Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

LAMP > GI Disease > Flashcards

GI Disease Flashcards

(72 cards)

Start Studying
1
Q

How do you diagnose acute pancreatitis?

A

For diagnosis of acute pancreatitis, need 2 of 3:
– Abdominal pain characteristic of disease
– Amylase and/or lipase elevated at least 3x upper limit of normal (ULN)
– Characteristic imaging findings

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

Why is lipase (compared to amylase) often preferred in diagnosing pancreatitis?

A

• Lipase is preferred: more sensitive and
more specific for acute pancreatitis
• Neither enzyme has accepted prognostic value
• Lipase remains elevated longer than amylase
• Current recommendations are for lipase measurement alone.

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

How does sensitivity/specifity compare for diagnosis of pancreatitis w/ lipase and amylase?

A

Lipase: 90/93
Amylase: 78/92

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

What else besides acute pancreatitis can cause elevations in pancreatic enzymes?

A
  • Macroamylasemia/macrolipasemia
  • Renal failure
  • Acute appendicitis
  • Cholecystitis
  • Intestinal ischemia or obstruction
  • Peptic ulcer disease
  • Gynecological disease
  • Diabetes (higher lipase, so diagnostic cutoff is >3-5 ULN, but no consensus on actual value)
  • Parotid/salivary gland disease (amylase only)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are causes of acute pancreatitis?

A
  • Gallstones and alcohol are most common
  • Hypercalcemia, hypertriglyceridemia
  • Post-ERCP, trauma/injury
  • Genetic pancreatitis(e.g.,CFmutations)
  • Drugs (e.g., azathioprine, sulfonamides, NSAIDs, steroid, tetracycline)
  • Viral infections (e.g., mumps, rubella, EBV, CMV, hepatitis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

bruising around umbiliccus

A

cullens

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

bruising around spleen/flank

A

greys

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

What are first tier LFTs?

A 
• Transaminases
– ALT, AST
• Bilirubin
• Alkaline phosphatase, γ-glutamyl transferase (GGT)
• Albumin
• Prothrombin time/INR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are second tier LFTs?

A 
• Hepatitis viral serologies and molecular
tests
• Fe, ferritin, Cu
• Alpha-1 antitrypsin
• Autoantibody tests
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the three classifiaitons of liver disease?

A
  1. hepatocellular injury/necrosis (damage/death to hepatocytes)
    ALT,AST > AP
  2. Cholestatic (obstruction of bile outflow from liver)
    AP > ALT or AST
  3. Infiltrative (neoplasm, amyloid)
    elevated AP w/ normal ALT, AST or AP > ALT, AST
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are transaminases and how do they differ?

A

• ALanine aminotransferase (ALT) (SGPT)
• ASpartate aminotransferase (AST) (SGOT)
• These “leak” from damaged hepatocytes
• ALT is more SPECIFIC for LIVER disease
– AST is found in MUSCLE and RED
– With extensive muscle breakdown, both ALT and AST rise
• ALT has a LONGER half-life

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

Where does AP come from?

A 
• Present on hepatocyte membrane
bordering the bile canaliculi
• Isoenzymes: liver, bone, placenta
– Elevation is not a specific marker for liver disease
• Bone, GI, kidney
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

When would you order GGT?

A

to confirm a liver source

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

What are reference intervals for AST/ALT?

A

• AST 0-45 U/L, female; 0-55 U/L, male
– Children higher to age 2
• ALT 0-50 U/L, female; 0-70 U/L, male

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

What are reference intervals for AP?

A

• Alkaline phosphatase 40-150 U/L

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

What are markers of liver function?

A

• Albumin
– Half-life of 21 days, but can fall more rapidly with severe inflammation
– Can fall with renal or GI losses, or burns
• Prothrombin time (PT, INR)

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

What causes an acute rise in transaminases?

A 
HepA/B
Drug induced hepatitis
Alcoholic
Ischemic (shock liver)
Acute duct obstruction
Wilson disease
Autoimmune hepatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Diagnostic test: Hep A

A

IgM anti-HAV

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

Diagnostic test: Hep B

A

HBsAg, IgM angti-HBc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Diagnostic test: drug induced hepatitis

A

improvement on stopping

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Diagnostic test: alcoholic

A

liver bx
improvement iwth abstinence
AST:ALT >2
AST <400

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Diagnostic test: shock liver

A

improvement iwth restoration of circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Diagnostic test: acute duct obstruction

A

cholangiography

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Diagnostic test: wilson disease

