EXAM REVIEW Flashcards

1
Q

What is our first line treatment for mild moderate ABX colitis?

what about if no improvement within 5-7 days?

How about severe disease?

A

Metronidazole 500 mg PO TID x 10 days (alternate is vancomycin 125 mg PO (oral) QID x 10 days)

severe: straight to PO vancomycin!

Treatment – Fulminant Disease:

Vancomycin 500 mg PO (or IV if unable to do PO) QID

AND

Metronidazole 500 mg IV q8 hrs

AND

Vancomycin PR 500 mg QID (in 500 mL Normal Saline as enema)

And Early surgical consultation!! patients w/ fulminant or toxic megaton who do not improve within 48-72 hrs need surgery to prevent perforation!

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2
Q

colonic diverticula: what do they look like in compared to normal colon tissue?

A

the outpouchings are asymptomatic and the color looks the same under colonoscopy as far as color etc

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3
Q

how do you treat diverticulosis?

A

no specific tx or workup, BUT Recommend increase in dietary fiber and water

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4
Q

what are our colorectal cancer screening PREVENTION tests?

how about DETECTION tests?

A

– Cancer Prevention Tests
• Colonoscopy* (preferred)
• Flexible Sigmoidoscopy
• CT Colonography

– Cancer Detection Tests
• Fecal Immunochemical Test aka FIT* (preferred)
• Hemoccult SENSA
• Fecal DNA

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5
Q

TIMELINES FOR THE FOLLOWING?

– Cancer Prevention Tests
• Colonoscopy* (preferred)
• Flexible Sigmoidoscopy
• CT Colonography

– Cancer Detection Tests
• Fecal Immunochemical Test aka FIT* (preferred)
• Hemoccult SENSA
• Fecal DNA

A

– Cancer Prevention Tests
• Colonoscopy* (preferred) - 10 years @ 50 y/o (45 in AA’s)
• Flexible Sigmoidoscopy - every 5-10 years
• CT Colonography - every 5 years (COL JONES SAID CT COLONOGRAPHY BEFORE FLEX SIG**)

– Cancer Detection Tests
• Fecal Immunochemical Test aka FIT* (preferred) ANNUAL TEST for those who turn down colonoscopy & other preventative tests
• Hemoccult SENSA - ANNUAL
• Fecal DNA - every 3 years

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6
Q

Higher Risk Patients – Family History Positive

A

single 1st degree relative w/ CRC OR advanced adenoma diagnosed at age >= 60 years same as grade 2b average risk (what does that mean?)

single 1st degree relative w/ CRC or advanced adenoma under 60 y/o or TWO 1st degree relatives w/ CRC or advanced adenomas =

screen every 5 years beginning at age 40 y/o or 10 years younger than youngest diagnosed relative

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7
Q

38 y/o woman for routine PE - generally healthy, active, non smoking - upon questioning she reveals her brother had colon cancer at 49… when do we do her screening?

A
  • colonoscopy at 39 y/o (10 years prior)
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8
Q

Based on those guidelines - which recommendation given to asymptomatic 50 y/o male who declines initial colonoscopy?

A

CT colonography every 5 years

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9
Q

Most likely DX for patient with/ Cramping, RLQ pain, maialise, weight loss, fatigue, non blood diarrhea, developed a fistula in the last year?

A

It’s the transmural disease associated with fistula - CRON’s disease

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10
Q

How do you separate from Cron’s from UC?

A

UC is not transmural and is bloody diarrhea and always starting rectum up so will be left sided always, but the pain could be LLQ or LUQ and maybe further up the colon

for Cron’s - instructor loves the word FLARES or intermittent bouts that are insidious (sneak up)

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11
Q

Which exam is most important to eval SB involvement for work up for Crohns?

A) colonscopy B) plain film C) capsule endoscopy

A

C - capsule endoscopy is the best option

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12
Q

phlegmon vs abscess on physical exam?

A

phlegmon should not be TTP and have a negative heel tap.

abscess will have the acute presentation of localized peritonitis with fever, abdominal pain and tenderness (TTP & + heel tap)

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13
Q

what is the lab test for IBS?

A

there isn’t one! we eliminate all organic etiologies first!!

*Also remember that this is a chronic condition. An acute onset of symptoms is suspicious for an etiology other than IBS.

• Diagnostic Testing:
– Routine screening labs
• CBC, CMP, UA
– Screening for Celiac disease in IBS-D (celiac diarrhea)
– Plain abdominal films in IBS-C (x-ray constipation)
• *Extensive diagnostic testing is not typically indicated unless the patient history and/or symptoms potentially indicate an organic etiology.

