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Gastrointestinal Flashcards

1
Q

Study to order if pt presenting with dysphagia/regurg for solids AND liquids

A

Probably a motility disorder

Get barium swallow

Want to see how throat looks when pt swallows, aka the peristalsis function & motility

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2
Q

Study to order if pt is presenting with dysphagia - initially to solid foods only but now cannot tolerate liquids or soft foods either?

A

Order an EGD - you want to look at the tissues!

Think if a tumor was growing…initially huge chunks of stead would cause a problem but then as the tumor grew larger & obstructed more you’d have problems with soft foods & liquid too!

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3
Q

Study to order when identifying a motility disorder of the esophagus?

List motility disorders of the esophagus

A

Order a barium swallow - want to see the peristalsis (AKA MOTILITY) of the esophagus!

Achalasia (inc LES pressure 2/2 idiopathic loss of nerves)

Nutcracker esophagus (excessive pressure during peristalsis - manometry = inc pressure during peri)

Diffuse esopageal spasm - esophagram shows CORKSCREW - stabbing chest pain worse w/ hot or cold liquids/food

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4
Q

Gold standard dx achalasia

A

Manometry

Increased LES pressure > 40 mmHg

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5
Q

EGD of nutcracker will show?

A

NORMAL

Get manometry for dx - will show inc pressure during peristalsis

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6
Q

Barium swallow (esophagram) nutcracker esophagus?

A

NORMAL

Get manometry for dx - will show inc pressure during peristalsis

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7
Q

Initial study to order for dysphagia to solids

A

EGD

If looking for tissue abnl - ring/web, cancer (dysphagia for solids only) –> EGD

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8
Q

Initial study to order for dysphagia to both solids and liquids (at onset)

A

Barium swallow esophagram

If dysphagia to solids and liquids from onset then probably a motility disorder

For identifying abnormal motility disorder - make the SWALLOW - aka barrium swallow

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9
Q

Clinical presentation & Dx diffuse lower esophageal spasm

A

CP: Stabbing chest pain, worse w/ hot or cold liquids/foods

Dx: Barium esophagram - CORKSCREW

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10
Q

Drugs that lower the esophageal pressure

(and therefore used to treat disease - achalasia, nutcracker, diffuse esophageal spasm - 2/2 increased esophageal pressure)

A

CCB
Nitrates
Botox injections
Sildenafil

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11
Q

Diagnosis of nutcracker esophagus

A

Manometry - increased pressure during peristalsis

EGD and barium swallow will be NORMAL (will probs have already ordered at least a barium swallow to see why person is having difficulty swallowing liquids and solids)

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12
Q

Who gets eosinophilic esophagitis?

A

MC IN KIDS

ATOPIC PT (allergies, asthma, etc…lots of IgE!)

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13
Q

Dx of eosinophilic esophagitis

A

Dx:
EGD - can be normal
+/- multiple corrugated rings on the esopagus
+/- white exucates

Tx:
Remove foods that incite allergic response, inhaled ICS WITHOUT spacer - want to go to throat not lungs

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14
Q

MCC pill-induced esophagitis

A

Bisphosphonates
KCl
Iron pills
Bb, CCB

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15
Q

Hallmark of infectious esophagitis

A

ODYNOPHAGIA = PAIN

CMV = large superficial shallow ulcers - GANCYCLOVIR 
HSV = small deep ulcers - ACYCLOVIR 
Candida = linear yellow-white plaques - FLUCONAZOLE
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16
Q

What is the diagnostic test of choice for a evaluating a person with acute chron’s disease?

A

UGI series with small bowel follow thru

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17
Q

What is plummer-vinson syndrome?

A

It is the triad of:

  1. dysphagia
  2. esophageal webs
  3. iron-deficiency anemia

MC in Caucasian women 30-60

Can also have atrophic glossitis, angular cheilitis

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18
Q

What is an esophageal web?

A

Thin membranes in the mid-upper esophagus - may be congenital or acquired

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19
Q

What is a schatzki ring? What are they associated with?

A

It is a LOWER esophageal web/constriction at the squamocolumnar junction

MC a/w sliding hiatal hernias, but may be a complication of corrosive esophageal injury (chronic GERD = stricture)

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20
Q

CP Schatzki ring, esophageal web?

A

Dysphagia to SOLIDS (mainly) - liquid can get by the ring for the most part

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21
Q

Dx Schatzki ring, esophageal web?

Tx?

