CSI 17 - Acute Abdomen Flashcards

1
Q

in what demographics can a pain free acute abdomen occur in?

A

Old people

Children

Immunocompromised

Last trimester of pregnancy

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2
Q

After the initial diagnostic procedures (Hx, Exams Ixs, labs, etc), what other pathways or methods may you use to help determine cause of an acute abdomen IF the symptoms doesn’t neccesitate immediate surgery

A

Further abdo exams by a physician with more xp

Diagnostic laparoscopy

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3
Q

what conditions can laparascopy be used therapeutically

A
  • Appendicitis
  • Cholecystitis
  • Lysis of adhesions
  • Hernia repair
  • many gynaecological causes of an acute abdo
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4
Q

what diagnostic algorithms or tools can help to further stratify risk of appendicitis

A

Appendicitis Inflammatory Response (AIR) score

Novel Pediatric Appendicitis Risk Calculator (pARC)

Need further prospective studies to evaluate clinical use

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5
Q

How has the attitude of narcotic analgesia changed over time regarding it’s use in patient’s with an acute abdomen

A

Before: it was discouraged as they thought it would mask the symptoms or exam findings and hence miss diagnosis

Now: evidence shows it doesn’t hinder management and improves pt comfort.

Fentanyl or one of it’s analouges is a useful agent used due to it’s potency and short half life

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6
Q

Give reasons as to why old people present atypically with abdo pain

A

They have long standing co-morbidiites hence cannot mount the appropriate physiological response (due to comorbidities or meds treat it).

Deteriorating CNS or PNS

  • CNS- dementia and hence can’t communcate symptoms effectively
  • PNS - alter perception of pain/temperature
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7
Q

Give reasons as to why pregnant people present atypically with abdo pain.

Explain any response needed?

A

Pregnancy have different physiology and hence making diagnosis very difficult.

Enlarged uterus compress abdo organs and there’s laxity of abdo walls: makes it difficult to localise pain and can blunt peritoneal signs

Pregnant people mauy have mild physiological leukocytosis (this finiding is non-specific in women with acute abdo).

Concerns about imaging (CT or Xrays)

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8
Q

what is the amount/threshold of radiation that hasn’t been linked to maternal or foetal defects?

A

less than 5 rads

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9
Q

what are the abdominal sources/causes of an acute abdomen?

From most common to least common

A

Intestinal Obstruction

Peritonitis secondary to infection

Inflammatory conditions that present with peritonism

Haemorrhage (e.g. ectopic pregnancy)

Ischaemia (Mesenteric ischaemia or ovarian torsion)

Processes associated with contamination of GI contents (e.g. perforated duodenal ro gastric ulcer)

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10
Q

What should you do if you see a pt with peritonitis secondary to infection?

what is needed?

A

Surgical emergency- LAPARATOMY

Don’t wait for diagnostic studies

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11
Q

what are the causes of obstruction (leading to an acute abdomen)

A

Adhesions (most common)

Incarceration of hernia (2nd msot common) and most common in people without prior abdo surgery

Volvulus, Gallstones, Intussuception

Congential anatomical abnormalities

Cancer

IBD

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12
Q

Inflammation may be an aetiology for an acute abdomen.

Give causes of inflammtion

A

Cholecystitis,etc

Diverticulitis

Meckel’s diverticulitis

IBD- pain due to inflammation itself or secondary obstruction

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13
Q

Perforation may be an aetiology for an acute abdomen.

Give causes of perforation

A

Gasstric or duodenal ulcers

Boerhaave’s syndrome and

Mallory weiss tear

Can lead to oesophageal laceration and GI haemorrhage

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14
Q

what are the gynacological causes of an acute abdomen

A

Ectopic pregnancy hence always do a pregnancy test for women in child bearing age

Others are:

  • Ruptured overian cyst
  • Ovarian torsion
  • Pelvic inflammatory diseases
  • Endometriosis
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15
Q

what are the vascular causes of an acute abdomen.