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14
Q

IBS Diagnositic criteria?

A

Diagnostic criteria:

≥ 3 months of abdominal pain or discomfort and altered bowel habits AND The abdominal pain is associated with 2/3 of the following:

  1. Relieved with defecation
  2. Onset associated with change in defecation
    frequency
  3. Onset associated with change in stool appearance
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15
Q

How does the dietary modification differ from IBS-D to IBS-C?

A

Diarrhea - trial elimination of LACTOSE and GLUTEN

Constipation - increase fiber and fluid (fiber low dose titrating to effect and discontinuing if not tolerated well)

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16
Q

Pt w/ Past MHx of UC which involves recto sigmoid to splenic flexure - bloody diarrhea, tenesmus, fecal urgency, treated with Oral Mesalamine (used oral b/c they didn’t tolerate topical) Mesalamine (Common Trade Names: Asacol, Pentasa, Rowasa) - now symptoms have returned, afebrile, isolated LLQ… how do you treat?

A

repeat the oral Mesalamine (already DOC) - it worked before so use it again - use the oral or rectal (not topical)

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17
Q

Older patient from hernia repair - several days in hospital - RL pneumonia which is treated with ceftriaxone - patient gets C diff - how do you treat?

A

go straight to oral vancomycin for 10 days QID 125 mg orally (don’t do surgery or mess around with them just tx)

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18
Q

Mild vs Moderate vs Severe UC

Stool frequency

Pulse

Hematocrit

Weight Loss

Temp

ESR

Albumin

A

Moderate (mild go down and severe above)

Stool frequency: 4 - 6 daily

Pulse: 90 - 100

Hematocrit: 30 - 40%

Weight Los: 1-10%

Temp: 99-100

ESR: 20 - 30

Albumin: 3 - 3.5

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19
Q

clinical presentation

mild to moderate vs Severe UC

A

Severe: has LLQ pain NOT relieved by defication, but as far as labs we will see SEVERE HYPOALBUMINEMIA!!!!

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20
Q

How often do we screen for UC?

A

colonoscopy w/ biopsy every 1-2 years STARTING 8 years AFTER Diagnosis

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21
Q

will we find anemia with IBS?

A

NO!! iron deficiency anemia think cancer

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22
Q

Most appropriate first line Tx for IBS?

A

Lifestyle modifications and reassurance

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23
Q

What are the indications for ERCP??

A

FILL THIS IN HERE FROM THE REVIEW IF YOU KNOW WHAT HE WAS SAYING, but short answer is in choledocolithiasis you usually do an US first (severe biliary colic, RUQ or epigastric pain, N/V, and Jaundice)… followed by ERCP is always indicated for stone removal even when it’s asymptomatic… it’s often followed up with a laparoscopic cholecystectomy

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24
Q

When I’m looking at lab test and I want to look at alcohol abuse in liver disease which two tests are important? I.e. What tests are always associated with alcohol liver disease? -

A

AST and ALT (most helpful in establishing alcohol disease)

AST and ALT
Look up how to do the 2:1 ratio’s (he said don’t over think it and don’t go too deep)

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25
Q

Patient that is jaundiced with an elevated unconjugated bilirubin - what would cause that?

A

hemolytic reactions (breaking down RBC’s)

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26
Q

Which one of these labs is elevated? 50 y/o pt w/ Malaise , RUQ pain, no bloody diarrhea, yellow skin, smoke 2 packs a day, past day or so his cigarettes started tasting bad to him, which labs are elevated?

A

Elevated transaminases (make you not want to smoke)

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27
Q

Of the following markers: most likely positive in patient with active hep B infections? could also be what others?

A
  • Hepatitis B surface antigen (HBsAg) – serologic hallmark of HBV infection (so most likely)
  • detection of IgM anti-HBc usually regarded as an indication of acute HBV infection
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28
Q

Is HBcAg detectable in serum?

A

NO core antigen not detectable, must BIOPSY to get it!

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29
Q

When do we see anti-HBs?

A

after clearance of HBsAg and/or successful vaccination

30
Q

indicates viral replication and infectivity in Hep B? What happens when it’s present for over 3 months?

A

Hepatitis B e antigen (HBeAg) indicates viral rep and infectivity….

