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Clinical Lab > Gastroenterology Labs > Flashcards

Gastroenterology Labs Flashcards

1
Q

Why do we do a GI tract work up

A

Why do we do a GI tract work up
-direct visualization (endoscopy and colonoscopy) can be expensive and invasive
-dyspepsia
-ulcer disease- MC cause h. pylori
-celiac disease
-GI tract bleeding
-colorectal cancer

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2
Q

dyspepsia causes

A

Causes:
- GERD
- peptic ulcer ds
-ulcer disease
- gastritis
-H. pylori

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3
Q

H. pylori diagnostic lab tests

A

Biopsy during endoscopy - MOST ACCURATE DX
-Histology
-Urease enzyme - H. pylori produces this
-PCR
- grow culture

Breath test: Non-invasive
-Urea labeled with radioactive carbon
-If urease is present the urea will be split into ammonia and radioactive carbon
-Test can also be used to prove eradication

Stool test: H. pylori antigens

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4
Q

celiac disease

A

Descrption:
-immune mediated disorder
-triggered by gluten

Who to test:
- pts with malabsorption
- first degree relative
- elevated aminotransferase level (AST/ALT)
-type 1 DM with GI symptoms

Tests:
-IgA tTG antibodies test with total IgA > Sen and Spec of 98% -> if you have a very high suspicion you can still bx if neg
-Biopsy for confirmation (gold standard)
-if neg workup: consider non-celiac gluten sensitivity

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5
Q

approach to celiac disease disorder

A

ORDER IgA tTG with total IgA: dont need to know specifics
-basically if neg and still high sus -> bx
-if positive-> still bx
-IgA tTG + and total IgA normal -> small bowel bx
-IgA tTG and total IgA normal -> unlikely dx -> if suspect celiac disease remains do a bx
-IgA deficiency -> order IgG deaminated gliadin peptide -> if + -> small bowel bx
-> if neg and suspect celiac disease remains -> small bowel bx

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6
Q

upper GI bleeding causes

A

Causes:
-CANCER
-Esophageal varices- caput medusa, ascites
-Peptic ulcer disease- NSAIDs use
-GERD
-Gastritis
-Duodenitis

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7
Q

lower GI bleeding causes

A

Causes:
-CANCER (colorectal)
-Hemorrhoids
-Anal fissures
-Inflammatory bowel disease- know diff between crohns and ulcerative colitis
-Diverticulitis

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8
Q

Ulcerative Colitis vs Crohns

A

UC:
- colon and rectum
- only the innermost lining of the colon -> bloody
- continuous inflammation
- bloody diarrhea

Crohns:
- mouth to anus (mostly small bowel)
- skip lesions/patchy inflammation
- transmural

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9
Q

GI bleed work up

A

1) endoscopy or colonoscopy for biopsy
2) CBC- check for anemia
3) fecal occult blood test

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10
Q

colorectal cancer (2nd leading cause of death) tests

A

Colonoscopy- every 10 years

Fecal immunochemical test (FIT) with DNA:
- sensitivity 79% (20-30% missed with a false negative!)
- test annually

Fecal occult blood test
- only 20-50% identified with colon cancer

CT colonography
flexible sigmoidoscopy

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11
Q

liver function

A

Conjunction- bilirubin
Metabolism- thyroid and steroid hormones
Storage- amino acids, carbohydrates, lipids, vitamins, minerals
Synthesis:
- protein (proteins LFTs, albumin)
- coagulation factors (2,5,7,9,10)
- transport proteins
- bile acids from cholesterol
- PT/INR elevated with liver disease due to decreased coagulation factors

Excretory
Detoxification : drugs and toxins

“ChatGPT Makes Studying Seriously Extremely Difficult”
- Conjunction
- Metabolism
- Storage
- Synthesis
- Excretory
- Detoxification

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12
Q

direct vs indirect bilirubin

A

Indirect (unconjugated = not water soluble)
- bilirubin in the blood ; NOT URINE
- elevated in hemolytic anemia, genetic disorders,

