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Gastro Intestinal Diseases (Lower GIT Congenital Disorders (Congenital…
Gastro Intestinal Diseases
*Esophageal Diseases
*Hematemesis Differentials
chronic vs acute
sinister cancers vs acute bleeding
Esophageal Varices
portal hypertension forces blood to pool in the esophageal veins
--> risk for rupturing
background of liver cirrhosis --> blood can't perfuse to the 3 zones of the liver --> gets shunted
Esophageal Ulcers
forceful Hematemesis
Mallory-Weiss mucosal tears
Booerhave Syndrome
--> transmural tear in the esophagus
--> air / fluid leaks into the abdomen and other structures (lungs)
*Mallory Weiss Syndrome
severe and chronic emesis (vomitting) --> tears esophagus mucosa
usually on background of chronic alcoholism and vomiting (Bulimia)
Gastro-esophageal Reflux Disease (*GERD)
Acute
Esophagitis
Chronic
Barrett's Esophagus
10% of chronic GERD
metaplasia: stratified squamous
--> glandular (gastric) + Globlet Cells
IRREVERSIBLE
Diagnosis
endoscopy --> visible coolumnar lining above EG junction
biopsy --> metaplasia
Pathophysiology
increased gastric pressure
gastric acid moves past LES (lower esophageal sphincter)
stratified squamous cells damaged --> basal layer hyperplasia
repair --> fibrosis --> stricture
Signs & Symptoms
heartburn = "burning" chest pain
dysphagia
Causes/Risk Factors
overweight
stress
age --> usually > 40 yrs old
can also get during pregnancy
alcohol
medications (tetracyclines, etc.)
Silent GERD
presents with nocturnal cough and throat hoarseness
*sequelae and complications of GERD
3 main complications of GERD
1 = Esophageal ulcers
--> P/C with odynophagia (pain on swallowing)
--> change of baseline GERD symptoms
2 = Esophageal strictures
--> from chronic GERD
--> collagen fibrosis in the esophagus closes the lumen tighter
--> get sensation of food getting stuck
3 = Barret's esophagus
--> most insidious
--> especially since it is silent and no change of baseline symptoms of GERD
Clinical Cases
Clinical Case
Clinical Case
Notes
:
note that
*Congenital/Mechanical
Esophageal Disorders
Esophageal Achalesia
failure of the LES (lower esophageal sphincter) to relax
emesis (vomiting), dysphagia (difficulty swallowing), and odynophagia (pain in swallowing) common
Esophageal Atresia
esophagus closes off
--> leads nowhere
Esophageal Fistula
esophagus connects to another organ or other part of the GIT other than the stomach
Esophageal Stenosis
smaller lumen
*Hiatus Hernia
also para-esophageal hernia
(part of stomach above diaphragm)
Pathophysiology
lower part of esophagus protrudes through esophageal hiatus of the diaphragm
pushes on pleural cavity, increased pressure
ischemia
necrosis
Treatment
surgically push back/remove the hernia and suture extended hiatus
*Zenker Diverticulum
in the esophagus
Elderly father MIKE meets younger Crocodile Dundee
-->
"CRIKEE that's a big ZENKER!"
present with foul smelling breath
can get recurrent aspiration pneumonias
--> food forced into the trachea
Zenker Barium Swallow
3 Sreps of Physiological *Swallowing
1 =
CN 10 = vagus
=
tongue lift
--> pushes the food up at back of tongue and into the oropharynx
--> ALL other tongue movements = CN 12 = hyoglossus
--> think HYOgloss = HYPO lowers the tongue and everything else
--> Vagus main digestor
2 =
cricopharyngeal
muscle contraction
--> involuntary
--> pushes the food into the esophagus
3 =
peristalsis
and
LES
relaxes
Tongue Anatomy and OSA
all motor to tongue from CN 12 = hypoglossal
--> "up and out and roll"
exception is CN 10 control styloglossal for lifting the tongue to swallow
Notes
:
vagus nerve = CN 10 makes OSA worse
--> since it lifts the tongue against the oropharynx
CN 12 = hypoglossal makes OSA better since lowers tongue
IBS (Irritable Bowel Syndrome)
IBS (Irritable Bowel Syndrome)
Signs and Symptoms
cycles of constipation and/or diarrhea
pain & bloating
30-40% of patients have depression and/or anxiety
Treatment
Goal
: treat the dominant symptom:
constipation & diarrhea
pain & bloating
Anti-Spasmotics
from different classes, but all end in "-ine"
Unknown MOA Smooth muscle relaxants
--> Mebeverine
Calcium Channel Blockers
don't want to effect the heart
--> use
Dihydropyridines
("Damn Pyrates Knife Nicked My Fellow!")
