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Y2 - CSI > Anna Pritchard > Flashcards

Anna Pritchard Flashcards

Abdominal Pain

1
Q

What does the introduction video reveal about Anna Pritchard?

A

Brought to A&E - suffering with occasional abdominal pain over the last year

Worsened over last 24hrs

Disrupting her sleep

Feeling nauseous as well

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2
Q

What symptoms does Anna Pritchard talk about in the case video?

A 
Bad abdominal pain
Started last night after eating Thai food for dinner 
Slowly getting worse
Slept terribly
Sharp
Middle and top of tummy
Laughing makes it worse
Sudden onset
Nothing like this before
Stomach pain on and off for a year but not as bad as this
Gets worse when she eats well
Nausea - vomited once 
No diarrhoea
No fever
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3
Q

What does Anna Taylor think the abdominal pain is?

A

Improperly cooked chicken from the Thai food she and her son ate - so food poisoning

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4
Q

What is Anna’s PMH?

A 
Borderline diabetes
Should loose weight and eat better 
No allergies
No regular medications
Took a paracetamol last night
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5
Q

What is found in the lifestyle history?

A

Works in a bank
Glass of wine most nights
3-4 bottles a week
Non-smoker

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6
Q

What is the doctors plan of action?

A

Examine
Run bloods
Painkillers
Will come back and explain what’s going on

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7
Q

What does acute abdomen refer to?

A

Rapid onset of severe symptoms that may indicate potentially life-threatening intra-abdominal pathology required urgent surgical intervention

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8
Q

In who can pain free acute abdomen occur in?

A

Older people
Children
Immunocompromised
Last trimester of pregnancy

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9
Q

How may acute abdominal pain present in A&E?

A

Be located in any quadrant of the abdomen
Be intermittent, sharp or dull, achy, or piercing
Radiate from a focal site
Be accompanied by nausea and vomiting.

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10
Q

What should immediate assessment focus on?

How can this be achieved?

A

Distinguishing patients with true acute abdomen that requires urgent surgical intervention from patients who can initially be managed conservatively

Patient with acute surgical pathology may deteriorate rapidly - need to be closely monitored

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11
Q

How is acute abdomen diagnosed?

A

History
Physical examination
Radiography
Laboratory results

If diagnosis still unclear:
Further abdominal examination by experiences physician
OR
Diagnostic laparoscopy

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12
Q

What else is a laparoscopy used for?

A

Therapeutic measure (i.e. treatment for)

Appendicitis
Cholecystitis
Lysis of adhesions
Hernia repair
And many gynaecological causes of an acute abdomen
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13
Q

What can help stratify the risk of appendicitis in patients presenting with acute abdominal pain?

A

The Appendicitis Inflammatory Response (AIR) score

The Pediatric Appendicitis Risk Calculator (pARC)

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14
Q

Is narcotic analgesia given to undiagnosed patients with an acute abdomen?

A

Yes - improves patient comfort e.g. fentnyl or one of its analogues die to potency and short half-life

Hoever, previously this was discouraged as it way believed that that symptoms would be masked, the examination hindered, and, therefore, the correct diagnosis missed

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15
Q

In what groups does abdominal pain present atypically and why?

A

Older people =
More co-morbidities
Higher risk for more severe disease due to decreased immune function
Dementia (communicating issues)
PNS dysfunction - alter perception of pain and temperature

Pregnant women =
Enlargement of uterus displaces and compresses abdo organs
Physiological leukocytosis
Hesitancy to conduct radiographs

Immunocompromised

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16
Q

What are the common differential diagnoses for an acute abdomen?

A

Adhesions
Incarcerated/strangulated hernia
Cholecystitis
Gastric ulcer

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17
Q

What are the uncommon differential diagnoses for an acute abdomen?

A

Volvulus
Intussusception
Duodenal ulcer
Ruptured ovarian cyst

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18
Q

What are the abdominal causes of an acute abdomen (from most common to least)?

A

Intestinal obstruction
Peritonitis secondary to infection e.g. pelvic infection, appendicitis - surgical emergency
Haemorrhage
Ischaemia
Contamination by gastrointestinal contents

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19
Q

What may other conditions may present similar to / as peritonitis?

A

Inflammatory conditions - e.g. diverticulitis, pancreatitis, and cholecystitis

Vascular processes - e.g. aortic dissection or ruptured abdominal aortic aneurysm

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20
Q

What are some causes of obstruction causing an acute abdomen ?

A 
Adhesions - most common 
Hernia incarceration = 2nd most common in patients without prior abdo surgery
Volvulus 
Gallstones
Intussusception
Congenital anatomical abdormalities
GI neoplasm
IBD
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21
Q

What are some causes of inflammation causing an acute abdomen?

