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Clin Med, Path, Pharm > Test 3 > Flashcards

Test 3 Flashcards

1
Q

Used to treat Ogilvie syndrome

A

NPO, NG tube, Neostigmine

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2
Q

What is neostigmine’s MOA?

A

reversible ACh inhibitor, indirectly stimulates nic. and musc. receptors to cause colonic contraction.

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3
Q

Side effect of neostigmine?

A

bradycardia

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4
Q

Continuous dilation of small intestine and colon

A

Ileus

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5
Q

Most common cause of acute intestinal obstruction?

A

Adhesions

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6
Q

What is the difference in pain presentation from closed loop obstruction and strangulation?

A

Closed loop obstruction with functioning ileocecal valve causes cramping and midabdominal pain with colicky behavior. Strangulation is more steady, severe, and localized.

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7
Q

High pitched hyperactive bowel sounds like “tinkling”

A

Acute intestinal obstruction

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8
Q

What two things do you have to establish with obstructions?

A

Strangulation vs nonstrangulation

Partial vs complete obstruction

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9
Q

What imaging do you order for an obstruction?

A

Abdominal x-ray is step on. Look for transition point. If x ray doesn’t work, go with CT abdomen and pelvis with IV and PO contrast.

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10
Q

How do you treat a strangulated obstruction?

A

Must do surgery. Only time you can avoid surgery is if there’s no strangulation, no increasing abd. pain, and no increasing WBC

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11
Q

What is the most common abdominal emergency in early childhood?

A

Intussusception

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12
Q

Where do intussusceptions usually occur?

A

ileocecal junction

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13
Q

What is the classic triad associated with intussusception?

A

Pain, currant jelly stool, sausage shaped abdominal mass on the right side.

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14
Q

What do you have to do before treating an intussusception?

A

Have an NG tube placed. Observe afterward in hospital for 12-24 hours.

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15
Q

What do you do for a SMALL BOWEL intussusception?

A

Usually nothing, many will resolve spontaneously.

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16
Q

Elliptical incision removal, rubber band ligation, laser phototherapy, cryosurgery, and infrared coagulation are treatment examples of what condition?

A

hemorrhoids

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17
Q

A tear in the anoderm distal to the dentate line, becomes chronic in 40% of patients

A

Anal fissure

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18
Q

If an anal fissure has raised edges, is it acute or chronic?

A

Chronic. If it was acute it would look like a paper cut

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19
Q

Constant pain, fever, malaise, patch of redness, indurated skin, mass on exam

A

Anal abscess

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20
Q

When do you give antibiotics to a pt with an anal abscess?

A

Only if they are immunosuppressed or have Crohn’s

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21
Q

What is the most common cause of anal fistulas?

A

Anal abscess. Originate from infected anal crypt gland.

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22
Q

Intermittent rectal pain after having an I/D

A

Anal fistula

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23
Q

Where are the highest rates of colorectal cancer?

A

Australia, New Zealand, Europe, North America. More common in males

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24
Q

What kind of polyps are the worst case scenario for getting CRC?

A

Sessile Villous Adenomatous Polyps

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25
Q

If an adenomatous polyp is found, when do you repeat colonoscopy?

A

Every 3-5 years

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26
Q

CRC screening in someone with family hx of 1st degree relative?

A

age 40 or 10 years before youngest family diagnosis <60

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27
Q

CRC screening in someone who has adenomatous polyps >1cm, villous, or tubulovillous polyps?

A

age 40 or 10 years before youngest polyp diagnosis <60

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28
Q

CRC screening in someone who had abdominal radiation?

A

Begin screening 10 years after radiation or age 35, whichever is later

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29
Q

CRC screening for African American patient?

A

Start at 45 because they have the highest CRC rates and a 20% higher mortality, and it occurs at a younger age

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30
Q

When should you perform a DRE on routine physical exam?

A

Anyone over 40

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31
Q

Lynch Syndrome (HNPCC) has a predominance of _______ sided lesions

A

Right sided.

Extracolonic cancers are very common

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32
Q

CRC screening for someone with lynch syndrome?

A

Every 2 years starting at age 25

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33
Q

How do we know if someone has Lynch?

A

3+ relatives with documented CRC, one of which is a 1st degree reltaive; one+ cases of CRC < age 50; CRC involves at least 2 generations

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34
Q

CRC risk factors that DO NOT change screening recommendations?

