used for patients who become unwell from perforation or abscess formation)
  • IV opioids and anti-emetics (metoclopramide 10mg IV)
  • Fluids: Hartmann’s, 500ml bolus in 15 mins if no known HF, LF, KF
  1. Appendicitis Inflammatory Response (AIR):
  2. Paediatric appendicitis risk calculator (PARC): this and the above have the least number of false positives. Used for suspected appendicitis
  3. Alvardo Score: predicts the likelihood of appendicitis
17
Q

Differentiate between acute cholecystitis and acute cholangitis

A

Cholecystitis is an inflammation of the gallbladder wall, usually caused by obstruction of the bile ducts by gallstones
Cholangitis is inflammation of the bile ducts

18
Q

What are the 3 types of stones implicated in cholecystitis and cholangitis

A

Cholesterol stones: Large, solitary; caused by age and obesity: Most common in the west- approx. 90%. Light yellow- dark green/ brown

Bile Pigment stones: Small, friable and irregular; caused by haemolysis. Dark coloured stones made of bilirubin and calcium salts (Black- haemolytic conditions, Brown- mostly found in the presence of bile stasis)

Mixed stones: A combination of cholesterol, calcium salts and pigment stone

19
Q

Risk factors for cholecystitis/ cholangitis

A

FORTY FAT FEMALE FAIR FERTILE

Crohn’s disease
DM/ obesity/ metabolic syndrome
Diet: high in triglycerides, refined carbohydrates and low fibre
Family history: monozygotic twins= higher risk
Genetic: ABCG8.Pd19H- increases cholesterol secretion. UGT1A1 in male carriers of gilbert syndrome (mild disorder where liver does not properly process bilirubin)
Increasing age: Peak age of occurrence= 70-79 years

Medication: 
-	Somatostatin analogues 
-	Glucagon-like peptide 1 
-	Ceftrixazone  
NAFLD
Prolonged fasting or weight loss: causes gallbladder hypomotility and increases cholesterol excretion in bile 
Use of hormone replacement therapy
Pregnancy/ Exogenous oestrogen: Increasing levels of oestrogen heighten cholesterol saturation of bile therefore women are more likely to develop sludge and gallstones. COCP in younger females
20
Q

Cholecystitis/ Cholangitis symptoms

A

Cholangitis: RUQ pain which radiates to the back: typically 30mins< x < 8 hours. May radiate to right shoulder
Pain lasting less than 30 mins is less likely to be biliary colic
- Biliary colic: steady, severe (intensity >5 on a scale of 1-10) pain on RUQ of abdomen lasting 15-30mins

Acute cholecystitis: In addition includes fever and tenderness in RUQ
Post prandial pain

21
Q

What is the main difference between biliary colic and cholangitis?

A

The inflammatory component in cholangitis:

Charcot’s triad: Local peritonism, fever, increased WCC

22
Q

Signs OE- cholangitis and cholecystitis

A

Leukocytosis: xs WBCs
Jaundice: Mirizzi’s syndrome: Stone in the GB progress to obstruct the bile duct
Acute Cholangitis: Charcot’s triad: RUQ Biliary pain , jaundice and fever
Local periotonism: Murphy’s sign: 2 fingers on RUW will cause pain and arrest on inflammation: only positive if same test on left side does not cause pain
Phlegmon (20% of patients)- RUQ mass of inflamed adherent omentum + bowel
Obstructive jaundice+ cholangitis: yellowish discolouration of the skin, dark urine and pale stools: if the stone moves to the cbd

23
Q

Cholecystitis and cholangitis investigations

A

FBC: Elevated WBC may suggest acute cholecystitis, cholangitis or pancreatitis
LFTs: Brief biliary obstruction with subsequent stone passage causes an early transient rise in ALT before ALP rises, GGT may rise
Serum lipase/ amylase: for pain located primarily in epigastric area with(/out) radiation to back could suggest acute pancreatitis= 3 times the upper limit of normal . In acute cholangitis: shows involvement of lower part of common bile duct. LFTs show picture of obstructive jaundice (ALT levels <100 IU/L with jaundice, ↑ ALP)

AUS (1st line): 95% sensitive: will show a thick walled shrunken GB, periocholecystic fluid, stones and CBD if filated >6mm
AXR: will show gallstones though their absence does not negate existence
MRCP/ EUS (Endoscopic ultrasound) if gallstones not suspected but suspicion remains high
Urinalysis
CXR
ECG: to identify tachycardia

24
Q

Acute cholangitis emergency management

Surgical management

A

Medical (BMJ best practice)

  1. IV broad spec abx: piperacillin/ tazobactam: 4.5g iv every 8 hours OR 500mg metronidazole + 400mg ciprofloxacin every 8 hours
  2. Biliary decompression and drainage within 12-24 hrs: ERCP with or without sphincterectomy + stent
  3. Pain management: Oxycodone 5mg orally/ (1-10mg IV) every 4-6 hours AND paracetamol 15mg/kg every 4-6 hours when required
  • Laparoscopic choledochotomy with T tube placement or early laparoscopic cholecystectomy with cbd exploration to be carried out within one week of
  • Percutaneous cholecystostomy to manage gallbladder empyema when surgery is contraindicated
25
Q

Acute cholecystitis management

A
  • IV analgesia + anti-emetics.
  • Commence antibiotics – cefotaxime 1g IV.
  • Nil by mouth
  • NG tube (if vomiting severe)
  • Refer to surgeons, consider laprascopic cholecystectomy