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PATH 375 > GASTROINTESTINAL, LIVER, BILIARY TRACT AND PANCREAS PATHOLOGY > Flashcards

GASTROINTESTINAL, LIVER, BILIARY TRACT AND PANCREAS PATHOLOGY Flashcards

1
Q

Most common craniofacial malformation in the newborn?

A

Cleft lip/palate

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2
Q

Why does a cleft lip/palate occur

A

Failure of fusion of fetal nasal and maxillary processes

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3
Q

Cleft lip/palate etiology

A

Genetic factors and some evidence for environmental (maternal medications, smoking, etc.)

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4
Q

How many cleft lip/palate cases are linked to genetic syndromes (example)

A

30% (The best known syndrome with cleft lip/palate is 22q11 deletion syndrome (DiGeorge syndrome))

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5
Q

Dental Carries (Tooth Cavities)

A

Erosion of the hard outer layer of the tooth (the enamel) by acids produced by bacteria

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6
Q

Risk factors for dental carries (tooth cavities)

A
  • Poor oral hygiene
  • Structural abnormalities (promoting plaque formation)
  • Sugary foods
  • Lack of saliva (to buffer bacterial acid)
  • Genetics?
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7
Q

Pulpitis

A

The cavity in the tooth enamel erodes through the dentin layer and into the the tooth pulp. This is when dental (painful) (bacteria can infect)

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8
Q

Gingivitis

A

Inflammation of the gums caused by bacterial plaques on and around the teeth (inflammation of the gums)

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9
Q

Periodontitis

A

Severe gingivitis where the gum retracts from the teeth

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10
Q

Effects of periodontitis

A
  • Teeth loosening or falling out
  • Bad breath
  • Infection spread to rest of jaw
  • Potential sepsis
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11
Q

Sepsis

A

Bacterial infection of the blood (can be life-threatening)

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12
Q

Potential effects from severe dental infections (e.x. pulpitis, periodontitis) where bacteria move into the blood

A
  • Sepsis
  • Bacteria can lodge (E.x. lodge on heart valves forming biofilms > infectious endocarditis)
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13
Q

Stomatitis

A

Inflamed/sore mouth

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14
Q

Recurrent aphthous stomatitis (‘canker sores’)

What is it? Cause?

A
  • Discrete, painful mouth ulcers that usually spontaneously resolve within 2 weeks
  • Unknown cause
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15
Q

Infectious stomatitis

A

Pocket of fluid bound by squamous mucosa

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16
Q

Infectious stomatitis (Herpes virus - ‘Cold sores’)

A

Typically starts as a vesicle initially, and may later ulcerate

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17
Q

Infectious stomatitis (Candida fungus - ‘oral thrush’)

Who does this effect?

A

Can affect infants, the immunosuppressed and users of inhaled corticosteroids

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18
Q

Oral cavity neoplasm

What cell type do they affect

A
  • Vast majority are squamous
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19
Q

Leukoplakia

A

Persistent white patch mouth lesion

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20
Q

Erythroplakia

A

Persistent red patch mouth lesion

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21
Q

Causes for mouth lesions

A

Heavy consumption of alcohol and with tobacco use (cause concern for squamous cell carcinoma)

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22
Q

Squamous cell carcinoma

A

Occurs when the oral squamous epithelium acquires genetic mutations, mainly from toxins, human papillomavirus (HPV) or
radiation

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23
Q

2 main types of squamous cell carcinoma

What types? Where do they tend to occur?

A

1) Associated with alcohol and tobacco use (tongue)
2) Associated with associated with HPV infection (oropharynx (tonsils location))
3) Other (radiation, UV, immunosupression)

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24
Q

squamous cell carcinoma progression

A

Dysplasia (increasing grade) > squamous cell carcinoma in situ > invasive squamous cell carcinoma > metastasis to neck regional lymph nodes and/or distant metastases

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25
Q

Sialadenitis

A

Inflammation of salivary glands (can lead to gingivitis)

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26
Q

Sialadenitis causes

2 types of causes and examples

A

Infectious causes:
- Bacterial ( S. aureus ), viral (mumps)

Non-infectious causes:
- Sjögren syndrome (autoimmune): inflammation of salivary and lacrimal glands
- Sialolithasis (stones in salivary gland)
- Therapeutic radiation

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27
Q

Salivary gland neoplasms

A
  • Benign (commonly pleomorphic adenoma)
  • Malignant (commonly mucoepidermoid carcinoma)
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28
Q

Hiatus hernia

What is it? cause?