A

Diabetes and alcohol use

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35
Q

CRC protective factors

A

Physical activity, Vitamin D, Fish consumption, ASA and NSAIDS, Postmenopausal hormone therapy

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36
Q

CRC that presents with fatigue, palpitation, iron deficiency anemia, and no change in bowel habits

A

Right sided, cecum

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37
Q

CRC that presents with obstruction, abdominal cramping, “apple core” lesion

A

Left sided

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38
Q

CRC that presents with hematochezia, tenesmus, narrow or “ribbon” stool. Anemia is uncommon

A

Rectosigmoid colon

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39
Q

TNM: T

A

depth of tumor penetration

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40
Q

TNM: N

A

Presence of lymph node involvement

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41
Q

TNM: M

A

Presence or absence of metastasis

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42
Q

What route does metastasis usually take? What’s an exception?

A

spread through lymph nodes and portal venous system. Liver is the most common site. distal rectal cancer can bypass portal system and reach lungs through paravertebral venous plexus.

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43
Q

Screening recommendation for IBD after pancolitis

A

8-10 years

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44
Q

Screening recommendation for left sided colitis

A

15 years

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45
Q

What do Kuppfer cells do?

A

Macrophages that break down dead RBCs found in liver.

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46
Q

The development of severe acute liver injury with encephalopathy and imparied syntehtic function (INR >1.5) in a patient without cirrhosis or preexisting liver disease.

A

Acute liver failure (<26 weeks)

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47
Q

Euphoria/depression, mild confusion, slurred speech, disordered sleep, may/may not have asterixis. Normal EEG

A

Grade 1 hepatic encephalopathy

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48
Q

Lethargy and marked confusion. Has asterixis. Abnormal EEG.

A

Grade II hepatic encephalopathy

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49
Q

Marked confusion, incoherent, sleeping but arousable, asterixis and abnormal EEG

A

Grade III hepatic encephalopathy

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50
Q

What labs should you order in someone you suspect with acute liver failure?

A

AST, ALT, Alk Phos, GGT, Total bilirubin, Albumin, INR, Acetaminophen level, Hepatitis panel, Ammonia level +/- BMP

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51
Q

How much do men and women have to drink to develop alcohol fatty liver?

A

> 60g of alcohol/day for men, >20g/day for women.
Men: 5 beers, 5 glasses of wine, 7 shots per day
Women: 4 beers, 2 glasses of wine, 2 shots per day

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52
Q

What imaging is best used to diagnose alcohol fatty liver?

A

Ultrasound.

LFTs are usually 2x ULN

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53
Q

Moderate elevations of AST and ALT less than 300. AST: ALT is at least 2:1.

A

Findings of Alcoholic hepatitis

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54
Q

What would you expect to find on biopsy in someone with alcoholic hepatitis?

A

Neutrophils

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55
Q

NAFLD without inflammation or fibrosis

A

Simple hepatic steatosis

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56
Q

NAFLD with necroinflammatory component

A

NASH

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57
Q

NAFLD with cryptogenic cirrhosis

A

non-alcoholic cirrhosis

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58
Q

Most common liver disorder in western industrialized countries?

A

NAFLD. Excessive importation of free fatty acids is related.

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59
Q

Screening recommendation for someone who has cirrhosis?

A

Transabdominal ultrasound every 6 months regardless of cause

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60
Q

Most common cause of death among patients with NAFLD

A

Cardiovascular disease

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61
Q

Incubates for 30 days, self limited. Rarely leads to fulminant hepatic failure. Does NOT become chronic. What will normalize first, LFTs or bilirubin?

A

Hepatitis A.
LFTs normalize first,
then bilirubin will normalize

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62
Q

Labs for hep A?

A

ALT>AST, often > 1000. Bilirubin will peak AFTER ALT and AST peak.
Gold standard: IgM anti-HAV. will be positive at the onset of symptoms.

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63
Q

Urticarial rash, petechiae, arthralgias/arthritis of small joints followed by constitutional symptoms that take over

A

Hepatitis B

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64
Q

Lab testing during acute phase of hep b?

A

Viral hepatitis B panel, Hep C, HIV testing.

ALT>AST

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65
Q

First thing that will be positive after HBV infection and will only be positive in someone who CURRENTLY has the virus

A

HBsAg

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66
Q

Checks if someone is immune to HBV virus

A

Anti-HBs (antibody to hep b surface antigen)

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67
Q

Nonspecific marker of acute, chronic, or resolved HBV infection. Tells you the real virus was there.