A

Barium esophogram (swallow) = diagnostic test of choice

Tx: Endoscopic dilation of the area if symptomatic without reflux

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22
Q

CP Boerhaave syndrome? Definitive diagnostic study?

A

Boerhaave = FULL THICKNESS rupture of DISTAL esophagus

CP: Retrosternal chest pain worse with deep breathing & swallowing, hematemesis

PE: Crepitus on chest auscultation due to pneumomediastinum

Dx: Definitive dx study = CONTRAST esophagram - positive = + leakage

Chest CT may be ordered first - shows pneumomediastinum, esophageal thickening

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23
Q

“Red wale” markings & cherry red spots are suggestive of what?

A

These are endoscopic esophageal variceal descriptions in which they are at very high risk of bleeding soon

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24
Q

When is a TIPS indicated in an esophageal varices bleed?

A

If bleeding despite endoscopic or pharmacologic treatment

C/I: Hepatic encephalopathy, infections

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25
Q

Mainstay of management to prevent rebleeds?

A

Nadolol

MOA: Decrease portal venous pressure with NON-selective beta blockers

Isosorbide

MOA: Long-acting nitrate (vasodilator) that reduces esophageal pressure

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26
Q

Type I hiatal hernia

A

“sliding” hernia = MC type (95%) - when GEJ comes loose & stomach w/ GEJ slide into the mediastinum (increases reflux)

Management: similar to GERD

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27
Q

Management of GERD

A
  1. Lifestyle modifications (elevation of HOB, avoid recumbency for three hours after eating, eating small meals, avoiding certain foods (fatty, spicy, citrus, chocolate, caffeinated), decrease ETOH intake, weight loss, smoking cessation
  2. “As needed” pharmacological therapy - OTC antacids, H2 blockers
  3. Initiation of scheduled pharmacological therapy - PPIs

**If alarm sx at any point (dysphagia, odynophagia, weight loss, bleeding) then order EGD

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28
Q

Alarm symptoms GERD

A

Dysphagia
Odynophagia
Weight loss
Bleeding

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29
Q

Gold standard GERD dx

A

24 hour ambulatory monitoring

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30
Q

Type II hiatal hernia

A

“rolling” hernia = when fundus of stomach protrudes thru diaphragm with GE junction remaining in anatomic location ….may lead to strangulation so ..

Tx = surgical repair of the defect to avoid complications

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31
Q

H. pylori triple thearpy

A

Clarithromycin
Amoxicillin
PPI

(CAP)

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32
Q

H. pylori quadruple therapy

A

Tetracycline
Metronidazole
PPI
Bismuth subsalicylate

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33
Q

Duodenal or gastric ulcers more common?

A

Duodenal 4x more common

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34
Q

All patients with a gastric ulcer need a ?

A

EGD w/ Bx to rule out malignancy

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35
Q

Alarm symptoms PUD

A

> 50 YO, dyspepsia, history of gastric ulcer, anorexia, weight loss, anemia, dysphagia

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36
Q

Follow up on gastric ulcer

A

ALL GU MUST BE FOLLOWED UP WITH ENDOSCOPY TO RULE OUT MALIGNANCY AND DOCUMENT HEALING!!!

Done 8-12 weeks after therapy initiation

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37
Q

Dyspepsia 2/2 duodenal ulcer - characteristics

A

Better w/ food
Worse 2-5 hours after eating
Worse at night

**Nocturnal sx clasically a/w duodenal ulcers

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38
Q

Gastric ulcers - characteristics of sx - onset

A

Food-provoked dyspepeia - bad pain soon after eating (30 min - 1 hr)

Weight loss (b/c afraid to eat)

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39
Q

Gold standard PUD dx

A

Endoscopy w/ bx

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40
Q

Causative factors, age, incidence, benign or malignant, pain worse or better with meals

Gastric vs duodenal - compare above characteristics

A

Duodenal:

  • Cause - inc in DAMAGING factors (acid, H. pylori)
  • Age - MC in younger pt (30-55)
  • Incidence- 4x MC, BENIGN
  • Pain BETTER w/ meals, worse 2-5 hours after meals

Gastric:

  • Cause - decrease in mucosal protective factors (dec mucus, bicarb, prostaglandins, NSAIDs)
  • Age - MC in OLDER pt (55-70)
  • Pain WORSE w/ meals (& for 1-2 hrs after too)
  • LESS common, 4% are MALIGNANT
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41
Q

What is the most important risk factor for gastric carcinoma?

A

H. pylori

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42
Q

MC type of gastric cancer

A

ADENOcarcinoma - gAstric

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43
Q

What is linitis plastica?