A

Inflammatory causes include - cholecystitis, appendicitis, acute pancreatitis, and acute diverticulitis and Meckel diverticulitis

Ulcerative colitis and Crohn’s disease may present with abdominal pain secondary to the inflammatory process or due to the complication of obstruction

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22
Q

What are some gynaecological causes causing an acute abdomen?

A

Pregnancy test to rule out ectopic pregnancy

Female reproductive organs e.g. ovarian cyst, ovarian torsion, pelvic inflammatory disease, and endometriosis

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23
Q

What are some vascular causes causing an acute abdomen?

A

Vascular pathologies resulting in intra-abdominal haemorrhage = abdominal aortic dissection, ruptured aortic aneurysm, and ruptured splenic artery aneurysm

Ischaemic causes = acute mesenteric ischaemia and infarction, ischaemic colitis, splenic infarct

Sickle cell crisis = vaso-occlusive episode

Budd-Chiari syndrome involves hepatic venous outflow obstruction - presents with hepatomegaly and ascites

Abdo wall haematoma - may be spontaneous, secondary to trauma e.g. exercise, coughing or procedure

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24
Q

What are some causes of infection leading to an acute abdomen?

A

Infective processes involving intra-abdominal organs e.g. hepatic abscess, hepatitis, gastroenteritis, infectious colitis, typhlitis, neutropenic enterocolitis

Psoas abscess = more common due to tuberculous obscess - extends from lunbar vertebra to the psoas muscle

Fitz-Hugh Curtis syndrome, a complication of pelvic inflammatory disease, comprises right upper quadrant abdominal pain associated with perihepatitis

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25
Q

What are some metabolic causes leading to an acute abdomen?

A

Metabolic causes = uraemia, diabetic ketoacidosis, Addisonian crisis, and hypercalcaemia

Inherited metabolic disorders = acute intermittent porphyria and hereditary Mediterranean fever

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26
Q

What can cause toxicity within the body leading to an acute abdomen?

A

Heavy metal poisoning = medical/environmental/occupational exposure to, e.g. mercury, lead, or arsenic

Narcotic withdrawal from opioids = abdo cramping pain

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27
Q

What urological causes can lead to an acute abdomen?

A

Men = testicualr torsion

Men and women = kidney stones, pyelonephritis

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28
Q

What may be some other causes leading to an acute abdomen?

A

Radiation enteritis

Spider bites

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29
Q

What processes can lead to contamination by GI contents?

A

Perforated duodenum

Perforated gastric ulcer

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30
Q

What should be done while awaiting the results of lab tests?

A

Surgical consult - made before further diagnostic testing - surgeon determines where operative or non-operative management is needed
IV access
Vitals monitored and corrected

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31
Q

When should surgery be conducted with limited pre-op evaluation?

A

In patients exhibiting evidence of hypovolaemic shock with a known or suspected haemoperitoneum (haemorrhage / blood in the peritoneal cavity)

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32
Q

What else needs to be done in patients with a potential ongoing haemorrhage / hemoperitoneum?

A

2 large bore IV lines places
Urgent typing and cross-matching of blood
Fluid resuscitation - initial = 2L of isotonic fluids
O-neg given until cross-matched blood is available
Condider antifibrinolytic e.g. tranexamic acid

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33
Q

How do patients with a ruptured abdominal aortic aneurysm / aortic dissection present?

How are these patients managed?

A

Presenting with abdominal pain radiating through to the back and a pulsatile abdominal mass

Careful fluid management with goal of maintaining systolic BP at 80-90 mmHg 
Urgent blood typing and cross-matching
Routine lab blood tests 
Emergent vasculr surgery consultation
Prophylactic antibiotics
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34
Q

What is the issue with overly aggressive fluid replacement?

A

Exacerbates bleeding via:
Dilutional and hypothermic coagulopathy
Lowering blood viscosity
The increased perfusion pressure from the expanded volume can lead to secondary clot disruption

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35
Q

What is the management plan if a perforation, diverticulitis or appendicitis is suspected?

A

Broad-specrum atibiotics (Abx) - due to contamination from perforation = rapid deterioration to sepsis

Urinalysis and culture samples ideally done before starting Abx

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36
Q

What should be conducted when females of childbearing age present with abdo pain?

A

Pregnancy test to exclude chance of ectopic pregnancy

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37
Q

What is the management plan if ectopic pregnancy is suspected?

A

2 large bore IV cannulae placed in case of rupture
Blood typing and cross-matching
Urgent gynaecological consultation

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38
Q

How might a mesenteric ischaemia present clinically?

A

Abdominal pain disproportionate to the signs on physical examination
Usually in older patients with - history of smoking, peripheral vascular disease, and/or a. fib

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39
Q

What is the management place for a mesenteric ischaemia?

A

Oxygen
Fluid resuscitation
Empirical antibiotics
Urgent surgical and interventional radiological consultations

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40
Q

What is the approach to reaching a clinical diagnosis?

