Transcript Block 5 cm * gastro exam 2, lectures 13-27

There are 67 title slides.
There are 207 total slides.
I won’t be doing anything for Dr. Gregg’s lectures.
This version is unedited (sorry for typos and errors).
1
1.
2.
3.
4.
5.
Know anatomy / blood supply for the colon, sigmoid and rectum
Diverticular disease complications
Initial Treatment of acute lower GI bleed
Hinchey classes
Diverticuli treatment
2
iClicker Questions from Lecture 13
3
Which of the following represents the
primary function of the colon?
A. Recycling
of salts and water
B. Absorption of branched chain amino acids
C. Processing of bile salts into bile acids
D. Absorption of fat
4
What is the origin of blood supply to the
right colon?
A. Celiac
Trunk
B. IMA
C. Splenic
artery
D. SMA
5
The portal vein is made up of the
confluence of what two veins?
Inferior mesenteric vein & superior mesenteric vein
B. Hepatic vein & inferior mesenteric vein
C. Splenic vein & superior mesenteric vein
D. Splenic vein & inferior mesenteric vein
A.
6
Sigmoid diverticulum are:
True diverticulum
B. False diverticulum
A.
7
Name two complications of
diverticulosis?

Diverticula Can...
1. Do Nothing (majority)
2. Bleed
3. Get Infected
8
Which of following is NOT complication of
diverticular disease
A. Bleeding
B. Abscess
C. Peritonitis
D. Pain
E. Colon
cancer
9
73 yo old present with rectal bleeding.
Tachycardic and HoTN. Suspect diverciular
bleed. What si the most important first
step after physical exam?
A. Immediate
laparotomy with sigmoid colon resection
B. Admission with IV abx
C. Resuscitation with IV fluids/blood
D. Place rectal tube or decompression
E. Consulatation with GE for colonoscopy
10
43 yo female with LLQ pain, febrile (102.5)
and leukocytosis (WBC 21.5). You suspect
diverticulitis. Best imaging study?
A. Colonoscopy
B. Nuclear
medicine scan
C. Abdominal ultrassound
D. CT scan of abdomen and pelvis with oral and IV
contrast
E. Plain abdominal xrays
11
1. Know anatomy / blood supply for the
colon, sigmoid and rectum
12
Arterial supply to colon

Ascending colon
 Ileocolic artery AND right colic arteries (branches of SMA)

Transverse colon
 Middle colic artery (branch of SMA)

Descending colon and sigmoid colon
 Left colic and sigmoid arteries (branches of IMA)

Remember SMA and IMA anastamose at the marginal
artery
13
Arterial supply to rectum

Proximal rectum
 Superior rectal a. (continuation of IMA)

Middle rectum and distal rectum
 R/L middle rectal aa. (branches of internal iliac aa.)

Anorectal junction and anal canal
 Inferior rectal aa. (branches of internal pudendal aa.)
14
15
16
17
18
2. Diverticular disease complications
19
 Do
nothing (majority)
 Bleed
 Get infected
20
3. Initial Treatment of acute lower GI bleed
21
How do you treat Diverticular Bleeding?
 Stabilize/Resuscitate

Give Blood if Needed

Colonoscopy

Arteriography

Bleeding Scan
{stop coumadin}
22
4. Hinchey classes
23
Hinchey Classification
Class
Description
Jason
0
Inflammation of Colon
Mild
I
Localized Abscess
Moderate
II
Pelvic Abscess
Severe
III
Purulent peritonitis
Bad
IV
Feculent peritonitis
Real Bad
24
5. Diverticuli treatment
25
Class
Description
Treatment
0
Inflammation of Colon
Oral Antibiotics
I
Localized abscess
Oral/IV Abx
II
Pelvic Abscess
Drainage + IV Abx
III
Purulent peritonitis
Lap vs. Open
Washout
IV
Feculent peritonitis
Resection + Ostomy
26
How do you treat Hinchey 0?

PO Antibiotics (10-14 days)
 Ciprofloxacin 500mg PO BID + Metronidazole 500mg PO
q8h
 Alt: Augmentin 875mg PO BID
27
How do you treat a Hinchey 1?

IV Antibiotics
•
Pipercillin/Tazobactam
•
Eratopenem
•
Bowel Rest
28
How do you treat Hinchey 3 or 4?

Resuscitation

IV Antibiotics
 Pipercillin/Tazobactam
 Eratopenem

Class 3 – consider washout – open vs. lapro

Class 4 – resection and colostomy
29
When do you operate on diverticulitis?

Early: Hinchey 3 or 4

Late: Recurrent Symptoms
 Surgery is INDICATED for worsening disease!
30
1. Know your bugs
31
1.
2.
3.
4.
Best screening method for CA
Risk factors for colon CA
Screening age recommendations
Know about FAP – risks, complications
32
1. Best screening method for CA
33
Colonoscopy





Complete exam of colon and rectum
Biopsy of lesions or complete removal
Requires thorough cleansing of colon
Requires sedation
Remains “gold standard” for colorectal screening
34
2. Risk factors for colon CA
35
RISK FACTORS
Age – 90% >50 y.o.
 Personal or family history of polyps or colon cancer
 Inherited genetic syndromes
 Inflammatory bowel disease

36
Other possible diet/life style risks







Red meat consumption
High fat consumption
Alcohol
Smoking
Obesity
Less active
Diet poor in fiber
37
Colorectal cancer
Males > females
 African Americans - highest incidence and mortality in
US
 Ashkenazi Jews one of highest CRC risks of any
ethnic group

38
3. Screening age recommendations
39
Risk category
Screening method
Age to begin
Average risk
Choose one of following:
FOBT annually
Flexible sigmoidoscopy every 5 yrs
FOBT annually + flex sigmoidoscopy every 5 yr
Air contrast BE every 5-10 yr
Colonoscopy every 10 yr
50 yr
Family history
Choose one of following:
Colonoscopy every 10 yr
Air contrast BE every 5 yr
40 yo or 10 yr before dx of
youngest family member,
whichever is earliest
HNPCC
Colonoscopy every 1-3 yr
Genetic counseling
Consider genetic testing
21 yr
FAP
Flexible sigmoidoscopy or colonoscopy every 1-2 yr
Genetic counseling
Consider genetic testing
Puberty
Ulcerative
Colitis
Colonoscopy with biopsies for dysplasia
Every 1-2 yr
7-8 yr after dx pancolitis
12-15 yr after dx of left sided
colitis
40
USPSTF – US Preventative Services Task Force




The USPSTF recommends screening for colorectal cancer (CRC) using fecal occult blood
testing, sigmoidoscopy, or colonoscopy, in adults, beginning at age 50 years and continuing
until age 75 years. The risks and benefits of these screening methods vary.
Grade: A Recommendation.
The USPSTF recommends against routine screening for colorectal cancer in adults age 76 to
85 years. There may be considerations that support colorectal cancer screening in an
individual patient.
Grade: C Recommendation.
The USPSTF recommends against screening for colorectal cancer in adults older than age
85 years.
Grade: D Recommendation.
The USPSTF concludes that the evidence is insufficient to assess the benefits and harms of
computed tomographic colonography and fecal DNA testing as screening modalities for
colorectal cancer.
Grade: I Statement.
41
4. Know about FAP – risks, complications
42
FAP – Familial Adenomatous polyposis