A
  • Displacement of portion of the stomach above the diaphragm
  • Cause unkown (genetics?)
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29
Q

Types of hiatus hernias

Types; definition; prevalence

A

Sliding hernia:
- 95% prevalence
- Sliding of gastroesophageal junction and cardia of stomach upwards

Paraesophageal hernia:
- 5% prevalence
- Portion of stomach protruding upward and
forming pocket beside esophagus (caused by prior surgery)

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30
Q

Achalasia

What is it? Effects?

A

Degeneration of the ganglion cells in the
myenteric plexus (distal esophagus)

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31
Q

Achalasia effects

A

Prevents the lower esophageal sphincter
from relaxing and decreases peristalsis in
the distal esophagus (dysphagia)

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32
Q

Achalasia causes

A
  • Primary cause unknown
  • Can occur secondary to parasitic infection
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33
Q

Varices

A

Dilation of submucosal veins of the distal esophagus

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34
Q

Varcies effects

A

The dilated veins can rupture, which can lead to life threatening bleeding

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35
Q

Varcies causes and treatment

A

Cause: Hepatic cirrhosis (causes hypertension in the portal vein system is the commonest cause)

Treatment: Endoscopically or with medications

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36
Q

Esophagitis

A

Inflammation of the esophagus (mainly of the squamous lining)

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37
Q

Gastroesophageal Reflux Disease (GERD)

A

Reflux of gastric contents into esophagus that causes a chemical esophagitis

Increased pressure in the stomach + insufficient lower esophageal sphincter tone

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38
Q

Gastroesophageal Reflux Disease (GERD) causes

A

Very numerous causes and risk factors are known, common ones include: smoking, alcohol abuse, obesity, pregnancy, excessive caffeine use

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39
Q

Esophagitis causes

A
  • GERD
  • Infectious causes: viral (herpes simplex virus), fungal (Candida)
  • Ingestion of irritating substances (some pills/medications, bleach, others)
  • Inflammatory conditions/allergy (eosinophilic esophagitis)
  • Various autoimmune diseases
40
Q

Barrett Esophagus

A
  • A complication of GERD (exacerbated by excessive alcohol and/or tobacco use)
  • Due to chronic irritation
  • The intestinal metaplasia has a risk of progression to dysplasia and then to esophageal adenocarcinoma
    -Some patients with Barrett esophagus require biopsy screening for early detection and treatment of dysplasia/adenocarcinoma
41
Q

Most common esophageal carcinomas

Types; location; risk factors

A

Squamous cell carcinoma
- Upper-mid esophagus
- Risk factors: alcohol and tobacco

Adenocarcinoma
- Distal esophagus
- Risk factors: GERD and Barrett esophagus; obesity and smoking also

42
Q

Signs/symptoms of esophageal carcinoma:

A
  • Occult gastrointestinal bleeding (anemia)
  • Unintentional weight loss
  • Progressive difficulty swallowing (dysphagia)
  • Pain on swallowing (odynophagia)
43
Q

Gastritis

A

Inflammation of the mucosal lining of the stomach (acute or chronic)

44
Q

Acute gastritis

Type of lymphocytes; causes

A
  • Neutrophils present
  • Causes: Drugs (aspirin), alcohol, severe
    physiologic stress (burns, trauma, etc.)
45
Q

Chronic gastritis

Lymphocytes; causes

A
  • Increased lymphocytes and plasma cells
  • Causes: Helicobacter pylori infection and autoimmune gastritis (two most common); also autoimmune/inflammatory conditions
46
Q

Gastropathy

A

Injury to the stomach lining in the setting of little or no inflammation
- Erosion or ulceration
- Causes: chemical; vascular injuries; physiological stress

47
Q

Peptic ulcer disease

A

Ulceration of gastric or duodenal mucosa in the
setting of acute or chronic gastritis

Causes: H. pylori, reduced mucosal barrier, drugs, others

48
Q

Peptic ulcer disease complications

A
  • Hemorrhage > melena, iron deficiency anemia, hematemesis
  • Perforation > peritonitis
  • Penetration > ulcer penetrates into pancreas
  • Scarring > stenosis > obstruction
49
Q

Helicobacter Gastritis

What is it (cause)? Risk factors?

