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Big Ol' Patho. > Acute Pancreatitis + Liver Cancer + Pancreatic Cancer + KIDS > Flashcards

Acute Pancreatitis + Liver Cancer + Pancreatic Cancer + KIDS Flashcards

1
Q

What is acute pancreatitis?

What occurs?

A

• Inflm of pancreas
• Very serious problem, can potentially cause death
• Auto digestion – not auto-immunity; digestion through enzymes
- Is self-limiting

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2
Q

What composition is pancreatic tissue (re: endocrine and exocrine)
What is the significance of this with the cause of acute pancreatitis?

A

o 99% of pancreas is exocrine tissues, other component is endocrine islets of langerhans

Lots of enzymes produced by pancreas!!

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3
Q

If acute pancreatitis is self-limiting, does this mean we don’t treat it?

A

o Just because is self-limiting doesn’t mean not very serious! Have to adequate manage the disease as it progresses or it becomes very dangerous

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4
Q

Et of pancreatitis?

A
  • Alcohol abuse (~70%)
  • Gallstones
  • Idiopathic (~10%) – something causes injury to pancreas and then it undergoes inflm
  • Others: pancreatic trauma, drugs (these are far less important than earlier causes)
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5
Q

Explain how alcohol is involved as a cause of acute pancreatitis

A

1) Ingestion causes inc in pancreatic section
2) When you drink alcohol, it constricts sphincter in PANCREATIC duct….

..Not sure exactly how this causes problem?
- Book says relationship is unclear but previous two factors are known.

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6
Q

Patho of acute pancreatitis

A
  • Normally pancreatic Es actived in duodenum, normal activation in presence of bile
  • Bile flow obstruction → premature activation of Es (as bile flows up pancreatic duct) → Es damage at pancreas to both exocrine and endocrine cells….causing auto digestion, hemorrhage + necrosis
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7
Q

Does the pancreas have a large functional reserve?

A

do not have large functional reserve…will become highly problematic with only small amounts of functional damage

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8
Q

What can trigger acute pancreatitis?

Manifestations?

A
  • Acute onset
  • May follow alcohol binge or large meal
    (alcohol = inc secretion + constriction of sphincter)
  • Severe abdm pain - Epigastric, radiates to back
  • Third spacing
  • Vascular collapse & shock possible
  • Elevated blood amylase & lipase
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9
Q

Why does AP lead to third spacing

What is a possible complication of this?

A

Inflm is going to lead to hyperemia, exudate formation, fluid moving out of organ into intersitial area + then to body cavity…possibly hypovolemia, hypovolemic shock, death
(explains vascular collapse and possible shock in AP?)

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10
Q

What would be an important test in diagnosis of AP?

A

•Test serum markers: Blood amylase & lipase

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11
Q

Blood amylase & lipase – which is the most important if we can only do one?

A

Amylase is also produced in the mouth while lipase is specific to the pancreas

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12
Q

Tx of AP

A
  • Based on severity
    1) Mild: 1 wk recovery
    o NPO (Why?) – eating inc secretions of pancreatic enzymes and bile exacerbating issue
    o Treat pain
    o Fluids/electrolytes
    o Correct metb abn (is going to affect insulin, glucagon etc as well, speaking of endocrine role of pancreas here)

2) Severe: ICU
o Renal, circ, hepatobiliary support (as complications manifest in other organs)
o IV opiates (for pain)

•Sx? May be needed for stones, hemorrhage

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13
Q

Liver cancer

What two kinds of tumours? Subdivisions of these?

A

Primary

  • Hepatocellular carcinoma
  • Cholangiocarcinomas
  • Adenomas

Secondary

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14
Q

Secondary tumors more common why?

A

Properties of the liver:
Inc size, portal drainage, inc perfusion
….large, highly vascularized organs prone to be secondary site of metastasis

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15
Q

Hepatocellular carcinomas

  • how common?
  • Origin?
  • Etiology?
A

90% of primary tumours

  • Hepatocytes
  • Et linked to:
    1) Chronic liver disease (eg: hep)
    2) Environmental toxins (arsenic)
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16
Q

WHy is chronic liver disease etiological factor in liver cancer?

A

viral DNA inserted into host DNA, causing mutations

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17
Q

Manifestations of hepatocellular carcinomas?

A

i. Insidious onset
ii. Then masked by underlying liver disease (only if d/t chronic liver disease - if have underlying disease (hep C), will see manifestations for the Hep C, which are similar to the CA manifestations…may not look for and detect CA)

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18
Q

Tx of hepatocellular carcinomas?

A

i. Poor prognosis (if advanced at Dx)
ii. Partial hepatectomy (tumour + some surrounding tissue)
iii. Chemo and radiation (palliative) – even if poor prognosis, doing what you can to make person as functional as possible

19
Q 
Liver adenomas
Who does it tend to occur in?
Origin?
Special consideration for these?
Tx?
A

 Tends to occur in women, 20-30yrs esp in those on contraceptive pill
 Origin = hepatocytes
 Tumour is extremely vascular – high risk of hemorrhage if any of vessels perforate
 If take early intervention w sx and withdraw hormones (from pill), have very good prognosis

20
Q

Cholangiocarcinomas

Origin?
Who is more prone?

A

Origin in bile duct epithelium

Those with chronic inflm of duct epith are more prone to this

21
Q

Where do METASTATIC (2ndry) TUMOURS in liver cancer typically come from?

A

From colon, lung, breast tumours

22
Q

Manfestations of metastatic or secondary tumours in liver cancer?

A

oThose of liver disease:
Hepatomegaly, ascites, abdm pain common
o Anorexia, fever, weight loss

23
Q

Why do fever and weight loss occur with 2ndry tumours in liver cancer?