Autosomal dominant
Lifetime colorectal cancer risk – 100%
 >100 polyps
 APC gene
 1/8000-29000

Complications
 Gardner’s, Turcot’s syndrome
 Polyps multiple areas


Rx – confirmatory genetic testing
Tx – colectomy
43
44
1.
2.
3.
4.
Meds causing constipation
Red flag symptoms
OMT for constipation
Diagnosing and symptoms of celiac disease
45
Dr. J’s Questions – end of lecture 17
46
5 yo presents with diarrhea x 2 days. What would
be some physical exam findings that would help
distinguish primary diarrhea vs. constipation?
Constipation can also cause diarrhea leading to misdiagnosis
 The liquid stool is able to come around the solid stool thus
giving us diarrhea in the setting of constipation (ENCOPRESIS)
 Physical exam is key to distinguish between the two

 Does the abdomen feel soft with good to hyperactive bowel sounds?
○ Not likely constipation
 Does the abdomen feel firm to hard with decreased bowel sounds?
○ Likely constipation
47

38 yo female with chronic constipation presents with
new onset HTN. Which med would be avoided for
treatment of HTN?
 CCB, BB, diuretics
48
72 yo female presents with constipation. Flat
plate of abd shows large bolus of stool in
ascending colon. Which vertebral segment
would you want to concentrate on to improve
autonomic activity in this area?

T10-T11
49
What would be some red flags in a patient with
symptoms of IBS?
50
Symptoms Usually not seen
 Onset
at a later age
 Bleeding, unless hemorrhoids present
 Fever
 Weight loss
 Persistent severe pain
 Nocturnal pain
 Malnutrition
 Steatorrhea
What pathologic findings would you expect in a
patient with celiac sprue?
Villous atrophy
 Hyperplastic crypts

 Proliferation
of lymphocytes and plasma cells
52
1. Meds causing constipation
53
Causes of constipation - medications
 Laxative
overuse

 Calcium channel blockers
 Beta blockers
 Diuretics
 Opioids
 Morphine
 Codeine





Antacids - those with
aluminum
Antispasmodics
Antidepressants
Iron supplements
Calcium supplements
Blood pressure medications



Anticonvulsants (some)
Certain sedatives
Certain tranquilizers
2. Red flag symptoms
55
Red flags
Bleeding, unless hemorrhoids present
 Fever

 WEIGHT
LOSS
Persistent severe pain
 Malnutrition
 New Onset Constipation in patients >40 =Colon
cancer until proven otherwise!

3. OMT for constipation
57
Constipation - treatment
 Diet
 OMT
 Increase fiber
 Focus on autonomic
 Increase fluid intake
hyperactivity
○ T10-11 for right colon
○ T12-L2 for left colon
 Mesenteric release
 Abdominal ganglion
release
 Increase activity
 Decrease intake of
milk, coffee, tea, and
alcohol
4. Diagnosing and symptoms of celiac
disease
59
Celiac Sprue
Celiac Disease or Gluten-Sensitive enteropathy
 Inability to tolerate gliadin (alcohol-soluble fraction of
gluten)

 Causes Immune response
 Damages mucosa of intestines
 Maldigestion and malabsorption occurs
Gluten is found in wheat, barley and rye
 Age seen is bimodal (8-12 months then 20-40 years old)
 Seen more frequently in patients with Type 1 DM, Downs
Syndrome or Turner Syndrome

4a. Diagnosing celiac disease
61
Celiac Sprue - DIAGNOSIS

Antibody testing
 Immunoglobulin A anti-tissue transglutaminase antibody
(IgA TTG)
 Antiendomysial IgA antibodies

Duodenal Biopsy for confirmation
 Involves the mucosa of the SMALL intestine
 Atrophic villi
 Hyperplastic crypts
 Proliferation of lymphocytes and plasma cells
4b. Symptoms of celiac disease
63
Celiac Sprue - SYMPTOMS
 GI
SYMPTOMS
 EXTRAINTESTINAL
 Diarrhea
 Anemia
 Flatulence
 Osteopenia / osteoporosis
 Borborygmus
 Neurological symptoms to
 Abdominal pain
include parasthesias,
sensory loss or seizures
 Skin disorders including
dermatitis herpetiformis
 Hormonal disorders
(amenorrhea, infertility)
 Weight loss
 Weakness and fatigue
secondary to poor nutrition
1.
Know your bugs.
65
1.
Know your bugs.
66
1.
Be familiar with the cases in the slides
67
Case #1
A 33 year old male develops severe, watery, nonbloody diarrhea on an airplane trip from Singapore to
the United States.
 He is taken to the ER from the airport and found to be
severely dehydrated, even though his diarrhea has
been going on for only a few hours.
 He is admitted, given IV hydration and improves to be
discharged 3 days later.

Case #1

What is your differential diagnosis?
 What is the most likely diagnosis?

What are the main organism(s) you would be concerned
about?
 How can you differentiate between organisms –
○ By symptoms?
○ By microscopy?
What is the mechanism that causes the diarrhea in this
case?
 What is the treatment for this disease process?

Question

The most likely diagnosis in this case is which of the
following?
A.
B.
C.
D.
E.
Cholera
EHEC Enterocolitis
Pseudomembranous colitis
Shigellosis
Typhoid fever
A = CORRECT
 Cholera is an important cause of potentially life threatening diarrhea in the
developing world where fecal contamination can reach drinking water supplies.
The diarrhea characteristically develops explosively, and patients may be critically
dehydrated within hours of onset of the disease. In developed countries, the
patients are treated with IV fluids; in developing countries, oral hydration with
water containing glucose and salt.
B
 Enterohemorrhagic E. coli (EHEC) diarrhea causes bloody diarrhea in the
absence of pus and fever
C
 Pseudomembranous colitis is usually caused by Clostridium difficile and is
associated with antibiotic usage
D
 Shingelosis causes bloody diarrhea with fever and pus
E
 Typhoid fever is an enteric fever and not a diarrhea. It causes fever, prostration,
abdominal pain, constipation and rash
Question

The organism most likely to be causing this patient’s
symptoms would be from which of the following
genus?
A.
B.
C.
D.
E.
Bordetella
Clostridium
Escherichia
Salmonella
Vibrio
A

Bordetella pertussis  pertussis or whooping cough
B

Clostridium difficile  pseudomembranous colitis, which is a
nosocomial, antibiotic associated diarrhea
C

E. coli (toxigenic strains) can cause diarrhea very similar to that
of cholera, but do NOT cause cholera
D
Salmonella enterica subp. Typhi  typhoid fever. Non-typhoidal
salmonella causes occasionally bloody diarrhea associated with
ingestion of contaminated poultry
E = CORRECT
 Cholera is caused directly by Vibrio cholerae, which is a gm (-)
curved rod with polar flagella

