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HD&T > Quiz 7 (info for 3rd midterm) > Flashcards

Quiz 7 (info for 3rd midterm) Flashcards

1
Q
  1. Chemical esophagitis-
A

irritants to squamous mucosa

  • corrosives, smoking, alcohol, chemotherapy
  • acute inflammation and possible ulceration
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2
Q
  1. Infectious esophagitis-usually immunosuppressed (often Herpes, Candida, and cytomegalovirus [CMV])
A
  • Often ulcers
  • CMV:
  • Affects entire GI tract
  • Neonates acquire thru birth canal or infected breast milk
  • Adults acquire through sexual transmission or needles
  • Multiple discrete, well-circumscribed superficial ulcers.
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3
Q
  1. Reflux Esophagitis
A

a. Relaxation of gastroesophageal sphincter
b. Symptoms: Burning, Excessive salivation, Choking
c. Aggravating factors: obesity, pregnancy, drug (decrease esophageal pressure: alcohol/tobacco, narcotics, nicotine patch) use
d. Medical treatment: antacids, H2 blockers, PPI -lose weight, stop smoking/drinking e. lifestyle treatment: lose weight, stop smoking and drinking
e. Complications: ulceration, stricture, Barrett esophagus (long tongues of extended columns of epithelium cells into esophagus)

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4
Q
  1. Reactive (erosive gastritis) gastropathy in stomach
A

a. Induced by: alcohol, NSAIDS, iron, Stress, bile reflux

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5
Q
  1. Acute injury in stomach
A

a. Acute gastritis—asymptomatic with possible significant blood loss

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6
Q
  1. Acute peptic ulceration in stomach
A

a. Nausea, vomiting, NSAIDs, stress

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7
Q
  1. Chronic gastritis in stomach
A

a. H. pylori gastritis-duodenal and pyloric ulcers; may lead to cancer
b. Autoimmune gastritis

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8
Q
  1. Peptic Ulcer Disease in stomach
A

a. H. pylori and NSAIDs causative
b. Increased acid
c. Punched our ulcers-potential for perforation and hemorrhage
d. Likely also involved in adenocarcinoma development

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9
Q
  1. Autoimmune atrophic gastritis
A
  • Genetic factors
  • No ulcers
  • Decreased gastric acid
  • Intestinal metaplasia
  • Long-term effects relate to malabsorption of B12 (pernicious anemia) `
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10
Q

a. Hyperplastic, sporadic polyps

A

• Response to gastric injury, around ulcers

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11
Q
  1. Gastric carcinoma
A

• Looks like intestinal tissue, and diffuse • Some have hereditary connection

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12
Q

C. Small bowel, colon

A
  1. Intestinal obstruction a. Usually mechanical (80%) b. Neoplasm and infarction (20%)
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13
Q
  1. Hirschsprung disease
A

• Congenital defect in colonic innervation • Failure to pass meconium

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14
Q

a. Celiac sprue selected diahhreal disease

A

• Immune mediated

—triggered by ingestion of gluten

  • Malnutrition:
  • Fe, B12 malabsorption
  • Atrophic glossitis
  • Dental effects: enamel defects, delayed too eruption, recurrent aphthous ulcers, cheilosis,
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15
Q

b. Lymphocytic colitis selected diahhreal disease

A

• Increased intraepithelial lymphocytes

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16
Q

c. Irritable bowel syndrome

A

• Relapsing pain, bloating, relapsing and alternating constipation/diarrhea • Diet, abnormal motility and stress are factors • No gross microscopic abnormalities

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17
Q

d. Infectious self-limiting colitis selected diarrheal disease

A

• Caused by microorganisms such as salmonella, E. coli, shigella, clostridium

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18
Q

e. Pseudomembranous colitis,

A

cells slough off • Usually caused by clostridium difficile • Spread via person to person • Often follows broad spectrum antibiotic therapy • Most common nosocomial infection in older adults