A

Anti-HBc

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68
Q

Positive tells you there was a recent infection of HBV within the last 6 months

A

IgM anti-HBc

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69
Q

Marker of high degree of infectivity in someone who has the real virus

A

HBeAg (hep b envelope antigen)

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70
Q

May be present in an infected or immune person. Suggests a low viral titer and low degree of infectivity

A

Anti-HBe

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71
Q

HBsAg positive for >6 months. Serum HBV DNA >100,000 copies. Persistent/intermittent elevation of AST/ALT levels.

A

Chronic hepatitis B

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72
Q

What genotype of HBV is most likely to become chronic?

A

genotype C

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73
Q

Labs in chronic hep B

A

May be normal. During exacerbations, ALT may be as high as 50x ULN

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74
Q

Who should get screening ultrasounds Q6-12 months with hep B?

A

Cirrhosis, family hx, africans, disease >40 years with persistent/intermittent serum elevations

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75
Q

What are the most common genotypes of HCV in the US?

A

Genotype 1a and 1b, also the most difficult to treat (75% of cases)

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76
Q

Where would you find genotype 4 HCV?

A

Africa

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77
Q

75% of patients with Hep C were born when?

A

1945-1965

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78
Q

How likely will Hep C become chronic?

A

60-80% of patients become chronically infected. Of those, over a quarter will develop cirrhosis.

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79
Q

Screening recommendation if IVDU or HIV + MSM for hep c

A

Annual testing

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80
Q

Screening recommendation for hep c if born between 1945-65

A

once in lifetime

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81
Q

What test do you order for routine Hep C screening?

A

HCV antibody test. If positve, check HCV RNA to confirm.

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82
Q

Acute Hepatitis C occurs how long after exposure to the virus?

A

2-26 weeks. Average is 7-8 weeks.

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83
Q

When will AST, ALT labs rise in comparison to RNA with hep c?

A

They will rise a few weeks before positive RNA can be detected.

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84
Q

HCV-RNA can be positive ___________ after exposure

A

days to 8 weeks

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85
Q

HCV antibody is positive as early as _______ after exposure.

A

8 weeks. Does not determine acute from chronic.

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86
Q

If you suspect acute hep C based on elevated LFTs and jaundice, check _______ immediately.

A

HCV RNA.

Check anti-HCV immediately and at week 12

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87
Q

When should you initiate treatment of acute hep C infection?

A

12 weeks after exposure to allow for possible spontaneous clearance. If you treat during the acute infection, they have a >80% chance of acquiring sustained virologic response.

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88
Q

In what case scenario would you NOT wait 12 weeks to treat hep C?

A

High inoculum volume, asymptomatic acute HCV. Genotype 1–treat for 24 weeks. Any other genotype treat for 12

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89
Q

Hep C RNA is different in acute and chronic infection how?

A

Acute–positive within 2 weeks and fluctuates

Chronic– remains steady. Increase in ALT precedes development of Ab

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90
Q

+RNA and high ALT, negative Ab

A

acute HCV more likely

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91
Q

+RNA, +Ab, normal or low ALT

A

Chronic HCV is more likely

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92
Q

What is the most common symptom of chronic hep C?

A

Fatigue

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93
Q

True or false: There is a strong correlation between LFTs and liver histology.

A

False

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94
Q

What are most symptoms from hep C from?

A

Development of cirrhosis.

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95
Q

What is the most common cause of death from hep C?

A

Complications of cirrhosis (portal HTN)

96
Q

What is the most common cause of death from hep B?

A

HCC

97
Q

What genotype of hep C has a higher ate of HCC?

A

1b

98
Q

What is the best predictor of progression to cirrhosis in hepatitis C?

A

Amount of inflammation and fibrosis on liver biopsy.

AA have slower progression

99
Q

What is genotype 1 treatment of hepatitis C?

A

Peginterferon, Ribavirin plus Protease inhibitor

100
Q

What are the hardest genotypes of hep C to treat?

A

1 and 4

101
Q

What are side effects of hep C antivirals?

A

Flu-like symptoms, anemia, neutropenia, thrombocytopenia, rash, hair loss, thyroid dysfunction, mood changes

102
Q

Protease inhibitors that disrupt replication of HCV that has shown to increase viral response especially in patients who have genotype 1 or who have failed therapy before

A

Boceprivir and Telaprevir

103
Q

When would you give telaprevir without boceprivir?