Direct (conjugated)
- hepatocytes done the work and packaged; problem is after liver synthesis
- can be excreted: dark urine
- elevated in liver disease, obstructions in liver, gall bladder, pancreatitis
-pancreatic cancer- extrahepatic blockage

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13
Q

liver: excretory function

A

-bilirubin comes from broken down hemolysis of RBCs (90-120 days)
-recycle it in liver
-unconjugated -> conjugated bilirubin -> excreted into the bile
-store in galbladder
-bile: aid in digestion of lipids

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14
Q

AST: aspartate animotransferase when is it decreased and increased

A
  • shows signs of hepatocellular damage: AST/ALT elevated when liver is “screaming”

Decreased:
- liver congestion
- high cholesterol

Increased:
- liver ds
- alcohol abuse
- MI: AST
- kidney infection/disease

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15
Q

ALT: alanine aminotransferase

A
  • indicates hepatocellular damage
  • more specific for liver function
  • elevated: liver ds
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16
Q

AST : ALT ratio

A

ETOH induced liver disease: AST> ALT
- AST:ALT value greater than 2
- SLAST: alcohol liver issue

… when specific to liver ALT is higher but with alcohol AST is higher

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17
Q

liver enzymes: lactate dehydrogenase (LDH) when is it elevated

A

elevated:
- cardiac
- RBC hemolysis
- renal disease

-could be many things
-non specific

18
Q

Hepatic shock

A

Hepatic shock: acute liver dysfunction from lack of blood flow
- ill patients
-more common in pts with hemodynamic disorders
-preventable with early treatment of underlying disease.
-There is no definite treatment -> manage conservatively
-Hepatic shock in patients can increase the mortality rate

19
Q

biliary tract: alkaline phosphatase (ALP)- when is it increased

A

Liver diseases:
-Cirrhosis
-Hepatitis
-Biliary obstruction

Bone Diseases:
-Bone Tumors
-Osteoporosis
-Rickets
-Padget’s disease- lytic lesions on all of bones
-Hyperparathyroidism
-Malignancies (leukemias & Lymphomas)

ALP:
-found in highest concentration in liver, bile ducts, and bone

20
Q

ALK Phos - when is it decreased

A

DECREASED:
-Wilson’s Disease
-Hyperphosphatasia
-Aplastic Anemia
-Pernicious Anemia
-Cretinism
-Chronic myelogenous leukemia (CML)

WHAP - CC

ALP: indicates cholestasis, inflitrative ds, billiary obstruction

21
Q

mc cancers that metastases to bone

A

-breast
-prostate

22
Q

biliary tract: gamma-glutamltransferase (GGT) when is it increased vs decreased

A

“LLL PP B Elevate GGT -> consecutive GGt think the 3L, 2 P, B pattern”
-lung cancer
-liver ds
-lupus (Systemic lupus erythematosus)
-pancreatitis
-prostate cancer
-breast cancer

Decreased:
-hyperthyroidism
-hypothalamic dysfunction

23
Q

Indicators of hepatocellular damage - which LFTs?

A

AST
ALT
LDH - non specific

24
Q

Cholestasis or billary obstruction - which LFTs are elevated

A

ALP
GGT
Bilirubin
Bile acids
5’- nucleotidase

25
Q

____ is used along with _____ to determine disease source

A

GGT is used along with Alk phos to determine disease source

GGT: indicates cholestasis or BILLIARY OBSTRUCTION
- Used along with elevated Alk Phos (ALP) to determine the disease source.
- If both are elevated = indicative of hepatobiliary disease
- if ALP is elevated and GGT is normal -> NOT billiary issue

26
Q

total bilirubin causes

A

Hepatic causes:
-hepatitis
-cirrhosis
-alcoholic liver disease

Can occur anywhere in pathway of metabolism

27
Q

indirect bilirubin causes

A

Pre-hepatic causes:
-hemolysis
-Newborns
-Malaria
-Sickle cell anemia
-Thalassemia
-Hemolytic uremic syndrome

Indirect = unconjugated
- issues with increase in RBC hemolysis OR
- issue with reduced liver reuptake or processing

28
Q

direct bilirubin causes

A

Post-hepatic causes:
-gallstones
-bile duct strictures
-biliary atresia
-pancreatic cancer
—-
direct = conjugated
- issues with excretion of conjugated bilirubin into the bile
- either: biliary obstruction OR
- hepatocellular dysfunction

29
Q

Albumin - what causes it to be low?

