Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

HDAT > week 10 > Flashcards

week 10 Flashcards

(50 cards)

Start Studying
1
Q

chemical esophagitis

A

-irritants to squamous mucosa
• corrosives, smoking, alcohol, chemotherapy
• acute inflammation and possible ulceration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

infectious esophagitus

A

usually immunosuppressed (often Herpes, Candida, and cytomegalovirus [CMV])
• 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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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 (protein pump inhibitor)
- lose weight, stop smoking/drinking
e. lifestyle treatment: lose weight, stop smoking and drinking
e. Complications: ulceration, stricture (narrowing), Barrett esophagus (long tongues of extended columns of epithelium cells into esophagus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

reactive gastropathy

A

erosive gastritis) gastropathy

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

acute gastritis

A

asymptomatic with possible significant blood loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

acute peptic ulcceration

A

a. Nausea, vomiting, NSAIDs, stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

chronic gastritis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

peptic ulcer disease

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

  1. Includes gastric and duodenal ulcers
    a. Causes:
    (1) Inflammation of epithelium
    (2) Erosion
    (3) Infection by H. pylori (70-80% incidence)
    b. 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
    c. Treatments:
    (1) Suppress acidity to heal sores (but not cure)
    • Antacids, PPIs, H2 blockers
    (2) 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
    Bacteria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

autoimmune atrophic gastritis

A
  • Genetic factors
  • No ulcers
  • Decreased gastric acid
  • Intestinal metaplasia
  • Long-term effects relate to malabsorption of B12 (pernicious anemia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

polyps gastric

A

a. Hyperplastic, sporadic

 Response to gastric injury, around ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

gastric carcinoma

A
  • Looks like intestinal tissue, and diffuse

* Some have hereditary connection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

small bowel obstruction

A 
sually mechanical (80%)
b.	Neoplasm and infarction (20%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

hirschprung diseases

A
  • Congenital defect in colonic innervation

* Failure to pass meconium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

celiac sprue

A

diarrhea• Immune mediated—triggered by ingestion of gluten
• Malnutrition:
 Fe, B12 malabsorption
 Atrophic glossitis
 Dental effects: enamel defects, delayed too eruption, recurrent aphthous ulcers, cheilosis,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

lymphocytic colitis

A

diarrhea. • Increased intraepithelial lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Irritable bowel syndrome

A

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

a. 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
b. Treatment:
(1) Typically symptomatic (i.e., deal with diarrhea or constipation with diet and anti-stress changes)
(2) 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

d. Infectious self-limiting colitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

crohns disease

A 
	Similar to ulcerative colitis
	It skips lesion and has intermediate constrictures
	Granulomas
	Fistulas and perianal disease (pain and drainage near anus)
	Also affects upper GI tract
	Transmural inflammation
	Fistulas, perianal
	Oral manifestation:
	0.5% have oral lesions
	Usually males
	Linear and deep ulcerations

(a)	Symptoms:
•	Chronic diarrheal problems
•	Can affect entire GI, but more intense in ileum and colon and intermittent areas with strictures between
-ulcerations
-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
(b)	Medications
•	Anti-inflammatories:
	Mesalamine (topical anti-inflammatory)
	Corticosteroids-act systemically
•	Metronidazole (antibiotic mechanism?)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

ulcertative colitis

A 
	More continuous especially in the colon
	No transmural inflammation
	No fistulas and not perianal
	Oral manifestation:
	Less common than in CD
	Usually males
	Edematous oral submucosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

colonic polyps

Study These Flashcards
A
  • Hyperplastic polyps- no malignant potential

* Adenoma- precursor to adenocarcinoma

22
Q

invasive colonic adenocarcinoma

Study These Flashcards
A
  • Responsible for 15% of all cancer related deaths in USA

* Dietary features: increased risk with low fiber, high intake carbohydrates/fats

23
Q

cholecysitis

Study These Flashcards
A

bile is common mechanism for excretion of toxins and drugs)
• Acute often caused by gallstones and obstruction. Can become chronic
• Cholestasis causes jaundice