recall Heart specific Non-dydropyridines
--> (Green Dill Tie)
--> verapamil & Diltiazem
Nicardipine (2nd Gen)
felodipine (2nd Gen)
Nifedipine (1st Gen)
Amlodipine (3rd Gen)
Anti-muscarnics
target M3 ACh receptors in GIT
anti-muscarinics are usually non-specific
--> Atropine
--> Hyoscine
--> etc.
Anti-Constipation (laxatives)
see
Constipation
for details
Bulk, Osmotic, Stimulant laxatives
feces softener (docusate sodium)
newer Cl- CIC2 channel stims
--> lubiprostone
Anti-diarrhea
anti-muscarinics --> target M3 receptors
Mu oppioid agonists (codeine=morphine & laporimide)
Lower GIT Tumours / *Cancer
see other notes
Lower GIT Groin *Hernias
*Inguinal Hernias
Indirect Inguinal
through the inguinal canal
Risk Factors
male
congenital
mostly babies where superficial inguinal ring doesn't close
Direct Inguinal
directly through the abdomen
NOT through the inguinal canal
Risk Factors
male
older people with weakened abdominal muscles
younger people with high strain on abdomen (weight lifting)
*Femoral Hernias
common in women
note the lacunar ligament gets weaker as women age
-->
"LACUNAR METADA..."
= think of Mario getting a femoral hernia because he is a GIRL
lacunar forms medial part of femoral ring
--> femoral hernia GI goes through
medial
to the Vein of
NAVY
Obstruction
Mechanical
80% by 4 MAIN defects
< 2 years old
Intussusception
"
telescoping
" of a segment of intestine into itself
--> remember "intussuss" means "into self"
> 2 years old
Herniation
caused by weakness usually
Volvulus
"twisting" of the intestine
occlusion of both lumen and blood vessels
Adhesion
to any part of the intestine or peritoneum
intestine needs to move freely
Remaining 20%
Cancer
Infarction
Non-mechanical
pancreatitis
Neurological
excess SNS activity/ loss of PNS/vagus
ex: gastroparesis
*Malabsorption Syndrome
note: can be malabsorption of anything, even water
first nutrient that is lost to malabsorption is fat
--> fat has the most complex absorption in the GI
--> tested for by SUDAN 3 stain for fat in feces
Signs and Symptoms
Diarrhoea
Steatorrhoea (floating fatty feces)
Weight Loss
Abdominal Discomfort/pain
Flatulence
*Malabsorption Differentials
note: can be malabsorption of anything, even water
first nutrient that is lost to malabsorption is fat
--> fat has the most complex absorption in the GI
--> tested for by SUDAN 3 stain for fat in feces
*Celiac Disease
Pathophysiology
immune response to gliadin protein
Villi destruction
mainly duodenum and Jejunum
Crypt Hyperplasia
Crypts get even deeper
genetic mutation of the HLA-DQ2 gene (used for APC = antigen presenting cells)
Diagnosis
Antigens
gliadin
positive for anti-tissue transglutaminase antibodies
1 - response to Gluten-Free Diet
Biopsy/Histology
villous atrophy in the proximal small intestine
Treatment
replace vitamins and minerals
Gluten-free Diet - NO:
wheat
rye
barley
(possibly) oats
Damage to mucosa is reversible
after 2 months of gluten-free diet
Gluten
2 main proteins that make up gluten:
--> gliadin and glutenin
Signs and Symptoms
Remember
"Celiacs have SAD Weight Loss"
Steatorrhoea (floating fatty feces)
Anemia
Diarrhoea
Weight Loss
Clinical Cases
Clinical Case
Notes
:
note that
Clinical Case
Celiac Disease Case
Bruner's Glands
unique to the duodenum
underneath the submucosa and secrete mucin to protect the duodenum from the acidic chyme from the stomach contents
Notes
note that a modified grain diet --> means you are modifying the grain in a diet, confused wording here
note on histology for Celiac disease in the duodenum the 2 keys are:
--> crypt hyperplasia
--> villous atrophy
Lactose Intolerance
Tropical Sprue
Pancreatic Diseases
Cystic Fibrosis
Signs and Symptoms
constant mucus build up in lungs and lower Resp
constant lower Resp Tract infection
