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Digestive System Module > Lecture 28 > Flashcards

Lecture 28 Flashcards

1
Q

Gall bladder pathology

A

Gallstones
Cholecystitis
Carcinoma of the gall bladder

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2
Q

Cholelithiasis

A

Gall stones
present in 10-20% of adults
80% of gallstones are “silent” - asymptomatic. indicental finding when scanning patient for something else, or assoc. w acute Cholecystitis
About 80% of gallstones contain crystalline cholesterol monohydrate and are called cholesterol stones
-The remainder are composed mainly of bilirubin and calcium salts and are called Pigment stones (patients with on going homolysis, chronic hemolytic conditions-inherited Hb synthesis disorders, alot of hemolysis and increased breakdown of bilirubin)

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3
Q

Pathogenesis: Cholesterol stones

A

Bile supersaturated with cholesterol
Conditions favour crystal formation
Cholesterol crystals remain in gall bladder long enough for stones to form (stasis)
-increase in size to the point of causing symptoms

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4
Q

Risk factors for choleslithiasis

A

The incidence rises with age and is greater in woman
-related to estrogen exposure, increased BMI
(fear, fat, female, 40)
Estrogenic influences (oral contraceptives, pregnancy) obesity and rapid weight loss favour stone formation
Gall bladder stasis favours stone formation
A family history of gallstones
Rare in under developed or developing societies (3rd world)
-more a condition of affluence

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5
Q

Gallbladder features

A

can be small or large

can be gravelly (small multiple stones)

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6
Q

Clinical consequences of Gall stones

A

May be asymptomatic (70-80% asymptomatic lifetime)
Symptomatic 1-3% per year
a)-Cholecystitis - acute/chronic (obstruction causing acute inflammation most common)
b)-Biliary colic - due to choledocholithiasis (obstruct bile duct, peristalsis normally occurring try to push stone forward, very painful (right upper quadrant abdominal pain to try overcome the obstruction). Blockage= extra hepatic obstruction = rise in bilirubin and liver enzyme (GGT and ALP)
-Complications of above: cholangitis (bacteria infection, gram -ve infection and inflammation in bile duct), obstructive cholestasis, pancreatitis (if stone goes right down to ampulla of vata blocking pancreatic duct)

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7
Q

Acute Cholecystitis

A 
Acute inflammation features: wall swollen, odematis, pink and erothematis, vasodilation of vessels, areas of hemoarrhage onto gb wall, some bile staining - see inflammatory cells (Neutrophils) under microscope
Most cases precipitated by gallstones
Acalculous cholecystitis - hard diagnosis (as patients have abdominal pain and features related to cholecystitis but no stones seen on imaging, so often excluding other pathologies)
Obstruction of the neck of the gall bladder or of the cystic duct
Chemical irritation (of mucosal lining setting up acute inflammation) appears to be the major factor with bacterial infection later (as a complication)
-not infection primarily, is inflammation of irritation of obstruction and bile salt, but can bacterial component to it
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8
Q

Acute abdominal pain abdo 02

A

“sudden onset abdominal pain. She finds the pain severe and she has been vomiting”

  • 40 and female (no BMI info) -risk group from cholelithiasis
  • abdominal pain and vomiting
  • could also be pancreatitis?
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9
Q

Clinical features of Cholecystitis

A

RUQ abdominal pain and tenderness (localised)
-often comes on after eating/fatty meals
-sometimes history of recurrent episodes of pain (transeitn blockage)
Febrile
Laboratory:
-Neutrophil leucocytosis (seen in any other acute inflammatory process (pancreatitis))
-Raised bilirubin, ALP and GGT if stone is in the common bile duct (extra hepatic obstruction)
-(amylase is going to be normal or mildly elevated- as pancreatitis more likely to be epigastric pain and tenderness and amylase is morelikely to be severely elevated)
Imaging- US ultra sound of gall bladder (look for stones and edema in wall of gal bladder to support diagnosis in conjunction with clinical and lab studies)

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10
Q

Chonic Cholecystitis

A

Chronic cholecystitis results from low-term association of gallstones and low-grade inflammation.
(multiple recurring acute inflammation/colecystitis)
Some cases have a history of repeated attacks of mild and acute cholecystitis
Pathology variable:
-wall thickened (not swollen and odematisis and erothematis, more shrunken down with scar tissue. -more chonic inflammatory response + repair pathway with fibrosis)
-gall bladder often contracted - but may be normal size or enlarged

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11
Q

Management sof Cholecystitis

A

Initial acute event:
-Many settle with conservative therapy: IV fluids, pain relief. (settle down inflammation. pot nasogastric tubes to settle down gastric secretions.)
-If suspicion of secondary infection (cholangitis or bacterial infection) then additional antibiotics
-Up to 25% may require acute surgical intervention
Long term:
-cholecystectomy - most now laparoscopic (more definitive therapy)
-quicker recovery
-look to do later as want inflammation to settler down. removing odematis and inflamed gallbladder would result in a higher risk of complications and risk of needing to convert to open laparotomy and cholecystectomy with longer recovery times

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12
Q

Choledocholithiasis

A

Choledocholithiasis is the presence of stone within the biliary tree
-cystic duct or common bile duct
–obstruction: biliary colic, allow bacteria to result in infection (due to stasis)
-ampulla- blocks common bile duct and pancreatic duct
–trigger pancreatitis
Complications:
1. Biliary obstruction colicky abdominal pain
2. Obstructive jaundice (raised bilirubin, dark urine and pale stools as additional complication)
3. Pancreatitis
4. Cholangitis
-3 + 4 inflammation and sepsis within bile ducts

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13
Q

Patient with jaundice abdo 13

A

“gone yellow” - jaundice, biliary tree, pancreas or liver
“suffers from bouts of abdominal pain, especially after eating”
-fatty meal, gallbladder contracts, stones tried to move down by peristalsis
-recurrent and pain
“his stool is pale and urine is dark”
-could be pancreatic pathology, tumour at pancreas head
-could also be stone in biliary duct
Investigations:
-Image further and manage appropriately

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14
Q

Cancers of the Biliary system

A

Carcinoma of the Gall bladder
Carcinoma of the Extrahepatic ducts
-Rare in biliary tree, but unfavourable prognosis cancers
-significant change in structure

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15
Q

Carcinomas of the Gallbladder Pathology

A

Most are adenocarcinomas
Most have invaded the liver by the time of diagnosis
Seen on older patients
-because high risk biology + advanced and beyond surgical intervention by time of diagnosis
Poor prognosis 5 yr OS 1%
-usually by time of presentations would have already had metastatic spread to liver (often)

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16
Q

Rectal bleeding Abdo 20:
A 55 year old NZ european man presents to his GP complaining of passing blood when he is passing a bowel motion. You are the trainee intern attached to the clinic and are asked to see him before the doctor. He is concerned because his father was diagnosed with bowel cancer in his 50s . Your own grandfather died of bowel cancer last week

A

family history

  • under 50 is rare for colorectal cancer (most commonly 60s), links to familial cancer
  • should see patients reflecting own experiences
  • “passing blood when he is passing a bowel motion”
  • “his father was diagnosed with bowel cancer in his 50s”
  • sigmoid or descending colon pot tumous, investigate with colonoscopy
17
Q

Adult with abdominal mass Abdo5:
A 52 year old NZ european woman presents to her GP with bloating of her abdomen, worsening over the last few months, associated with intermittent diarrhoea and 5kg weight loss. Her brother and father were diagnosed with bowel cancer in their 40’s

A
  • re how bowel cancer might present (symptoms alert to significant GI pahtology- weightliss, abdominal bloating, and change in bowel habits) -may suggest underlying colorectal malignancy
  • strong family history of colorectal cancer at young age - alerts to thinking about familial cancer
  • “bloating of her abdomen”
  • “intermittent diarrhoea and 5kg weight loss. Her brother and father were diagnosed with bowel cancer in their 40’s” - strong malignancy suggestion
18
Q 
Bowel obstruction (abdo 3):
A 68 year old NZ european/Maori man presents to the Accident and Medical centre with vomiting and abdominal distention. He has also noted that his bowels have not moved for 4 days and he is not passing wind
A

often how bowel cancer presents

  • strong suggestion of bowel obstruction
  • even though multiple potential causes, but frequently if tumour obstruction, may lead to small or large bowl (typically large bowel) obstruction
  • “vomiting and abdominal distention. His bowels have not moved for 4 days and he is not passing wind” - require further investigations
19
Q

