Acute Pancreatitis + Liver Cancer + Pancreatic Cancer + KIDS Flashcards
What is acute pancreatitis?
What occurs?
• Inflm of pancreas
• Very serious problem, can potentially cause death
• Auto digestion – not auto-immunity; digestion through enzymes
- Is self-limiting
What composition is pancreatic tissue (re: endocrine and exocrine)
What is the significance of this with the cause of acute pancreatitis?
o 99% of pancreas is exocrine tissues, other component is endocrine islets of langerhans
Lots of enzymes produced by pancreas!!
If acute pancreatitis is self-limiting, does this mean we don’t treat it?
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
Et of pancreatitis?
- 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)
Explain how alcohol is involved as a cause of acute pancreatitis
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.
Patho of acute pancreatitis
- 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
Does the pancreas have a large functional reserve?
do not have large functional reserve…will become highly problematic with only small amounts of functional damage
What can trigger acute pancreatitis?
Manifestations?
- 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
Why does AP lead to third spacing
What is a possible complication of this?
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?)
What would be an important test in diagnosis of AP?
•Test serum markers: Blood amylase & lipase
Blood amylase & lipase – which is the most important if we can only do one?
Amylase is also produced in the mouth while lipase is specific to the pancreas
Tx of AP
- 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
Liver cancer
What two kinds of tumours? Subdivisions of these?
Primary
- Hepatocellular carcinoma
- Cholangiocarcinomas
- Adenomas
Secondary
Secondary tumors more common why?
Properties of the liver:
Inc size, portal drainage, inc perfusion
….large, highly vascularized organs prone to be secondary site of metastasis
Hepatocellular carcinomas
- how common?
- Origin?
- Etiology?
90% of primary tumours
- Hepatocytes
- Et linked to:
1) Chronic liver disease (eg: hep)
2) Environmental toxins (arsenic)
WHy is chronic liver disease etiological factor in liver cancer?
viral DNA inserted into host DNA, causing mutations
Manifestations of hepatocellular carcinomas?
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)
Tx of hepatocellular carcinomas?
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
Liver adenomas Who does it tend to occur in? Origin? Special consideration for these? Tx?
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
Cholangiocarcinomas
Origin?
Who is more prone?
Origin in bile duct epithelium
Those with chronic inflm of duct epith are more prone to this
Where do METASTATIC (2ndry) TUMOURS in liver cancer typically come from?
From colon, lung, breast tumours
Manfestations of metastatic or secondary tumours in liver cancer?
oThose of liver disease:
Hepatomegaly, ascites, abdm pain common
o Anorexia, fever, weight loss
Why do fever and weight loss occur with 2ndry tumours in liver cancer?
o Unexplained weight loss will always cause hp’s to look for cancer
o Fever in absence of infection
Tx of 2ndry tumours in liver cancer?
*Has come from other cancer…
o Very poor prognosis –> Supportive and palliative
Who is pancreatic cancer more common in?
Black
Male
Smokers
How does pancreatic cancer rank in terms of deaths d/t cancer?
Leading cause of death from CA
•90% mortality within 1st year
Et/risk factors for pancreatic cancer?
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
Why is it surprising that the prognosis for pancreatic cancer is so poor?
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
Manifestations of pancreatic cancer?
• 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
Cause of jaundice and weight loss in pancreatic cancer?
unknown
Diagnosis and treatment of pancreatic cancer?
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
CLEFT LIP (CL)
What is it?
How common?
Cause?
- 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
CLEFT PALATE (CP)
What is it?
Et?
Prevalence?
Treatment?
- 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
Pyloric stenosis
What is it?
When does it occur?
How prevalent?
More common in?
- 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
Et of pyloric stenosis?
• 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
Patho and manifestations of pyloric stenosis?
- Hypertrophy → constriction → inflm → obstruction (content not getting into duodenum)
- Projectile vomiting, dehydration, malnourishment
Diagnosis of pyloric stenosis
Tx?
- Hx and Px - when you palpate in upper right quadrant, may be able to detect mass
- US
- Sx for tx
Gastroesophageal reflux in kids:
Is it common?
When does it typically occur?
What is the problem?
- 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?
Tx of GE reflux in children?
• 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)
HIRSCHSPRUNG DISEASE
Cause?
What occurs?
Tx?
• ~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)
INTUSSUSCEPTION
What occurs and where?
- Intestine invaginates into adjoining part
* Usually at ileocecal valve
Why does intussesception typically occur at the ileocecal valve?
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
Patho of intussesception:
• 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
Tx of intussusception?
• 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