Explain any relevant details

A

Haemorrhage caused by

  • ruptured AAA
  • Abdo aortic dissection
  • ruptured splenic artery aneurysm

Ischeamic:

  • AMI or ischeamic colitis
  • splenic infarct
  • Vaso-occlusive episoded of sickle cell crisis

Budd chiari syndrome - stop hepatic venous outflow and hence lead to hepatomegaly and ascites

Abdo wall haemtoma

  • occur spontaneously or
  • secondary to trauma , coughong, exercise or procedure
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16
Q

State and explain the infective causes of an acute abdomen

A

Psoas abscess- due to tuberculosis abcess spreading from lumbar vertebrae to psoa

Hepatitis/hepatic abcess

gastroenterirtis, infectious colitis

Typhilitis (neutropenic enterocolitis)

Fitz-Hugh syndrome: complication of pelvic inflammatory disease

  • you hsve RUQ pain associated with perihepatitis
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17
Q

what are the metabolic causes of acute abdomen

A

Uraemia

Diabetic ketoacidosis

Addisonian crisis

Hypercalcaemia

Genetic:

  • Acute intermittent porphyria
  • Hereditary Meditteranean fever
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18
Q

state what toxic substances can cause an acute abdomen

A

Heavy metal poisoning - caused by medical/environmental/occupational exposure to, mercury, lead, or arsenic.

Narcotic withdrawal from opioids may result in abdominal cramping pain.

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19
Q

what are the urological and other causes of acute abdomen

A

Urology

  • In men, testicular torsion should be considered.
  • In both men and women: kidney stones and pyelonephritis

Other

Radiation enteritis and spider bites

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20
Q

what are the general urgent considerations for pt with an acute abdoment

A

Whilst waiting for routine labs, consult a surgeon; it’s more efficient

IV access should be obtained and monitor vital signs

Correct any abnormalities (with fluids or blood products)

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21
Q

what should you consider for a pt exhibiting evidence of hypovolaemic shock with a known or suspected haemoperitoneum

A

Get to surgery ASAP (with limited pre-op evaluation)

Those with ongoing haemorrhage:

  • Give 2 large bore IV lines
  • Urgent typing and cross-mathcing of blood is needed
  • Fluid resuscitation

Initial resuscitation involves:

  • 2L of isotonic fluids
  • O negative uncross-matched blood can be given until cross-matched blood can be given
  • Maybe give antifibrinolytic like tranexamic acid
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22
Q

what should you consider regarding FLUIDs for a pt exhibiting evidence of aortic dissection or ruptured AAA?

Explain why

A

Careful fluid management (aim SBP to bebetween 80 and 90) or even lower if mentation is intact

This is becauses aggressive fluid replacment can lead to more bleeding via:

  • hypothermic and dilutional coagulopathy
  • Lowering blood viscosity
  • Increased perfusion pressure FROM FLUID expands volume and lead to sendoary clot disruption
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23
Q

what should you consider APART FROM FLUIDs for a pt exhibiting evidence of aortic dissection or ruptured AAA?

Explain why

A

O2

multiple peripheral or centraL venous access

Urgent blood typing and cross-matching

Routing labs tests

Vascular surgery consultation

Prophylactic Abx

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24
Q

what should you consider if a perforated viscus, appendicitis or cholecystitis is suspected

i.e what measures should you take quickly?

A

Give Broad spectrum Abx: contents of GI can lead to sepsis

Urine MCS and dip stick

Blood tests

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25
Q

what should you consider for a pt that is female of childbearing age.

what should you do now?

A

Preg test - exclude ectopic preg

if ectopic is suspected give 2 large bore IV cannulae (incase it ruptures)

Blood type and cross matching should be considered

Urgent gynaecological consultation is needed

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26
Q

what should you consider If a patient reports abdominal pain disproportionate to the signs on physical examination,

what disgnois should you think of and what should you offer

A

Consider mesenteric ischeamia esp in old ppl with Hx of:

  • Smoking
  • Peripheral vascular diseases
  • A-fib

Offer:

  • O2
  • Fluid resuscitation
  • Broad spectrum Abx
  • Urgent surgical and Interventional radiologist consultation needed
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27
Q

what are the common differentials for an acute abdomen?

*The list is not exhaustive but you should already the know the ones not listed*

A

Gastrointestinal malignancy

Hepatic abscess

Fitz-Hugh Curtis syndrome

Mallory-Weiss tear

Abdominal wall haematoma

Hereditary Mediterranean fever

Typhlitis (neutropenic enterocolitis

Narcotic withdrawal

Infectious colitis

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28
Q

what are the uncommon causes of an acute abdomen.