• Persistence of HBeAg beyond 3 months indicates increased likelihood of chronic HBV

31
Q

In Contrast to Hep A and B - what would Hep C infection look like? M

A

ore mild w/o any overt clinical symptoms which is why it’s so easily transmitted - severe GI symptoms? No… it’s associated with Hep C is associated with Cancer

32
Q

• High risk of conversion to chronic state

– Significantly increased risk of cirrhosis and carcinoma

A

Hep C

33
Q

Assume you found Hep C marker: Anti-HCV EIA
• If result is positive/equivocal, do which test do we do and what are we looking for? If that follow on test is positive what are observing in our patients I.e. which labs really matter?

A

HCV RNA test (PCR) – Presence of HCV RNA is confirmatory of Hep C (HCV)

If HCV is confirmed obtain renal panel and urinalysis
• To observe for p r o t e i n u r i a , h e m a t u r i a , a n d / o r r e d u c t i o n in glomerular filtration rate (GFR)

34
Q

He said Hep B is associated with pregnancy in the review… but the slides say this hep is associated with pregancy!

A

Hep E

35
Q

You’re testing patients with suspected hep C - hep C - what’s the most appropriate next step - what do you do next?

A

RNA PCR

36
Q

21 y/o pt otherwise healthy - high transaminases with no symptoms and slight hepatomegaly - got a new tattoo recently - from his friend w/ kit from Amazon?

A

most likely Hep C

37
Q

Which of the following is a LATE manifestation of hepatic encephalopathy?

A

AMS (person place time or event), somulance, confusion,

(sleep pattern inversion is EARLY so not this) other EARLY signs are hypersomnia, insomnia or inversion of sleep pattern, subtly impaired computations, exaggeration of normal behavior, metabolic tremors, muscular incoordination, asterixis (tremor of the hand with the wrist extended)…. later we have altered mental status

38
Q

56 y/o with cirrhosis ER due to AMS and confusion - hyper reflexia, pungent breath odor, asterixis (tremor of the hand with the wrist extended)… treat with?

A

Lactulose

39
Q

Ascites and think bacterial peritonitis - what’s most likely for bacterial ?

A

fever

40
Q

Systemic manifestations to cirrhosis - what’s a condition that’s related to portal hypertension and cirrhosis?

A

Caput medusae

41
Q

Risk of hepatocellular carcinoma?

A

cirrhosis - alcohol abuse

42
Q

Female with generalized puritis - AST and ALT elevated, ALP elevated, what’s wrong with the patient? Can’t stop scratching?

A

Biliary cirrhosis (scratching) - not carcinoma

43
Q

Hallmark of Wilson’s disease?

A

Kayser–Fleischer ring (KF rings) are dark rings that appear to encircle the iris of the eye. They are due to copper deposition in part of the cornea (Descemet’s membrane) as a result of particular liver diseases.

Wilson disease. … Wilson disease (WD) is an autosomal recessive inherited disorder of copper metabolism, resulting in pathological accumulation of copper in many organs and tissues. The hallmarks of the disease are the presence of liver disease, neurologic symptoms, and Kayser-Fleischer corneal rings.

44
Q

Budd chiari syndrome major syndrome?

A

SPIDER WEB VEINS?

Symptoms associated with Budd-Chiari syndrome include pain in the upper right part of the abdomen, an abnormally enlarged liver (hepatomegaly), yellowing of the skin and the whites of the eyes (jaundice), and/or ascites

Budd-Chiari syndrome involves obstruction or narrowing (occlusion) of the outflowing veins from either large regions of the liver or the entire liver. Blood clots or congenital webbing occur at the junction of these vessels with the large vein that carries the blood from the lower part of the body (inferior vena cava) to the right upper chamber (atrium) of the heart. This syndrome may begin gradually or abruptly.

45
Q

40 y/o male with optometry exam - notices ring around eyes - which disease and what would we expect to find in the serum and urine?

A

Wilson’s disease (decreased serum ceruloplasmin- cannot carry the copper out, but copper will still be increased in the urine because that’s not normally how it’s excreted)

46
Q

Treatment protocol for hemochromatosis and Wilson’s disease - what do we to with?

A

Chelators - tx is chelation of the copper

47
Q

Budd-Chiari Syndrome
• Hepatic Venous Outflow Tract Obstruction
– Results in post-hepatic portal HTN

what are the two types?

A

• Primary Budd-Chiari:
– Obstruction due to a predominantly venous
process (thrombosis or phlebitis)

• Secondary Budd-Chiari:
– Compression or invasion of the hepatic veins
and/or the inferior vena cava by a lesion that originates outside of the vein (eg, a malignancy

48
Q

what are the essentials of dx for budd-chiari syndrome?

test of choice?