A

ceruloplasmin
urine copper
slit lamp
liver Cu measurement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Diagnostic test: autoimmune hepatitis
anti-smooth muscle (f actin) | anti-LKM type 1
26
How high can ALTL be with acute hepatitis?
thousands
27
If ALT over 5000 consider....
acetaminophen hepatic ischemia unusual viruses like HSV
28
stones can cause transient elevations to...
1000s
29
alcoholic hepatitis cuases modest elevations to...
less than 400 (bili is often elevated more)
30
What are common cuases of chronic hepatitis?
HepC/B (anti-HCV, RNA, HBsAg) NASH (US, liver bx) Alscoholic liver disease (liver bx)
31
How do you define chronic hepatitis?
>3 mos transaminases usually 205 fold elevated pt can be asymptomatic
32
what characterizes cholestatic disrorders?
rise in AP and bili
33
blockage of microscopic ducts
primary biliary cholangitis
34
blockage of large ducts
obstruction ca of head of pancreeas stones
35
blockage of large and small dcuts
primary sclerosing cholangitis
36
What are common causes of cholestasis?
``` PBC PSC Large bile duct obstruction drug induced infiltrative/malignancy inflammation ```
37
Middle-aged women | Anti-mitochondrial antibody
Primary biliary cholangitis
38
Usually men 20-50; ulcerative colitis | Cholangiography
primary sclerosing cholangitis
39
Jaundice, pain | Ultrasound
large bile duct obstruction (stone, tumor)
40
Malignancy, sarcoid, amyloid | Ultrasound, CT
drug induced
41
adult bili ref range
.2 - 1.3
42
first 2 wks of life bili
0-11.7
43
bilirubinuria is = ...
lier disease
44
>85% insoluble, carried by albumin elevation means hemolysis
unconjugated/indirect
45
<15% soluble elevations mean liver disease (parenchyma/biliary tract)
conjugated/direct
46
When is jaundice visible?
bili > 2.5 mg/dL
47
What causes unconjugated hyperbilirubinemia?
• Hemolysis, resorption of a large hematoma, ineffective erythropoiesis (e.g., B12 deficiency) • Neonatal physiologic hyperbilirubinemia • Gilbert syndrome
48
What is Gilbert syndrome?
``` – Benign defect in UDPGT activity – 3-7% of the population, M:F 2-7:1 – Manifests in stress conditions, including fasting – Bilirubin < 6.0 mg/dL – LFTs normal, Hb normal – No treatment, just reassurance ```
49
What suggests conjugated hyperbijjlirubinemia?
– Suggested by abdominal pain, fever, palpable gall bladder – Ultrasound reveals duct dilation, unless very transient (e.g., passage of a gall stone) – A transient rise in aminotransferase levels can be seen with acute large duct obstruction
50
alcoholic hepatitis
* Hepatocellular injury * AST> 2xALT, but AST <400UL * Bilirubin increase and PT/INR better indices
51
What viruses classically cuase viral hepatitis?
Hep A, B (D,C,E) CMV EBV HSV
52
What should you exclude before diagnosing autoimmune hepatitis?
chronic viral hepatitis wilson disease assoc w/ Hashimotos thyroiditis
53
WHat is primary biliary cirrhosis?
* Typically middle aged women (40-60 yrs) * Presents with fatigue and pruritus * Increased levels of AP and IgM * Fat soluble vitamin deficiencies and metabolic bone disease, increased cholesterol (HDL), later increased bilirubin * Granulomatous infiltration of septal bile ducts * Anti-mitochondrial antibodies present in over 90-95%
54
Autoimmune hepatitis vs PBC
Autoimmune hepatitis: 7-10x ULN anti-smooth muscle Ab 90% PBC: 1-3xULN anti-mito 90-100%
55
What causes toxic hepatitis?
``` • Alcohol • Drugs – Predictable (e.g., acetaminophen) – Idiosyncratic (e.g., isoniazid) • Environmental – Vinyl chloride – Jamaica bush tea – Kava kava – Amanita phalloides or A. verna (mushrooms) ```
56
acetaminophen toxicity: 0-24 hrs
Anorexia, nausea, vomiting
57
acetaminophen toxicity: 24-72
Right upper quadrant abdominal pain (common) | AST, ALT, and, if poisoning is severe, bilirubin and PT (usually reported as the INR) sometimes elevated
58
acetaminophen toxicity: 72-96
Vomiting and symptoms of liver failure Peaking of AST, ALT, bilirubin, and INR Sometimes renal failure and pancreatitis
59
acetaminophen toxicity: >5
Resolution of hepatotoxicity or progression to multiple organ failure (sometimes fatal)
60
What is hte rumack matthew nomogram
Hours vs. Plasma acetaminophen (can determine if hepatotoxicity likely given level and how many hours out)
61
What causes Fe overload?
Herediatary hemochromatosis Multiple blood transfusions (talassemia major) Consider in adults w/ liver disease (men)
62
What should you consider in a pt with transferrin saturation >55% and ferritin > 200?
Fe overload Liver bx with Fe measurement
63
Where does Cu accumulate in wilsons disease?
liver | basal ganglia
64
defect in wilson disease
ATP7B gene (increased Cu absorption, decreased excretion)
65
What are sxs of Wilson diesase?
* Hepatitis, splenomegaly, hypersplenism, Coombs neg. hemolytic anemia, portal hypertension, neuro-psychiatric disease * Can cause chronic or fulminant hepatitis * Kayser-Fleischer ring seen on slit-lamp exam
66
Wilson disease is usually diagnosed in what population?
adolescent or young adult
67
Labs diagnostic of WIlsons?
* Increased urinary Cu (> 40 μg/24 h) * Low serum ceruloplasmin (<20 mg/dL; <5 mg/dL is diagnostic) (Cu binding protein) * Increased hepatic Cu (>250 μg/g dry wt.)
68
What is Crigler Najjar type 1?
* Very rare, newborns * Unconjugated hyperbilirubinemia * Bilirubin > 20 mg/dL * Fatal disease, kernicterus – Liver transplant * ABSENT UDPGT activity
69
What is Crigler Najjar type 2?
``` • More common than type 1 • Unconjugated hyperbilirubinemia • Can survive to adulthood • Bilirubin 5-25 mg/dL • Milder DEFICIENCY of UDPGT – Enzyme can be induced by phenobarbital ```
70
What are dubin johnson and rotor syndromes?
* Both are rare, benign disorders with asymptomatic jaundice * Often present in 2nd decade of life * Increased direct (conjugated bilirubin) * Dubin-Johnson caused by mutations in multiple drug resistance protein 2 * Rotor syndrome mechanism unclear
71
Neonatal jaundice affects what % of newborns?
60% acute encephalopathy > kernicterus
72
What causes neonatal jaundice
• Usually immaturity of conjugating enzymes • Other causes – Hemolytic disease (incl. HDN), bruising (e.g., cephalohematoma) – Breast feeding, especially if inadequate – Sepsis

LAMP (16 decks)

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