A

Only indicated for null responders.

Give both for genotype 1

104
Q

How do you treat Hep C in someone who can’t be on a protease inhibitor?

A

Treat with ribavirin and peginterferon for 48 weeks

105
Q

Hep C with evidence of cirrhosis sreening

A

Q6 month ultrasound

106
Q

Hep C without evidence of cirrhosis screening

A

Q12 month ultrasound

107
Q

How is hep D transmitted?

A

Sex, blood, bodily fluids. Needs hep B

108
Q

How is hep E transmitted?

A

Fecal-oral, rare in US. Test IgM anti-HEV

109
Q

Characterized by progressive hepatic fibrosis, distortion of hepatic architecture, forming regenerative nodules (incongruent surface of the liver)

A

Cirrhosis

110
Q

Most common causes of cirrhosis?

A

viral hepatitis, alcoholic liver disease, hemochromatosis, NAFLD

111
Q

Methotrexate, INH, and alpha-1 antitrypsin deficiency may cause what?

A

cirrhosis

112
Q

Causes of decompensated cirrhosis

A

Processing problems
Hormone Imbalances
Portal Hypertension

113
Q

How would someone have trouble processing bilirubin with cirrhosis?

A

If you aren’t making albumin, unconjugated bilrubin can’t bind to it to become water soluble and go to the liver.
Also, some people just can’t conjugate the bilirubin with glucuronic acid, or it can’t get out of the liver.

114
Q

Where will you notice jaundice first?

A

Under the tongue

115
Q

Why would someone have trouble processing ammonia with cirrhosis?

A

Amino acids produce ammonia when they’re metabolized, which has to be converted to urea by the liver. Sick liver can’t do this.

116
Q

Clinical result of liver’s inability to process ammonia?

A

hepatic encephalopathy

117
Q

How does ammonia cause encephalopathy?

A

Ammonia crosses BBB and is used by brain cells to convert glutamate to glutamine. Too much glutamine = increased osmotic pressure in brain cell = swelling = confusion

118
Q

What is the treatment of hepatic encephalopathy?

A

First line is Lactulose laxative. Goal is 2-3 loose stools/day.

119
Q

FSH stimulates what?

A

Sertoli cells to make sperm

120
Q

LH stimulates what?

A

Leydig cells to make testosterone

121
Q

What converts testosterone to estradiol?

A

Aromatase (made by the liver)

122
Q

spider angiomata, palmar erythema, and gynecomastia are a result of what?

A

High levels of estrogen, occurs in 2/3 of patients with cirrhosis.
Caused ultimately by too much aromatase and SHBG production by the liver.

123
Q

Hormone problems occur most often in what kind of cirrhosis?

A

Alcoholic cirrhosis

124
Q

serum LH, FSH levels high, serum testosterone low

A

Primary hypogonadism (testicle problem)

125
Q

Serum LH, FSH levels low or normal, serum testosterone low

A

Secondary hypogonadism. (pituitary/hypothalamus problem)

126
Q

How does liver disease cause portal hypertension?

A

decreases vascular radius from fibrosis, decreased production of NO, Body makes collaterals and connects to the systemic system through this

127
Q

Physical manifestations of portal HTN

A

Caput medusa, hemorrhoids.

Complications: ascites, esophageal varices, spontaneous bacterial peritonitis, hepatorenal syndrome

128
Q

Treatment of ascites

A

Salt restriction WITH diuretic. Should be on BOTH spironolactone and furosemide.

129
Q

Where do most esophageal varix hemorrhages occur?

A

Superficial to the GE junction

130
Q

Recommendation for screening for varices

A

All patients with cirrhosis should have EGD to document existence of varices. Negative–repeat Q2-3 years. Positive, repeat yearly.

131
Q

Those who have 1 eisode of bleeding have ______% chance of rebleed within ____.

A

60-80%, 1 year.

1/3 of further rebleeding episodes are fatal.

132
Q

Treatment of esophageal varices bleeding

A

LIgation during endoscopy. Nonselective beta blockers–propranolol (Indur) is the drug of choice. Reduces portal and collateral blood flow

133
Q

SBP is almost always seen in what disease?

