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Big Ol' Patho. > Peptic Ulcer Disease & Hepatitis > Flashcards

Peptic Ulcer Disease & Hepatitis Flashcards

1
Q

What is Peptic Ulcer disease?
Cause?
Where does it occur?

A
  • Ulcerative disorder
  • Helicobactor pylori infection
  • Occurs in stomach (20%) or duodenum (80%)
  • Primarily affects mucosa - Can affect deeper layers (if acid makes contact with them)
  • Remission and exacerbations
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2
Q

Why is PUD most common in the duodenum?

A

stomach not common b/c built with protection; buffering occurs in duodenum normally, but if not intact will result in ulcer

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3
Q

WHy do you see remission and exacerbations in PUD?

A
  • if thinking about food or eating, acid secreted
  • Should be acute problem b/c is completely curable but if individual doesn’t seek medical attention see recurring remission and exacerbations
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4
Q

How is H Pylori able to infect the stomach?

A
  • is transient visitor in the gut, not usually causing problems but can become problematic when produce niches for themselves (areas they colonize within stomach wall)
  • Survive in harsh environment by secreting adhesion proteins that help to attach to epithelial tissue and urease (enzyme the breaks urea to ammonia NH3 & CO2) that creates formation of bicarbonate, which acts as buffer within these niches
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5
Q

General etiology of PUD

- How are the presence of bacteria contributing the the formation of the ulcer?

A
  • Helicobactor pylori infection
  • Exact mechanisms by which these bacteria cause the ulcer is unclear
    o Inflm – when bacterial colonize, cause this
    o Hypergastrinemia – gastrin hormone signals secretion of HCl; bacteria stimulates secretion of gastrin, and thus more HCl (inc HCl secretion)
  • Other factors play a role, but are not etiological…
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6
Q

Risk factors for PUD?

A
  • HCl and biliary acid
  • Steroids and NSAIDs –
  • Chronic gastritis (d/t other bacterial infection or other – damages lining as well)
  • Smoking, alcohol, caffeine (aggravate symptoms once disease is in place)
  • Stress
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7
Q

Effect of steroids + NSAIDs as risk factors for PUD?

A

inc acid secretion and damages mucosal lining

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8
Q

How are HCL and biliary acid both considered etiological and risk factors in PUD?

A

etiology…have to have both the bacterial infection and the acid for the ulcer to form)

is risk factor in that it aggravates the ulcers once they exist

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9
Q

Risk factors AKA?

The opposite to this?

A

Offensive factors

Defensive factors

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10
Q

What defensive factors exist in r/t PUD?

A

o Regulation of acid secretion
o intact perfusion
o mucus
o regeneration of the mucosa (replenishment of cells, not speaking here of healing)

**these prevent the formation of peptic acid disease; normally these are able to outweight the action of the offensive factors…if then overcome by exceessive offensive factors, the disease will develop

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11
Q

Patho of PUD?

A
  • H. pylori infection
  • Inflm → tissue damage
  • Inc gastrin prod (hypergastrinemia?) → inc acid secretion → tissue damage
  • Defenses against gastric acid impeded by risk factors
  • Penetrating ulcer forms
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12
Q

Mnfts of PUD?

A
  • Abdominal pain: burning, cramping – often felt over the chest as well (and therefore cannot be defining feature of diagnosis)
  • Nausea, vomiting (not very common presentation, is not d/t pain but rather GI symptom here)
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13
Q

Complications of PUD?

A
  • Perforation of the ulcer
  • Hemorrhage
  • Gastric or duodenal obstruction – D/t edema, spasm (of muscle) or scar tissue contraction
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14
Q

Complication of perforation of the ulcer?

A

can end up with peritonitis as complication of this

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15
Q

Would you expect to see frank or occult blood in stool of individual with PUD?

A

high up in GI tract, would find OCCULT blood in stool (not frank) because of this location

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16
Q

Explain mechanism by which edema causes obstruction in PUD?

A

in lumen, not tissue edema, from exudate and mucus + air in the bowel….pressure increases in that area of the gut

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17
Q

Is scar tissue considered metaplasia?

A

No, because not considered normal tissue

Metaplasia = replacing normal tissue with normal tissue

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18
Q

Dx of PUD?

A
  • Hx
  • UBT (urea breath test), serology, fecal Ag
  • Barium swallow →
  • Endoscopy
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19
Q

How does a UBT work?

A

o Urea —–→ NH3 + CO2
o Trying to track the C molecule in urea –> person given solution with labeled carbon urea solution, which goes into stomach, if H. Pylori is present it will be producing urea -→ it will be converted to CO2 and ammonia, CO2 will also be labeled….this CO2 will be taken into blood and exhaled (person asked to exhale 2 hours after ingestion and exhales into 2 bags…then this air is checked for marked C in CO2.
o If person doesn’t have H. Pylori in gut and given urea solution, will only excrete
o ONLY time you’ll have urea is when H. Pylori is present! And urea is required for radioactive C to be seen.

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20
Q

What is serology?

A

looking for antibodies in the blood

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21
Q

How would you detect H. Pylori in the stool?

A

antigens (proteins) that are related to H. Pylori

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22
Q

Tx of PUD?

A

• Antacids? – will relieve pain temporarily by neutralizing acid
• Triple regimen: (to eradicate the bacteria and treat ulcers at the same time) – 2 possibilities
o H2RA (H2 receptor antagonist to block gastric secretion) + 2 Abx
o PPI (blocks H+ secretion) + 2 Abx

• Sx for complications (sometimes)

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23
Q

Why are H2RAs used in PUD?

Examples of H2RA?

A

o Histamine receptors blocked by H2RA b/c histamines facilitate acid secretion (histamine can’t bind so acid is not secreted)
o H2RA examples = zantac + tagamet

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24
Q

Action of PPIs?

A

block secretion/pumping of H+ ions

need more detail on this?

25
Q

Examples of PPI’s

A

losec, pariet, nexium

26
Q

Typical 3X regimen for PUD?

Typical treatment length?

A

losec, amoxil + flagyl = 1st line tx

→ losec carried on beyond 7-10day ABx regimen b/c ulcers still there and going to continue to be aggravated by acids (several weeks to months)

27
Q

Etiology of Hepatitis

A

• Can be one of several factors
• Microbes – bacteria, viruses, fungi, parasites can all cause hepatitis
o Primarily viruses (most common) = viral hepatitis
• Drugs (chemical, recreational, etc…hepatotoxic drugs cause inflm here) = toxic hepatitis
• Autoimmunity = autoimmune hepatitis

28
Q

Kinds of viral hepatitis?

A

Hepatitis A, B, C, D, E (caused by 5 separate viruses)
• Also have Hep F and G – these currently not considered to be threats
• Epstein Barr Virus and Cytomegalovirus both can cause hep too

29
Q

Are the types of viral hep similar or different? How so?

A 
•	Similar mnfts
•	Differences: 
 1) Virus and transmission
 2) Incubation period
 3) Severity of the disease (mnfts similar but severity differs based on virus)
30
Q

Does damage to the liver easily cause a loss in fx?

A

• Liver has very large functional reserve, and therefore must damage much of it before fx is entirely impaired

31
Q

Refer to Day pg 1214, Table 40-4 for comparison of hep types

A

++

32
Q

Hep A

A
  • Largely transmitted via oral-fecal route
  • Mild
  • Acute form (does not have chronic state)
  • Pt recovers on own, not typically requiring tx
  • “Carrier state” → pt carrying microbe but not displaying symtoms; are still infective and can pass disease along
  • add detail from chart
33
Q

Hep B

A
  • More severe than A
  • 10% - 15% are chronic
  • Can have carrier state
  • Can transmit through saliva
  • add detail from chart
34
Q

Hep C

A
  • 80% are chronic (means this is worst version of the disease)
  • Remission and exacerbations
  • Often leads to cirrhosis (is complication)
  • Transmission through blood and blood products, semen
  • add detail from chart
35
Q

Patho of Viral hepatitis?

A

• 2 mechanisms in all types
1) Infection stimulates IR → inflm & necrosis
2) Viral injury (explain) → necrosis – viruses enter cells and lyse them
• Hepatocyte necrosis
–> Dec liver function (hepatocytes specifically targeted by virus)
–> Vascularture & ducts damaged - Inflm damages vasculature and ducts (bile and otherwise) along with other tissues

• Healing in ~4 months (most self-limiting)

36
Q

• *Review structure of bile ducts and liver structure!

A

++

37
Q

3 phases of viral hep manifestations

A

1) Prodromal
2) Clinical aka Icterus
3) Recovery phase

38
Q

Prodromal Phase of viral hep?