A

Obtain comprehensive history
Perform thorough medical examination
Lab tests and imaging to support clinical findings

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41
Q

What is important to include when obtaining a history from the patient?

A

SOCRATES

Time of onsent and current duration of pain

Location of pain and consideration of patient’s perception of the anatomical distribution of their symptoms

Whether pain is referred

Characteristics of the pain - intermitten, sharp, dull achy, piercing

Associated systemic or gastrointestinal symptoms, including fever, chills, nausea, and vomiting

Time of last bowel movement

Type and time of last meal or other oral intake

Presence or absence of anorexia

Previous medical and surgical history

History of IBD

Women = date of their last menstrual period, use of contraception and current prgnancy status

Medications taken to alleviate symptoms

Cardiac history

Family history

History of trauma

Travel history

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42
Q

What does the time of onset and current duration of abdominal pain indicate about the diagnosis?

A

Sudden-onset umbilical pain radiating to right iliac fossa = acute appendicitis

Long-term epigastric pain = gastric ulcer; sudden worsening = perforation of the ulcer; sudden epigastric pain following vomiting (usually a severe episode) or oesophagogastroduodenoscopy may indicate oesophageal perforation (Boerhaave’s syndrome)

Previous instances of similar pain = recurrent condition, e.g. cholecystitis, pancreatitis or diverticulitis, with increasing frequency and severity indicating disease progression

43
Q

What does the location of the abdominal pain indicate about the diagnosis?

Epigastric pain
LUQ
RUQ
LLQ
RLQ
(Peri)umbilical pain
A

Epigastric pain = gastric ulcer / perforation, pancreatitis, perforated oesophagus, or Mallory-Weiss tear, cholelithiasis, MI

Left upper quadrant pain = splenic infarct or ruptured splenic artery aneurysm, pyelonephritis, kidney stones, or perforation or malignancy of the colon

Right upper quadrant pain = hepatitis, hepatic abscess, Fitz-Hugh Curtis syndrome, perforation or malignancy of the colon, pyelonephritis, or kidney stones, acute appendicitis in pregnant women due to displacement by uterus

Left lower quadrant pain = sigmoid volvulus (esp. in elderly), diverticulitis, Crohn’s disease, ulcerative colitis, kidney stones, gastrointestinal malignancy, psoas abscess, an incarcerated / strangulated hernia, or gynaecological concerns, including ovarian torsion or cyst rupture, ectopic pregnancy, or pelvic inflammatory disease (PID)

Right lower quadrant pain = appendicitis, kidney stones, gastrointestinal malignancy, psoas abscess, an incarcerated / strangulated hernia, or gynaecological concerns, including ovarian torsion or cyst rupture, ectopic pregnancy, or PID

Periumbilical (behind the belly button) pain = appendicitis (may radiate to the right lower quadrant) or acute mesenteric ischaemia. Other causes of central abdominal pain include leaking or ruptured abdominal aortic aneurysm and small bowel obstruction

44
Q

What does persistent lateralised pain indicate?

A

Persistent lateralised pain = condition associated with ascending or descending colon, kidney, gallbladder or ovary

45
Q

Why is it important to ask about radiation of pain? What can radiation indicate?

A

Radiation of pain: the presence and pattern of radiation can suggest potential etiology

Pain of renal colic frequently radiates from the flanks downward into the groin.

Pain with radiation to the back can indicate pancreatitis, abdominal aortic dissection, or ruptured abdominal aortic aneurysm

46
Q

What are some classic reffered pain sites and what do they indicate?

A

Right scapula pain = gallbladder disease, liver disease, or irritation of right hemidiaphragm (e.g., right lower lobe pneumonia)

Left scapula pain = cardiac disease, gastric disease, pancreatic disease, splenic disease, or irritation of left hemidiaphragm

Scrotal or testicular pain (usually pain is radiating from either costophrenic angle to the groin) = kidney stones or ureteral disease

47
Q

What do different characteristics of pain indicate?

A

Kidney / ureteric stones = severe, with the patient unable to find a comfortable position

Adhesions and icarcerated / strangulated hernias = intermittent and colicky

Abdominal aortic dissection = severe, sharp, or tearing in the thorax or abdomen

Cholecystitis and cholelithiasis = excerbated by eating (esp. fatty) food

48
Q

What GI conditions are often reported with additional associated systemic and/or GI symptoms? e.g. fever, chills, nausea, vomiting

A

Cholecystitis, a ruptured duodenal ulcer, gastric ulcer, appendicitis, acute mesenteric ischaemia, PID, acute diverticulitis, hepatic abscess, hepatitis, abdominal wall haematoma, or spider bites

49
Q

What other GI systems review questions are important to ask and why?

A
  1. Time of last bowel movement = e.g. with an obstruction may not be for a while
  2. Nature of recent stool
  3. Type and time of lasyy meal / oral intake
  4. Presence / absence of anorexia = e.g. apprndicits, obstructive processes, diverticulitis, hepatic abscess, radiation enteritis, and infectious colitis
50
Q

What in the PMH is important to ask and why?