A

ESLD

134
Q

Labs for diagnosing cirrhosis

A 
Alk Phos elevated but less than 3X ULN 
Worse INR, worse hepatic dysfunction.  
Hyponatremia is common.
CBC:  Thrombocytopenia is most common
Anemia
Splenomegaly
135
Q

Anemia from iron deficiency from acute or chronic GI blood loss

A

Microcytic

136
Q

Anemia from folate deficiency

A

Macrocytic

137
Q

What is the best imaging study to order to diagnose cirrhosis?

A

Abdominal ultrasound.

LIver biopsy is the gold standard, but not usually needed.

138
Q

What does a fibrotest or fibrosure test assess?

A

Takes a bunch of factors into account to classify if patients have mild fibrosis, significant fibrosis, or indeterminate

139
Q

Rapid, noninvaisve ultrasound done using a special probe to measure hepatic tissue stiffness.

A

Elastography

140
Q

Classification system used to determine severity of liver disease according to ascites, bilirubin and albumin, prothrombin time, and degree of encephalopathy. Used to determine who should have hepatic dose adjustments.

A

Child Pugh

141
Q

Prognostic model to help estimate disease severity, survival, and transplant. Measures bilirubin, creatinine, INR.

A

MELD score.

Avg score for transplant is 20, avg time to transplant is 321 days.

142
Q

Primary cancer of the liver that occurs mostly in patients with underlying chronic liver disease and cirrhosis.

A

Hepatocellular Carcinoma

143
Q

What is the trend of HCC?

A

Doubled in last 20 years, increasing in AA population. Mostly men and Caucasians.

144
Q

Most common physical sign of HCC?

A

Hepatomegaly

145
Q

Diagnosis of HCC?

A

Abdominal ultrasound. Can use CT or MRI to clarify, then diagnosis is made on biopsy. Uses TNM classification to stage.

146
Q

Common bile duct ends where?

A

Sphincter of Oddi

147
Q

How does common bile duct drain into duodenum?

A

Ampulla of Vater or major duodenal papilla

148
Q

Exocrine function of pancreas?

A

Digestive enzymes from Acinar cells and ductal cells

149
Q

What do acinar cells do?

A

Stimulated by CCK, releases trysinogen, lipase, and amylase

150
Q

What does lipase need to be totally active?

A

colipase and bile salts

151
Q

What do ductal cells do?

A

Release bicarbonate by stimulating secretin. Helps buffer acidic fluid from entering the duodenum from the stomach

152
Q

Endocrine function of the pancreas?

A

Langerhan’s cells.
Beta cells—Insulin
Alpha cells – Glucagon
Delta cells – Somatostatin

153
Q

What is the most common cause of pancreatitis?

A

Gallstones! Cause 40% of all cases.

Cause reflux of bile into pancreatic duct and edema

154
Q

Causes of acute pancreatitis

A

Alcohol (30%), idiopathic (30%), triglycerides >1000 mg/dL, Post-ERCP

155
Q

Acute onset. Persistent, severe epigastric pain. May have radiation to the back that is partially relieved by sitting up or bending forward. Most have N/V.

A

Acute pancreatitis

156
Q

Pain is localized with abrupt onset, colicky

A

Gallstone pancreatitis

157
Q

Painless disease with unexplained hypotension in post-op or critical care pt

A

Pancreatitis

158
Q

Mild ttp in epigastrum

A

Mild pancreatitis

159
Q

Diffuse, intense pain, may have ileus secondary to inflammation. Look for Cullen’s sign and Grey-Turner’s sign

A

Severe pancreatitis

160
Q

Lab findings for pancreatitis: Serum amylase

A

rises within 6-12 hours of onset, half life of 10 hours, normal in 3-5 days. Amylase 3x ULN is magic number. Alcoholic pancreatitis and hyperTG will possibly have normal amylase.

161
Q

If a patient presents to the ER >24 hours after onset of pancreatitis, what test may be more helpful?

A

Serum lipase. Rises 4-8 hours after onset, peaks at 24 hours, normal in 8-14 days. Better test in someone with alcoholic pancreatitis.

162
Q

Imaging for acute pancreatitis

A

Abdominal and chest x rays

If you need to go further, CT abdomen with IV contrast

163
Q

What is the colon cutoff sign?

A

lack of air distal to splenic flexure due to spasm of descending colon in response to pancreatic inflammation. Indicates severe disease.

164
Q

What is the diagnostic criteria of pancreatitis?

A

Need to meet 2 of the following 3:

  1. Acute onset of persistent, severe epigastric pain often radiating to the back
  2. Elevation of serum lipase or amylase 3X ULN
  3. Characteristic findings on CT, MRI, or U/S
165
Q

What % of patients with acute pancreatitis will develop severe pancreatitis?