Tumours of colon and rectum

A

Cancers of colon major health problem in NZ (lung is largest as often inoperable and biology of disease)
Most common cancer in NZ
Second most common cause of cancer death in NZ after lung cancer
Benign tumours- mainly polyps
Malignant tumours - mainly adenocarcinomas (ulcerating lesion with rolled edges, pot. necrotic)
-Adenoma with adenocarcinoma ( risen out of previous benign tumour.
-all adenocarcinomas all arise from benign adenoma that will then progress into a adenomacarcinoma

20
Q

Most common cancers

A
  1. Colorectal 14.6% (2716 cases)
  2. Breast 13.3% (2479 cases)
  3. Prostate 13.3% (2471 cases)
  4. Melanoma 10.8% (2017 cases)
  5. Lung 8.9% (1659 cases)
21
Q

Leading causes of cancer death

A
  1. Lung 18.2% (1451)
  2. Colorectal 15.3% (1222)
  3. Breast 8.2% (652)
  4. Prostate 7.1% (564)
  5. Pancreas 4.1% (353)
22
Q

Polyps

A

A circumscribed growth or tumour which projects above the surrounding mucosa
Need (excised) biopsy to determine nature
-Non neoplastic polyps (benign overgrowths/small tumours that rise above mucosa, all clinically look similar)
-Neoplastic polyps - adenoma

23
Q

Non-neoplastic Polpys

A

No malignant potentials. No follow ups required. Reassuring. Incidental findings

  1. Hyperplastic polyps
    - small
    - benign (no potential to progress into adenocarcinoma)
    - usually asymptomatic (found in patients having screening colonoscopy, or being investigated for other reasons (biopsy report back indicating))
    - normal bowel morphology, just an over growth of mucosa
    - do not have malignant potential
    - small 3-6mm, common
  2. Inflammatory polyps
    - seen in IBD, overgrowth
    - reactive change/response of mucosa (small overgrowths/polyps)
    - Benign, (pseudopolyps)
24
Q

Neoplastic polyps

A

Adenomas:

  • Benign polyps with malignant potential (e.g. HMPCC) (familial adnomas pulposus carcinomas)
  • Most age >50, M=F
  • Familial predisposition
  • Epithelial Proliferation with variable degrees of dysplasia (abnormal growth)
25
Q

Neoplastic Polyps: pathology

A

Adenomas 3x main types

  1. Tubular adenomas- most common, mostly tubular glands
    - epithelium relatively normal
  2. Villous adenomas- villous projections, often large (flatter base) and sessile
    - higher propensity to trans form
  3. Tubulovillous adenomas- mixture of above
26
Q

Polyps clinical

A

Most asymptomatic
May bleed (if in distal part of bowel, w. blood in bowel motions), mucosal discharge
If larger: -altered bowel habit
-bowel obstruction(unusual)

27
Q

Adenoma to Carcinoma sequence -overview

A

Benign:
Hyperproliferation –>
Adenomatous Polyps: Small –> Large –>
Severe dysplasia (pre-cancerous polyp) –>
Malignant:
Adenocarcinoma –>
Cancer
-start as small adenoma, grow and expand, and develop through acquisition of multiple molecular changes of epithelium (becomes more dysplastic) to progress into adenocarcinoma
- for screening strategies: removal of adenomas will reduce risk of patient developing adenocarcinomas
1.familial colorectal cancer patients put in regular colonoscopy patient to pick up early development of adenomas and remove before progression through to invasive adenocarcinoma
2. If patient is know to have adenomas, follow up endoscopies looking for adenocarcinomas in the future

28
Q

Adenoma’s risk of transformation into carcinoma

A

Polyp size- rare if 4cm
Degree of dysplasia
-greater abnormality of maturation of epithelium