A

o Unexplained weight loss will always cause hp’s to look for cancer

o Fever in absence of infection

24
Q

Tx of 2ndry tumours in liver cancer?

A

*Has come from other cancer…

o Very poor prognosis –> Supportive and palliative

25
Q

Who is pancreatic cancer more common in?

A

Black
Male
Smokers

26
Q

How does pancreatic cancer rank in terms of deaths d/t cancer?

A

Leading cause of death from CA

•90% mortality within 1st year

27
Q

Et/risk factors for pancreatic cancer?

A

Et unclear but linked to…
o Smoking (major risk) – contains organ-specific carcinogens
o Alcohol
o DM
o Chronic pancreatitis (are predispositions)
o Age (>50 yr) – very rare to see in individuals younger than this; this r/t cumulative exposure with cumulative damage
o Poor diet

28
Q

Why is it surprising that the prognosis for pancreatic cancer is so poor?

A

not arising in the functional cells, but rather in the ducts (functional cells in pancreas not malignant themselves)…so it is hard to explain why the prognosis is so poor

29
Q

Manifestations of pancreatic cancer?

A

• Manifestations d/t mass rather than dec fx (pressure, not loss of glucagon, insulin, etc)

  • Jaundice
  • weight loss
  • abdm pain (classic mnfts)

*these delay dianosis by leading astray

30
Q

Cause of jaundice and weight loss in pancreatic cancer?

A

unknown

31
Q

Diagnosis and treatment of pancreatic cancer?

A

Dx:
• Ultrasound & CT
• most will have already metastasized by time of dx
Tx:
•Pain control is key (prognosis very poor so little you can do)
• Sx (primary approach…tumour must be in very early stage to have this be successful) – if has metasized, will have sx with palliative care
• Chemo not used – not very successful

32
Q

CLEFT LIP (CL)

What is it?
How common?
Cause?

A
  • Indentation to deep fissure
  • Maxillary and nasal structures do not fuse (wk 5-8 is period of sensitivity)
  • Uni or bilateral, can be midline or on either/both sides
  • ~1 in 700 births
  • Teratogens – etiology clear cut….= Smoking, viral infec (in mother), folic acid deficiency

•CL AND CP often together

33
Q

CLEFT PALATE (CP)

What is it?
Et?
Prevalence?
Treatment?

A
  • Back in roof of mouth
  • Incomplete fusion of palatine structures (wks 9-12)
  • Malformed nasal structures? (likely will happen but not in all cases)
  • Strong link to smoking in pregnancy
  • ~1 in 2000 births

• Sx

34
Q

Pyloric stenosis

What is it?
When does it occur?
How prevalent?
More common in?

A
  • Muscle hypertrophy & constriction at pylorus – opening into duodenum obstructed
  • 2-8wks of age (after birth)
  • ~1 in 1000 births
  • 4:1 male to female ratio
35
Q

Et of pyloric stenosis?

A

• Idiopathic
• Linked to:
1) Hypergastrinemia (elevated gastrin in blood, leading to inc HCl secretion) – in infant, stomach and duodenum not adequately protected…suggested this occurs to compensate for protective measure (?)

2) PGE (prostaglandin E) – babies given IV infusion of this?
3) erythomycin exposure

36
Q

Patho and manifestations of pyloric stenosis?

A
  • Hypertrophy → constriction → inflm → obstruction (content not getting into duodenum)
  • Projectile vomiting, dehydration, malnourishment
37
Q

Diagnosis of pyloric stenosis

Tx?

A
  • Hx and Px - when you palpate in upper right quadrant, may be able to detect mass
  • US
  • Sx for tx
38
Q

Gastroesophageal reflux in kids:
Is it common?
When does it typically occur?
What is the problem?

A
  • Common GI problem (in kids) ~50%
  • Very common up to 3 months or so
  • Neuromuscular Et (is functional, not structural, neuromuscular issue)
  • Reflux via lower esophageal sphincter
  • Gastric contents move into esoph→ esophagitis?
  • Will be issue of nourishment b/c child may avoid/minimize ingestion → growth problems?
39
Q

Tx of GE reflux in children?

A

• Mostly self-limiting (~1 yr)
o Symptomatic treatment → may need H2RA or PPI
o Modify feeding – small meals, thicken food, positioning
o Fundoplication? (to fortify sphincter, in extreme cases)

40
Q

HIRSCHSPRUNG DISEASE
Cause?
What occurs?
Tx?

A

• ~1 in 5000 births

  • RET gene mutation, Chr 10 → codes for proteins that are involved in cell signaling for cell formation in many tissues including neural tissue
  • In this disease, segment of colon lacks parasympathetic ganglia (specialized neurons) → no peristalsis (localized to affected area) → accum of contents → colon distension → abdm distension (→ risk for perforation)

•Tx: aganglionic segment removed (joins other ends)

41
Q

INTUSSUSCEPTION

What occurs and where?

A
  • Intestine invaginates into adjoining part

* Usually at ileocecal valve

42
Q

Why does intussesception typically occur at the ileocecal valve?

A

smaller part of intestine (ileum) moves into larger part (cecum), so it’s easier for this to occur here

Pressure building in ileum pushes it into the cecum

43
Q

Patho of intussesception:

A

• Invagination → obstr → inflm → edema → ischemia – edema d/t exudate moving into lumen, ischemia occurs as luminal pressure increases → vessels in wall affected by this

Necrosis, perforation & peritonitis possible

44
Q

Tx of intussusception?

A

• Hydrostatic reduction
– use water-soluble contrast medium (so can see on x-ray) and air pressure,

don’t use barium anymore (causes issues of constiption, etc)

o Have to very careful not do this if perforation exists

•Some require sx

Big Ol' Patho. (17 decks)

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