A

Previous medical and surgical history

Focusing on prior abdominal or pelvic surgeries: prior surgery increases the likelihood of an obstruction secondary to adhesions

Is patient mmunocompromised due to infections such as HIV, or are taking medicine for systemic inflammatory conditions such as lupus or rheumatoid disease, and whether they have received chemotherapy and/or radiation

History of IBD e.g. could be colitis due to IBD

For women = last menstrual period, contraception used, current pregnancy status

Medications taken

Cardiac history

Social history e.g. alcohol intake

History of trauma

Travel history

51
Q

What are the important aspects of a physical examination?

A

Measurement of vital signs = blood pressure, temperature, and pulse rate

The physical examination should be performed in the order:

  • Inspection
  • Auscultation
  • Percussion
  • Palpation
  • Other important examinations: rectal, pelvic, scrotal
52
Q

What can inspection of the abdomen in a physical examination reveal?

A

General assessment of how ill the patient appears should be made

Pain and moving around unable to find a comfortable position = renal colic

Atill and reluctant to move = peritonitis

Abdominal scars = previous and current pathology and the likelihood of adhesions

Contour of abdomen = generalised distension or local bulges that may accompany bowel obstruction, hernia, or mass

Skin changes, particularly over hernia sites = strangulation with blanching erythema, discoloration, or even ulceration in late stages

Periumbilical discoloration (Cullen’s sign) or bruising of the flanks (Grey Turner’s sign) indicates haemorrhagic pancreatitis

53
Q

What can auscultation of the chest and abdomen in a physical examination reveal?

A

Small or large bowel obstruction:
Early = hyperactive ‘tinkling’ bowel sounds
Late = reduced or absent bowel sounds, often in combination with a markedly distended abdomen

Chest auscultation may reveal increased vocal resonance and reduced breath sounds consistent with pneumonia, or reduced heart sounds and/or a pericardial rub associated with pericarditis

Bowel sounds may be absent in a patient with a perforated viscus, haemoperitoneum, or other conditions with peritoneal inflammation

54
Q

What can abdomen examination involving observation, palpation and percussion suggest?

A

Observation = abdomen may be distended with abdominal obstruction; patient may be lying still if they have peritonitis.

Palpation =
Rigid abdomen = acute abdomen and implies severe peritoneal irritation with reflex involuntary guarding, generally only encountered with perforated peptic ulcer (with generalised release of gastric acid)
Rebound tenderness = appendicitis, diverticulitis, irritation of the parietal peritoneum, advanced obstruction and volvulus
Murphy’s sign = cholecystitis
Palpable and irreducible hernia = incarcerated hernia
Palpable masses = cholecystitis, appendix mass, intussusception, or aortic aneurysm (pulsatile)

Percussion =
Pain = peritoneal inflammation
Used to detect the presence of shifting dullness

Although uncommon, situs inversus and mid-gut malrotation should be considered for patients with left-sided abdominal pain

55
Q

When might a rectal examination be necessary and what would the findings suggest?

A

Necessary for presence of occult or frank blood, pain, or mass (faecal impaction, tumour, prostate, pelvic abscess)

Blood in stool suggests = acute diverticulitis; volvulus; intussusception

Blood in rectum and stool = haemorrhoids, upper gastrointestinal bleeding, or lower gastrointestinal tumours

56
Q

When might a pelvic examination be necessary and what would the findings suggest?

A

Necessary in women if pain is lower abdomen =
May assist in the diagnosis or exclusion of ovarian torsion, an ectopic pregnancy, or PID

Necessary in men for scrotal / testicular exam =
Tenderness = epididymitis, testicular torsion, inguinal hernias, testicular masses

57
Q

What lab tests are ordered to support clinical findings?

A

Initial tests for all patients
FBC = leucocytosis seen in anything ending in itis
U&E = stage of intetsinal obstruction, elevated glucose in pancreatitis, serum urea elevated in aortic dissection / aneurysm
Urinalysis = UTI, stones
Pregnancy test in women of all reproductive ages

Further lab tests =
Comprehensive metabolic panel e.g. LFTs
Coagulation studies
Serum amylase and lipase = elevated in acute pancreatitis
Serum lactic acud = acute mesenteric ishcaemia

58
Q

What imaging tests may be ordered to support clinical findings?

A

Plain abdominal x-ray = fast, inexpensive
Non-specific but can show obstruction, stones, calcification

Erect chest x-ray = if perforation suspected
e.g. free air under diaphragm

CT of abdomen = for almost all surgical abdo cases

Ultrasound = reveal stones, ectopic pregnancies, torsed ovary, abdominal aortic aneurysm

MRI = limited use, maybe for aortic dissection

59
Q

When might a laparoscopy be considered and why?