*Again list is not exhausitve, the others are too niche that you would guess them in the SBA*

Link

A
  • Volvulus
  • Intussusception
  • Duodenal ulcer
  • Ruptured ovarian cyst
  • Ovarian torsion
  • AMI/ ishcameic colitis
  • Hypercalcaemia
  • Aortic dissection
  • Ruptured AAA
  • DKA
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29
Q

what does long standing epigastric pain suggest?

A

Gastric ulcer

A sudden worsening suggests perforation

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30
Q

what does sudden epigastric pain following vomiting and/or OGD suggests?

A

Oesophageal perforation

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31
Q

what does it suggest for areas of the pain in the diagram that present gradually or more progressively

A
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32
Q

If a pt has similar pain before but now it’s come back, what does it suggest?

A

This may suggest a recurrent condition, such as cholecystitis, pancreatitis or diverticulitis, with increasing frequency and severity indicating disease progression.

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33
Q

what does RUQ pain signify

A

Cholelithiasis, cholecystitis, hepatitis, hepatic abscess,

Fitz-Hugh Curtis syndrome,

Perforation or malignancy of the colon,

Pyelonephritis, or kidney stones.

Acute appendicitis in a pregnant woman due to displacement by the enlarging uterus.

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34
Q

what does LLQ pain indicate?

A

Sigmoid volvulus (typically older patients), diverticulitis, IBD kidney stones, gastrointestinal malignancy,

Psoas abscess,

incarcerated / strangulated hernia,

gynaecological concerns,:

  • ovarian torsion or cyst rupture,
  • ectopic pregnancy, or pelvic inflammatory disease (PID).
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35
Q

what are the causes of periumbilical pain?

A

Appendicitis before radiating

Acute mesenteric ischeamia

Leaking or ruptured AAA

Small bowel obstruction

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36
Q

What does persistent lateralised pain indicate?

A

condition associated with ascending or descending colon, kidney, gallbladder or ovary.

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37
Q

what does the diagram show about radiation

A
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38
Q

what does referred pain to the follwoing indicate?

Right scapula

Left scapula

Scrotal/Testicular pain

A

Right scapula:

  • Gallbladder disease, liver disease,
  • irritation of right hemidiaphragm (e.g., right lower lobe pneumonia)

Left scapula:

Cardiac disease, gastric disease, pancreatic disease, splenic disease, or irritation of left hemidiaphragm.

Scrotal or testicular pain:

  • Usually from loin to groin: kidney stones or ureteral disease
    *
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39
Q

what are other important information to consider when a pt presents with abdominal pain

A

Character: Aortic diseection is a sharp, tearing pain.

Other associated symptoms like fever, chills, N&Vomiting shows:

  • Cholecystitis , etc
  • spider bites, abdominal wall haematoma

Time of last bowel movement: important for construction

Nature of recent stool

Time and type of last meal or oral intake

Presence of anorexia:

  • Appendicitis
  • radiation enteritis
  • hepatic abscess

PMHx, FHx, SHx, DHx

last menstrual period

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40
Q

why is it important to ask about history of cardiac disease for a pt with an acute abdo

A

CVD predispose to AAA

History of A-fib can lead to acute mesenteric ischaemia

41
Q

why is travel history important?

A

whether the patient has visited an area endemic for amoebiasis (hepatic abscess),

or areas that have insanitary conditions (gastroenteritis and infectious colitis).

42
Q

what does it signify if a pt is still and relunctant to move?

A

More typical for peritonitis

43
Q

Apart from patients with marked obstruction, in what patients would you see absent bowel sounds

A

perforated viscus,

haemoperitoneum, or other conditions with peritoneal inflammation.

44
Q

On palpation, what does it signify if a pt has peritonitis with reflex involuntary guarding?

what about rebound tenderness?

A

Peptic ulcer disease

Rebound tenderness:

  • appendicitis, diverticulitis
  • any condition that causes inflammation of the parietal peritoneum
45
Q

what does it signify if you palpate the following on a pt?

  • Irreducible hernia
  • Palpable masses
A

Irreducible hernia signify incarcerated hernia

Palpable masses:

  • cholecystitis
  • appendix mass
  • intussusception
  • aortic aneurysm
46
Q

what should you consider (although uncommon) if a pt presents with left sided abdominal pain?

A

Situs invertus and/or mid-gut malrotation

47
Q

what should you consider for a pelvic examiantion?

what signs should you look for?