A

RUQ pain and tenderness (tender painful hepatomegaly)
Ascites
occlusion/absecne of flow in hepatic veins and/or inferior vena cava
Jaundice and Spenomegaly (from slides)

test of choice is color doppler ultrasound

49
Q

how do we treat budd-chiari syndrome?

A

admit the pt! then

50
Q

What is Charcot’s Triad? Which disease has this triad and what is it due to?

how about Reynolds pentad? Which disease?

A

Charcot Triad:
– RUQ Pain
– Fever/Chills
– Jaundice
• Sometimes referred to as “Ascending Cholangitis”
– Due to the ascent of bacteria from the duodenum via the opening of the bile duct

Acute Cholangitis • Reynolds Pentad:
– RUQ Pain
– Fever/Chills (rigors)
– Jaundice
– Altered Mental Status
– Hypotension
• Indicates  Acute Suppurative Cholangitis
– Surgical emergency!
51
Q

Patient comes in for routine exam for physical… she Female undergoes RUQ ultrasound - for slightly raised transaminases - few stones in gallbladder - what do you do?

A

tell the patient to diet and exercise and they can continue on WITHOUT a referral

52
Q

34 y/o male goes to ER for acute onset of n/v chills 130/82, pulse 96, low grade fever 100.4 (listen to fever classifications here) - PE says he’s ill appearing - positive Murphy’s sign w/o palpable liver or gallbladder and no jaundice - do we ADMIT this patient and how do we treat?

A

Admit this pt…. Give IV fluid, IV abx, and consult surgeon for admission (NEEDS CONSULT***)

53
Q

40 y/o male RUQ pain , N/V, yellowish skin 4 hours ago, 130/82, temp 99 - ill appearing pt (so must admit) - no hepatomegaly and - jaundice and scleral icterus -

A

he has choledocolithiasis

54
Q

In contrast to treatment of cholelithiasis - how to treat choledocolithiasis?

A

must do ERCP even w/o symptoms

55
Q

Reynolds syndrome adds what two to Charcot’s triad?

A

HOTN and AMS (look to see if it’s explained in another question)

56
Q

43 y/o female with 6 month hx of vague RUQ discomfort - not related to meals - dull discomfort - pt type I diabetes - pt rarely drinks - only takes acetaminophen - no family hx of chronic liver disease and no blood transfusions -after ordering labs- mild AST ALT and ALP rise - normal iron - lipid panel has markedly triglyceridemia (cholesterol) she has slightly elevated HBsAg - most likely cause?

A

non alcoholic steatohepatitis (NASH form of NAFLD non alcoholic fatty liver disease) ….compare HB sAg only slightly elevated means that it’s not Hep B… it can be there and she got the surface antigen of Hep B from the vaccine!

most patients asymptomatic
-if symptoms usually fatigue, malaise, vague RUQ discomfort… NAFLD usually found because of elevated aminotransferases (or incidental finding of hepatic steatosis on abdominal imaging for diff reason)

57
Q

what are the most common causes of NAFLD?

A

obesity
diabetes
hypertriglyceridemia (as a part of metabolic syndrome)

most patients are asymptomatic, will have elevated aminotransferases, hepatomegaly, or steatosis on US

most patients asymptomatic
-if symptoms usually fatigue, malaise, vague RUQ discomfort… NAFLD usually found because of elevated aminotransferases (or incidental finding of hepatic steatosis on abdominal imaging for diff reason)

58
Q

normal lab findings for NAFLD? How do we diagnose definitively?

A

Lab findings:
– Elevated transaminases
• 1:1 AST:ALT ratio – Elevated ALK PHOS

• Hepatic ultrasonography & BIOPSY
– Evidence of steatosis

• Must rule out other causes of fatty liver disease
– excessive consumption of alcohol (confirmed via biopsy though because cannot rule out alcohol even when they say this… also, imaging does not distinguish steatosis from steatohepatitis only biopsy does

59
Q

Ransoms criteria - presentation - what is it used for?

A

predicts severity of acute pancreatitis

AGE.    >55
WBC    >16,000
BG     >200
LDH    >350
AST    >250

After 48 Hours we compare initial to 48hr levels of the following
Hematocrit ——– fall by >10%
BUN —————— increase by >5 mg/DL despite fluids
Serum Ca ——- <8 mg/dL
PO2 —————- < 60mmHg
Base deficit —— > 4 MEq/L
Fluid sequestration — > 6L

60
Q

Acute Pancreatitis

• Laboratory Findings:

A

– ↑↑Serum amylase and lipase (3x upper limit)
• Lipase increases earlier, remains elevated
longer & has higher sensitivity for pancreatitis (SO WE PREFER LIPASE)

– CBC – Leukocytosis
– CMP:
• Elevated BUN – Hepatic Panel
• Elevated ALK PHOS & Bilirubin

– Elevated CRP – marker of inflammation

61
Q

Suspected carcinoma of the pancreas - Clinical Presentation and hallmark finding?