A

Caused by infection by Helicobacter pylori (fecal oral transmitted; bacterium hides in the gastric mucus)

Risk factors:
- Longstanding infection risk factor for malignancy

50
Q

Parietal cells

A

Produce HCl and intrinsic factor

51
Q

Chief cells

A

Produce pepsinogen

52
Q

G cells

A

Produce gastrin

53
Q

Autoimmune Gastritis

A

Immune system recognizes parietal cells as foreign and destroys them

54
Q

Autoimmune Gastritis effects

A
  • Stomach and fundus chronically inflamed
    and atrophic
  • Parietal cells destroyed (and chief cells as bystanders)
  • G cells produce lots more gastrin
55
Q

Autoimmune Gastritis consequences

A

1) Inability to Absorb B12
2) Increased Risk of Gastric Adenocarcinoma
3) Increased Risk of Gastric Well Differentiated Neuroendocrine Tumor

56
Q

Autoimmune Gastritis consequence: Inability to Absorb B12

A
  • No intrinsic factor > the body cannot absorb vitamin B12 > megaloblastic anemia
  • Chronic lack of vitamin B12 can also lead to
    irreversible nerve damage

Treatment:
* Diagnosis of autoimmune gastritis
* Supplementation with vitamin B12

57
Q

Autoimmune Gastritis consequence: Increased Risk of Gastric Adenocarcinoma

A
  • Chronic inflammation, atrophy
    and intestinal metaplasia in the fundus/body
    increases risk of gastric adenocarcinoma
  • High levels of gastrin are produced by G cells because of the lack of stomach acid being produced
  • Elevated gastrin > carcinogenesis
  • Solution: Biopsy screening for intestinal
    metaplasia and early gastric adenocarcinoma
58
Q

Autoimmune Gastritis consequence: Increased Risk of Well-Differentiated Neuroendocrine Tumor

A

High production of gastrin → proliferation of stomach endocrine cells → neuroendocrine tumor

Solution: Good prognosis (low risk of spread) → removal

59
Q

Gastric adenocarcinoma risk factors

A
  • H. pylori gastritis
  • Autoimmune gastritis
  • Nitrosamine exposure
60
Q

Gastric adenocarcinoma histological classification

A

Intestinal type: forms polypoid mass or tumor
Diffuse type: Spreads over wall
Mixed type: Bit of both

61
Q

Gastric adenocarcinoma metastasis

A
  • Lymph node
  • Bilateral ovarian spread
62
Q

Gastric lymphoma most common type

A

MALT lymphoma

63
Q

MALT lymphoma

Progression? Cause?

A

Progression: Slow (low grade) but can transform into high grade

Cause: H. pylori infection

64
Q

Meckel’s Diverticulum

A

Developmental disorder of small intestine where a portion of the vitelline duct remains open (rule of 2: population affected; developing symtopms; etc.)

65
Q

Celiac disease

A

Gluten allergy (products of gluten breakdown trigger allergic response)

  • Malabsorption results from damage to small intestine mucosa (excess lymphocytes in epithelium; atrophy of villi; inflammation)
66
Q

Inflammatory Bowel Disease

A

2 diseases characterized by recurrent inflammation of the intestines: Crohn’s and Ulcerative Collitis

67
Q

IBD etiology

A

Uknown

68
Q

Crohn’s and UC similarities

A
  • Common in caucasians
  • Familial predisposition
  • Extra-intestinal manifestations (arthritis, skin lesions, liver)
  • Predispose to dysplasia and carcinoma
69
Q

Crohn’s Disease

A

Inflammation involving all layers of the bowel wall (causes deep ulcers, strictures, fistulas, and adhesions)

70
Q

Crohn’s Disease

Location; inflammation pattern; granulomas

A

Location: Often right colon and small intestine (anus involved; rectum spared)

Inflammation pattern: Patchy and discontinuous

Granulomas: Many cases have granulomas in the bowel wall

71
Q

Ulcerative Colitis

A

Inflammation involving only the mucus (shallow ulcers) → may stop peristalsis if severe

72
Q

Ulcerative Colitis

Location; Inflammation pattern; granulomas

A

Location: Starts in the rectum and proceeds proximally (rectum and left colon)

Inflammation pattern: continuous

Granulomas: No

73
Q

Diverticular disease

A

Outpouching of the bowel that forms a blind ended segment

True diverticula: Meckel diverticulum (all layers of the bowl wall)
False diverticula: Acquired (only mucus)

74
Q

Diverticulus disease complications

A

Diverticulosis = Many diverticula
- Wall of the diverticula is quite thin → bleeding

Diverticulitis = Inflammation of diverticula
- Pouches become obstructed with stool → bacteria trapped → inflammation

75
Q

Colorectal adenocarcinoma

Commoness? Risk factors? Cause? Metastasis method? Assessment?