A

15-25%

166
Q

What tool is used to predict severity of pancreatitis?

A

Ranson’s criteria about mortality.
Looks at age (>55), WBC (350), AST (>250). (GA LAW)
After 48 hrs:
HCT fall, BUN inc, low Calcium, pO2, base deficit, fluid sequestration (C. HOBBS)

167
Q

If a patient with acute pancreatitis feels better, do they have to come in for follow up?

A

Yes, in a month to make sure complications don’t occur.

Acute peripancreatic fluid collection, acute necrotic collection, pseudocyst, walled-off necrosis

168
Q

Treatment of pancreatitis

A

Recognize severity first.
Mild–NPO
Mod-Severe: PO intake not tolerated because of inflammation and extrinsic fluid collections.
No recommendation for prophylactic antibiotics

169
Q

No problems with exocrine/endocrine function or digestion. Diffuse morphology

A

Acute pancreatitis

170
Q

Digestion, endo/exocrine problems. Morphology is patchy with focal infiltrate and fibrosis.

A

Chronic pancreatitis.

171
Q

Causes of chronic pancreatitis

A

Most common: alcohol abuse
Smoking, hereditary pancreatitis (marked increase of pancreatic adenocarcinoma)
Obstructed duct, systemic disase, idiopathic

172
Q

Common denominators of chronic pancreatitis

A
  1. Hypersecretion of protein that is NOT compensated by bicarb (ductal bicarb secretion impaired)
  2. Inflammatory and patchy histology changes in exocrine pancreas
173
Q

What is the predominant feature of chronic pancreatitis?

A

Abdominal pain

174
Q

How much of the pancreas needs to be lost to have pancreatic insufficiency? What other problems can develop?

A 
90%
Diabetes Mellitus (insulin requring, affects alpha and beta cells), fat and protein deficiency
175
Q

“classic triad” of chronic pancreatitis

A
  1. Pancreatic calcifications
  2. Steatorrhea
  3. DM
176
Q

What is the best imaging for chronic pancreatitis? What is the worst?

A

Best: MRCP–uses no radiation, no contrast
Worst: Ultrasound (least sensitive and specific)

177
Q

What should you suspect when total bilirubin and alk phos are elevated in pancreatitis?

A

Obstruction from fibrosis, stricture, stone/calcification or edema

178
Q

When should you take pancreatic enzyme supplementation?

A

First bite of a meal.

Examples are Pancreaze, Creon, Ultresa

179
Q

How does CCK cause pain?

A

Releasing factors stimulate duodenum to release CCK. CCK stimulates pancreas to secrete digestive enzymes, which also degrade the releasing factors. When no enzymes are produced, releasing factors are never degraded so the pancreas keeps trying to make more enzymes. Result is pain from way too many digestive enzymes.

180
Q

Pain management for pancreatitis

A

TCA + short course of opiates and NSAIDs for 3 weeks.

181
Q

Where do most pseudocysts occur and what can it cause?

A

2/3 are in the tail of the pancreas.

Abd. pain, obstruction, vascular occlusion, spontaneous infection, pseudoaneurysm (digestion of nearby vessel)

182
Q

Treatment of pseudocysts

A

Drainage if >6 cm or persisted for >6 weeks

183
Q

Postprandial pain and early satiety

A

Duodenal obstruction

184
Q

Pain and elevated LFTs

A

Bile duct obstruction

185
Q

95% of malignant neoplasms in pancreatic cancer arise from where?

A

Exocrine elements.

85% of tumors are adenocarcinomas arising from ductal epithelium.

186
Q

Generalized pain or epigastric/back pain. May be intermittent and worse with eating, worse at night. Weight loss, anorexia, diarrhea, steatorrhea, vomiting, may see Virchow’s nodes, etc

A

Pancreatic cancer

187
Q

Where do most pancreatic tumors occur?

A

Head of the pancreas (60-70%)

These are more likely to present with jaundice, steatorrhea, and weight loss

188
Q

How do you diagnose pancreatic cancer?

A

Can’t just rely on symptoms. Need to do imagine and liver function testing. Transabdominal U/S, CT scan
Confirm with biopsy

189
Q

What is the role of tumor markers in pancreatic cancer?

A

CA19-9 is related to tumor size.

Degree of elevation at presentation and post-op setting associated with prognostic predictions.