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19
Q
  1. Inflammatory Bowel Disease a. Crohn’s disease:
A

• Similar to ulcerative colitis • It skips lesion and has intermediate constrictures • Granulomas • Fistulas and perianal disease • Also affects upper GI tract • Transmural inflammation • Fistulas, perianal

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20
Q

Oral manifestation of Chrons

A

• Oral manifestation: ➢ 0.5% have oral lesions ➢ Usually males ➢ Linear and deep ulcerations

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21
Q

b. Ulcerative colitis

A

• More continuous especially in the colon • No transmural inflammation • No fistulas and not perianal

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22
Q

Oral manifestation of ulcerative colitits

A

➢ Less common than in CD ➢ Usually males ➢ Edematous oral submucosa

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23
Q

Colonic polyps

A

• Hyperplastic polyps- no malignant potential • Adenoma- precursor to adenocarcinoma

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24
Q

Invasive colonic adenocarcinoma

A

• Responsible for 15% of all cancer related deaths in USA • Dietary features: increased risk with low fiber, high intake carbohydrates/fats

25
Q

Hepatic Cholecytitis

A

• Acute often caused by gallstones and obstruction. Can become chronic

  1. Cholecystitis (bile is common mechanism for excretion of toxins and drugs)
  2. Cholestasis causes jaundice
26
Q

B. Liver diseases-summary-these diseases can go on to cirrhosis

A
  1. Fatty liver • Caused by ETHOH, obesity and diabetes Mel. 2. Hepatitis • Caused by virus, drug or autoimmune 3. Biliary disease 4. Metabolic disease 5. Vascular
27
Q

Hepatitis constituent

A
  • Liver made up of hepatocytes, duct cells and blood vessels
  • Organization: Portal tracts contain the triad (portal triad) of bile ducts, portal veins (bring blood from gut with nutrients and recently consumed drugs), hepatic artery from the heart. Blood goes to the sinusoids and enriches hepatocytes, then goes to central vein and drains back to the heart to be recycled. Blood from different sources mix in the sinusoids drains into the “central veins” and exits to the hepatic vein that goes to the heart
  • Hepatocytes do all of the metabolic work of the liver and absorb nutrients and drugs.
    • Most hepatotoxic events occur around the ‘central vein’

• Drugs are the #1 cause of liver toxicity!

  • Biopsy of liver can be potentially dangerous due to major hemorrhaging
28
Q

Liver details

A
  1. Fatty (fat globules in hepatocytes) liver-steatosis

• Worst destruction is fibrosis. It leads to collagen scar and permanent injury. End stage is cirrhosis

  • Causes—alcohol, obesity and diabetes (known as the metabolic syndrome)
    2. If hepatocytes die in large sheets, the areas fill up with blood. Blood can build up due to heart failure and cause backflow around the central vein
    3. If cannuliculi in liver fill with bioe due to cholestasis, the person becomes jaundiced (often caused by drugs)
    1. Acute more lobular, chronic is more portal with fibrosis and collagen bridges
29
Q

Hepatitis

A
  1. Hepatitis is inflammation of liver. If caused by viruses can be contagious and dentists must be very careful with these patients • Can also be caused by toxins and drugs • Acute can often resolve itself. Chronic less likely to recover (fibrosis often a part of this) • Acute caused by Hepatitis A and E viruses (1-3months)

• Hep.B and C viruses start with acute hepatitis and progress to chronic with fibrosis progressing to cirrhosis and hepatocellular carcinoma: tend to be the more severe

30
Q

Memorized table

A
31
Q

Hep B and C

A
  1. Hep C virus found in >170 million carriers worldwide
    • Acute phase usually asymptomatic and not diagnosed
    • Chronic phase, Ab present at 5-20 weeks
    • 60% related to parenteral exposure
    • Caused by RNA virus
    • Can lead to hepatocarcinoma
    • No vaccines
  2. Heb B virus, 2 billion chronically exposed in world, 350 infected. 15-25% of infected will go into chronic phase and most will die from complications. Can lead to cancer of liver (hepatocarcinoma)

-important to get vaccinated.