A

In a apitent who is:

  • Clinically stable
  • No indication for therapeutic surgical intervention
  • No apparent cause for their abdominal pain after non-invasive procedures
  • No relative or absolute contraindication to surgery

Can be used as diagnostics or therapeutics

60
Q

What are the common differentials for abdominal pain?

A 
Adhesions
Incarcerated/strangulated hernia
Cholecystitis
Gastric ulcer
Appendicitis
Ectopic pregnancy
Pelvic inflammatory disease
Acute pancreatitis
Acute diverticulitis
Ulcerative colitis
Crohn's disease
Cholelithiasis
Gastrointestinal malignancy
Hepatic abscess
Fitz-Hugh Curtis syndrome
Mallory-Weiss tear
Abdominal wall haematoma
Hereditary Mediterranean fever
Typhlitis (neutropenic enterocolitis)
Narcotic withdrawal
Hepatitis
Gastroenteritis
Infectious colitis
Sickle cell crisis
Endometriosis
Testicular torsion
Kidney stones
Pyelonephritis
61
Q

What are the uncommon differentials for abdominal pain?

A 
Volvulus
Intussusception
Duodenal ulcer
Ruptured ovarian cyst
Ovarian torsion
Abdominal aortic dissection
Ruptured aortic aneurysm
Acute mesenteric ischaemia (AMI) and infarction
Meckel's diverticulitis
Psoas abscess
Oesophageal perforation (Boerhaave’s syndrome)
Ischaemic colitis
Ruptured splenic artery aneurysm
Budd-Chiari syndrome
Splenic infarct
Uraemia
Diabetic ketoacidosis
Addisonian crisis
Hypercalcaemia
Acute intermittent porphyria (AIP)
Radiation enteritis
Heavy metal poisoning
Spider bite
62
Q

Mrs Pritchard has presented with acute abdominal pain

What are the top 5 differentials of this presentation?

A

Gastric ulcer - that has now ruptured

Acute pancreatitis

Cholecystitis / gallstones

Gastritis

Biliary Colic

63
Q

On examination:
Tenderness in the right upper quadrant
Normal resp and cardio examination
Combined with her history, this raises suspicion that the source of her pain is from her hallbladder (GB) - specifically due to gallstones (cholelithiasis)

What are the 3 main diagnoses linked to gallstones?

A

Biliary colic

Cholecystitis

Ascending cholangitis

64
Q

What are the differences between:

Biliary colic

Cholecystitis

Ascending cholangitis

A

Biliary colic - constant pain that lasts for less than 6hrs, triggered by fatty food that causes contraction of the GB, colicky pain as the gallstones are present at the neck of the GB and they try to pass out through the ducts into the duodenum / GI system
No inflammation or infection so blood tests should turn up normal

Cholecystitis - pain and fever, inflammation of gallbladder (GB) due to gallstone lodging in the cystic duct
Positive Murphy’s sign - place hand on upper right quadrant and ask patient to breathe in - GB hits hand and causes patient to stop breathing from the pain
Tachycardia
Blood tests show - raised WCC, raised CR, (due to inflammation), ALP may be mildly raised by bilirubin always normal

Ascending cholangitis - pain, fever, and jaundice, inflammation of the bile duct system as gallstone moves back up to block the common hepatic duct (no drainage of the liver)
Tachycardic
Hypotensive 
Confusion
Deranged LFTs
Raised bilirubin
65
Q

Why does ascending cholangitis present with Charcot’s triad? (pain, fever, jaundice)

A

Blockage in hepatic duct
No drainage of liver
So no drainage of albumin
= Jaundice

Fever from inflammation
Pain from gallstone trapped in hepatic duct

66
Q

Normal HR, BP, RR, Sats (on room air), Temp

Normal Hb
High WCC
High neurophils
Normal platelets

Normal creatinine
Normal urea
Normal postassium 
Normal sodium
High CRP

Normal AST
Normal ALP
Normal bilirubin

So what is the most likely differential for Mrs Pritchard looking at her blood test results?

A

Acute cholecystitis due to normal LFTs

67
Q

What investigation is used for suspected gallstones?

A

USS - ultrasound scan

68
Q

How are gallstones formed, and what are some of the risk factors for gallstone disease?

A

Gallstones may be formed from:
Not enough emptying GB regularly
Excess bilirubin - cause crystalisation of bile
High cholesterol levels - excess cholesterol clumps together to form stones
High calcium - bile salts clump together

Risk factors =
5Fs - Female, Fat, Fair, Fourties, Fertile (oestrogen increases biliary cholesterol production)
Genetic risk factor
Haemolytic anaemia - abnormally increased RBC breakdown = raised bilirubin 
Hyperlipidaemia - from fatty diet 
Malabsorption of bile salts
Obesity - increased cholesterol
Some drugs / medications
OCP - oral contraceptive pill
Crohn's or IBS
Recent weight loss
69
Q

What is bile made up of?