Question

The toxin causing the patient’s symptoms is thought to
act by which of the following mechanisms?
A.
B.
C.
D.
E.
It inactivates eEF-2 and inhibits eukaryotic cell protein
synthesis
It blocks release of acetylcholine
It interferes with the 60S ribosomal subunit and inhibits
eukaryotic cell protein synthesis
It produces defensins that allow the organism to withstand
oxygen dependent and independent killing
It stimulates an adenylate cyclase by ADP-ribosylation of GTP
binding protein
A

Used by Corynebacteria diphtheriae and Pseudomonas aeruginosa. The
diptheria toxin targets heart, nerve and epithelial cells. The Pseudomonas
exotoxin A targets liver cells.
B

Used by Clostridium botulinum  flaccid paralysis
C


Used by Shigella dysenteriae and enterohemorrhagic E.. Coli
Both cause bloody diarrhea
D
Used by Salmonella typhi to avoid intracellular killing
E = CORRECT
 Virbrio cholerae produces cholera toxin  ADP-ribosylates the GTP binding
proteins Gs-alpha  activation of adenylate cyclase with increased cAMP and
increased efflux of Cl – and water into the gut. The mechanism of action is
similar to that of the E. coli heat labile toxin.

Question

A 35 year old male presents with a 2 hour history of watery
diarrhea and abdominal cramps. He ate some leftover fried
rice that was on his counter from a lunch the day before.
Stool exam shows gram-positive, motile encapsulated
bacilli. What would be the most likely cause of his
symptoms?
A.
B.
C.
D.
E.
Bacillus cereus
Clostridium perfringens
Escherichia coli
Shigella spp.
Staphylococcus aureus
A = CORRECT
 B. cereus = gram (+), motile, encapsulated bacillus that
produces enterotoxins in the gut  diarrhea and abdominal
cramping
B
 Clostridium perfringens not motile
C
 E. coli not gram (+) bacilli
D
 Shigella spp. not gram (+) bacilli
E
 Staphylococcus aureus not gram (+) bacilli
Case #2

A 32 year old female presents to the office 10 days
after returning from a trip to Mexico. She complains
of foul-smelling, watery diarrhea that floats in the
toilet. She also is having bloating and flatulence.
She denies fevers, chills or any vomiting. She is
otherwise healthy.
Case #2
What is in your differential?
 What lab tests would you like to order to help with
diagnosis?

Case #2
On stool examination,
you note the following as
seen in this
photomicrograph.
 What is the most likely
diagnosis?
 What are some
complications of
untreated disease?
 What is the treatment for
the patient?

Question
A 27 year old male presents to the office 8 days after
hiking in the wilderness in Oregon. He complains of foulsmelling, watery diarrhea. He also has fatigue and
malaise. Exam of the stool reveals flagellated
trophozoites.
 The most likely cause of his symptoms would be which of
the following?

A.
B.
C.
D.
E.
Entamoeba coli
Entamoeba histolytica
Giardia lamblia
Schistosoma mansoni
Strongyloides stercoralis
A

Entamoeba coli – nonpathogenic amoeba sometimes found in stool
B
Entamoeba histolytica – invasive  amebic dysentery. Pathology primarily of colon, but it can cause
abscesses in other organs (liver and brain). Stools may show trophozoite forms or typical spherical cysts.
Characterisically spherical in shape, measure 10-20 micrometers in diameter and granular cytoplasm
containing up to 4 nuclei.
C = CORRECT
 Giardia lamblia – pathogenic flagellated protozoan that causes both epidemic and sporadic disease. Has a
wide range of clinical presentations, from asymptomatic infection to protracted diarrhea and steatorrhea.
Primarily infects stomach and small intestine when contaminated water is ingested. Dx is generally made by
examing stool specimens for trophozoites or cysts. Stools may contain oval or elliptical cysts, which are
thicked walled and measure 8-14 micrometers in diameter.
D
 Schistosoma mansoni is a blood fluke. Acute infection presents with fever, weight loss, abdominal pain, and
lymphadenopathy. Late disease demonstrates portal HTN, variceal bleeding, and pipestem fibrosis of liver
E
 Strongyloides stercoralis is an intestinal helminth (threadworm). Acquired when the infectious larva penetrates
bare skin. Infections have wide range of presentations. Can be asymptomatic, or organsims can cause GI
symptoms (abdominal pain and diarrhea). They can cause pulmonary symptoms during the migration through
the lungs. In immunosuppressed individuals, can cause hyperinfection, a life threatening condition (capable of
autoinfection)

Question
A 27 year old male presents to the office 8 days after
hiking in the wilderness in Oregon. He complains of foulsmelling, watery diarrhea. He also has fatigue and
malaise. Exam of the stool reveals flagellated
trophozoites.
 What would be the most likely source for this infection?

A.
B.
C.
D.
E.
Raw oysters
Undercooked pork
Undercooked eggs
Undercooked hamburger patties
Contaminated water
A

Raw oysters – found with cafovirus, Plesiomonas, and Vibrio
spp.
B

Contaminated undercooked chicken – found in
Campbylobacter spp
C

Undercooked eggs – found in Salmonella
D
Contaminated undercooked hamburger patties – EHEC
(Enterohemorrhagic E. coli)
E = CORRECT
 Contaminated water

Question
A 27 year old male presents to the office 8 days after
hiking in the wilderness in Oregon. He complains of foulsmelling, watery diarrhea. He also has fatigue and
malaise. Exam of the stool reveals flagellated
trophozoites.
 What is the most appropriate treatment for this patient?

A.
B.
C.
D.
E.
Ciprofloxacin
Doxycycline
Metronidazole
Oral vancomycin
Primaquine
A

Cipro = fluoroquinolone – Tx LRT infections, UTIs, and sinus, skin and bone/joint infections caused by
susceptible bacteria. Acts by inhibiting DNA gyrase and topoisomerase IV.
B
Doxycycline (a TCN) – Tx infections caused by bacteria (Chlamydia, Rickettsia, and Mycoplasma).
Bacteriostatic abx with mild to moderate gram (-) and gram (+) coverage. Doxy = alternative Tx for
certain bacterial infections in patients who have PCN allergies and can be used in conjection with
quinine to treat chloroquine-resistant malaria caused by Plasmodium falciparum. It is also an alternative
drug for prophylaxis against 4 spp of Plasmodium that cause malaria in humans. Acts by inhibiting
protein synthesis via binding to the 30S ribosome subunit.
C = CORRECT


Metronidazole is active against several protozons (Giardia lamblia, Entamoeba hystolitica, and
Trichomonas vaginalis) and against anaerobic bacteria. Metro or tinidazole are recommended as 1st line
Tx for Giardia infections. Acts by disrupting bacterial DNA and inhibiting nucleic acid synthesis.
D

Oral vancomycin – Tx of staphylococcal enterocolitis or for abx-assoicated pseudomembranous colitis
(caused by Clostridium difficile). Vancomycin – inhibitor of bacterial cell wall synthesis and known as
time-dependent kilelr of bacteria (must maintain adequate blood levels over extended periods of time to
exhibit bacteriocidal effects
E

Primaquine – active against the intrahepatic hypnozoites of Plasmodium ovale and Plasmodium vivax.
Acts by disrupting Plasmodium mitochondria.
Case #3
Multiple members of a wedding party are seen in the
ER within a 2 day period because they developed
vomiting and diarrhea.
 Symptoms seem to last 24-48 hours and individuals
recover uneventfully.