  • Caused by DNA virus
  • Cirrhosis (chronic phase)= portal hypertension;
  • causes ascites 85% of time in chronic phase with cirrhosis
32
Q

Cirrhosis

A
  1. regenerative hepatocyte nodules; fibrosis surrounding nodules
33
Q
  1. Autoimmune hepatitis unusual
A

- found in obese females predominantly

  • Rapid response to steroids
  • 80% have extensive fibrosis
34
Q
  1. Fatty liver disease:
A

Caused by ETOH, obesity, diabetes mellitus etc.

  1. (not an inflammatory disease:
35
Q
  1. Metabolic disease:
A
  • Often associated with iron overloads
  • Wilson’s disease: copper metabolic defect goes to hepatitis then cirrhosis
36
Q
  1. Gastroesophageal reflux disease (GERD) is chronic; ‘acid reflux” is acute (isolated incidents
A

​Episodes referred to as heartburn and occurs daily in 7% of population

  1. Aggravating factors: empty stomach, inclined, increased age, obesity, fatty foods, caffeine/alcohol/smoking, large meals, some drugs
  2. Relief: small meals, reduced fat, reduced weight, elevate head of bed, avoid aspirin/NSAIDs
  3. Dental tips:
  • Protect teeth from erosion by gastric acids (i.e., mouth guard, neutralize acid with basic solution, don’t brush teeth after gastric juices are in mout-i.e., acidic
37
Q
  1. Medications to neutralize HCL
A
  1. Antacids-neutralize gastric HCl
    * Types: magnesium salts (can cause diarrhea); bicarbonate (causes gas); calcium carbonate (chalky and constipation); aluminum salts (not very effective)
38
Q
  1. H2 receptor blockers-not effective at the H1 receptors (i.e., not good antihistamines)-reduce gastric secretions by blocking H2 receptors in gut
A

​Types (available both OTC and by Rx):

  • Cimetidine (Tagamet)
  • Ranitidine (Zantac)
  • Famotidine (Pepcid)
  • Side effects: headaches, diarrhea, drowsiness
39
Q

Proton pump inhibitors (PPIs) –available OTC and by Rx

A
    • Mechanism: disrupts hydrogen exchange for K in parietal cells, which blocks production and release of HCl into gut.
    • Side effects: diarrhea, interferes with digestion, increases food allerges, oral sores/ulcers
40
Q

PPI often combined with ..?

A
  • Often combined with H2 blockers
    1. Products
  • Omeprazole (Prilosec)
  • Omeprazole + sodium bicarbonate for fast release (Zegerid)
  • Lamsoprazole (Prevocid)
  • Esomeprazole (Nexium)
41
Q
  1. Peptic Ulcer disease (causes)
A
  1. Includes gastric and duodenal ulcers
  2. Causes:
  3. Inflammation of epithelium
  4. Errosion
  5. Infection by H. pylori (70-80% incidence)
42
Q

Peptic Ulcer disease (symptoms)

A
  1. Symptoms:
  • Epigastric burning, alleviated by eating or antacids
  • Pain worse on empty stomach and at nigh
  • Pain often mistaken for a heart attack and vice versa
43
Q

Peptic ulcer tx

A
  1. Suppress acidity to heal sores (but not cure)
    * Antacids, PPIs, H2 blockers
44
Q

Cure if h.pylori related peptic ulcer

A
  1. Cure if H pylori-related –H pyloria is contagious especially within family members
  • Prevpac; combination of lansoprazole (a PPI) and the antibiotics amoxicillin and clarithromycin
  • Milk of Magnesia (magnesium based) may also help kill
    *
45
Q

Sites of nutrient absorbtion

Stomach

duodenum

jejnum

ileum

colon

A

water, alcohol

fe,ca,mg,na,fats,water,proteins vitamin

carb, protein

bile salt, b12, Cl

Water, electrolytes

46
Q

Laxative for constipation

A
  1. Constipation (mobility too slow, too much water absorption)
  2. Pharmacology: Laxatives:
  • Bisacodyl
    • Stimulant of smooth muscles
    • Fast acting
    • OTC
    • Suppository/oral
    • Cramps
  • Docusate
  • Water retention in stools, softens stools
  • OTC (e.g., Dulcelax)
47
Q

Diarrhea definition and medications

A
  1. Diarrhea
  2. Loose, watery stools- motility too fast, not enough absorption
  3. Consequence: dehydration, malnutrition-worse in young and elderly
  4. Medications:
  5. Loperamine- Imodium; mild opioid agonist: if severe, can use strong opioid agonists
  6. Bismuth subsalicylate (e.g., Pepto-bismol)
  7. Anti-cholinergics such as atropine
48
Q

IBS symtpoms

A
  1. Symptoms:
  • No structural defect –not sure of the exact cause
  • Typically episodic pain and bloating
  • Could be 5HT-dependent neuromuscular disorder
  • 20% of population have suffered (most common GI disorder)
  • Most common in young adults and ~50 Years old—possible association with stress and poor diet
49
Q

IBS tx and drugs

A
  1. Treatment:
  2. Typically symptomatic (i.e., deal with diarrhea or constipation with diet and anti-stress changes)
  3. Drugs: only linaclotide (Linzess) is FDA-approved for IBS with constipation
  • It is a guanylate cyclase-C agonist-it increases bowel movement, fluid secretion and reduces pain
  • Side effects: diarrhea, gas
50
Q
  1. Inflammatory Bowel Disease (IBD: < 1% of population)
  2. Spectrum of disorders
  3. Crohn’s disease
  4. Symptoms:
A

Chronic diarrheal problems

  • Can affect entire GI, but more intense in ileum and colon and intermittent areas with strictures between

-swelling and scarring

  • Hypogastric pain
  • Perianal fissures/fistules
  • Higher incidence of arthritis
  • Fatty liver
  • Possible genetic link
  • Perhaps abnormal inflammatory response to normal flora
  • Has remission
  • Increase incidence of colon cancer
51
Q

Inflammatory bowel disease meds

A
  1. Medications
    * Anti-inflammatories:
  • Mesalamine (topical anti-inflammatory)
  • Corticosteroids-act systemically
  • Metronidazole (antibiotic mechanism?)
52
Q
  1. Ulcerative colitis
A
  • Similar to Crohn’s disease but limited to colon and more generalized (no strictures)
  • Medications are similar to Crohns disease
53
Q

dental implication of hepatitis

A

HBV infection most significant occupational dental

hazard (vectors: blood, saliva, nasopharyngeal secretions)

b. In mouth, highest concentration is gingival sulcus

c. Manifestations (infections and bleeding based):

  • Lichen planus
  • Periodontal disease
  • Candidiasis
  • Increased oral bleeding
  • Increased incidence of type II diabetes
  • Sjogrens syndrome
54
Q
  1. Chronic hepatitis (e.g., hepatitis B and C)
A

a. e.g., infection, drugs, autoimmune diseases

55
Q

managing hepatitis

A
  • Accidental exposure:
  1. Carefully wash wound-don’t rub (embeds viruses)
  2. Use antiviral disinfectant (e.g., iodine or chlorine formulations)
  3. Initiate HBV vaccine series
    * Don’t be judgmental
56
Q
A
57
Q
  1. Hepatocellular carcinoma
A
  1. Most deadly cancer
  2. It has been increasing due to increases in the incidence of Hep B and C
58
Q
  1. Evaluation of hepatitis severity:
A
  1. Grade= degree of inflammation
  2. Stage= degree of fibrosis-this is the most important for prognosis-extreme if it progresses to cirrhosis that includes collagen surrounding hepatic nodules (hepatocytes)

HD&T (7 decks)

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