Steatorrhoea (floating fatty feces)
Weight Loss
Diagnosis
Sweat test
CFTR pump needed in sweat
glands to pump water out of sweat
large amounts of Cl- in sweat is good
indicator of Cystic Fibrosis
Pathophysiology
mutation in the CFTR gene
*Initial tests for malabsorption
always check fat absorption first
*Whipple Disease
"OLDER men love FOAMY WHIPPed cream IN the CAN"
Lower GIT Congenital Disorders
Congenital Hirschsprung Disease
think
"NO SPRING" to get the feces moving
Aganglionosis of Myenteric plexus (ENS)
--> loos of ENS to GIT smooth muscles
--> loss of peristalsis and motility
constipation and "
megacolon
" proximal to the lost ENS
usually rectum and distal colon
Key Features:
M > F
10% are Down's Syndrome (Trisomy 21)
RET gene (gene NOT on Ch 21) --> oncogene
Present with:
constipation
unable to pass meconium
Congenital Meconium Illeus
obstruction in the illeum
can't pass mesocnium
Key Features:
15% are Cystic Fibrosis Syndrome (Trisomy 21)
Present with:
viscous meconium
reason why CF implicated (CFTR in pancreas)
Congenital Atresia (=closure / occlusion)
GIT narrows and closes off at some point
Esophageal, duodenal
not common in the colon
Present with:
inability to pass meconium at birth
can't eat/throwing up
Vascular occlusion causing intestinal atresia (death or occlusion)
called "apple peal" atresia
Case example:
Notes
:
note that small intestine atresia, especially when there is a portion of small intestine that is missing
--> this is due to vascular occlusion to that area
--> the areas receives no blood and hence dies off
Congenital Imperforate Anus
anus is missing or blocked
Key Features:
relatively common
Present with:
inability to pass meconium at birth
Congenital Diverticula
*Meckel's Diverticulum
most common congenital disorder of the small intestine in the population (2% overall = fairly common)
think "Angela Merckel is in the 2%"
--> Meckel's Diverticulum
whenever you see a kid < 2 years old presenting with painless bleeding
--> this is Meckels D until proven otherwise
--> actually very common = 2%
Clinical Cases
Clinical Case
Clinical Case
Notes
:
note that
Meckel's Diverticulum
Meckel is a type of ectopy
Case presentation:
Notes
:
note that Meckel's Diverticulum can be made of many different types of cells from throughout the upper GI tract
--> in this case it is pancreatic cells
--> most commonly Merkles have gastric cells within them
Merkel is an example of ectopy
ectopy = is where there are normal cells from another part of the body in a different location
--> DUE to incorrect embryological development
--> it happens at borth and is not due to a cell trying to change in response to environment or toxins
this is different than metaplasia that occurs in many cancers and things like Barret's esophagus that later lead to cancer
Meckel's Diverticulum
think "Angela Merckel is in the 2%"
Case presentation:
Notes
:
Rule of 2s for Meckel's Diverticulum
--> especially near the illeocecal junction
compare and contract Meckel's and Zencker's Diverticula
Meckel's is a true diverticula = meaning it has all 3 normal layers of the GI tract
--> mucosa, submucosa and muscular layers
Zenker's is a pseudo diverticula = meaning it is missing the muscular layer of the GI tract
Congenital Meckel's Diverticulum
Rules of 6 - 2s
< 2 yrs old
2 feet proximal from illeocecal junction
2% of population
2 inches long
2M : F
2 ends = MECKELs or SINUS
--> PATENT duct or CYST
MD cells and histology
note that MD has 2 specific remnents from gastric and pancreatic cell tissue
--> gastric cells
--> pancreatic cells
heterotopic tissue = presence of a particular tissue type at a non-physiological site,
--> co-existing with original tissue in its correct anatomical location.