Case #3

In the differential would be






Norwalk virus – cruise ships
Echovirus – fall/winter
Astrovirus - winter
Rotavirus group A – young kids
Adenovirus
What would be the key distinguishing factors for each of
these viruses related to
 Ages affected
 Signs and symptoms
 Complications
Question

An outbreak in a daycare of children with watery
diarrhea, vomiting, low-grade fever and anorexia occurs
involving 6 children. The diarrhea is copious and some
of the children are hospitalized due to dehydration.
Which of the following properties would you expect to
find in the responsible virus?
A.
B.
C.
D.
E.
Enveloped icosahedral, DNA
Enveloped icosahedral, non-segmented RNA
Naked icosahedral, DNA
Naked icosahedral, non-segmented RNA
Naked double-stranded, segmented RNA
A

Enveloped icosahedral, DNA. Herpesviridae (HSV 1 and 2), caricella, herpes zoster,
EBV, CMV, Roseola infantum, Kaposi sarcoma) – examples of enveloped icosahedral
DNA virus
B

Enveloped icosahedral, non-segmented RNA. Flavivirus family (yellow fever, dengue,
St. Louis encephalitis, HepC) and Togavirus family (rubella, Western equine
encephalitis, Eastern equin encephalitis, and Venetuelan encephalitis).
C

Naked icosahedral, DNA. Paroviridae (B-19 virus) and Papillomaviridae (human
papillomavirus), Polyomaviridae (BK virus, JC virus), and Adenoviridae (adenoviruses).
D
Naked icosahedral, non-segmented RNA. Calcivirus family (Norwalk agent, Noro-like
virus), Herpevirus family (HepE), and Picomarvirus (polio, ECHO), enteroviruses,
rhinoviruses, Coxsackie viruses, HepA)
E = correct


Naked double-stranded, segmented RNA. These children likely have a rotavirus
infection – common cause of hospitalizations for diarrhea in young children.
Presentation is typical – self limited, risk of severe dehydration. Rotavirus (member of
Rotavirus family); contains segmented double-stranded RNA within naked icosahedron
Question

A mother brings her 2 month old infant to the ER because he
appears unable to properly swallow his formula. On physical
exam, generalized weakness is noted in the infant. Upon
questioning of the mother, she notes that she has been
sweetening the infant’s formula with honey over the past few
days. Which of the following is produced by the organism
most likely responsible for the infant’s symptoms?





IgA protease
Endotoxin A
Lecithinase
Lipopolysaccharide
Spores
A
B
C
D
E = CORRECT
 Spores – botulin toxin
1.
2.
3.
4.
5.
Mineral absorption
Differentials for gas, bloating, episodic diarrhea
Distinguish intestinal hormones
Omega-3 supplements affecting disease activity
Short bowel complications
93
1. Mineral absorption
94
Primary functions of the Digestive system


Most processes are involuntary, controlled by nervous system and hormone
communication
Mechanical
 Chewing
 Propulsion -muscular contractions mix and move the food (peristalsis).


Chemical digestion
Chemical breakdown of food
 Enzymes, acid, secretions
 Absorption – transport of digested molecules, vitamins, minerals, water into blood.
 Defecation – elimination of unused foodstuff ( feces)
GI tract flow: transit time is 24 to 72 hours
Food  bolus  chyme  feces
Minerals primarily
absorbed in small
intestine
(duodenum,
jejunum, some in
ileum)
(02)Absorption of Vitamins and Minerals





Fat-soluble vitamins are absorbed via micelles, water-soluble
forms of vitamins A, E, and K supplements can be absorbed in
the absence of bile acids
Some water-soluble vitamins use passive and facilitative
diffusion
B12-Intrinsic Factor complex requires intrinsic factor receptor in
the distal ileum for absorption of B12
Mineral absorption is more complex, particularly for the cation
minerals which are usually chelated to a ligand (i.e. usually an
acid, organic acid or amino acid). This form is more easily
absorbed by intestinal cells.
Diet- (foods)- can effect the bioavailability of minerals to us.
(02&03)Vitamins and minerals continued






Iron and zinc absorption depends on the needs of the host
Animal sources are better absorbed than plant sources
because of the interactions with the phytates and oxalates
present in plant-based foods
**Zinc absorption is impaired with increased amounts of
calcium, magnesium and iron
**Calcium absorption is regulated by vitamin D
Cobalt absorption is increased in people with iron deficiency
but compete and inhibit one another’s absorption
**Supplemental amounts of iron or zinc can decrease
absorption of copper
Malabsorption syndromes

Malabsorption disorders are most detrimental to nutrition status
 Nutrient deficiencies - multiple
 Weight loss
 Serious complications

Disorders associated with malabsorption









Genetic disorders e.g. Celiac disease, Crohn’s disease
Pancreatic disorders e.g. pancreatic insufficiency, Cystic Fibrosis
Intestinal disorders e.g. Ulcerative colitis
Intestinal infections e.g. Clostridium difficile
Liver disease (bile insufficiency)
Surgeries
Rarely involves single nutrient
Treatment of malabsorption disorders may also stress nutritional
status
Bariatric patients –are at risk of malnutrition because of
malabsorption and must be evaluated frequently. These patients in
particular may have issues with dumping syndrome, mineral
absorption, B12 and protein absorption or losses.
2. Differentials for gas, bloating, episodic
diarrhea
100
Lactose Intolerance

Causes: genetic or secondary deficiency of lactase
(hypolactasia)
 Secondary: infection, inflammatory disorders, HIV, or malnutrition





Affects ~ 70% population worldwide, especially African
Americans, Asians, South Americans
Diagnosis: history, lactose tolerance test or breath hydrogen test
Inability to digest lactose into galactose and glucose
Undigested lactose enters into the colon where bacteria ferment
it to short-chain fatty acids, carbon dioxide and hydrogen gas
Patients will often complain of bloating, gas, and may have
episodic diarrhea.
Celiac disease -continued
Children present with more GI symptoms (diarrhea,
steatorrhea, bloating) poor weight gain
 Frequently misdiagnosed as irritable bowel syndrome
(IBS), lactase deficiency, gallbladder disease
 Intestinal mucosa damage

 Malabsorption of nutrients, anemia, osteoporosis, vitamin or
mineral deficiencies, dermatitis hepetiformis (itchy skin rash)

Gluten intolerance: individuals who have symptoms and
may or may not have CD
 Nausea, abdominal cramps, diarrhea
3. Distinguish intestinal hormones
103
(03)Major GI Hormones