A

98% water, bile salts, bilirubin (formed from breakdown of RBCs), cholesterol and normal electrolytes present in plasma

Gallstone formed from super saturation of bile

What the gallstone is made of depends on age, gender, ethnicity, genetic predisposition

70
Q

What are the different 3 types of gallstone?

A

Cholesterol gallstones = poor diet, obesity = due to excess cholesterol
Yellow-green

Pigmented stones = excess bile pigment production
Bilirubin breakdown products (from breakdown of RBCs)
Small, dark, numerous

Mixed stones

71
Q

What are complications caused by gallstones?

A

GB rupture - may lead to sepsis

GB cancer - cholangiocarcinoma due to chronic inflammation

Acute ascending cholangitis - gallstone travels backwards and blocks hepatic duct (sometimes it blocks the common bile duct instead)

Acute gallstone pancreatitis - gallstone travels and blocks pancreatic duct (increased amylase and lipase - these are released into the bloodstream rather than travelling to the ilium)

Gallstone ileus - fistula opens between GB and ilium, gallstones travel via fistula into bowel and obstructs it usually where the small bowel meets the large bowel = narrowest point fo the bowel (v. rare)
Leads to vomiting, severe abdo pain, etc.

72
Q

What is the treatment of asymptomatic VS symptomatic gallstones?

A

Asymptomatic = no treatment

Symptomatic = laparoscopic cholecystectomy = requires written consent form

73
Q

What do you need as a surgeon to gain valid consent for laparoscopic cholecystectomy?

A
  • Voluntary - no coersion
  • Patient needs to have capacity - need to be able to understand, retain, weigh up and communicate their decision
  • Informed consent - all info provided

• The patient’s diagnosis and prognosis
• The right of the patient to refuse treatment and make their own decisions about
their care
• Alternative options for treatment, including non-operative care and no treatment
• Advice on lifestyle that may moderate the disease process
• The purpose and expected benefit of the treatment
• The nature of the treatment (what it involves)
• The likelihood of success
• The clinicians involved in their treatment
• Potential follow-up treatment
• The material risks inherent in the procedure and in the alternative options discussed
• Give the patient time to make the decision - depends on urgency of situation
• For private patients, costs of treatment and potential future costs in the event
of complications

  • Knowledge of procedure
  • Explain diagnosis
  • Treatment options
  • Purpose of procedure
  • Risks
74
Q

A core part of informed consent is explaining the risks and complications of a surgical procedure

What are the risks and complications with a laparoscopic cholecystectomy?

A

General surgical risks / complications:

  • General anaethesia
  • Infection
  • DVT / PE (increased risk of blood clots due to inactivity of muscles during the procedure)
  • Bleeding
  • Scar may not heal properly
  • Chronic pain (as pain may not subside)
  • Anaphylaxis / allergy to medication

Risks / complications specific to a cholecystectomy:

  • BIle leakage - from bile duct injury
  • Damage to nearby structures e.g. bile ducts, liver, small intestines
  • Gallbladder perforation
  • May need to be converted into an open surgery

Early complications:

  • Keep wounds dry and clean
  • Subhepatic abscess post-op

Late complications:

  • Worried about hernias
  • Worried about poor wound healing
75
Q

How does a laparoscopic cholecystectomy work?

A

4 small incisions made in the abdomen for insertion of long surgical instruments and a surgical video camera

Surgeon views GB and surrounding structures on a monitor connected to the camera

Surgeon manipulates long surgical instruments from outside the body while viewing the procedure on the monitor

76
Q

What is the gallbladder (GB) and what is its purpose?

A

Small organ
Part of the biliary system - attached via the cystic duct
Liver produces bile that is then drained into the GB and released during digestion into the small intestine (stimulated by fatty foods and proteins in the duodenum)
Bile is stored and concentrated in the GB

77
Q

What is the purpose of bile?

A

Formed in the liver

Essential for digesting fats, excreting cholesterol

78
Q

What happens if there is dynfunction in the physiology of the GB?

A

Production of gallstones - from imbalances in the constituents of bile and biliary sludge secondary to GB hypokinesis

Gallstones can block the biliary tree = inflammation of other organs and GB

79
Q

What is the liver on a cellular level (i.e. what is the physiology of the liver)?

A

The liver is a large organ located in the right upper quadrant of the abdomen

Composed of hepatic lobules = hexagonally shaped functional units of the liver

Lobules composed of hepatocytes, or liver cells

Hepatocytes = important in the production and secretion of bile

Hepatic lobules also contain a central vein and portal triads at the periphery consisting of branches of the bile duct, portal vein, and hepatic artery

Epithelial lined sinusoids run between the hepatocytes and connect the peripheral vasculature to the central vein

The bile produced by the hepatocytes is drained in the opposite direction of blood flow to the periphery of the lobule by small channels known as the Canals of Hering

They are lined by simple cuboidal epithelium and ultimately drain the bile into the bile ductule of the portal triad, which will go on to drain into the bile duct

80
Q

What is the GB on a celluar level (i.e. what is the physiology of the liver)?