A

Diffuse thickening of the stomach wall w/ “leather bottle” appearance due to gastric cancer infiltration = WORSE type

Superficial spreading = best prognosis/type of gastric cancer

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44
Q

CP gastric cancer

A

EARLY SATIETY!!!
(tumor filling up stomach = full easier…duh)

Iron-deficiency anemia 2/2 small amt bleeding

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45
Q

Signs of mets gastric ca

A

Supraclavicular LN = VIRCHOW
Umbilical LN = sister mary joseph

Ovarian mets = krukenburg tumor

Left axillary LN = IRISH sign

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46
Q

Bilirubin metabolism - prehepatic, intrahepatic, posthepatic

A

Pre-hepatic -
Bilirubin produced by heme metabolism (2/2 RBC destruction). Heme degraded by macrophages in RES = green biliverdin to –> bilirubin (red/orange) -this unconjugated bilirubin is sent to liver for conjugation & excretion

Intrahepatic -
Hepatocytes conjugate the bilirubin w/ enzyme UGT. This conjugated bilirubin (d. bili) is now water soluble (for bile excretion)

Post-hepatic -
D. bili is mixed in with bile, transported thru biliary & cystic ducts to be stored in GB.

Conjugated bilirubin cannot cross intestinal wall. It is converted to urobilinogen which is oxidized by gut bacteria to stercobilin (give stool brown color), converted to urobilin in kidney & excreted in urine (give urine it’s color). Small amt converted back & reabosorbed for further use in biliary system (via enterohepatic circulation)

Therefore in disease where there is excess DIRECT (conjugated) bilirubin, it is excreted in the urine & stool –> if you have a biliary obstruction it prevents secretion of large portions of conjugated bilirubin from being excreted in stool which is normally given its brown color by the stercobilin. It stays in the blood, & goes to kidney where converted to urobilin –> The urinary excretion is not blocked so a lot of excretion from blood is shifted to urine = DARK urine & LIGHT stools in conjugated hyperbilirubinemia.

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47
Q

Why is dark urine & light-colored stool seen with conjugated (direct) hyperbilirubinemia?

A

In disease where there is excess DIRECT (conjugated) bilirubin, it is excreted in the urine & stool –> if you have a biliary obstruction it prevents secretion of large portions of conjugated bilirubin from being excreted in stool which is normally given its brown color by the stercobilin.

It stays in the blood, & goes to kidney where converted to urobilin –> The urinary excretion is not blocked so a lot of excretion from blood is shifted to urine = DARK urine & LIGHT stools in conjugated hyperbilirubinemia.

Urobilin is what gives urine its characteristic yellow color!

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48
Q

Why can you see dark urine with hemolysis (causes almost all cases of indirect (unconjugated) hyperbilirubinemia?

A

Because you have hemaglobinuria so the hemoglobin that’s being lysed from the RBC gets peed out in your urine…the dark urine is from that NOT from bilirubin

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49
Q

Increase bilirubin WITHOUT increased LFTs… = ?

A

Think inherited bilirubin metabolism disorders (Gilbert’s (dec UGT activity), or Crigler-Jajjar = NO UGT activity, dubin johnson - can’t excrete from hepatocyte)

Gilbert’s is v common!

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50
Q

Dubin johnson syndrome?

A

Isolated (mild - 2-5) conjugated hyperbilirubinemia (b/c hepatocytes can conjugate but not excrete the bilirubin how they’re supposed to = all conjugated bilirubin stuck in liver = dark

Dubin = DDD (3D’s)
Dubin
Direct
Dark liver

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51
Q

Indirect hyperbilirubinemia is 2/2?

A

Indirect = HemolysIIIIs & gIIIIIlbert’s!

Have I’s in them! Indirect starts w/ an I!

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52
Q

Cholestatic pattern of liver injury

A

Inc alk phos
Inc GGT
Inc bilirubin

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53
Q

Hepatocellular pattern of liver injury

A

Inc ALT & AST > others

ALT more sensitive for Liver dz

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54
Q

Which of the liver function tests is most sensitive for biliary injury?

A

GGT

But not specific

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55
Q

Increased ALP without increased GGT

A

Bone or gut issue not liver issue

Remember alk phos is also found in intestinal mucosa & bone

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56
Q

Inc ALT > 1000 AND + ANA…thinking?

