post midterm: 1 Flashcards by ce huff

How is the liver involved in bile production?

RBC breakdown > Bile > fat digestion

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What kind of proteins does the liver make?

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

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How does the liver play a role in immune system?

makes proteins for immune system

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what role does liver play in storage?

glycogen, vit B12 and D

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

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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Give 3 examples of more “indirect” liver tests?

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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what are the 2 main categories of hepatitis?

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

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

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

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

True

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

Stomach (gastric) ulcer: 40 – 70

Duodenal ulcer: 25 – 55

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

true

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

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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2 most common causes of peptic ulcer disease?

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

Gram negative pathogen

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

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

False, dec.

-developing nations have high inc.

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

false

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

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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how do you tx h pylori?

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

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

Ulceration
Hemorrhage
Perforation
Death

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

Older age
History of ulcers
Corticosteroid use
Higher NSAID dose

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

How do NSAIDs induce ulcers?

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

what is only cox 2 selective drug on market?

celebrex/celecoxib

*do not use with heart problems

cox 1 vs cox 2?

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

Cox – 2:
Mediates inflammation

2 main tx for antacid therapy?

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!

what is the diff bw ulcerative colitis vs Crohn's

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

what is underlying cause of IBD?

* 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

do you see malabsorption of nutrients with ulcerative colitis?

no, colon just resorbs water

is ulc colitis usually more acute or chronic?

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

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

true but rare

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

true

what kind of lab findings do you expect with IBD?

* Anemia * Leukocyosis (active disease, abscess) * Elevated sed rate/CRP * Hypoalbuminemia (malnutrition)

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

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

what are some hepatitic complications of IBD?

- Fatty liver, chronic active hepatitis, cirrhosis - Sclerosing cholangitis-uncommon, inflamm of bile ducts -Gallstones-increased risk Crohn’s disease

what are some ocular manifestations of IBD?

``` **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)

what's one possible tx for IBD?

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

what is celiac disease?

- Intolerance to gluten | - Small bowel inflammation

what might be some clinical presenting signs of celiac?

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

How to dx Celiac?

* Antibody tests to screen - Tissue transglutaminase IgA * small bowel biopsy to confirm diagnosis

celiac disease is associated with what other conditions?

autoimmune: type 1 DM, autoimm thyroid - genetic - seen in Down and turner ``` *Elevated liver function tests Dermatologic manifestations (Dermatitis herpetiformis) Arthritis ```

celiac most common in what pop?

women and younger

what is underlying cause of IBS?

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

what is normal range of BMs?

3 BM/day to 3 BM/week

what are some IBS symptoms?

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

possible tx for IBS?

Antidepressants (including low dose tricyclics) | Antispasmotics