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Year 3 Medicine > Acute abdomen pathology > Flashcards

Acute abdomen pathology Flashcards

1
Q

Twisted ovarian cyst: underlying pathology

A
  • the cyst within the ovary is attached by a pedicle of blood vessels which becomes twisted thus increasing the pressure
  • first venous blood flow is obstructed then over time with further twisting arterial supply can also be affected
  • decreased venous return leads to congestion as blood is still being pumped in
  • the ovary becomes haemorrghagic but also necrotic because even though blood is coming in it’s not well perfused
  • generally underlying pathology is in the ovary
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2
Q

Twisted ovarian cyst: causes

A
  1. mature cystic teratoma
  2. lesion
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3
Q

Mature cyst teratomas

A
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4
Q

Mature vs immature teratoma

A
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5
Q

Where do most ecotopic pregnancies occur?

A

Fallopian tube (90%)

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6
Q

Causes of ectopic pregnancies in the fallopian tube

A
  • 50%: identifiable lesion such as chronic salpingitis from pelvic inflammatory disease, or adhesions from appendictis, endometriosis, or previous laparotomy
  • 50%: no cause can be identified
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7
Q

How does chronic salpingitis cause ectopic pregnancies?

A
  • chronic salpingitis- inflammation of the fallopian tubes
  • generally the fertilized ovum would travel to the uterus but the inflammation of fallopian tubes impairs its movement so it gets implanted in the fallopian tubes instead
  • the fertilised ovum grows within the narrow tube–>tube bursts–>haemorrghage
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8
Q

How common is ectopic pregnancy?

A

1/150 pregnancies result in ectopic implanation.

but most can’t survive in extrauterine environments- except if it’s in the fallopian tubes.

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9
Q

Most common complication of ectopic pregnancy in fallopian tube

A
  • fallopian tube bursts–>haemorraghe
  • often 6 week safter previous menstrual period
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10
Q

Clinical presentation of ectopic pregnancy

A
  • normal sympoms of pregnancy- morning sickness, amenorrhoea, swollen breasts, positive pregnancy test
  • intermittent lower abdominal pain before sudden onset severe pain
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11
Q

Mechanisms and causes of intestinal obstruction

A
  1. WITHIN LUMEN- eg Meconium ileus (in children with CF)
  2. WITHIN WALL- eg Tumours eg Adenocarcinoma
  3. EXTRINSIC- eg Caecal volvulus
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12
Q

What is meconium?

A

The earliest stool of the infant consisting of material they’ve ingested while in utero. Expelled after birth

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13
Q

What is meconium ileus?

A
  • occurs in children with cystic fibrosis
  • children may be born with meconium ileus due to the viscid consistency of the meconium in CF
  • the viscid nature of meconium leads to obstruction
  • in later life they develop meconium ileus equivalent (MIE) sydrome

(UNIQUE TO CF)

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14
Q

Colonic adenocarcinoma

A
  • forms in an annular ring like fashion around the bowel wall
  • leads to constriction and ultimately obstruction
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15
Q

Colonic adenocarcinoma histology

A
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16
Q

What is volvulus? Which part of the GI tract does it occur in?

A
  • Twisting of the bowel
  • In adults, it cccurs with equal frequency in the small intestine (around a twisted mesentry) and colon (around sigmoid or caecum which are more mobile)

**it’s not the mesentry that twists around the bowel, it’s the bowel that twists around itself and the mesentry**

  • In children (less common) it occurs mostly in small intestine
  • results in ischaemia and the buildup of gas and fluid in the portion of bowel affected
  • ultimately can result in necrosis or gangrene
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17
Q

How do you treat volvulus?

A

-requires immediate surgical intervention

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18
Q

Presentation of volvulus

A
  • abdominal pain
  • distention
  • COMPLETE constipation
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19
Q

Clinical presentation of intestinal obstruction

A
  • abdominal pain: true colic is intermittent central gripping pain.
    a) small bowel: every 2-20 minutes
    b) large bowel: every 30 minutes
  • vomiting
  • distention
  • absolute constipation
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20
Q

What is an abscess?