Gastrin

Mechanical contact with food
on the stomach /small intestine
mucosa stimulates the release
of gut peptide

Cholecystokinin (CCK)
 Released from G cells in the pyloric
region of the stomach
 Thoughts, food, caffeine, distension
of the antrum…cause  HCL and
pepsinogen release

Secretin 
 Released from proximal duodenum
 Opposes the action and secretion
of gastrin.
 Stimulates  release of water and
bicarbonate
 Released in the proximal
duodenum in response to HCL, fats,
peptides and AA’s--->pancreatic enz
and gallbladder contraction
 In the brain CCK inhibits food
intake.
GI hormones continued
2 incretin hormones that decrease blood glucose levels.
GIP (Glucose –dependent insulinotrophic polypeptide)
(+insulin) results in delayed gastric emptying and satiety
cues.
 GLP-1(Glucagon-like polypeptide) - (+ insulin & glucagon)

GI Hormones

Motilin
 Released from the duodenal mucosa and
 Promotes gastric emptying and GI motility.
 Erythromycin (antibiotic) acts to stimulate motilin receptors
and are use to treat delayed gastric emptying.

Somatostatin
 Released by D cells of the antrum and pylorus
 Primary roles are inhibitory and antisecretory
106
4. Omega-3 supplements affecting disease
activity
107
Diseases of the Small Intestine
IBD

Medical Management
 Corticosteroids, Antibiotics, Immunosuppressants

Nutrition Management
 Tube feeding / Parenteral Nutrition may be necessary
 Foods as tolerated ( this is varies by individual) usually lactose





free meals and low fat meals are better tolerated.
Multivitamin and mineral supplement, especially folate, B12, and
B6
Omega-3 supplementation—shown to decrease disease activity
Consider use of prebiotics and probiotics
Small frequent feedings are better tolerated than large meals
If steatorrhea present, MCT may be useful for adding calories
5. Short bowel complications
109
Diseases of the Small Intestine
Short bowel syndrome

Loss of 70% to 75% of the small bowel usually results
in SBS:
 100 to 120 cm of small bowel without a colon
 50 cm of small bowel with the colon intact
Causes weight loss; diarrhea; decreased transit time;
malabsorption; dehydration; loss of electrolytes;
hypokalemia
 note section on SBS in Krause’s text

Diseases of the Small Intestine
Short Bowel Syndrome (SBS)
Resection of the major parts of the small intestine
(treatment for Crohn’s disease, small intestinal cancers
etc.) can result in multiple nutrient deficiencies, fluid &
electrolyte balance
 Intestinal adaptation is the process of intestinal recovery
leading to improved absorptive capacity. Ileum has
greater adaptive capacity then jejunum.

 There are permanent effects on B12, nutrition and bile acid
reabsorption if ileum removed--worsens fat malabsorption and
diarrhea
 Removal of the ileocecal valve (sphincter) may result in
infiltration of colonic bacteria into small intestine causing
bacterial overgrowth
MNT for SBS

Medical Nutrition Therapy




Immediately after surgery: fluid & electrolyte replacement (intravenous)
First weeks: rehydration of diarrheal fluid losses
PN (TPN) gradually reduced as oral feeding resumes
Introduction of oral feedings as soon as possible to promote intestinal
adaptation
○
○
○
○
Sips of liquid formulas progressing to larger amounts
Solid foods as tolerated
Small, frequent feedings
Low-fat, high carbohydrate diet if steatorrhea is present (watch for dumping
syndrome)
○ Vitamin and mineral supplements
○ Low-oxalate diet to reduce risk of kidney stone formation
1.
2.
3.
4.
5.
Indications for hyperal
Complications of parenteral nutrition
Calories in IV solutions
Refeeding syndrome complications
PN in alcoholic patients
113
1. Indications for hyperalimentation
114
Parenteral Nutrition Indications (partial list)













GI tract not functional/ massive bowel resection
Radiation enteritis
Diffuse peritonitis
Intestinal obstruction – unable to bypass
Intractable vomiting / Intractable diarrhea
Inadequate intestinal absorptive area
High output enterocutaneous fistula (>500ml) and inability to gain enteral
access distal to the fistula site.
GI ischemia – severe
Ileus
Persistent GI hemorrhage
GI tract not accessible
Nutrient needs are > what can be met through the GI tract (in catabolic
patients, Cystic Fibrosis…)
Acute pancreatitis, with jejunal delivery of nutrients ( more in chp 30)
2. Complications of parenteral nutrition
116
Complications associated with PN
1.
2.
3.
Catheter-related problems - like sepsis,
pneumothorax, air embolus, catheter malposition…
Metabolic abnormalities - hyper and hypoglycemia,
glycosuria, elevation hepatic enzs…
Gastrointestinal complications – fatty liver,
cholestasis, atrophy of GIT (tx with trophic feedings)
Compilicaitons associated with PN
( see box 14-6, pg. 319 in Krause’s text)
Mechanical
 Access, line insertion, line
occlusion, phlebitis
 Pumps
Infectious
 Contamination, catheter / line,
sepsis
Metabolic
 Glucose control
 Fluid and electrolytes, Acidbase
 Renal and Hepatic
 Nutrient deficiency / excess
 Bone diseases
Gastrointestinal
3. Calories in IV solutions
119
Nutritional Requirements
Quick calculations

Fluid
 30-40 ml/kg
 Reduce in RF, CHF

Total Calories (Kcals)
 20-30 kcals/kg
BMI:
>25 20 -24.9
Metabolic state: hypo normal
Kcal/kg:
<20 20 -25
<20
hypercatabolic
>25
Avoid over feeding
Permissive under feeding ( 15 -20kcal/kg)
Parenteral Nutrition Rx Calculation







Balanced Parenteral Nutrition Rx: CHO ~ 50% Total Kcals, PRO
~20% Total, & IV Lipids/Fat ~30% Total Kcals.
Lipid kcal goal = 1800 Total Kcals x 30% = 540 kcals/2 Kcals/ml
(20% IVLE)= 270 ml IVLE/d
Protein Goal= 105 gm/d x 4 kcal/g= 420 kcals/d.
Lipid + Protein Kcals= 960 kcal/d. Subtract from Total kcal for CHO
kcals/d= 840/3.4= 247 g Dextrose/d.
PN volume goal/infusion rate= ~2100 ml/d. 2100/24 hrs= ~90 ml/hr.
To obtain % per volume of Dextrose & Amino Acids divide gms of
each by total volume.
PN Rx for Calorie and Volume Goal= Dextrose 12% + Amino Acids=
5% + 270 ml (or 54 g) 20% IVLE/d at 90 ml/hr.
Above PN Rx provides: 1853 kcal/d, 48% CHO, 23% PRO, 29%
IVLE, Dextrose Infusion rate= 2.6 mg/kg/min, & 2160 ml/d.
Dextrose

3.4 kcals/gm IV dextrose
 (4 kcals/gm glucose orally)

Maximum adult oxidation rate is 7mg/kg/min
 Usual amount is 2 to 5mg/kg/min
 Ex: 70kg: 2-5 mg/kg/min x 70kg x 1g/1000mg x 1440min/day =
202 gm to 504 gm of dextrose over 24hrs
 40% to 50% of total calories
Lipid





Lipids serve as a concentrated form of energy (9 kcal/gm).
Lipid emulsions are available in 10%, 20% and 30%
concentrations.
Lipid emulsions should not be used in patient’s with egg
allergy
Providing 20% -30% of total calories as lipids should give
~1gm fat/kg of body weight.
Do not exceed 2.5 gm lipid emulsion/kg body weight in most
patients
 1g/kg/day in critical ill septic patients
4. Refeeding syndrome complications
124
Refeeding Syndrome
Definition: Metabolic and physiologic consequences
associated with the depletion, repletion, and compartmental
shifts of electrolytes and alterations in glucose metabolism
and fluid status.
 At risk patients: Hx of severe wt. Loss (> 10% of UBW),
cachexia, poor nutritional intakes (substance abuse,
economically deprived, anorexia nervosa)
 Initial serum labs are WNL but total body stores of
electrolytes are depleted.

Management of Refeeding Syndrome







Empiric thiamine, folate, and B12 (cofactors in metabolism)
Aggressive treatment of abnormal electrolytes, esp. K, Phos, Mg
prior to and during nutrition therapy
Daily monitoring of I/O, weight, electrolytes
Slow initiation of NS with advancement over several days as pt
tolerates therapy. Cautious underfeeding usually required.
Repletion of low levels of K, Mg, Phos prior to advancing NS
therapy
Careful selection of NS therapy
Consideration of all sources of dextrose Kcals-IV fluids, drips,
meds.
Transition off of PN

Sudden stop
 Risk of hypoglycemia (especially if insulin in bag)
 Taper stop ( this is better generally)
 Cut rate 50% for 1 – 2 hours then d/c

To enteral feeds
 TF @ 20 mL/hr before PN taper
 Stop PN when > 75% needs via enteral support (peds)

To oral feeds
 Diet @ 25% (Clears not adequate) before PN taper
 Stop PN when > 60% needs via oral diet
5. PN in alcoholic patients
128
Nutritional Requirements
Goals of PN Therapy
 Stop further nutritional losses*
 Maintain adequate nutritional stores
 Slow repletion of cachectic patients
PN is not for acute correction
 Malnutrition
 Fluid
 Electrolytes
 Micronutrients
However PN is a powerful tool in beginning to start renourishing a
patient.
*for example when treating alcoholics be careful to assess their
nutritional status before loading them up with dextrose. Alcoholics
often have liver disease – and the liver has a big role to play in our
carbohydrate metabolism.
1.
2.
3.
4.
5.
Cytokines in gut mucosa related to celiac
HLA genotype and mechanism for pathogenesis of celiac
IL15 role in celiac
NOD2 and Crohns dz
t-cells, IL13, TH1 in Crohns dz
130
1. Cytokines in gut mucosa related to celiac
131

IL-15
 IEL infiltration with CD8+ T cells
 Inhibits TGF-beta  reduce Treg population

IL-21
 Inhibit Treg

IFN-alpha
 Death of enterocytes via Tc cells

IFN-gamma
 Tissue damage

TNF-alpha
 Apoptosis
132
Celiac Disease and IELs

Hallmark of Celiac Disease is IEL
infiltration by CD8+ T cells
 Different from IBD
 IELs are believed to participate in
pathogenesis by mediating destruction of
epithelium
○ Gluten alters IEL cells leading to production of
IL-15 and expression of nonclassical MHC
Class I molecules
○ Increase in IL-15 leads to expression on
IELs for these nonclassical MHC and to the
activation of the IELs which kill the epithelial cell
IL-15 Drives IEL-Mediated Epithelial Cell Damage
• Promotes survival ( Bcl)
•  IFN- secretion
IL-15
•  Granzyme/Perforin
•  CD94/NKG2C (HLA-E)
CD8+ TCR+
•  CD94/NKG2D (MIC, ULBP)
• Block suppression of Treg cells
• Maturation of DC
Contribution of IFN- & IL-21 to Celiac Disease
Gliadin-specific Th1
IFN-
TNF-
•  Cytotoxic
targets
• Apoptosis
•  MHC I
• EC death
2. HLA genotype and mechanism for
pathogenesis of celiac
136
2a. HLA genotype for pathogenesis of celiac
137
Negatively Charged Gluten Peptides Bind to
HLA-DQ2 Molecules
Glutamine  Glutamic acid
Celiac Disease
Clinical Presentation
HLA-DQ2 homozygotes 5X higher risk
• Disorder s. intestine – malabsorption, villous
atrophy & intolerance to gluten
–
–
AKA gluten-induced enteropathy
95% of celiac disease patients have susceptibility HLA
genotype:
o
DQ1*0501, DQ1*0201 (70% of twins have disease)
2b. Mechanism for pathogenesis of celiac
140
Celiac Disease Immunologic Features
Celiac Disease is a T cell mediated immune
disease of the small intestine triggered by
gluten.




Antigen: Gluten (gliadin and glutenins)
It is associated with HLA-DQ2 or HLA-DQ8
restricted lamina propria CD4+ T cells that
recognize gluten and secrete interferon-gamma.
Gliadin is a substrate of tissue transglutaminase
(transforms positively charged glutamines to
negatively charged glutamic acid)
Increased B Cell activity
 Antibodies against Gliadin (IgA-AGA, IgG-AGA)
 Endomysial antibody (IgA-EMA)
 Tissue transglutaminase (IgA-tTG)
3. IL15 role in celiac
142
IL-15 Drives IEL-Mediated Epithelial Cell Damage
IL-15
CD8+ TCR+
•
•
•
•
•
•
•
Promotes survival ( Bcl)
 IFN- secretion
 Granzyme/Perforin
 CD94/NKG2C (HLA-E)
 CD94/NKG2D (MIC, ULBP)
Block suppression of Treg cells
Maturation of DC
4. NOD2 and Crohns dz
144
Inflammatory Bowel Disease
Clinical Presentation
• Ulcerative colitis
–
–
–
–
–
–
Affects the colon
Bloody diarrhea
Abdominal pain
Fever
Weight loss
Anti-neutrophil cytoplasmic antibody (ANCA)
(70%)
• Crohn’s disease (terminal ileum)
–
–
–
–
–
Affects any part of GI tract
Fever
Abdominal pain
Diarrhea (w/o blood)
Fatigue
– NOD2 is predisposing factor (rel. risk =
38)
NOD 2
Recognizes muramyl-dipeptide
(MDP) a breakdown product of
peptidoglycan
 Expressed in monocytes,
macrophages, dendritic cells, GI
epithelial cells
 Mediates MDP-induced activation
of NF-kB

 Results in activation of pro-
inflammatory cytokines, chemokines,
and antimicrobial factors
Muramyl Dipeptide (MDP) - Ligand for NOD2
M = N-acetyl muramic acid
G = N-acetyl glucosamine
• NOD2
stimulation by
LPS
• GI tract
contains lots
of gram (-)
bacteria with
an LPS
5. T-cells, IL13, TH1 in Crohns dz
149
Lack of Treg Control
For Th1 & Th17 Apoptosis in CD
Is Crohn’s really a classic Th1 response?
IL-23 - a pro-inflammatory cytokine
Tp
CD4+CD25-
IL-12
(p40/
p35)
+ Antigen
Th1
IFN
TNF-
IL-4
Th2
IL-4
IL-5
IL-10
Effector T Cells IL-13
IL-23 (p40/p19)
Th17
IL-1
IL-6
TNF
IL-17
macrophage
Th1 & Th17 Cells Drive Inflammation in CD
1.
2.
3.
4.
Cytokine difference in Crohns vs. UC
Mucosal damage causes for UC
Autoimmune liver damage mechanism and cells involved
Pathologic changes in celiac disease
153
1. Cytokine difference in Crohns vs. UC
154
Cytokine profiles (mRNA and protein)
Ulcerative colitis
 IFN
 TNF
 IL12 absent (EBI3+)
 IL5 +
 IL13+
 IL2 +/ IL4 absent
Crohn’s
 IFN (>UC)
 TNF (>>UC)
 High IL12 (EBI3 absent)
 IL5 absent
 High IL23/IL17
 IL2+/ IL4 absent
There is insufficient evidence to support a classical Th1/Th2
paradigm in UC and CD
2. Mucosal damage causes for UC
156
NKT Cells (IL-13)
Drive Mucosal Damage in UC
3. Autoimmune liver damage mechanism
and cells involved
158
[ CTLA-4]
[ TNF]
[ Fas]
Mechanism of
Liver Damage
Inflammatory NKT Cells
May Drive Liver Damage
Proposed Pathogenic Mechanisms
Mechanism
Target antigens
Molecular mimicry
MHC risk factors
Non-MHC risk factors
Deficiencies in immunoregulatory
cells
Nature
Principal features
Cytochrome 2D6,
tRNP(Ser)Sec80
Formiminotransferase cyclodeaminase
UGT
anti-LKM1
anti-SLA
anti-LC1
anti-LKM3
Homologous amino acid sequences between
genomes of HCV, CMV, and HSV-1 and
cytochrome 2D6, and SMA and ANA
Cross-reacting autoantibodies
Concurrent immune diseases
DRB1*0301, DRB1*0401 (N. America, n. Europe)
DRB1*0404, DRB1*0405 (Mexico, Japan, China) Influence susceptibility, phenotype, and severity in
DRB1*1301 (South America)
different ethnic groups
DRB1*07, DQB1*0201(type 2 AIH)
CTLA-4 gene polymorphism
TNFA*2 gene polymorphism
TNFRSF6 gene polymorphism
Tyrosine phosphatase CD45 mutation
Vitamin D receptor polymorphism
Affects clinical phenotype
Regulatory CD4+CD25+ T cells
NKT cells
Deficient number and function impair suppression
of CD8+ T cells
Lymphocytes Are Present in Areas of Interface Hepatitis
T Regulatory (Treg)
Cell Number & Function Impaired
Liver-Specific AutoAbs
Circulate & Coat Liver Cells
AutoAbs Against Liver Membrane Ags
•
High levels of liver-specific lipoprotein (LSP)
−
Anti-asialoglycoprotein receptor (ASGPR)
o
o
Titres correlate with liver damage
Plasma membrane protein exclusive to hepatocytes
4. Pathologic changes in celiac disease
165
Celiac Disease
Clinical Presentation
• Gluten in the diet:
–
–
–
–
–
–
Failure to thrive (children)
Weight loss
Abdominal distention
Bloating
Chronic diarrhea
Abnormal tests for absorption function
• Jejunal biopsy specimen:
– Blunting & flattening of mucosal
surface
– Villi absent or broad & short
– Elongated crypts
– LP infiltrated by mononuclear cells
– Lesions regress w/ gluten-free diet
1.
2.
Presentation and diagnosis of Hirschprungs
Treatment of constipation in kids
167
Key points

The rectum empty of feces and Explosive discharge of
foul-smelling feces and gas- Hirschsprung disease

Gold standard for Hirschsprung disease- rectal
biopsy

Down Syndrome- Hirschprung disaease- association

Definition of constipation

First line of therapy of constipation- beside diet
modification- osmotic agents- polyethylene

glycol
Encopresis could be mistaken for diarrhea
168
1. Presentation and diagnosis of
Hirschprungs
169
1a. Presentation of Hirschprungs
170
Clinical Manifestations
Distended abdomen
failure to pass meconium
and/or bilious emesis (neonatal period)
Failure to thrive with hypoproteinemia
Stool
dilatation intraluminal pressure blood flow
Proliferation of bacteria
enterocolitis (Clostridium
difficile, Staphylococcus aureus, anaerobes, coliforms)
diarrhea, abdominal tenderness
 Sepsis and signs of bowel obstruction
 Tympanitic and distended- with a large fecal mass






171
Clinical Manifestations

Ultrashort-segment
 Gganglionic segment is limited to the internal sphincter
 Ganglion cells are present, anorectal manometry is
abnormal

Long-segment
 Involving the entire colon
 The extent determined accurately by biopsy at the time of
laparotomy
172
Rectal examination
 Normally
placed anus - finger snug
 Rectum empty of feces
 Explosive discharge of foul-smelling feces and gas
The stools can consist of small pellets, be ribbon-like, or have a
fluid consistency
 Retained feces may be associated with pain and fever
 Urinary retention with enlarged balder or hydronephrosis

173
1b. Diagnosis of Hirschprungs
174
Diagnosis
 Gold
standard - rectal biopsy (stained for
acetylcholinesterase)

Hypertrophied nerve bundles that stain positively for
acetylcholinesterase with an absence of ganglion cells
 Unprepared contrast enema – an abrupt narrow
transition zone - proximal and distal colon
Compare rectum to that of the sigmoid colon
 10% of newborns have a normal contrast study

175
2. Treatment of constipation in kids
176
Constipation

Constipation: Two or fewer stools per week OR passage
of hard, pellet-like stools for at least 2 weeks.

Functional Constipation: Two or fewer stools per week,
voluntary withholding of stool, and infrequent passage of
large diameter, often painful, stools.

Encopresis: Fecal Incontinence caused by leakage of
retained stool.
Functional Constipation/Encopresis
Treatment

Disimpaction – Enemas, Glycerin suppositories or oral
laxatives.
 Polyethylene glycol (PEG) 1.5g/kg/day

Maintenance
 Diet modification – water, fiber, fruit juices
 Behavioral Therapy – scheduled toilet times
 Laxatives - Polyethylene glycol 1g/kg/day,
Lactulose 1-3 ml/kg/day, Glycerin suppositories

Long treatment course with frequent relapses
178
Constipation – oral medications
Osmotic agents - lactulose (a synthetic disaccharide),
sorbitol, and polyethylene glycol (PEG 3350)
 Lubricants - mineral oil
 Stimulants - promote enhanced colonic transit (eg,
senna, bisacodyl) avoided as long-term therapy

179
1.
2.
3.
4.
Locations of anal fissures
Define fistula
Workup and treatment of hemorrhoids
Anatomy of anal glands
180
1. Locations of anal fissures
181
Pathophysiology

Tear/split of the anoderm
 Constipation
 Straining

Pain cycle begins spasm of anorectal sphincter musculature
 Cyclical
 Nonhealing
 Scar formation
Relative ischemia inhibits healing
 Chronic Fissure

 Present for >30d,
 Develop sentinel skin tag or hypertrophied anal papilla secondary to
scarring from fissure itself
182
Diagnosis (Anal Fissure)
 Primary - caused by repeated trauma and muscle spasm of
anal canal
 LOCATION
○ 90% in POSTERIOR MIDLINE
○ Anterior anal fissures seen more commonly in women
 Secondary - related to other disease states (Crohn’s,
Syphilis, leukemia, TB)
 Location
○ Lateral within anal canal
 Treat primary disease to heal fissure
 Always suspect possible neoplasm
183
2. Define fistula
184
Anal fistula, or fistula-in-ano…

…is an abnormal connection between the
epithelialised surface of the anal canal and the
perianal skin. Anal fistulae originate from the anal
glands, which are located between the two layers of
the anal sphincters and which drain into the anal
canal. ...
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Fistula
Anatomy & Pathophysiology

Fistula/Fistula in Ano
 Non Anatomical Communication b/w epithelial surfaces
 Connection between the anal canal and skin
 Cryptoglandular theory
○ Suppuration of the anal glands is origin of most anorectal infections
 Most fistula arise as a sequelae of abscess
○ Hx of abscess with drainage
○ Drainage required hole to drain abscess
○ Now the drained abscess = fistula (leaks pus out)

Associated disease process
 Crohn’s – disastrous, complicated operation
○ Will see multiple fisultae
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Anatomy & Pathophysiology
Four Categories - defined by relationship with external sphincter
1. Intersphincteric
 45% of cases
 Tract passes between sphincters
2.
Transsphincteric
 30% of cases
 Tract extends through external sphincter
3.
Suprasphincteric
 20% of cases above internal sphincter
4.
Extrasphincteric
 5%
 Extension of an ischiorectal abscess that has eroded into rectum
above level of sphincter
 Most originate as a caudad extension of a pelvic infection or malignant
process
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3. Workup and treatment of hemorrhoids
188
3a. Workup of hemorrhoids
189
Signs and Symptoms
Internal hemorrhoids

Blood per Rectum (BRBPR)
 Can be bright red to dark or clots
 Usually painless
Rectal itching and irritation
 Rectal fullness or discomfort (tenesmus)
 Mucous discharge
 Prolapse through anal canal

 Can become incarcerated, with thrombosis and/or necrosis
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Diagnosis

Examination of the perianal area
 Protrusion, swelling, erythema, masses, openings, drainage
 Can see external hemorrhoids or prolapsing internal hemorrhoids

Digital Rectal Exam
 Can check for gross blood, mass, tenderness
 Can be limited by pain with thrombosis of external hemorrhoids or
fissure

Anoscopy is mandatory for viewing internal hemorrhoids
 Unless thrombosed, they cannot be palpated with digital exam


Prolapse may be induced with Valsalva maneuver
Endoscopy should be performed to exclude proximal disease
if appropriate.
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Diagnosis
Classification of Internal Hemorrhoids
 First degree
 Bleeding, enlarged, nonprolapsing

Second degree
 hemorrhoid prolapses, but reduces spontaneously

Third degree
 Hemorrhoid prolapses but requires manual reduction to return

Fourth degree
 Hemorrhoid prolapses and is not reducible(may strangulate)
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Diagnosis
193
Diagnosis
194
3b. Treatment of hemorrhoids
195
Medical Therapy
First Line Treatment for 1st and 2nd degree hemorrhoids (and possibly 3rd)
 Increase fiber intake – addresses constipation – metamucil, fibercon, etc
 Increase fluids water 8x
 Avoid constipation, straining
 Changing toilet habits
 The toilet is not a library.
 Sitting or straining on toilet increases intraabdominal pressure, pushes pelvic contents
down, engorges pelvic veins


Suppositories, creams and salves have a little effective role in treating
hemorrhoidal disease except for providing some relief from swelling and
relieving itching.
Sitz Baths
 Warm water universally eases many painful perianal conditions

Ice may relieve the pain of acute thrombosis of external hemorrhoids
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Nonoperative Rx: Internal Hemorrhoids
Reserved for patients with grades 2 or 3 after failed trial of medical therapy
 Grade 4 hemorrhoids will not resolve with nonoperative or medical therapy
 Treatment is directed at symptoms
 Methods to eliminate problematic internal hemorrhoids include nonoperative
techniques:
 Rubber band ligation
 Sclerotherapy injection
 Infrared photocoagulation
 Laser ablation - rare
 Cryotherapy – no longer done
 All of these methods are non operative treatments and should be performed
for all first, second- with few third degree internal hemorrhoids that do not
respond to medical therapy
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
Internal Hemorrhoids
Extent of symptoms determines treatment regardless
of grade. Bleeding/irritation/soilage
 Most non-operative treatments have similar efficiency
when administered by an experienced clinician

 Rubber band ligation is most common utilized in the United
States.

Non-operative techniques, such as rubber band
ligation, have recurrence rates of 30-50% within 5-10
years.
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Non surgical Treatment
Internal Hemorrhoids
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Surgical Treatment:
Internal Hemorrhoids
Surgical resection is reserved for who fail non-operative
therapy or noncandidates for conservative management
(severe bleeding, etc)
 Hemorrhoidectomy - full-thickness excision of mucosa and
sub-mucosa and involved venous column without injury to
underlying muscle.

 Both external and internal hemorrhoids are removed
 Usually try to take no more than 2 columns

Open vs. Stapled Hemorrhoidopexy
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Surgical Treatment:
Internal Hemorrhoids
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Surgical Treatment:
External Hemorrhoids - thrombosis
Identify, local anesthesia, and excising overlying skin
and underlying veins
 After 48 hrs – minimal benefit to excision
 Enucleation of the thrombosis alone may result in
recurrence
 Suturing the wound closed is not necessary

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Hemorrhoidectomy
Complications are rare, <5% of cases
 Most Common Complication

 Urinary Retention
 Others include:
 Bleeding
 Infection (rare)
 Recurrence
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4. Anatomy of anal glands
204
Anatomy

Anal Glands
 Empty into the anal canal at the level of the Dentate line

Extension into one or more potential spaces
 Perianal
 Intersphincteric
 Ischiorectal (Horseshoe Abscess)
 Supralevator
205
Anatomy
206
Pathophysiology
•
Cryptoglandular theory
• Suppuration of the
anal glands is origin of most
anorectal infections
•
Approximately 10% of anorectal abscesses will
originate from non cryptoglandular source, including:
Crohn's disease, atypical infection, malignancy, or
trauma.
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