A

characterized by lack of energy in body

a. Lethargy, myalgia
b. Fever, abdm pain
c. Anorexia, nausea, vomiting (GI symptoms)

39
Q

Why is the prodromal phase characterized by a lack of energy?

A

liver fxs to process things ingested to make into product that can be utilized for energy

40
Q

Why does viral hep present with fever and abdm pain?

A
  • manifestations of infection and inflm

- abdm pain d/t swelling of capsule (which capsule??), which presents with pain

41
Q

When does the clinical phase of viral hep symptoms begin?

A

5-10 days after prodromal

42
Q

Symptoms of clinical phase of viral hep?

A
  • Manifestations worsen
  • Jaundice
  • Pruritus
  • Enlarged and tender liver
43
Q

Why does jaundice result in viral hepatitis?

A

++Look up the process of RBC breakdown!!

common mnft of liver disease; accumulation of bilirubin in the circulation, deposited in ALL tissues (seen in skin and sclera because there are superficial)

i. Globin = protein – broken down into amino acids and recycled
ii. Heme – one intermediate is bilirubin → under physiologic conditions, liver processes this further and it’s excreted through the gut
iii. If liver unable to fx properly can’t process all of bilirubin

44
Q

Why is pruritus seen in hep?

A

d/t deposit of bile salts in the integument (liver involved in synthesis of bile)

45
Q

Enlarged liver aka?

Why does this manifest in viral hep?

A

Hepatomegaly

- enlarged liver d/t swelling

46
Q

What occurs during the recovery phase of symptoms of viral hepatitis?

A

a. Acute mnfts subside (~3wk)

b. Full recovery within ~16 wk

47
Q

How is recovery from viral hepatitis measured?

A

seen through ALT and AST returning to normal (lower) levels) – enzymes will be seen to be elevated when damage occurs b/c when cells in liver die, they release the content…liver is heavily involved in metabloism so these enzymes live in the hepatocytes

48
Q

Tx of viral hep?

A

• Rest in order to decrease energy requirement of in the individual
• Modify diet (smaller meals, those rich in calories and low in fat)
• No alcohol or other hepatotoxic drugs
• Relief from pruritus
• Not intervening aggressively – no antivirals needed. Treated like cold of flu.
• Post exposure prophylaxis: address personal hygiene (healing process will advance), given gamma-globulins (),
o Hep A and B vaccines
o Hep C: hygiene, gamma globulins + anti-virals

49
Q

Why is rest part of tx of viral hep?

A

(which in turn decreases workload of the liver as it is so heavily involved in metabolism)

50
Q

Why modify diet for viral hep?

A

– this decreases workload of the liver b/c liver responsible for making bile, which is required for emulsifying fats

51
Q

Autoimmune hep:

  • Acute or chonic?
  • Etiology
  • 2 types?
A
  • Severe, chronic form
  • Idiopathic?? (sometimes)
  • Complex trait etiology
  • HLA genes on chromosome 6
  • Enviro (viruses and chemical agents) are trigger
  • 2 Types: I and II
52
Q

Which type of autoimmune hep is more common?

A

Type 1

53
Q

Which demographic is most affected by autoimmune hep?

What mechanism of injury?

A

• 30% in women

ANAs & anti-smooth muscle Abs (ANA = anti-nuclear antibodies) are those that inflect damage here; walls of smooth muscle in vessels and ducts targeted here

54
Q

What demographic is most affected by Type 2 autoimmune hep?

WHat is targeted here?

A
  • 2-14yrs – young kids affected

* Abs against cytosol and microsomes

55
Q

Cytosol?

Cytoplasm?

Microsomes?

A

o Cytosol = fluid and microstructure component of the cytoplasm
o Cytoplasm = everything between nuclear and cellular membranes
o Microsomes = vesicles that budd off cysternal(?) ends of the endoplasmic reticulum for transport

56
Q

Manifestations of autoimmune hep?

A

Range from asympt to mnfts of liver failure

57
Q

Dx of autoimmune hep?

A
  • Primary goal: want to exclude viral hepatitis & other liver disease
  • Specific test done to confirm diagnosis: Inc in gamma globulins
58
Q

Treatment of autoimmune hep?

A
  • Immunosuppressant drugs: want to suppress Ab production

* Liver transplant? (for those nonresponsive to drugs and have pressing problems)

Big Ol' Patho. (17 decks)

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