A

Localised area of necrosis (walled off)

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21
Q

Pathophysiology of acute appendicitis

A
  • FAECOLITH (hardened stool) blocks the lumen of the appendix
  • the appendix then CONTRACTS to try and push the faecolith out
  • this increases the PRESSURE within the bowel wall
  • increased pressure leads to ISCHAEMIC CHANGES–>lack of blood flow to the wall–>increased susceptibility to bacterial infections which then causes inflammation
  • common organisms: E. Coli, Streptococci,
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22
Q

Describe the pathological progression of appendictis

A
  • earliest lesion superficial ulceration of the mucosa (if it’s more extensive then it can lead to necrosis)
  • ischaemic processes further away from blood supply are more serious
  • interference with circulation leads to necrosis and perforation which can spread to the peritoneal cavity
  • if infection becomes walled off it can lead to a LOCALISED ABSCESS. This can then spread leading to generalised peritonitis (which you wanna avoid)
  • ulceration stops at mucosal surface
  • symptoms associated with obstruction are poorly localised, pain associated with peritonitis differ
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23
Q

Where does ulceration of the appendix occur?

A

Only at mucosal surface

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24
Q

Describe Appearance of appendix when its a) normal vs b) in appendictis

A

a) shiny, red, fresh
b) dull, grey, granular

25
Q

Picture of normal appendix

A
26
Q

Picture of appendix in appendictis

A
27
Q

Microscopic appearance of acute appendictis

A

Classic features of inflammation: neutrophils, dilatation

28
Q

Microscopic appearance of appendix mucosal ulceration

A

There’s also an abscess here (localised within appendix atm)

29
Q

Clinical presentation of appendicitis

A
30
Q

Pathophysiology of perforated diverticulitis

A
  • common in western societies
  • diverticulum: outpouching of the bowel.
  • It’s an area of weakness. increased pessure in that area can drive the mucosa through the these areas of weakness–>infection and perforation
    i. e. perforation of the diverticulum leads to diverticulITIS
31
Q

What contributes to formation of the diverticula in the bowel wall

A
  • weaknesses in bowel wall
  • high lumenal pressure in the bowel
32
Q

What does hyperaemic mean?

A

More blood

33
Q

Clinical presentation of perforated diverticulitis

A
  • severe left iliac fossa pain
  • nausea, vomiting, constipation, loss of appetite
  • patients are usually pyrexial and have tachycardia
  • may be a tender indistinct mass parallel to the inguinal ligament
34
Q

Causes of chronic and acute peptic ulcers

A

Chronic

Helicobacter infection

NB: someone with a chronic peptic ulcer could still present acutely

Acute

  • NSAIDs
  • alcohol
  • smoking
35
Q

What are most deaths with peptic ulcers due to?

A

Perforation of the ulcer

36
Q

Clinical presentation of ruptured peptic ulcer

A
  • epgastric PAIN
  • patients with acute peptic ulcer present with acute pain of short duration but may have had previous similar episodes interspersed with periods of relief which last for months or even years
37
Q

What level does AAA usually occur?

A

Below the renal arteries

38
Q

Two types of AAA

A
  1. Saccular- outpouching
  2. Fusiform- diffuse swelling
39
Q

Pathophysiology of AAA

A
  • atheromatous wall
  • often with thrombi on top of the plaque i.e. overlying mural thrombi
  • aneurysm may rupture into the peritoneal or retroperitoneal tissue- almost always fatal
40
Q

Picture of AAA

A
41
Q

Microscopic view of AAA

A
42
Q

Which layer of the blood vessel does AAA form in? And where does the thrombus form?

A

The plaque is within the tunica intima (innermost layer).