A

Commoness: Top 3 most common malignancy and cause of death for men and women

Risk factors: General (age, obesity, smoking, etc.)

Cause: tend to be IBD-associated; genetic syndromes)

Metastasis method: via lymphatics or blood

Assessment: Colonoscopy screening (neoplastic colon polyps)

76
Q

Jaundice/Hyperbilirubinemia

A

A symptom (not disease) describing yellow discolouration of the skin, eyes and mucosa

77
Q

Jaundice classification

A
  • Pre-hepatic (E.x. hemolysis of RBC releases bilirubin)
  • Hepatic (E.x. liver damaged → bilirubin build up)
  • Post-hepatic (E.x. bile cannot be excreted)
78
Q

Bilirubin

Function; “life cycle”

A

Bilirubin helps digest fats

Hemoglobin breakdown → heme and globulin → heme loses iron → bilirubin → binds to albumin → conjugated in the liver →excreted into bile

79
Q

Hemochromatosis

A

Autosomal recessive disorder of iron metabolism preventing the liver from regulating iron

80
Q

Hemochromatosis effects

A

Iron builds up and leaves scaring, liver failure, increased carcinoma risk

81
Q

Hepatitis A

Transmission; effects; symptoms; vaccine

A

Transmission: Fecal-oral
Effects: Acute infection (if severe → liver failure)
Symptoms: asymptomatic or mild
Vaccine: Preventative

82
Q

Hepatitis B

Virus type; transmission; effects; symptoms; vaccine

A

Virus type: DNA
Transmission: Fluid
Effects: chance of chronic infection; scarring and cirrhosis; carcinoma
Symptoms: 2/3 asymptomatic
Vaccine: Preventative

83
Q

Hepatitis C

Virus type; transmission; effects; symptoms; vaccine

A

Virus type: RNA
Transmission: Fluid
Effects: likely chronic infection; cirrhosis; major risk factor of carcinoma
Vaccine: None

83
Q

Hepatitis E

Virus type; transmission; effects

A

Similar to A
Virus type: RNA
Transmission: Fecal-oral
Effects: Acute

84
Q

Hepatitis D

A

Requires co-infection with hepatitis B (similar transmission and symptoms; greater liklihood of liver failure)

85
Q

Cirrhosis

A
  • Common end stage of many liver diseases (chronic liver disease causing scarring)
  • Liver is not able to regenerate and perform normal functions (Resulting in: portal hypertension, jaundice, bleeding, etc.)
86
Q

Clinical features of cirrhosis

A

JAG H BEEP:
- Jaundice (cannot metabolize bilirubin → yellow coloration)
- Ascites (low serum albumin and portal hypertension → fluid in peritoneal cavity)
- Gynecomastia (cannot detoxify estrogen → male breasts)
- Hematemesis (esophageal bleeding → vomiting/passing blood)
- Bleeding (No clotting factors →easily bruise)
- Edema (low plasma oncotic pressure (no albumin) → swelling)
- Encephalopathy (cannot remove toxins → unconsioucness)
- Pleural effusion (low albumin → fluid in pleural cavity)

87
Q

Gallstones (cholelithiasis)

A

Stones in gall bladder

88
Q

Types of gallbladder stones

A
  • Cholesterol stones (most common)
  • Pigment stones
  • Mixed stones
89
Q

Cholesterol stones

What are they? Risk factors?

A

Excess cholesterol secretion by the liver

Risk factors (4 F’s): Female, Over Forty, Fertile, Fat

90
Q

Cholelithiasis complications

A
  • Cholecystitis
  • Stones obstruct bile duct (jaundice; ascending cholangitis)
  • Obstruction of bowel
  • Risk factor for gall bladder cancer
91
Q

Chronic Pancreatitis

What is it? Causes? Effects?

A

Persistence of inflammation (after original inciting agent removed)

Potential causes: Cystic fibrosis, alcohol

Effects: fibrosis, exocrine/endocrine insufficiency

92
Q

Pancreatic ductal adenocarcinoma (PDAC)

Diagnosis?

A

Very difficult to detect early (usually asymptomatic) eventually presents with jaundice because of obstruction of the common bile duct

At diagnosis: Often already metastatic; poor prognosis

93
Q

Pancreatic well differentiated neuroendocrine tumors (WDNETs)

A

Malignant tumors arising from endocrine cells of pancreatic islets

Diagnosis: Better prognosis than PDAC, but can metastasize and kill

94
Q
A

PATH 375 (4 decks)

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