A

The gallbladder wall is composed of several layers

Innermost mucosal layer is made up of columnar epithelium with microvilli = increase surface area which is useful for concentrating bile

Beneath the mucosa is a lamina propria, a smooth muscle layer, and an outer serosal layer due to its intraperitoneal location

81
Q

How does the GB and biliary system develop from the foregut?

A

End of 4th week of embryogenesis = appearance of hepatic diverticulum

Hepatic diverticulum goes on to become the liver, extrahepatic biliary system, and a portion of the pancreas

The superior bud of the diverticulum develops into the gallbladder

At week six, the common bile duct and part of the pancreas rotate around the duodenum. The bile ducts undergo plugging with epithelial cells and recanalization of their lumens, with the common bile duct and cystic duct connecting by week seven

By week twelve, the gallbladder is no longer solid and the liver is secreting fluid through the patent bile ducts that now empty into the duodenum. The development of the biliary system is extremely complex and can lead to numerous variations in its structure

82
Q

What is cholecysto-enteric fistula?

A

Abnormal connection between the GB and intestines, can lead to a rare form of small bowel obstruction

83
Q

Function:

Para 1

A

The function of the gallbladder is to store and concentrate bile, which is released into the duodenum during digestion. Bile is an alkaline fluid continuously produced by the liver whose primary function is to aid in digestion and absorption of lipids, as they are not soluble in water. It is composed of cholesterol, bilirubin, water, bile salts, phospholipids, and ions. The cholesterol excreted into bile eliminates most of the cholesterol in the body.

84
Q

Function:

Para 2

A

Specialized enteroendocrine cells called I-cells are located in the duodenum and jejunum. When these cells are stimulated by fatty acids and amino acids released from the stomach, a peptide hormone called cholecystokinin (CCK) is released. CCK has two main functions pertaining to the gallbladder. Its first function is to stimulate the smooth muscle of the gallbladder to contract and release bile into the biliary tree. The second function of CCK is to simultaneously signal the muscular sphincter of Oddi to relax. After leaving the gallbladder, bile flows down the common bile ducts into a confluence with the main pancreatic duct called the ampulla of Vater. From there, it travels through an opening called the major duodenal papilla into the second portion of the duodenum. The flow through the papilla is controlled by the opening and closing of the sphincter of Oddi. When not stimulated by CCK, the gallbladder relaxes and fills with bile. Outside of the gallbladder, CCK stimulates pancreatic secretions necessary for digestion and delays further emptying of the stomach. Release of CCK is inhibited by the hormone somatostatin which functions to turn off digestion.

85
Q

Function:

Para 3

A

Bile acids are synthesized in the liver from cholesterol precursors. The rate-limiting step of bile acid production is catalyzed by cholesterol 7α—hydroxylase. The bile acids are conjugated to the amino acids glycine and taurine and become soluble bile salts. These bile salts are important in the process of emulsifying lipids in the intestine. As the lipids are metabolized into free fatty acids and monoglycerides in the digestive tract, they are then packaged into micelles made up of bile salts that act as surfactants. Bile salts are able to do this because of their amphipathic nature. Their hydrophilic portions interact with water making them soluble, while their hydrophobic portions keep lipids contained in the center. The hydrophilic portions are also negatively charged, which repels them from other bile salts and keeps the lipids small and easy to digest. Cholesterol and phospholipids are also contained in the structure of the micelles. The bile salts are reabsorbed in the distal ileum of the small intestine and recycled back to the liver in a pathway called the enterohepatic circulation.

86
Q

Function:

Para 4

A

Bilirubin is a yellow pigment that is produced as a breakdown product of heme contained in red blood cells. This compound is initially unconjugated and insoluble in water. The unconjugated bilirubin, also called indirect bilirubin, is taken up by the liver and conjugated with glucuronate via the enzyme UDP-glucuronosyltransferase. The then conjugated bilirubin, also known as direct bilirubin, is then excreted into the bile in a soluble form. The bilirubin contained in bile will eventually travel through the gastrointestinal system and give urine its yellow color and stool its brown color via the breakdown products urobilin and stercobilin, respectively. If bile is unable to enter the duodenum, the buildup of bilirubin leads to jaundice, which is the yellowing of the skin, eyes, and mucus membranes, as well as acholic (pale) stools.

87
Q

What is the initial test to diagnose most disorders of the GB?

A

Abdominal ultrasound

Or sometimes a CT in an emergency setting to evuluate the abdo pain

88
Q

Why are x-rays not as useful as an ultrasound?