A

Autoimmune hepatitis

+ANA
+ smooth muscle ab
+ Increased IgG

= Autoimmune issue

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57
Q

Labs for viral or toxic ACUTE liver injury

A

ALT> AST –> both very high

AST & ALT > 1000 –> think ACUTE viral hepatitis

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58
Q

Labs consistent with CHRONIC liver injury

A

Increased INR

Low albumin

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59
Q

Cholelithiasis - CP, RF, Dx, Tx

A

CP: Colicky, sudden onset, INTERMITTENT RUQ abd pain after big fatty meal, lasting 30 min - several hours

RF: Family history, native american = strongest factors. Also Fat, fair, female, forty, fertile etc

Dx: Ultrasound

Tx:
ASX –> observe
Symptomatic –> Elective cholecystectomy

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60
Q

Choledocolithiasis - CP, complications

A

Gallstone in CBD a/w ductal dilation

CP: ASX = MC (>50%) - may be incidental finding when doing studies for other reasons or during evaluation of abnormal LFTs on routine testing

Complications: Acute pancreatitis, acute cholangitis

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61
Q

Initial test ordered choledocolithiasis

A

Trans-abdominal US

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62
Q

Diagnostic test of choice choledocolithiasis

A

ERCP - dx & tx - extract the stone

63
Q

Acute cholangitis - what is it? Etio

A

Biliary tract infection 2/2 obstruction in the CBC - MC due to GN organisms that ascend from the duodenum

E. coli MC, klebsiella, enterobacter species, anaerobes or enterococcus also common

64
Q

Gold standard dx acute cholangitis

A

Cholangiography via ERCP

65
Q

Management acute cholangitis

A

ABX:
Monotherapy - unasyn, zosyn
Dual - Cipro/flagyl, ceftriaxone/flagyl etc

Stone extraction:
Preferred via ERCP

66
Q

Gold standard dx for acute cholecystitis

A

HIDA scan

+ HIDA = non-filling of GB

67
Q

Management cholecystitis

A

NPI, IV fluids, ABX, cholecystectomy w/in 72 hours, laparoscopic preferred whenever possible

68
Q

Who gets acute acalculous cholecystitis?

A

MC occur in the seriously ill (post op, ICU patients) 2/2 prolonged fasting, dehydration, TPN, GB stasis, burns, DM etc

It’s due to GB sludge not stones

69
Q

Si of chronic cholescystitis -

A

Strawberry GB

Porcelain GB (premalignant condition)

70
Q

Acute hepatic failure = what?

A

Rapid liver failure manifesting as hepatic encephalopathy with coagulopathy common

71
Q

MCC acute liver failure

A

Acetaminophen overuse or overdose

Also drug reactions (Isoniazid, rifampin, pyrazinamide), viral hepatitis, budd-chiari (hepatic v. obs), Reye syndrome (ASA use during viral infection in kids) etc

72
Q

Management of hepatic encephalopathy

A

Lactulose - converted to lactic acid, neutralized the ammonia

Rifaximin, neomycin - reduces GUT bacteria that produce ammonia in the GIT

Protein restriction (proteins are broken down into ammonia)

73
Q

What is the only definitive treatment for acute liver failure?

A

Liver translplantation

74
Q

Which viral liver infection is a/w spiking fevers?

A

Hepatitis A

75
Q

CP viral hepatitis

A

Malaise, arthralgias, URI sx, anorexia (liver won’t let you eat if it’s sick!!!), N/V, abdominal pain, +/- acholic (clay) stools

76
Q

CP fulminant hepatitis 2/2 acute viral hepatits

A 
Encephalopathy
Coagulopathy
Jaundice
Edema
Ascites
Asterixis 
Hyper-reflexia
77
Q

MC source of Hep A

A

Asx children < 6 YO = mc source for adults

Also from drinking contaminated water/food during international travel b/c it spreads via FECAL oral route - just like Hep E

78
Q

You can only catch Hep D if you have?

A

Hep B

Specifically HepB surface antigen (acute hep B infection) to allow dual Hep D entry

= Direct cytopathic effect = more severe hepatitis & faster progression to cirrhosis

79
Q

Hep C labs in acute hep C infection

A

Use HCV RNA

HCV RNA will be positive w/in 6 weeks of infection

May have Anti-HCV ab –> but unlike Hep B, anti-HCV antibodies does not indicate cure (can have chronic Hep C if still positive for HCV RNA > 6 months)

80
Q

Hep C labs indicating resolved infection

A

HCV RNA NEGATIVE

+/- Anti-HCV Ab

81
Q

Hep C lavs indicating chronic hepatitis

A

HCV RNA positive for > 6 months

AND Anti-HCV positive

Even tho developed ab, your body couldn’t control & now you have a chronic Hep C infection (occurs in 80% of pt infected)

82
Q

Screening for HCC

A

Via serum alpha-fetoprotein & US

83
Q

First serologic evidence of Hep B infection

A

+ Hep B surface antigen

84
Q

Hep B serologies consistent with distant resolved infection or vaccination?