A

For most women with lower abdo pain

Can help to exclude or diagnose ectopic pregnancy, PID, ovarain torsion.

PID:

  • cervical motion tenderness
  • adnexal tenderness
  • Bimanual exam or USS may show tibo-ovarian abscess

Ectopic preganancy:

  • Palpable adnexal mass with/wtihout tenderness
  • vaginal beleding on speculum examination

Ovarian torsion:

  • severe, unilateral adnexal tenderness that is often palpable
  • Urgent gynae review is needed
48
Q

what should you bear in mind for a scrotal or testicular exam?

A

Tenderness can suggest epidydimitis or testicular torsion

Testicular torsion :

  • Need doppler ultrasound quickly (to check perfusion) and urgent urology review
  • Surgical detorsion is recommended less than 6 hrs from presentation

USS can help seperate hydrocoeele (due to patent process vaginalis) and identify testicular masses

Check inguinal canals on BOTH sides for hernias

49
Q

what does hypoCL or HypoK+ occur in ?

what about glucose?

urea

A

latter stages of intesitnal obstruction

Glucose: pancreatitis if insulin is compromised

Urea:

  • Aortic dissection
  • AAA
  • renal srteries are compromised
50
Q

If diagnosis is not definitive from the physical examination, laboratory analysis, or radiographic evaluation, why are the following tests helpful?

e.g

  • LFT
  • Coagulation studies
  • Serum amylase
  • Lactic acid
A

LFTs (and basic comprehensive panel)

Coagulation studies:

  • For all pts with suspected vascular causes like AAA, AMI etc
  • Unstable pts esp if surgery is indicated.

Serum amylase and lipase:

  • Pancreatitis (3 times mroe than normal)
  • Lipase is better indicator as it last longer in blood (2wks compared to 5 days)
  • Have a low threshold for admitting as it can be missed

Consider other conditions that need surgery even if tests are normal

Serum lactic acid (VBG):

  • if mesenteric ischaemia is suspected
  • serial measurements should be used for resuscitation
51
Q

what are the other conditions that can also mildly elevate amylase

A

Ectopic pregnancy, intestinal obstruction, and perforated duodenal ulcer.

Although amylase levels are not used to diagnose or monitor these condition

52
Q

What can a plain AXR show?

A

Show obstruction and dilation

Radio-opaque stones indicative of cholecystitis , pancreatitis or kidney or ureteric stones.

AAA:

  • aortic wall calcification on kidney, ureters or bladder
  • loss of psoas shadow: shows a ruptured AAA

these findings with the clinical picture is sufficient to proceed to surgery

53
Q

when shoukd you perform an Erect CXR and what can it show?

A

if perforation is suspected

  • rule out pneumopeitoneum
  • if pneumoperitoneum is visible - need surgical consult immediately

may also be a useful pre-op tests for anaesthetists and id often performed in conjuction with plain AXRs

54
Q

what is the indication of CT?

what about pregnant women?

A

Any surgically related causes of an acute abdomen : e.g. cholecystitis, etc

If pt with ruputre AAA is too uinstable to be moved, use an USS

Can be used in pregnant women but need obs&gynae consult first to check fetal viability (24 wks)

55
Q

describe the usefulness of ultraosound ,

what will it show for the following dieases?

  • Cholecyctitis
  • Pelvic - ectopic pregnancy
  • Ovarian torsion

what else can it show?

A

For cholecystitis , can show :

  • gallstones
  • thickened gall bladder wall (more than 4 mm)
  • pericholecystic fluid.

Pelvic utraosund for ectopic pregnancy:

  • show blood or pseudogestational sac in utero
  • ectopic pregnancy
  • complex mass in adnexa

ovarian torsion:

  • doppler USS may show reduced or absent blood flow to torsed ovary

Can also show presence and size of AAA and presnece of fluid or blood within the peritoneum (esp for unstable pts)

56
Q

what is the significance of Focused Assessment with Sonography for Trauma (FAST)

A

A limited ultrasound examination directed solely at identifying the presence of free intraperitoneal or pericardial fluid and is used principally in trauma situations.i

57
Q

in what pts may a laparoscopy be considered?

A
  • 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.