A

LOW albumin causes: synthetic liver dysfunction
-Liver diseases
-Malnutrition
-Kidney diseases
-Burn injury(dont need to know)
-if albumin is low you have more fluid shifts -> swelling

Bro ABU LMK - ALBUMIN: “think abu from aladdin bc hes chill”
-liver ds
- kidney ds
- malnutrition
- burn

30
Q

Synthetic liver functions: what are the main products

A
  • albumin
  • transthyretin/prealbumin: signs of malnutirition
  • coagulation factors: I, II, V, VII, X
31
Q

HBsAg negative, anti-HBc negative, anti-HBs negative

A

HBsAg, anti-HBc, anti-HBs negative
-susceptible

32
Q

HBsAg neg, anti-HBc pos, anti-HBs pos

A

HBsAg neg, anti-HBc pos, anti-HBs pos
resolved HBV infection

33
Q

HBsAg neg, anti-HBc neg, anti-HBs pos

A

HBsAg neg, anti-HBc neg, anti-HBs pos
vaccinated

34
Q

HBsAg pos, anti-HBc pos, anti-HBs neg

A

HBsAg pos, anti-HBc pos, anti-HBs neg
-active HBV infection (usually chronic)
-if anti-HBc IgM present, may represent acute infection

35
Q

HBsAg neg, HBcAB pos, HBsAb neg

A

HBsAg neg, HBcAB pos, HBsAb neg
-distant resolved infection (MC)
-recovering from acute infection
-false pos
-occult hepatitis B

HBcAB is the same as anti-HBc

36
Q

tests used in dx of hepatitis C

A

tests used in dx of hepatitis C
-anti-HCV EIA neg / HCV RNA neg- not infected
-anti-HCV EIA pos / HCV RNA neg- resolved HCV infection
-anti-HCV EIA neg / HCV RNA pos- early acute HCV infection or chronic HCV infection in immune compromised person
-anti-HCV EIA pos / HCV RNA pos- acute or chronic HCV infection

37
Q

acute pancreatitis description + sx

A

Autodigestion by its own enzymes

Sx:
-epigastric pain
-nausea/vomiting
- back pain
-severe: fever, hypotension, tachycardia

38
Q

acute pancreatitis causes + dx

A

Causes:
- biliary tract obstruction
- alcohol abuse
- idiopathic

Dx: LIPASE or amylase elevation greater than 3x normal
-LIPASE has 95% sensitivity and specificity (more organ specific)
-take dx together with clinical presentation

39
Q

chronic pancreatitis causes and clinical presentation

A

Causes:
-multiple acute pancreatitis events
- alcohol consumption
- malnutrition
- cystic fibrosis in children

Clinical presention:
-impaired glucose tolerance testing or DM
- abdominal pain
- weight loss
- pancreatitic calcifications
-steatorrhea

40
Q

chronic pancreatitis DX and complications

A

DX:
-endoscopic US
-endoscopic retrograde cholangiopancreatography (ERCP): visualize ducts and identify strictures/stones -> RISK of causing ACUTE PANCREATITIS EVENT
- amylase and lipase levels -> do not tell the story ** DO EUS or ERCP

Complication:
-cellular destruction leading to scar tissue then causing pancreatic DUCT OBSTRUCTION
-can destroy endocrine function- cause DIABETES!

41
Q

exocrine pancreatic neoplasms

A

CA 19-9 tumor marker for pancreatic cancer:
-70-90% sensitivity
-68-92% specificity
-dependent on tumor size
-elevated in other GI cancers

42
Q

tumor marker for pancreatic cancer

A

CA 19-9

Clinical Lab (17 decks)

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