A

+ Hep B surface ANTIBODY

85
Q

Serologies consistent with successful Hep B vaccination

A

+ Hep B surface ANTIBODY

Negative for Ab to core, envelope
Negative for all actual antigens (surface, envelope antigen)

86
Q

Hep B serologies consistent with acute Hep B infection

A

Hep B surface antigen +

aCute infection: IgM against Hep B Core (Anti-HBc)

87
Q

Chronic Hep B infection categorized as?

A

Hep B surface antigen positive for > 6 months

88
Q

Presence of Hep B envelope antigen a sign of ?

A

Active viral replication & increased infectivity

Present > 3 months = high likelihood of developing chronic HBV

(only 10% of adults do but 90% of perinatally acquired Hep B –> chronic)

89
Q

Labs consistent with chronic replicative Hep B

A

Anti HBs negative
Anti Hbe negative

HbsAg +
HbeAg +

Anti Hbc + (IgG)

Basically your immune system sucks & didn’t make antibodies to anything it was supposed to. So all antigens still positive (except core b/c not acute inf anymore) and all antibodies are negative

90
Q

Labs consistent with chronic non-replicative hepatitis

A

HbsAg +
HbeAg -

Anti-Hbc + (IgG)
Anti-Hbe +
Anti-Hbs -

91
Q

HbsAg -
Anti-HBs -

Anti-HBc IgM +

HbeAg -
Anti-Hbe -

A

Window period

Anti - core IgM = first antibody to appear

92
Q

HbsAg+
Anti-Hbs -

Anti-Hbc + (IgM)

HbeAg +/-
Anti-Hbe +/-

A

aCute hepatitis

Anti-Hep B core IgM antibodies AND
Hep B surface antigen positive

**Establishes infection & infectivity

If it is replicating already then Hep B envelope antigen will be positive & if body has made Ab to that then anti- Hbe will be as well - depends on when serologies were ordered & how fast immune system reacts

93
Q

HbsAg -
Anti-Hbs +

Anti-Hbc + (IgG)

HbeAg -
Anti-Hbe -

A

Recovery (resolved)

Antibodies to the surface antigen and core without any actual active viral antigens present in blood = body controlled the infection & killed every viral particle with those antigens

94
Q

HbsAg -
Anti-Hbs +

Anti-Hbc -

HbeAg -
Anti-Hbe -

A

Immunization

Antibodies to surface w/o antibodies to core b/c vaccine doesn’t contain any core viral material only surface

95
Q

HbsAg +
HbeAg -

Anti-Hbc + (IgG)
Anti-Hbe +
Anti-Hbs -

A

Chronic non-replicative hep b

Remember this is after 6+ months of labs staying like this b/c > 6 months = chronic hep b by definition

96
Q

HbsAg +
AntiHbs -

Anti-Hbc + (IgM)

HbeAg +
Anti-Hbe -

A

Chronic replicative Hep b

Remember this is after 6+ months of labs staying like this b/c > 6 months = chronic hep b by definition

97
Q

Prevention of Hep B

A

Vaccin given @ 0, 1, & 6 months

98
Q

Hepatic vein obstruction known as? MC in who? Primary vs secondary?

A

Budd-chiari syndrome

Mc in women in 20’s-30s

primary - hepatic vein thrombosis (MC)
secondary - hepatic vein or IVC occlusion (exogenous tumor suppression)

99
Q

Classic triad budd-chiari

A
  1. Ascites
  2. Hepatomegaly
  3. RUQ abd pain
100
Q

Dx budd-chiari - screening

A

Ultrasound

101
Q

Gold standard dx budd-chiari

A

Venography

performed if HIGH suspicion and negative non-invasive testing

102
Q

Tx budd chiari

A

Shunts (tips)

Balloon angioplasty w/ stent (if stenotic or obstruction of ivc = hepatic v occ)

Pharmacologic - anticoagulation - if acute thrombus < 4 weeks, not involving the IVC

Manage ascites - diuretics, low sodium, paracentesis

103
Q

HCC dx, tx

A

Ultrasound

Inc alpha-fetoprotein

Tx: Surgical resection

AVOID FNA to prevent seeding

104
Q

Cirrhosis definition

A

Irreversible liver fibrosis with nodular regeneration 2/2 chronic liver disease

105
Q

Si/sx hepatic encephalopathy

A

AMS - confusion, lethargy (ammonia)
Asterixis
Fetor hepaticus (sweet musty odor)
Inc ammonia levels

106
Q

General sx & physical exam severe liver cirrhosis

A

Sx: Fatigue, weakness, weight loss, anorexia

Si: 
Spider angiomas
Palmar erythema
Ascites 
Caput medusa 
Gynecomastia 
Muscle wasting 
Jaundice 
Bleeding 
Dupuytren's contractures
107
Q

CHILD-PUGH staging parameters

A

0-3 points for each - values listed + 3 points

Total bili > 3
Serum albumin < 2.8
PT INR > 2.3
Ascites moderate - severe
Hepatic encephalopathy Grade III-IV
5-6 pt = class A = 100% 1 yr 85% 2yr survival
7-9 pt = class B = 81% 1-yr, 57% 2-yr
10-15pt = class C = 45% 1-yr, 35% 2-yr
108
Q

Anti-mitochondrial antibody is hallmark in which disease?

A

Primary biliary cirrhosis

= Idiopathic AI d/o intrahepatic sm bile ducts

109
Q

Primary biliary cirrhosis -what is it? MC in? Sx? hallmark? tx?

A

Idiopathic AI d/o intrahepatic sm bile ducts

MC In middle-aged women (40-60)

Fatigue = 1st sx, then pruritis, RUQ, hepatometaly, jaundice

Dx: Hallmark = Anti-mitochondrial antibody, labs w/ cholestatic pattern

Tx =

  1. Ursodeoxycholic acid - dec progression
  2. Cholestyramine & UV light for pruritis
110
Q

Primary sclerosing cholangitis = what? MC in who? A/w with which disease?

A

AI progressive cholestasis 2/2 diffuse fibrosis of intrahepatic AND extrahepatic ducts

MC in YOUNG MEN 20-40 YO …notice whereas PBC is MC in middle-aged WOMEN…

PSC = UC –> MC a/w IBD - esp ULCERATIVE COLITIS. Inc risk of cholangiocarcinoma.

Dx ERCP, labs w/ cholestatic pattern

Tx: Liver transplant = definitive, stricture dilation to relieve sx, meds not beneficial

111
Q

Kayser-flescher rings?

A

COPPER deposits in eye 2/2 wilson’s disease = rare autosomal recessive mutation = inadequate bile excretion of copper

112
Q

Wilson’s disease? What? Dx, Tx

A

What:
Rare autosomal recessive mutation =
inadequate bile excretion of copper = abnormal deposits in brain, cornea, kidney (Wilson BRA-CO-KI = his name)

CP: Parkinson-like sx 2/2 basal ganglia cCu deposition, personality & behavioral changes, liver disease, corneal deposits

Dx: Decreased ceruloplasmin, inc urinary copper excretion

Tx:

  1. D-penicillamine (chelates copper) - also chelateds vitmain B6 (pyridoxine), so give to prevent depletion
  2. Zinc
113
Q

Ransons criteria used for? Parameters?

A

Deciding whether to admit someone w/ acute pancreatitis

Glucose > 200
Age > 55
LDH > 350 
AST > 250 
WBC > 16

0-2= severe pancreatitis unlikely, 2% mortality
> 3 = severe pancreatitis likely, 15% mortality

114
Q

MCC chronic pancreatitis in kids

A

Cystic fibrosis

Remember pancreatic insufficiency = one of three MC clinical manifestations of CF - pancreatic duct gets clogged = loss of exocrine function

115
Q

MC pancreatic cancer

CP
PE
Dx
Tx

A

Ductal adenocarcinoma, most in head

pAncreatic = Adenocarcinoma

painless jaundice, wieght loos = CP
Pruritis 2/2 inc bile salts in skin, anorexia, acholic stools, dark urine (CBD obs)

PE - courvosier’s sign – palpable NON-dtender distende gallbladder a/w jaundice

Dx - CT scan = initial TOC. ERCP most sensitive test.

Tx: whipple

116
Q

Tumor markers for pancreatis cancer

A

CEA
CA 19-9 (p looks like a P)

Ovarian is CA-125 (5 looks like an O)

117
Q

Painless rectal bleeding in 2 YO boy

A

Meckel’s diverticulum

Management = surgical excision if sx

118
Q

First line imaging SBO

A

Plain films - KUB will show air fluid levels in a step ladder pattern

119
Q

First line imaging paralytic ileus

A

Plain ABD radiograph - uniformly distended lops of small and large bowel

120
Q

Celiac dz - CP, dx

A

CP:
1. Malabsorption - diarrhea, abd pain, distension, steatorrhea, growth delays

  1. Dermatitis herpetiformis (pruritic, papulovesicular rash on extensor surface, neck, trunk & scalp)

Dx:
+ endomysial IgA Ab
+ transglutaminase Ab

121
Q

Definitive dx celiac

A

Small bowel biopsy

122
Q

Test of choice lactose intolerance

A

Hydrogen breath test

123
Q

Mc sites of a volvulus?

A

Sigmoid colon

Cecum

124
Q

Initial TOC volvulus

A

Endoscopic decompression of the bowel

125
Q

Characteristics of IBS - typical pt, diagnostic criteria

A

Pt: Young woman, early 20s

Dx criteria:
Recurrent abd pain on average at least 1x/week in the last 3 months with at least 2/3:

  1. Pain is related to defecation
  2. Pain onset a/w change in stool frequency
  3. Onset a/w change in stool form
NO BLOOD
NO ANOREXIA 
NO WEIGHT LOSS
NO NOCTURNAL SX (if nocturnal sx then IBD not IBS) 
NO family hx CRC, IBD, celiac sprue

Tx: Lifesytle changes - no smoking, dec fat & processed food, sleep, veggies

Diarrhea sx - dicyclomine (antispasmodic) or antidiarrheal - loperamide

Constipation sx - prokinetics, bulk-forming laxatives, saline or osmotic laxatives, lubiprostone

126
Q

Management of chronic mesenteric ischemia

A

Bowel rest, surgical revascularization (angioplasty w/ stenting or bypass)

Dx was via angiogram

127
Q

Definitive dx acute mesenteric ischemia

A

Angiogram

128
Q

Ishcemic colitis 2/2?

A

Low perfusional states - shock, shunting blood from organs = areas of ischemia in colon (watershed)

CP: LLQ pain (if sigmoid ischemic) w/ bloody diarrhea

Tx: Restore perfusion (IVF)

129
Q

Toxic megacolon definition, causes

A

Non-obstructive extreme colon dilation (>6cm)

Seen in :UC, chron’s pseudomembranous colitis, infectious, colitis, ischemic colitis etc

Tx: bowel decompression, bowel rest, NGT, ABX, fix electrolytes

130
Q

UC/CD a/w which rheumatological d/o? Skin d/o?

A

Seronegative spondyloarthropathies, aknylosing spondylitis

Erythema nodosum (also in sarco)

131
Q

Right sided colon ca presentation

A

change in bowel habits
+FOBT
Anemia
Diarrhea

132
Q

Left-sided colon ca

A 
Present LATER (left colon = bigger) 
Large bowel obstruction 
\+ change in stool diameter 
Hematochezia
133
Q

CRC Tx - localized vs mets

A

Local - surgical resection

134
Q

Dx colon ca, labs

A

Colonoscopy w/ bc = Dx TOC

elevated CEA, Iron-def anemia

135
Q

Elevated CEA = ?

A

COLON cancer - monitored during treatment too

CRC = CEA

136
Q

Indirect inguinal hernia is lateral or medial to the inferior epigastric artery?

A

LATERAL

Originates at weak spot in the INTERNAL (deep) part of the inguinal ring/canal & travels down thru ring & patent process vaginalis into the scrotum

137
Q

Direct inguinal hernia is lateral or medial to the inferior epigastric artery?

A

MEDIAL

Originates due to weakness in the floor of the inguinal canal - plows thru hesselbach’s triangle

138
Q

Anal fissure

A

Longitudinal paper-cut like tear in anoderm = anal pain at rest exacerbated by BM assoc w/ anal bleeding

Hx anal pain brought on by BM that lasts hours-days afterwards,, assoc w/ some bleeding, confirmed by PE

139
Q

Dx hemorrhoids

A

PE and/or anoscopy, DRE

140
Q

CP Anal abscess

A

Diffuse, tender, erythematous, indurated and fluctuant area within/near the buttocks
Pain is CONSTANT, can have problems sitting, NOT a/w BM (unless along wall)

141
Q

CP Anal fistula, MCC

A

MCC:
Non-healing (chronic) anorectal abscess of anal crypt gland in 40 YO M

CP:
Non-healing anorectal abscess following I&D

Intermittent rectal pain worse w/ BM sitting, activity

Malodorous perianal drainage, perianal skin excoriated/inflamed

May feel palpable cord leading to opening

142
Q

Tx Anal abscess/fistula

A

I&D followed by WASH

Warm-water cleansing
Analgesics
Sitz baths
High-fiber diet

143
Q

PKA common in? CP? Dx? Tx?

A

Common in BLONDE, blue-eyed with FAIR skin

CP:
Vomiting, mental delays, irritability, convulsions, eczema, inc DTR

Screening:
PKU heel stick at birth

Dx:
Urine w/ mousy odor

Tx:
Lifetime dietary restriction of phenylalanine (found in milk, cheese, nuts, fish, chicken, meats, eggs, legumes, aspartame in sodas

144
Q

Vitamin A involved with which bodily functions?

A

Vitamin A involved in: Vision, immune function, embryo development, hematopoiesis, skin & cellular health (epithelial cell differentiation)

VISION, SKIN, IMMUNE SYSTEM

145
Q

CP Vitamin A def

A 
CP: 
Xerophthalmia 
Night blindness
Poor wound healing
Dry skin
Poor bone growth

squamous metaplasia in conjunctiva, resp epithelium, urinary tract

BITOT’s SPOTS on eyes = white spots on conjunctiva due to squamous metaplasia of the corneal epithelium

146
Q

Vitamin C (ascorbic acid) def RF

A

Diet lacking raw citrus & green veggies, smoking, alcoholism, elderly, malnourished

147
Q

Vitamin C CP

A

= SCURVY = 3 H’s

Hyperkeratosis - hyperkeratotic follicular papules surrounded by hemorrhage

Hemorrhage - vascular fragility due to abnormal collagen production w/ recurrent hemorrhages in gums, skin & joints, impaired wound healing

Hematologic - anemia, glossitis, malaise, weakness, increased bleeding time

148
Q

Vitamin D def children

A

Rickets = soft bones = bone bending (Bowed legs), fx, costochondral thickening (rachitic rosary), dental problems, muscle weakness, developmental delay

Tx Ergocalciferol (vitamin D2)

149
Q

Vit D def adult

A

Osteomalacia

Diffuse bony pain
Muscle weakness
Fractures

LOOSER LINES - radiolucencies on xray

Tx Ergocalciferol (vitamin D2)

150
Q

B1 deficiency - 3 big clinical manifestations

A

ETOH = MCC

CP:

  1. BERIBERI
    - Dry = CRAN = muscle cramps/wasting, Reflexes impaired symmetrically, ANorexia, Neuropathy (peripheral, paresthesias)
    - Wet = HOHF, dilated CMP
  2. Werkicke’s encepholapthy TRIAD - AGO - Ataxia, global confusion, ophthalmoplegia (paralysis or abnl of ocular mu)
  3. Korsakoff’s dementia - irreversible - short term memory loss (50 first dates), confabulation
151
Q

Riboflavin def

A

Ribovlafin = B2

Def = Oral-ocular-genital syndrome

Oral = lesions of mouth, magenta-colored tongue, angular cheilitis, pharyngitis

Ocular = photophobia, corneal lesions

Genital = scrotal dermatitis

Noticing a pattern here with b vitamins…if have to then guess a mucosal membrane issue or nervous system issue or skin issue…

152
Q

Niacin def

A

Niacin = B3

Def = PELLAGR - 3D;s= diarrhea, dementia, dermatitis

Noticing a pattern here with b vitamins…if have to then guess a mucosal membrane issue or nervous system issue or skin issue…

153
Q

Pyridoxine def

A

Pyridoxine = B6 def

Etio: isoniazid, OCP

B6 def = PERIPHERAL NEUROPATHY, seizures, headache

Stomatitis, cheilosis, glossitis, glaky skin, anemia

Noticing a pattern here with b vitamins…if have to then guess a mucosal membrane issue or nervous system issue or skin issue…

154
Q

B12 def - etio, CP

A

Etio - pernicious anemia, strict vegans, malabsorption (ETOH, chron, atrophic gastritis (dec IF prod)

CP: Neurologic sx similar to neurosypalis 2/2 degeneration of posterior cord - loss of proprioception (clumsy, stumbling around, flap feet, looks like neurosyphilis)

Macrocytic, megaloblastic anemia

Tx IM (malabsorptive issues) or oral B12 (dietar issues)

Shillings test tells the difference

*PANCE by subspecialty (22 decks)

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