190
Q

What stimulates the gallbladder?

A

CCK

Vagus and splanchnic nerves

191
Q

Where is ALT found? What is it correlated with?

A

Found in high concentrations of the liver, low concentrations in heart and kidney.
ALT and trunk fat are related–more central adiposity may have falsely elevated ALT

192
Q

Where is AST found? What is it correlated with?

A

Found in tissues of high metabolic activity. Heart, liver, skeletal muscle, kidney, brain, pancreas, spleen, lungs.
Level of elevation correlates with number of damaged cells and time since injury. Evaluates liver and heart disease

193
Q

What can cause increased AST?

A

Acute MI, liver disease, tissue trauma (infection, hyperthermia, brain trauma, injury), Hypothyroidism

194
Q

Where is Alkaline Phosphatase found? What does it correlate with?

A

Originates in bone, liver, placenta.
Tumor marker, index of liver and bone disease.
Rises with biliary tract obstruction AND rise is out of proportion to AST, ALT elevations.
Liver disease, hyperparathyroidism, CHF, CKD, ulcerative colitis

195
Q

True or false: There is no increase in AP with osteoporosis.

A

True

196
Q

GGT will be elevated when? When do you check it?

A

Elevated Alk Phos can be from bone or liver. Cehck GGT–will be elevated with liver disease but normal with bone disease

197
Q

GGT is associated with what?

A

Sensitive to amount of alcohol consumed in chronic drinkers, elevated in all forms of liver disease/liver cancer

198
Q

Disproportionate elevation in serum ALT and AST compared to ALP

A

hepatic cause

199
Q

Disproportionate elevation in serum ALP compared to ALT and AST

A

biliary cause

200
Q

AST>ALT (2:1)

A

Alcohol

201
Q

ALT>AST

A

Hepatic cause

202
Q

How long do LFTs need to be elevated to be chronic? How high to be mild?

A

Chronic: 6 months +
Mild: Less than 5X ULN

203
Q

Work up of chronic LFT elevation?

A
  1. Identify meds that can cause this
  2. Assess alcohol abuse
  3. Hepatitis?
    4.
  4. Consider NASH
204
Q

Risk factors for developing gallstones

A 
Female, 40, fat, fertile (pregnancy)
Rapid weight loss
Genetics (native americans)
Cirrhosis
HyperTG
Gallbladder stasis from DM, TPN, spinal cord injury, use of octreotide
205
Q

What is the biggest contributing substance to biliary sludge?

A

Cholesterol

206
Q

Gallstone disease will have what kind of PE findings, labs?

A

normal

207
Q

Biliary colic that is actually usually constant, dull/achy in RUQ or epigastrum, radiate to back or right shoulder, diaphoresis, n/v, NOT made worse with movement, lasts 30 minutes, plateus in an hour. Entire attack lasts less than 6 hours.

A

Gallstone disease, biliary colic

Visceral in origin, GB wall is not inflamed

208
Q

Chest pain, general abd. pain, belching, fluid regurgitation, abd. distention/bloating, retrosternal burning, n/v

A

atypical presentation of gallstone disease

209
Q

What if you were expecting to see gallstones on ultrasound and didn’t?

A

Repeat in a few weeks

210
Q

4-6 hours of prolonged biliary colic, assocaited fever, pain and peritoneal inflammation, abnormal labs

A

acute cholecystitis

211
Q

fever, leukocytosis, hypotension, mental status changes

A

Acute cholangitis (complication of choledocolithiasis)

212
Q

What will you find on CCK Cholescintigraphy in pt with functional gb d/o?

A

Low ejection fraction

213
Q

Treatment of gallstones with biliary symptoms

A

Elective cholecystectomy because this will prevent repeated attacks and complications. Pain management with NSAIDS or IV Keterolac (Toradol). May use opioids if cannot take NSAIDS but ALL opioids increase tone at sphincter of Oddi

214
Q

RUQ pain, fever, leukocytosis associated with gallbladder inflammation/gallstones.
+ Murphy’s sign (pain on palpation of GB)
Will lay still since movement makes it worse

A

Acute cholecystitis

215
Q

Looks the same as acute cholecystitis but NOT associated with gallstones

A

Acalculous cholecystitis

216
Q

Result of mechanical irritation or recurrent GB attacks, end result is fibrosis and thickening of GB

A

Chronic cholecystitis

217
Q

What is a porcelain gallbladder?

