post midterm: 1 Flashcards

1
Q

How is the liver involved in bile production?

A

RBC breakdown > Bile > fat digestion

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2
Q

What kind of proteins does the liver make?

A
  • transport: ex TBG transferrin, albumin
  • coag factors
  • makes proteins that help with fluid oncotic pressure
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3
Q

How does the liver play a role in immune system?

A

makes proteins for immune system

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4
Q

what role does liver play in storage?

A

glycogen, vit B12 and D

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5
Q

what is often the best Proteins made by liver are often the best measure of liver function?

A

Proteins made by liver are often the best measure of liver function

  • Serum proteins: Albumin, globulins, total protein
  • Coagulation protein function: Prothrombin time (protime or PT)
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6
Q

Give 3 examples of more “indirect” liver tests?

A

1) Transaminases “liver function tests” (LFT’s)
Monitor liver injury; exist in other cells as well (eg muscle)
-AST / SGOT
-ALT / SGPT
-GTT – most specific to liver
2) Bilirubin: colors bile, causes jaundice when elevated
-Increases with hemolysis, biliary obstruction, liver dysfunction
3) Alkaline phosphatase:
Increase with disease of bile ducts (w/ ↑ bilirubin), bone disorders

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7
Q

what are the 2 main categories of hepatitis?

A

1) biliary: Blockage of bile ducts e.g. gallstone

2) hepatocellular: Celluar injury from drug, toxin, virus, etc

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8
Q

how would biliary hepatitis show up on lab tests? hepatocellular hep?

A

biliary:
- Initial ↑ in bilirubin, alkaline phosphatase
- Later ↑ in transaminases (AST, ALT)
- Secondary liver injury

hepatocellular:
-Initial ↑ in transaminases (AST, ALT), bilirubin (causes jaundice)
May recover
Later ↑ in PT; ↓ protein levels (albumin, globulins, total serum protein)
Liver synthetic defects

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9
Q

T/F: peptic ulcer disease has a high rate of recurrence

A

True

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10
Q

stomach vs duodenal ulcers are more common in what age ranges?

A

Stomach (gastric) ulcer: 40 – 70

Duodenal ulcer: 25 – 55

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11
Q

T/F: peptic ulcer disease can be aggravated by meals or lack of meals

A

true

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12
Q

what kind of bleeding do you see with acute? subacute? chronic?

A

Acute: coffee ground emesis, Vomiting of gastric blood !EMERGENCY!
Acute/subacute: melena, Passing digested red blood in stool / black, tarry stool
Chronic: iron deficiency anemia

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13
Q

2 most common causes of peptic ulcer disease?

A

Helicobacter pylori infection
NSAID use

other:
Stress ulcer (acute/severe illness)
Gastrinoma (MEN I)
Antral G-cell hyperfunction
Tumors
Oral corticosteroid use**
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14
Q

H pylori is what kind of pathogen and able to evade host defenses how?

A

Gram negative pathogen

1) Secretes Urease (permits survival in acid stomach)
2) sticks to epithelial cells to evade immune response

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15
Q

T/F: peptic ulcer disease is inc in US?

A

False, dec.

-developing nations have high inc.

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16
Q

T/F: H pylori is always harmful and should be eliminated?

A

false

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17
Q

what are 3 options to test for/dx peptic ulcer disease

A

1) Gastric/duodenal biopsy (endoscopy)
2) Breath test (C-Urea)

3) Serology (ELISA antibody test)
* *however, the ab is there whether or not infection is present!

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18
Q

how do you tx h pylori?

A
Triple therapy:
-Anti-secretory therapy (proton-pump-inhibitor)
-Two (at least) antibiotics
Amoxicillin
Clarithromycin (Biaxin)
Metronidazole (Flagyl)
19
Q

what are some complications of NSAIDs that can result in peptic ulcer disease

A

Ulceration
Hemorrhage
Perforation
Death

20
Q

what are some possible risk factors for NSAID-induced ulcers (gastric, duodenal)?

A

Older age
History of ulcers
Corticosteroid use
Higher NSAID dose

Possible risks:
H. pylori co-infection, tobacco use, alcohol use
*MAYBE ADDITIVE?

21
Q

How do NSAIDs induce ulcers?

A

Diminished prostaglandin synthesis results in decreased epithelial mucus and bicarbonate, lower mucosal resistance to injury

22
Q

what is only cox 2 selective drug on market?

A

celebrex/celecoxib

*do not use with heart problems

23
Q

cox 1 vs cox 2?