Also for childbearing women with non-specific abdo pain and suspected appendicitis: (better prognosis and diagnosis)

58
Q

what are the features of a laparoscopy? (diagnostically AND therapeutically)

A

can be diagnostic and therapeutic for:

  • acute cholecystitis
  • perforated ulcer
  • appendicitis
  • lysis of adhesions

if procedure can’t be done laparoscopically or the pt cannot tolerate insufflation pressure then the case is converted to a laparotomy

59
Q

from F2F session

what are the systemic causes of epigastric pain, what shoudl you try to exclude in a pt with epigastric pain first

A
  • DKA
  • Addisonian crisis
  • Lead poisioning
  • Hypercalcaemia

Always try to exclude gastroenteritis for this patient (food poisoning)

  • Features are febrile, too much diarrhoea and vomiting
  • If suspected to have it secondary to takeaway ; report to public health England
60
Q

Physiologically speaking, when are ALP and AST raised?

A

ALP more likely to raised when there’s obstruction of the liver (esp bile)

AST raised when hepatocyte dies

61
Q

How are the overwhelming majority of gallstones found?

A

iNCIDENTALLY and they are asymptomatic

62
Q

what are the clinical features/cause of biliary colic

A

Dull RUQ pain

Symptoms last for LESS than 6 hrs (more likely to be constant)

No inflammation: blood tests is normal

Trigger by fatty food; stimulate CCK causes contraction of gall bladder

Nausea and vomiting

Normally caused by blockage of gallstones in the cystic duct or neck of gallbladder causing muscular contraction

63
Q

what are the clinical features/cause of acute cholecystitis

A

Severe constant RUQ pain or maybe epigastric

Murphy sign positive (do the same on the left hand side and confirm there’s no pain)

Pyrexia and tachycardia

Raised WCC, CRP

Sometimes, have a slightly raised ALP

Bilirubin is normal

Nausea and vomiting

64
Q

what are the clinical features/cause of acute cholangitis

A

Biliary outflow obstruction and infection of bile ducts (bacterial)

Gallstones may be found in CBD

CLINICAL SIGNS:

  • Jaundice
  • Severe pain
  • Rigors and fever
  • Tachycardic, febrlle and hypotensive
  • Raised WCC, CRP, ALP
  • Raised LFTs (raised BR and others)

Charcot’s triad (Jaundice, rigors/fever and RUQ pain)

Very high mortality

Reynold’s Pentad: if they have shock and altered mental status

Obstruction of bile from liver or gallbladder and infection (bacterial)

65
Q

what are the risk factors for gallstones

A
  • Forty
  • Female
  • Fat
  • Fertile
  • Fair (caucasian)
  • (High fat diet, maybe native American)
  • Haemolytic anaemia
  • Crohn’s disease (affect absorption of bile products in terminal ileum)
  • Oestrogen increase biliary cholesterol production and OCP can increase risk
66
Q

what investigation is used to see gallstones?

what will you see

A

USS

99% of gallstones don’t show up on AXR and CTs aren’t used

Features seen on USS:

  • Hyperechoic echoing and posterior acoustic shadowing
67
Q

what is the composition of bile and how does gallstones form?

what are the types of gallstones

A

Bile mainly made of water (98%). Others are BR, Cholesterol, bile salts and electrolytes

Gallstones result from supersaturation of bile, can differ in sizes.

The composition differs from age, diet and ethnicity.

Gallstone Crystallisation could be either from cholesterol (majority) or bilirubin (pigment) or both

68
Q

what are the features of cholesterol stones and give relavant risk factors

A

Cholesterol gallstones normally found alone, and can be yellow or dark green or brown colour.

They are large.

RF are:

  • poor diet and
  • obesity due to excess cholesterol
69
Q

what are the features and RF of pigment stones and mixed stones

A

Pigment stone:

  • made up of bilirubin breakdown products.
  • They are small, darker and numerous.
  • It can be from excess bile pigment production.
  • Can be black or brown

Black pigment: made up of calcium bilirubinate and more likely seen on X-ray

Brown: occur secondary to infectiojn

RF: haemolytic anaemia (for black pigment stones esp)

Mixed stones: combo of pigment and cholesterol , and bile salts

70
Q

what are the different locations of gallstones that can cause

  • Acute cholecystitis
  • Bilairy colic
  • Ascending cholangitis
  • Pancreatitis
A

Gallstones in neck of gallbladder or cystic duct you get cholecystitis

Hartman’s pouch can also cause it

Impacted stone with inflammation gives you cholecystitis

Gallstone found in CBD with infection causes ascending cholangitis

Gallstone in the neck of gallbladder or cystic duct can also cause bilary colic

Gallstone in pancreatic duct causes acute pancreatitis

71
Q

what are the complications of cholecystitis

A

Pancreatitis – block flow from MPD

Gallstone Ileus- rare

Gallstone cancer (cholangicarnicoma) due to long standing inflammation.

Gallbladder empyema : gallbladder gets blocked and lead to build up of pus

72
Q

Explain the pathophysiology of Gallstone Ileus

A

Gallbladder lies adjacent to duodenum

It is small bowel obstruction secondary to gallstones.

Overtime wall of gallbladder is eroded due to chronic inflammation and lead to fistula formation b/w gallbladder and duodenum (this occurs over a long time)

It occurs when gallstone enters duodenum and causes the blockage of small bowel.

Gallstone enters ileocaceal valve and cause small bowel obstruction

It takes TIME

73
Q

what is Mirrizi syndrome?

A

Stone in cystic duct or gall bladder neck that causes pressure on the hepatic ducts

You get obstructive jaundice. But imaging shows no gallstones in hepatic ducts

74
Q

what are the treatment guidelines for :

  • Asymptomatic gallstones
  • Biliary colic
  • Acute cholecystitis
A

Asymptomatic gallstones- no treatment

Biliary colic: avoid fatty food and other conservative treatment.

Cholecystitis: laparoscopic cholecystectomy

75
Q

what are the complications of laparoscopic cholecystectomy

  • General
  • Speciifc
  • Early
  • Late
A

General: Inherent to any op

  • Incision:
  • Bleeding, scarring
  • Infection at incision site
  • Chronic pain (Post -op pain may not subside, ie. post-cholecysectomy syndrome)
  • DVT and PE (due to inactivity of muscle as it’s paralysed, more time increases risk)
  • Anaesthetic risk : depends on comorbidity , age

Specific :

  • Vessel (cystic artery or hepatic artery) damage
  • Damage surrounding structures (bowel, bladder, ureter, liver) that can lead to haemorrhage
  • Bile duct injury- devastating
  • Bowel leakage/perforation
  • Laparascopic may be converted to open op and hence make bigger cuts

Early risk):

  • Straight after op, wound can get infected

Late:

  • Wound not heal properly and lead to hernia
76
Q

Explain and outline the procedure for a laparoscopic chiolecystectomy

A
77
Q

What are the guidelines for obtaining valid consent

GMC and RCS website is here for more info!!

A

You must have knowledge of the procedure to obtain valid consent

Explain diagnosis to them and all the effects

Make sure they have capacity. Give them time

Treatment options:

  • Include do nothing
  • Tell them all available
  • You cam recommend to pt but don’t force it

Purpose of treatment- needs to be written on consent form.

Tell risk:

  • Different people have varying tolerance for risk
  • Different risk are different for different people
78
Q

what are the components of brown and black pigment gallstones?

what diseases are they associated with?

A

Brown:

  • Infection of biliary tract (bacterial and helminth deconjugation of bilirubin glucoronides)
  • Found in asia

Black:

  • Consists of calcium bilirubinate
  • Found in haemolytic aneamia or
  • Pts with ineffective haematopoesis
  • Pts with cystic fibrosis
79
Q

what 3 mechanisms are important in the formation of cholesterol gall bladder stones

A

Cholesterol supersaturation

Gallbladder hypomotility

Kinetic, pro-nulceating protein factors

80
Q

what are the components of the majority of gallstones

A

Cholesterol (70%) in a matrix of bile pigments, calcium salts and glycoproteins.