A

Uncommon manifestation of chronic cholecystitis. GB becomes calcified, can identify on plain xray. increases risk of developing GB carcinoma (poor prognosis).
Always get cholecystectomy

218
Q

Labs for acute cholecystitis

A

Leukocytosis (may have abdnemia)
LFTs should be normal in uncomplicated case
U/S is test of choice. CT misses 1/5 of gallstones because they are the same radiodensity as bile

219
Q

What would you expect to see on ultrasound of acute cholecystitis?

A
  1. Gallstone in cystic duct
  2. GB wall thickening >2-4 mm
  3. Gall bladder distention
  4. Perichoecystic fluid
    5 . Air in gallbladder wall (gangrenous)
  5. Ultrasonographic murphy’s sign
  6. Dilation of common bile duct or intrahepatic ducts
220
Q

Role of Cholescintigraphy (HIDA Scan)

A

HIDA is injected and selectively taken up by hepatocytes and secreted into bile. Can visualize GB, cystic duct, CBD and small bowel within 30-60 minutes. test is considered positive if GB does not visualize within 60 minutes.

221
Q

Since acute cholecystitis will go away on its own in 7-10 days, why treat it?

A

Complications are common! Gallbladder gangrene with subsequent perforation is the most common. Patients need cholecystectomy.
Fistula and ileus can also happen.

222
Q

Antibiotic guidelines for acute cholecystitis

A

If WBC >12.5, clinical findings of temp >101.3, air in GB, elderly, immunocompromised

223
Q

What antibiotics are used to treat acute cholecystitis?

A

First line is monotherapy with Piperacillin/Tazobactam (Zosyn)
OR
Ceftriaxone (Rocephin) PLUS Metronidazole (Flagyl)
OR
Levaquin Plus Flagyl
NSAIDs (Toradol) for pain.

224
Q

What can chronic cholecystitis cause?

A

Increased risk of gallbladder cancer

225
Q

Risk factors for acalculous cholecystitis?

A

Prolonged fasting (endotoxin is released from bile)

226
Q

Increased serum bilirubin, alk phos, and GGT out of proportion to AST and ALT elevations

A

Choledocolithiasis

227
Q

Treatment of choledocolithiasis

A

Locate stone, remove it

Use ERCP. If can’t do ERCP, perform cholecystectomy

228
Q

Stone gets stuck in ampulla of Vater and blocks bile output. Stagnant bile becomes infected and bacteria spreads back up ductal system into liver. (bacterial translocation into biliary tract)

A

Asending cholangitis

229
Q

Most common offender of ascending cholangitis?

A

E. Coli! (Up to 50%)

Klebsiella, Enterobacter. Also some gram positives, anaerobes are rarely the sole infecting organism.

230
Q

Classic presentation of ascending cholangitis

A

Charcot’s triad (Fever, Jaundice, RUQ Pain)

Reynold’s Pentad (Charcot’s triad plus hypotension and altered mental status)

231
Q

What if you suspect acute cholangitis but they lack Charcot’s triad?

A

Transabdominal ultrasound. If positive on stones or CBD dilation, perform ERCP in 24 hours.

232
Q

Progressive inflammation, fibrosis, and structuring or med. and large intrahepatic and extrahepatic bile ducts. This condition has a strong association with what?

A

Primary Sclerosing Cholangitis

Strong association with ulcerative colitis (can occur years after colectomy for UC)

233
Q

Who is primary sclerosing cholangitis more common in? What is time of survival without liver transplant?

A

70% are men.

Average time is 10-12 years after diagnosis without liver transplant

234
Q

Fatigue, itching, intermittent fever, chills, RUQ pain. How do you diagnose this?

A

Primary Sclerosing Cholangitis
Cholangiography (ERCP, MRCP)
Biopsy can support but isn’t diagnostic

235
Q

Labs for primary sclerosing cholangitis

A

Cholestatic pattern on LFTs
Positive p-ANCA 80% of the time.
Negative antimitochondrial antibodies

236
Q

T-lymphocyte mediated attack on small intralobular bile ducts

A

Primary biliary cirrhosis

237
Q 
\+ Antimitochondrial antibodies
White women
Fatigue, pruritus, hyperpigmentation of skin
30-65 years old
Rheumatic symptoms
A

Primary biliary cirrhosis

Diagnose with liver biopsy and perform serum testing

Clin Med, Path, Pharm (12 decks)

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