Lab finding?

A

Clinical Presentation:
– Abdominal pain, jaundice, weight loss
• Vague, diffuse epigastric or LUQ pain
• Jaundice due to common bile duct obstruction by pancreatic head lesion

Courvoisier Sign
• Non-tender, palpable gallbladder

Lab finding: CA 19-9
• Serum tumor marker

62
Q

45 y/o male with insidious onset of gastric discomfort - in patient treatment for alcohol - 40 y smoking history - no longer drinks - yellowish discoloration of his sclera, patient lost weight - what type of cancer are we worried about ?

A

Pancreatic cancer

63
Q

63 y/o women acute onset abdominal pain - initially constipated, but now diarrhea - steady LLQ pain - 101.5 temp, abdomen tender, rebound tenderness - what’s the best test to confirm this diagnosis?

A

Abdominal CT

* WHAT”S THE DIAGNOSIS ?!?!!?!?!?!? ***

DIVERTICULUTIS!!! (Old lady w/ constipation was foot stomped in his lecture FYSA)

64
Q

42 y/o severe abdomen pain in epigastric region - 10/10 pain, N/V, 86/55 - pulse is 112, temp 101.5, rebound tenderness mid epigastric pain - bowel sound are absent, positive cullens sign - what’s the most common cause of this presentation?

A

what’s the most common cause of this presentation: Cholelithiasis and alcohol abuse

Presentation / Dx =
Acute Pancreatitis
• Most commonly due to gallstones or chronic alcohol abuse (> 2/3 of cases)

65
Q

56 y/o with abdominal pain 9/10, N/V, fever, clammy skin, Tylenol and fluids, on a hydrochlorothiazide (which causes increased Ca levels),

TTP in both upper quadrants, HR = 100, Past med hx = CHF, gallstones, etc. What’s the most likely Diagnosis and how do we treat?

A

ACUTE PANCREATITIS (increased calcium = increased coagulability)

“Tx for pancreatitis… bowel rest and fluids “

We ADMIT ALWAYS = mild and Severe get admitted

If it’s sever we need an early surgical consult.. if it’s mild we can keep them NPO to rest the pancreas, bed rest, and pain control with morphine (conventional says meperidine aka demerol)

66
Q

Which of the following is the best tx for an asymptomatic pt with metabolic syndrome… with elevated ALK PHOS, evidence of steatosis on hepatic US… best tx method?

A

Lifestyle modifications (stop drinking, diet, exercise)

Dont need to admit (HOWEVER IF YOU HEAR, ILL-APPEARING, YOU ADMIT)

67
Q

33 y/o female for annual physical… Hx of GERD, asthma, IBS, 1-2 drinks/week, never smokers, no drugs, PmHx=appendectomy, father had a heart (“lots of distractors”), mother has hx of UC…

What’s the appropriate screening age for this patient?

A

50!

UC is not a concern for her… “lots of distractors”

68
Q

68 y/o diabetic w/ sudden RUQ pn, radiating to the shoulder and leukocytosis w/ elevated transaminases if this patient doesn’t get the requisite surgical procedure… what is the most common complication?

A

diabetic = immunocompromised

Gangrenous cholecystitis

(associate gangrenous w/ diabetics….)

69
Q

_________ is by far the most common cause of persistent mildly to moderately elevated aminotransferase levels.

A

NAFLD

Nonalcoholic fatty liver disease

70
Q

Elevated ALT and AST levels, often greater than 1000 units/L (20 mckat/L), are the hallmark of hepatocellular necrosis or inflammation. Elevated alkaline phosphatase levels are seen in cholestasis or infiltrative liver disease (such as tumor, granulomatous disease, or amyloidosis). Isolated alkaline phosphatase elevations of hepatic rather than bone, intestinal, or placental origin are confirmed by concomitant elevation of…

A

.. gamma- glutamyl transpeptidase or 5′-nucleotidase levels. Serum gamma-glutamyl transpeptidase levels appear to correlate with the risk of mortality and disability in the general population.

The differential diagnosis of any liver test elevation always includes toxicity caused by drugs, herbal and dietary supplements, and toxins.