A
COX – 1: “Housekeeping”
Constitutive (always on)
Protects gastrointestinal mucosa
Enables platelet aggregation
Manages renal blood flow

Cox – 2:
Mediates inflammation

24
Q

2 main tx for antacid therapy?

A

1) proton pump inhibitors: H+ / K+ pump exchanges K and H (acid) at the gastric lumen
- pull in K, pump out H

2) H2 blockers: : targets histamine-mediated acid release
!however, there are multiple stimuli for gastric acid secretion ex: Histamine, gastrin, others!

25
Q

what is the diff bw ulcerative colitis vs Crohn’s

A

both are marked by inflamm, but in ulcerative colitis, it is limited to colon (Crohn’s could affect any part of GI tract)
-also, ulcerative colitis affects mucosa to submucose whereas crohn’s can affect mucosa through serosa and UC=colectomy is curative whereas can recur after surgery for Crohn’s

26
Q

what is underlying cause of IBD?

A
  • Inappropriate and ongoing activation of mucosal immune system
  • Association with abnormal immunological response to normal bacteria and/or pathogens

-Infiltration of lamina propria with immune cells (lymphocytes, macrophages)
Activated T-cells produce cytokines resulting in chemotaxis, immune response and tissue damage

-Genetic susceptibility

27
Q

do you see malabsorption of nutrients with ulcerative colitis?

A

no, colon just resorbs water

28
Q

is ulc colitis usually more acute or chronic?

A

Onset may be fulminant or indolent-basically there is a lot of variation, could be acute or chronic
Long term:
Exacerbations and remissions or chronic

29
Q

T/F: possible for Crohn’s to affect proximal GI tract like mouth?

A

true but rare

30
Q

T/F; can get Crohn’s that only affects colon

A

true

31
Q

what kind of lab findings do you expect with IBD?

A
  • Anemia
  • Leukocyosis (active disease, abscess)
  • Elevated sed rate/CRP
  • Hypoalbuminemia (malnutrition)
32
Q

Pts with IBD have a 30X higher risk for what other disease?

A

Ankylosing spondylitis:
however, AS activity unrelated to bowel Sx; no response to bowel Tx

**can also get colitis-associated arthritis involving larger joints:
Migratory and Disease activity follows bowel Sx and Tx

33
Q

what are some hepatitic complications of IBD?

A
  • Fatty liver, chronic active hepatitis, cirrhosis
  • Sclerosing cholangitis-uncommon, inflamm of bile ducts

-Gallstones-increased risk Crohn’s disease

34
Q

what are some ocular manifestations of IBD?

A
**Uveitis:
Often bilateral
Chronic
Females > males
***Patients with IBD + uveitis=75% have arthritis

**Episcleritis and scleritis: usually Crohn’s disease

**Night blindness=Vitamin A malabsorption (Crohn’s)

35
Q

what’s one possible tx for IBD?

A

Treatment: Anti-inflammatory therapy
-Corticosteroids (glucocorticoid)
Used acutely to induce remission, usually not maintenance

  • can use immune suppression drugs
  • can use TNF-blocking therapy or monoclonal ab
36
Q

what is celiac disease?

A
  • Intolerance to gluten

- Small bowel inflammation

37
Q

what might be some clinical presenting signs of celiac?

A
  • short stature
  • Bowel symptoms may be ignored or misdiagnosed (e.g. IBS)
  • mild but chronic malabsorption
    e. g. iron deficiency anemia
38
Q

How to dx Celiac?

A
  • Antibody tests to screen
  • Tissue transglutaminase IgA
  • small bowel biopsy to confirm diagnosis
39
Q

celiac disease is associated with what other conditions?

A

autoimmune: type 1 DM, autoimm thyroid
- genetic
- seen in Down and turner

*Elevated liver function tests
Dermatologic manifestations (Dermatitis herpetiformis)
Arthritis
40
Q

celiac most common in what pop?

A

women and younger

41
Q

what is underlying cause of IBS?

A

basically just know pathophysiology not well understood

  • Changes (? abnormal) gut motility
  • Increased gut sensitivity to stimuli / lower pain threshold
  • Possible alteration in immune function
  • Entity of post-infectious IBS
  • Abnormal visceral nervous function
42
Q

what is normal range of BMs?

A

3 BM/day to 3 BM/week

43
Q

what are some IBS symptoms?

A
  • Chronic abdominal pain
  • Irregular or altered bowel habits
  • Bloating and increased gas
  • Upper GI symptoms: heartburn, dyspepsia etc
44
Q

possible tx for IBS?

A

Antidepressants (including low dose tricyclics)

Antispasmotics