24
Q

liver diseases

Study These Flashcards
A 
1.	Fatty liver
•	Caused by ethanol, obesity and diabetes Mel.
2.	Hepatitis
•	Caused by virus, drug or autoimmune
3.	Biliary disease
4.	Metabolic disease
5.	Vascular
25
liver constituents
* Liver made up of hepatocytes, duct cells and blood vessels * Organization: Portal tracts contain the triad (portal triad) of (i) bile ducts, (ii) portal veins (bring blood from gut with nutrients and recently consumed drugs), and (iii) 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
26
steatosis
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)
27
liver disease details
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 bile due to cholestasis, the person becomes jaundiced (often caused by drugs) 4. Acute more lobular, chronic is more portal with fibrosis and collagen bridges
28
hepatitis general
5. 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 (1-3 months) • 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
29
hep C
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 (not digestive tract) exposure • Caused by RNA virus • Can lead to hepatocarcinoma • No vaccines
30
hep B
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 (fluid in peritoneal cavity) 85% of time in chronic phase with cirrhosis
31
regenerative hepatocyte nodule
fibrosis surrounding nodules
32
autoimmune heapatitis
unusual- found in obese females predominantly • Rapid response to steroids • 80% have extensive fibrosis
33
fatty liver disease
not an inflammatory disease: | • Caused by ETOH, obesity, diabetes mellitus etc.
34
metabolic disease
• Often associated with iron overloads • Wilson’s disease: copper metabolic defect goes to hepatitis then cirrhosis 12. Evaluation of hepatitis severity:
35
evaluation of hepatitis severity
* Grade= degree of inflammation * Stage= degree of fibrosis-this is the most important for prognosis-extreme if it progresses to cirrhosis that includes collagen surrounding hepatic nodules (hepatocytes)
36
hepatocellular carcinoma
* Most deadly cancer | * It has been increasing due to increases in the incidence of Hep B and C
37
GERD
1. Episodes referred to as heartburn and occurs daily in 7% of population 2. Aggravating factors: empty stomach, inclined, increased age, obesity, fatty foods, caffeine/alcohol/smoking, large meals, some drugs 3. Relief: small meals, reduced fat, reduced weight, elevate head of bed, avoid aspirin/NSAIDs 4. 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
38
antacids
neutralize gastric HCl • Types: magnesium salts (can cause diarrhea); bicarbonate (causes gas); calcium carbonate (chalky and constipation); aluminum salts (not very effective)
39
H2 receptor blockers
not effective at the H1 receptors (i.e., not good antihistamines)-reduce gastric secretions by blocking H2 receptors in gut • Types (available both OTC and by Rx):  Cimetidine (Tagamet)  Ranitidine (Zantac)  Famotidine (Pepcid) • Side effects: headaches, diarrhea, drowsiness
40
proton pump inhibitors PPI
available OTC and by Rx • 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 allergies, oral sores/ulcers • Often combined with H2 blockers (1) Products  Omeprazole (Prilosec)  Omeprazole + sodium bicarbonate for fast release  Lansoprazole (Prevocid)  Esomeprazole (Nexium)
41
stomach absorption
water and OH
42
duodenum absorption
Fe, Ca, Mg, Na, Fats, water, proteins, vitamins
43
jejunum absorption
carbohydrates, proteins
44
ileum absorption
bile salts, b12, Cl
45
colon apsorption
water, electrolytes
46
constipations
``` (mobility too slow, too much water absorption) a. Pharmacology: (1) Laxatives: • Bisacodyl  Stimulant of smooth muscles  Fast acting  OTC  Suppository/oral  Cramps • Docusate  Water retention in stools, softens stools  OTC (e.g., Dulcelax) ```
47
diarrhea
a. Loose, watery stools- motility too fast, not enough absorption b. Consequence: dehydration, malnutrition-worse in young and elderly c. Medications: (1) Loperamine- Imodium; mild opioid agonist: if severe, can use strong opioid agonists (2) Bismuth subsalicylate (e.g., Pepto-bismol) (3) Anti-cholinergics such as atropine
48
inflammatory bowel disease
crohns and ulcerative colitis
49
ulcerative colitis
* Similar to Crohn’s disease but limited to colon and more generalized (no strictures) * Medications are similar to Crohns disease
50
HBV dental complications
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 3. Chronic hepatitis (e.g., hepatitis B and C) a. e.g., infection, drugs, autoimmune diseases Management • Accidental exposure:  Carefully wash wound-don’t rub (embeds viruses)  Use antiviral disinfectant (e.g., iodine or chlorine formulations)  Initiate HBV vaccine series • Don’t be judgmental

HDAT (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions