Oz - Foot Stomps

Question 1

Anoscopy and sigmoidoscopy - in otherwise healthy patients w/o anemia, under age of 45 y/o w/ small volume bleeding, anoscopy and sigmoidosocpy are performed to look for anorectal disease, IBD, infectious colitis. If a lesion is found

For patients over 45 w/ small volume hematochezia…

Answer 1

THE ENTIRE COLON MUST BE EVALUATED WITH COLONSCOPY TO EXCLUDE TUMOR!

Question 2

what are most cases of antibiotic associated diarrhea from?

Answer 2

usually mild and self limited and NOT from C Difficile

“True colitis” is ALMOST always from C. diff

Question 3

how are most cases of antibiotic associated colitis diagnosed?

Answer 3

stool assay from lecture

Question 4

water
greenish
foul smelling
may have mucous in the stool
abdominal cramping
mild leukocytosis <15,000 WBC

Temperature of less than 100.4

Answer 4

mild moderate abx associated colitis

Question 5

what makes mild moderate abx associated colitis become severe?

Answer 5

profuse diarrhea
fever of 100.4 to 101.3
hypoalbuminemia: serum albumin < 3g/dL

PLUS 1 of the following:

abdominal pain with diffuse abdominal TTP

NO ABDOMINAL DISTENTION!

Question 6

what makes severe ABX colitis become fulminant?

Answer 6

SEVERE plus one of the following:

Fever over 101.3
admission to ICU
HOTN w/ or w/o vasopressors
ileus (ID'd on CT)
significant abdominal DISTENTION
WBC > 35k
serum lactate levels > 2.2 mmol/L
End organ failure

Question 7

remember that ABX associated colitis does not always manifest with true pseudomembranous colitis… it becomes so when?

Answer 7

when there is severe inflammation and manifests with raised yellow or off-white plaques up to 2cm in diameter scattered over the colonic mucosa

Question 8

how do we test for C diff? What is the SOC and what else in addition to Study of choice?

Answer 8

stool assay PCR which is the Study of Choice***

backup is Enzyme Immunoassay (EIA) in which you need two samples to complete the testing!

IN addition:

CMP (electrolytes)
Hypoalbuminemia

Question 9

when we have fulminant C diff what do we want to make sure we have?

Answer 9

contrast enhanced CT of the abdomen and pelvis to look for Toxic megacolon

Question 10

true colitis is ALMOST always from?

How is diagnosis established in most cases?

Answer 10

C. diff

stool assay

Question 11

ABX disrupt normal flora and allow C diff to flourish in the colon… what are the most common causative agents?

Answer 11

– Ampicillin
– Clindamycin
– 3rd Gen cephalosporins
– Fluoroquinolones
– **However** almost all antibiotics have been
implicated

Question 12

How can you tell if it’s ABX associated colitis mild to moderate versus severe vs fulminant as far as fever?

how about TTP and distention?

Answer 12

fever is

less than 100.4 = mild to moderate
100.4 to <101.3 = severe
>101.3 = fulminant

mild/moderate = cramping, but no TTP
severe = cramping + diffuse abdominal TTP (no distention)
fulminant = severe + Significant Distention and/or ileus

Question 13

Define Severe ABX colitis so well that you just need to know mild/mod is not as bad and fulminant is worse

Answer 13

Severe S/S =
profuse diarrhea and fever = 100.4 to <101.3
Hypoalbuminemia < 3g/dL

PLUS one of the following

Abdominal pain with diffuse TTP (no significant distention)
OR
Leukocytosis of 15k to 35k

Question 14

Define fulminant ABX colitis

Also remember these patients are about to die and need emergency tx

Answer 14

Severe plus one of the following:

– ICU (due to colitis)
– HOTN w/ or w/o required use of
vasopressors 
– Fever ≥ 38.5°C (101.3°F) 
– Ileus or significant abdominal distention
– AMS* 
– WBC ≥ 35,000 
– Serum lactate levels >2.2 mmol/L 
– End organ failure (mechanical ventilation, renal failure, etc.)

Question 15

what is the study of choice for ABX colitis?

Answer 15

stool assay of Polymerase Chain Reaction (PCR) is the Study of choice

backup is Enzyme immunoassay (EIA) and it requires two samples

Question 16

remember that pseudomembranous colitis is NOT always a result of ABX associated colitis

Answer 16

cool

Question 17

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

what about if no improvement within 5-7 days?

Answer 17

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

Question 18

An tibiotic Associated Colitis

Tr eatment – Severe Disease:

Answer 18

• Vancomycin 125 mg PO QID x 10 days

Question 19

Antibiotic Associated Colitis

Treatment – Fulminant Disease:

Answer 19

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!!

Question 20

Antibiotic Associated Colitis (any stage)

• Treatment – Relapse:

Answer 20

– Up to 25% will relapse within 14 days
– Repeat course of oral antibiotics (repeat what worked)
– Subsequent relapses require 7 week taper of
vancomycin (7 week taper)

– Adjuvant therapy
• Probiotics • Fecal transplantation

Question 21

Under NAFLD… our instructor made it sound like the two subdivided classifications lead to one another… what are they and what is the progression?

Answer 21

NAFL —> NASH

Nonalcoholic Fatty Liver —-> leads to NonAlcoholic SteatoHepatitis

Question 22

How is NALFD usually discovered?

Answer 22

Incidentally on abdominal imaging ordered for another reason altogether

OR

USUALLY because of elevated transaminases levels***

Question 23

How can we confirm that NAFLD is not due to alcohol consumption?

Answer 23

Biopsy of the liver!

Question 24

What is a hallmark of alcoholic steatosis “fatty liver” as far as lab findings and why? How about on PE what might they find?

Answer 24

2:1 AST to ALT elevation because of lack of Vit B6 which is the building blocks to make ALT (explains the decrease). Also will have elevated GGT levels*

On PE may find hepatomegaly (high% of patients have enlarged liver)

Question 25

What may alcoholic steatosis progress to? How would that differ as far as S/S’s?

Answer 25

Alcoholic steatosis many progress to alcoholic steatohepatitis

They S/S’s for alcoholic steatosis are usually asymptomatic maybe with hepatomegaly on PE….

… S/S’s of steatohepatitis are jaundice, anorexia, fever, and tender hepatomegaly with the potential for muscle wasting and abdominal distention or ascites later into the progression of the disease

Question 26

In alcoholic steatohepatitis… what must we rule out?

How do we do this?

Once they are admitted… how do we prophylactically treat gastric mucosal bleeding before it begins?

Answer 26

Rule out other causes of acute hepatitis

Obtain ultrasound and biopsy to rule out others causes

IV PPI as prophylaxis against gastric mucosal bleeding

Question 27

What is a late stage of hepatic fibrosis which has distortion and the formation of regenerative nodules?

What can they be a progression of I.e. what are common causes?

Answer 27

Cirrhosis

Commonly caused by:
Alcoholic Liver disease
Chronic viral Hep C or B
NAFLD
Hemochromatosis

Question 28

If you see micronodular on the exam and it’s describing cirrhosis what should you think IMMEDIATELY!?!

Answer 28

ETOH so cause of Micronodular = alcohol

Question 29

What happens to patients who continue to drink alcohol after they have been diagnosed with steatohepatitis?

What is the definition chronic alcohol intake?

Answer 29

Steatohepatitis will progress to cirrhosis

30-50 grams of alcohol DAILY intake for 10 YEARS = chronic alcohol intake

Question 30

Type of cirrhosis where the patient may be asymptomatic or have Vague signs and symptoms like:

anorexia
weight loss
weakness
fatigue

WHICH all of those cannot be tied to a particular disease based off s/s*

Answer 30

compensated cirrhosis (w/ or w/o varices?)

Question 31

What S/S develop when compensated cirrhosis becomes uncompensated? what causes them?

Answer 31

– Jaundice
– Pruritus
– Signs of upper gastrointestinal bleeding
(hematemesis, melena, hematochezia)—- Portal HTN
– Abdominal distension from ascites —- Portal HTN
– Confusion due to hepatic encephalopathy —– too much ammonia from failing liver

Question 32

what are some physical manifestations of uncompensated cirrhosis?

Answer 32

terrible breath
gyneocomastia
loss of sexual hair
testicular atrophy
ankle edema
rectal varices
ascites
dilated abdominal veins (caput medusae)
spider nevi
esophageal varices causing hematemesis or melena in the stool
decreased mental functioning / confusion. coma
Cruveilhier-Baumgarten murmur – venous hum that may be auscultated in patients with portal hypertension – best appreciated with the stethoscope placed on the epigastrium

Question 33

what is one late systemic manifestation of cirrhosis and what may it cause?

Answer 33

decreasing BP / MAP - syncope?

• Decreasing BP (MAP)
– Patients with established HTN may become
normotensive or even hypotensive – MAP = DBP + 1/3(SBP – DBP)
• Fatigue • Fever • Weight loss • Muscle wasting

Question 34

Cruveilhier-Baumgarten murmur

Answer 34

– venous hum that may be auscultated in patients with portal hypertension
– best appreciated with the stethoscope placed on the epigastrium

Question 35

Cirrhosis – Systemic Manifestations

Abdominal Findings?

Answer 35

• Ascites • Hepatomegaly • Splenomegaly
• Caput Medusae
– In portal hypertension, the umbilical vein, normally obliterated in early life, may open.
– Blood from the portal venous system may be shunted through the periumbilical veins into the umbilical vein and ultimately to the abdominal wall veins

• Cruveilhier-Baumgarten murmur
– venous hum that may be auscultated in patients with portal hypertension – best appreciated with the stethoscope placed on the epigastrium

Question 36

Cirrhosis – Systemic Manifestations

Dermatologic

Answer 36

• Jaundice 
• Spider Angiomata (spider telangiectasias) 
• Palmar Erythema 
• Nail changes
– Muehrcke nails and Terry nails 
• Nail Clubbing

Question 37

Cirrhosis –
Systemic Manifestations
Endocrine?

Answer 37

• Women
– Chronic anovulation is common, which may manifest as amenorrhea or irregular menstrual bleeding

• Men
– Hypogonadism manifested by impotence, infertility,
loss of sexual drive, and testicular atrophy
– Other signs of feminization
– loss of chest or axillary
hair
– Gynecomastia