A

Less sensitive - only calcified gallstones can be seen on a plain abdominal xray
Only 10% of patients with cholelithiasis have that

89
Q

What is a HIDA scan? Why is it used?

A

Hepatobiliary iminodiacetic acid (HIDA) scan AKA cholescintigraphy
Specific and sensitive diagnostic test

A radionuclide scan where a tracer is given intravenously and is taken up by hepatocytes in the liver
Tacer concentrates in the GB if the cystic duct is patent

90
Q

What lab tests are ordered in suspected GB disease?

A

CBC - complete blood count
CMP - complete metabolic panel
LFTs

91
Q

What is the pathophysiology of cholelithiasis and biliary colic?

A

Formation of gallstones in the GB - can be cholesterol (80%), pigmented or mixed

5 F’s = risk factors

Pigmented stones are broken down into brown and black stones
Black stones = composed of calcium bilirubinate = seen on radiography
Usually secondary to pathologies that cause haemolysis, as RBC breakdown is what causes the increased bilirubin in bile
Brown stones occur secondary to infection

92
Q

What are most gallstones?

A

Asymptomatic

93
Q

What is biliary colic?

A

Stone stuck in cystic duct = RUQ pain in response to fatty meals, as lipids stimulate the secretion of CCK, which causes painful contractions against the stone

94
Q

What is Choledocholithiasis?

A

Gallstone lodged in common bile duct = elevated liver enzymes as the liver cannot empty OR travel to pancreatic duct causing pancreatitis = elevated amylase and lipase

95
Q

What is the pathophysiology of cholecystitis?

A

Inflammation of GB
Commonly due to gallstone lodged in cystic duct = calculous cholecystitis
Without gallstone = acalculous cholecystitis = due to infection, low perfusion or biliary stasis
Causes prolonged abdominal pain with associated fever and leukocytosis
Untreated = infection
Repeated attacks = scarring and calcification of GB = risk of cancer

96
Q

What is the pathophysiology of cholangistic?

A

Inflammation of the bile ducts
Ascending colitis = secondary to infection
Biliary tree obstructed - bile stasis = bacterial growth

Charcot’s triad = jaundice (elevated bilirubin), fever, RUQ
+ hypovolaemic shock and confusion = Reynold’s pentad

97
Q

What is the clinical relevance of understanding the pathophysiology of these diseases?

A

Health coaching - reduce risk factors e.g. lose weight, healthier (low fat) diet
Can also predict side effects of drugs, e.g. OCP = increased cholesterol levels
Porduce drugs to improve risk factors e.g. reabsorption of bile, lower cholesterol levels in the body etc.
Surgical treatments e.g. performing laparoscopically by knowing the anatomy

98
Q

What are brown pigmented stones?

A

associated with infections of biliary tract (bacterial and helminthic deconjugation of bilirubin glucuronides)
more frequent in Asia.

99
Q

What are black pigmented stones?

A

Consist of calcium bilirubinate and found in= haemolytic anaemia, ineffective haematopoiesis, patients with cystic fibrosis

100
Q

What are the 3 mechanisms of cholesterol GB stones?

A
  1. Cholesterol supersaturation of bile
  2. Gallbladder hypomotility
  3. Kinetic, pro-nucleating protein factors
101
Q

How does cholesterol supersaturation occur?

A

Cholesterol = slightly soluble in water, made more soluble in bile through mixed micelles with bile salts and phospholipids, mainly phosphatidylcholine (lecithin)

Precipitation of cholesterol occurs when cholesterol solubility exceeds the (cholesterol saturation index >1)

Cholesterol crystals occur at low phospholipid : cholesterol ratios and at relative low phospholipid and low phospholipid and high bile salt concentrations

Multilammellar vesicles then fuse and may aggregate as solid crystals

102
Q

How does gallbladder hypomotility occur?

A

Supersaturated bile often is found in healthy individuals
Microcrystals formed are effectively flushed from the gallbladder during postprandial contractions

Incomplete GB emptying = increased lipid concentrations = cholesterol gallstones = seen in T2DM, etc.

103
Q

What are the kietic factors of cholesterol gallstones?

A

Formation of microcrystals in supersaturated bile is modulated by kinetic protein factors

Mucin = glycoprotein mixture secreted y biliary peithelial cells = crystallising promoting protein

104
Q

Venn diagram with stone in the middle, and 3 circles (cholesterol supersaturation, nucleation, and growth)

A

Cholesterol supersaturation = increased cholesterol, decreased phospholipids, decreased bile salts

Nucleation = increased promotors, decreased inhibitors, maybe presnece of helicobacters

Growth = increased residual volume and decreased motility

All 3 overlapping = gallstone = cholesterol crystals aggregate in bile supersaturated with cholesterol, nucleated in the presence of pronucleating factors such as mucin, and grow to stones in an enlarged GB with hypomility

Y2 - CSI (8 decks)

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