81
Q

Explain the mechanism behind cholesterol supersaturation in the formation of cholesterol gallstones

A

Cholesterol is slightly soluble in water but bile makes it solubele via mixed micelles (containing bile salts and lecithin)

Precipitation of cholesterol occurs when it’s solubilty exceeds its saturation index of 1 (shown by Gibbs Triangle)

Hence it crystallises at:

  • low phospholipid: cholesterol ratio
  • low phospholipid and high bile salt concentration

The multilammellar vesicles then fuse and may aggregate as solid crystals

82
Q

what does Gibbs triangle/ternary phase diagrams show regarding cholesterol supersaturation

A

Ternary phase diagrams shows molar bile salt-cholesterolphospholipid percentages

83
Q

Explain the mechanism behind Gallbladder hypomotilty regarding gallstones formation

what are the at risk groups

A

Those with cholesterol gall stones have gallbladder hypomotility

Incomplete emptying lead to increased total lipid concentrations

impaired emptying seen in:

  • diabetes
  • those with rapid weight loss
84
Q

Regarding gallbladder hypomotility, how does it relate to developing symptomatic disease when the stone has already formed

A

Risk of symptomatic disease higher for those that has higher/efficient gallbladder emptying

85
Q

Explain the mechanism of how kinetic factors can lead to formation of cholesterol gallstones

A

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

A number of inhibitory or promoting proteins have been described.

Mucin, a glycoprotein mixture that is secreted by biliary epithelial cells is the crystallization promoting protein in gallbladder sludge.

86
Q

Apart from emulsifying fat, what are the other functions of bile and where is the location of the gall bladder

A

essential for digesting fats, excreting cholesterol, and even possesses antimicrobial activity.

Gallbladder is found in the gallbladder fossa of the live rin the RUQ and is part of the extrahepatic biliary system

87
Q

As part of the hepatic lobule, what structure helps in drainig bile into the biliary tree?

what cells lines them

A

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.

88
Q

Extensively describe the layetrs of the gallbladder and the function

A

The innermost mucosal layer is made up of columnar epithelium with microvilli.

The 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.

89
Q

what are the functions off CCK

A

they are released by I cells in duodenum and jejunum in response to fatty aicds and amino acids

It causes contraction of gallbladder

It relaxes sphinxter of Oddi

It increases pancreatic exocrine secretion

90
Q

what enzyme catalyses the rate limiting step for the production of bile acids

A

cholesterol 7α—hydroxylase. (bile acid is made from cholesterol)

91
Q

Explain how bile acids aid in absorption of fats

A

Bile acids are amphipathic and hence emulsify fats into micells

The hydrophilic part is negatively charg and hence repel other bile acids

Micelles are then formed (containing cholesterol and phospholipids)

Bile salts then reabsorbed in terminal ileum to enterohepatic circulation

92
Q

What enzyme catalyses conjugation of Bilirubin and explain what occurs when BR cannot enter the duodenum

A

Enzyme is : glucuronate via the enzyme UDP-glucuronosyltransferase

You get Jaundice (yellowin of eyes, mucus membranes, etc) and pale stool (no stercobilinogen or urobilin made)

93
Q

Although a USS is the inital test of choice for looking at gallbladder disease, what test is most specific and sensitive diagnostic test for cholecystitis?

Explain why and when is it used?

A

hepatobiliary iminodiacetic acid (HIDA) scan, also known as cholescintigraphy.

IV nucleotide tracer that can go up to the gallbladder, it concentrates in gallbaldder if the cystic duct is patent.

It is typically performed in the setting of an ambiguous abdominal ultrasound with clinical suspicion of gallbladder pathology.

94
Q

How can aCCK be used a s a diagnositc test for gallbladdewr disease

A

CCK can be administered to test for the ejection fraction (EF) of the gallbladder.

An EF below 35% is considered abnormal and indicative of functional gallbladder disorder.

95
Q

what are the names of the enzyme for LFTs you can measure

A

AST

ALT

ALP

GGT- likely to be raised as it’s made by hepatocyte and epithelial cells lining the gallbladder

BR

96
Q

what is Choledocholithiasis ?

A

Choledocholithiasis occurs when a gallstone becomes lodged in the common bile duct..

This can affect LFTs and or pancreatic enzymes and may even lead to ascending cholangitis

97
Q

Apart from gallstones what are other causes of cholecystits seen in ill pts (Acalculous cholecystiits)

A

infection, low perfusion, or biliary stasis

98
Q

what drugs and conditions can increase risk of gallstones formation and explain why

A

OCP containing estrogen causes increased levels of cholesterol.

Somatostatin analogs such as octreotide block the release of CCK and lead to the formation of biliary sludge (gallbladder hypomotility)

Fibrates block the rate-limiting enzyme 7-alpha-hydroxylase causing increased cholesterol and decreased bile acid production.

Conditions:

  • Fasting- less CCK made
  • Those under parenteral nutrition- less CCK made