29
Q

Adenoma to Carcinoma Sequence

A

*most cancers have 5-6 different acquired genetic mutations required before see malignant phenotype
Normal colon: Germ line (inherited) or somatic (acquired) mutations of cancer suppressor genes (“first hit”) - APC at 5q21
Mucosa at risk: Methylation (epigenetic) abnormalities inactivation of normal alleles (“second hit”) - APC B-caterin
Adenomas: Proto-oncogene mutations - K-RAS at 12p12
Homozygous loss of additional cancer suppressor genes. Over expression of COX-2.
-p53 at 12p13. LOH at 18q21. SMAD 2 and 4.
Carcinoma: Additional mutations. Gross chromosomal alterations - Telomerase. Many genes
* have a screening programme, picking up mutated genes at early stage, take stool sample, lab take DNA analysis for particular DNA profile (colon cancer screening strategy with biomarker- potential intervention targeting these genes)

30
Q

Colorectal cancer

A

15% of all cancer deaths

Peak age 60-70, rare age Females rectal cancers

31
Q

Environmental risk factors for Colorectal cancer

A
  1. Diet (high red meat, low fibres, high CHO)
  2. High incidence in developed countries e.g. NZ, AUS, US
  3. ? Protective effect of aspirin and NSAID
32
Q

Pathology of Colon cancer

A

Adenocarcinoma
Variable differentiation (of cells)
Found caecum, ascending, transverse, descending, sigmoid, rectum (all parts of large bowel)
-Ulcerating tumour: fungating tumour, rolled edges, necrotic centre (bleeding)
Microscope: trying to form glandular structures, blue undifferentiating cells (high nucleocyte:cytoplasmic ratio)(tumour cells) alot of mytotic figures (inflammatory cells). Outgrown blood supply, Necrotic tissue

33
Q

Staging of Colorectal cancer

A

T= (local) extent of invasion of bowel wall
N= number of lymph nodes involved
M=metastatic disease present of not (if have metastastic disease local resection wont be curative, more systemic chemo therapy required)
-Prognosis determined by stage of tumour
-clinically important for optimal treatment, prognosis, extent

34
Q

Stages of Local colon cancer

A
  1. invade into mucosal wall
  2. deeply through mucosal wall
  3. Invading through external surface
  4. local spread of lymphatics and hematogenous spread into lymphatics
35
Q

Clinical Features of Colorectal cancer

A

Abdominal pain, mucous discharge, PR bleeding, change in bowel habit, bowel obstruction
Right sided tumours-may be present with iron deficiency anaemia due to occult bleeding
Spread to regional nodes, liver, lungs, bones
Constitutional symptoms e.g. weight loss, malaise

36
Q

Bleeding of Necrotic Caelcum

A

10-30ml daily
bleeds into bowel content
unlikely to be seen (more obvious if in sigmoid colon)
-but often have occult bleeding (not clinically apparent bleeding)
-instead have iron deficiency anaemia, as bleeding from right side of gut, every 1ml blood lost has 0.5ml of iron. only absorb 1-2ml of iron from diet.
-quickly get into negative balance and risk of developing iron deficiency
-male or female post menopausal, bleeding of GI tract or pathology of large bowel (particularly tumour of caecum)

37
Q

Familial Polyposis Syndromes

A

Group of inherited polyposis syndromes (familial adenoma polpyosis coli most common, number of polyposis)

  1. Autosomal dominant inheritance
  2. Predisposition to malignant transformation
    - in colon
    - other sites
  3. Study has given clues to molecular pathology of colorectal cancer
38
Q

Familial Adenomatous Polyposis

A

Multiple adenomas in colon and elsewhere in gut - most tubular adenomas

  • usually evident adolescence
  • transform into cancer
  • APC gene on chr5q21 (inherited germ line mutation on APC gene. Also involved in sporadic bowel cancer, adolescents and adults develop multiple polyps into colon, adenomas, high risk of transformation. would go into screening and maybe considered for prophiliactic colectomy)
  • Autosomal dominant
  • Prophylactic colectomy
39
Q

HNPCC Hereditary Nonpolyposis Colorectal Cancer (HNPCC)

A

Autosomal dominant inheritance
5% of all colorectal cancer cases
Consider if family history or young age of onset of cancer (under age of 50)
Progress adenoma to carcinoma but no increase in polyps
-regular screening programmes w. colonoscopies to look for early adenomas to reduce risk
Due to inherited mutation in DNA mismatch repair gene

Digestive System Module (38 decks)

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