There is a MURAL THROMBUS- thrombus on the WALL of the plaque–>this presses on the underlying tunica MEDIA

43
Q

Clinical presentation of AAA

A
  • SEVERE CENTRAL abdominal pain
  • radiates to the BACK, and GROIN (irritation fo genito-femoral nerve)
  • patient may collapse from the accompanying HYPOTENSIVE SHOCK (because of loss of blood) or SUDDENLY DIE
  • often the patient is a smoker with a history of angina, intermittent claudication,MI, TIA or stroke
44
Q

Range in severity of ischaemic bowel disease

A

Most severe: transmural infarction (death of whole thickness of bowel wall)

Medium severity: mural infarction (involvement of part of the bowel wall)

Least severe: mucosal infarction (just invovles the mucosa)

45
Q

Causes of ischaemic bowel disease

A

Arterial

  • arterial thrombosis: eg within coeliac artery
  • arterial embolism - due to mural thrombi elsewhere eg MI with thrombus embolising to the bowel

Venous

Virchow’s triad eg Factor V Lieden

Non-obstructive ischaemia

-SHOCK- blood being shunted away from GI tract

Misc

Volvulus- not only obstructs the bowel but also obstructs the blood supply

46
Q

Pathology of transmural bowel infarction

A
  • regardless of whether it’s arterial or venous infarction, it will appear haemorrghagic:
    a) venous: blood pumped in but not out so appears haemorraghic
    b) arterial: infarction due to lack of blood supply. but blood vessel suddenly opens up and blood rushes in
  • within 104 days intestinal bacteria produce gangrene and perforate the bowel
47
Q

Clinical presentation of mesenteric thrombus or embolism

A
  • pain of infarction is usually severe and continuous and quickly develops all the hallmarks of peritonitis
  • generalised pain accompanied by vomiting
  • history of angina, MI, intermittent claudication or stroke
48
Q

Aspects of biliary tract disease

A

a) acute cholecystitis
b) gallstones

49
Q

Pathophysiology of acute cholecystitis

A
  • often goes hand in hand with gallstones (in 90% of the cases)
  • so gallstones usually cause an obstruction to bile flow
  • the bile then builds up in the gall bladder and water keeps getting absorbed–>bile becomes concentrated
  • this leads to chemical damage of the gall bladder wall- eg phospholipase digests the mucous layer
  • wall is compromised–>bacterial invasion–>inflammation

(main diff between acute cholecystitis and appendictis is that in the former the damage is CHEMICAL whereas in the latter it’s PHYSICAL due to pressure)

50
Q

What are gallstones made of?

A
  • cholesterol: pale
  • pigment: dark
  • mixed
51
Q

Clinical presentation of biliary tract disease

A

a) acute cholecystitis
- sudden onset right upper quadrant pain radiating to the back close to the tip of the scapula
- continuous pain exacerbated by movement and respiration
- nausea and vomiting
- Murphy’s sign
b) Gallstones
- biliary COLIC- generalised severe upper abdominal pain
- not true colic as there are no remits between exacerbations
- nausea and vomiting

52
Q

What is Murphy’s sign?

A

Breathing in puts pressure on the gallbladder, leading to patient catching their breath at the point of maximum inhalation.

Test is positive if they don’t feel the same pain in the LUQ.

53
Q

Mechanism of pancreatitis

A

due to autodigestion of the pancreas by inappopriately activated enzymes (usually present in inactivated state)

  1. Proteases: proteolytic digestion of tissues
  2. Elastases: necrosis of blood vessels leading to haemorrghage
  3. Lipases: Fat necrosis

Ultimately the body responds to injury with inflammation!

54
Q

Histological features of acute pancreatitis

A
55
Q

Clinical features of pancreatitis

A
  • severe continuous epigastric pain
  • patient lies still and breathes shallowly
  • better when sitting forward
  • radiates to the back
  • frequent vomiting and retching
56
Q

What are renal stones made of?

A
  • 70% made of calcium (oxalate and phosphate)- thus can be picked up on Xray
  • can be made of uric acid or cystine
57
Q

What’s worse: large or small kidney stones?

A

Small!

Because they can pass into the ureters from the kidneys.

Bigger stones never leave the kidneys.

58
Q

Acute salpingitis

A
  • diff from chronic salpingitis
  • caused by ascending infection
  • more than 50% caused by gonorrhoea infection
  • may involve ovary
  • can lead to abscess formation (local necrosis with neutrophils)
59
Q

Clinical presentation of renal stones

A

Year 3 Medicine (9 decks)

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