--> In other words, it implies ectopic tissue, in addition to retention of the original tissue type.
Notes
:
Meckel's present usually with spontaneous and painless GI bleeding
can have pain though in the RUQ
--> Meckel's 2 inches proximal to the illeocecl valve and near the umbilicu = old vitilline duct
--> should always be a differential for children with RLQ pain along with appendicitis
Meckel like Vitiline abnormalities
"Vitaline is OMPHiously VITAL to my MECKEL"
"Vitaline is OPTHiously VITAL"
= Vitiline duct comes from the Omphalomessenteric duct
"VITAL to my Meckel"
- Vitiline duct --> MEckel diverticulum and others
"MECKEL = MIDDLE"
= midgut to umbillicus
--> remnant for OMPH Vitiline yolk sac
-->
"V in Vitiline = 7"
= Vitiline closes at 7 weeks
RULES OF TUS with the TU TU scoring BABY for the TRUE MECKELS DIVERTICULUM
the TRUE DIVER MECKEL dives from the YOLK STALK DIVING BOARD
between the YOLK STALK DIVING BOARD and the TRUE MECKEL DIVERTICULUM is the VIDEO DUCK recording the best dive in the world
Acute GIT Emergencies
Ischemic Bowel Disease
arteries usually to hindgut occluded
--> splenic flexure, descending, sigmoid, rectum
must operate within hours
Signs and Symptoms
sudden severe abdominal pain and tenderness
vomiting and bloody diarrhea
Risk Factors
> 50 yrs old
CVS diseases
Necrotizing Enterocolitis (NEC)
Signs and Symptoms
abdominal distension
bloody feces
circulatory collapse
Histological gas bubbles in submucosa (from invading bacteria)
Risk Factors
usually in premature babies
under-developed immune system + bottle feeding
Diverticulosis Disease
herniation/pouches of mucosa into the intestinal wall
very common --> 50% of people > 60 yrs old
usually not serious unless abscess forms or perforation
Diverticulitis
-when diverticula becomes inflamed
*Appendicitis
LRQ abdominal pain
initial visceral pain
--> dull and more diffuse on the abdomen
--> closer to the umbilicus usually
severe parietal peritonitis
--> pain is worse, sharp, more localized
--> moves closer to McBurney's point
Appendix Positions:
McBurney's Point = 2/3 from umbilicus to ASIS
--> where the vermiform appendix usually lies
14% Post-Ileal
10% Pelvic
Pelvic
is the most dangerous for appendicitis to spread through greater sac
dangerous in females --> spread to ovaries & ectopic pregancies
24% Subcecal
Paracecal
43% Retrocecal
Pre-Ileal
*Illeopsoas test for Appendicitis
have them do flexion at hip against resistance at the knee
positive test = if pain
--> could either be a psoas cysts or appendicitis / inflamed peritonitis
Clinical Cases
Clinical Case
Clinical Case
Notes
:
note that
Anus and Anal Canal Disease
Normal Structure
glandular tissue --> white line --> stratified squamous
Tumours
Carcinomas:
adenocarcinoma
basoloid carcinoma
squamous cell carcinoma
Melanoma (rare)
HPV (Human Papilloma Virus)
Diseases
STDs --> ex: syphillis
Hemmoroids
chronic sitting and constipation
pressure on veins surrounding anal canal --> form pockets of blood
within anal canal --> no pain
subcutaneous --> pain
Chron's Dsease
Anal Fissures
Anal Fistulas
Anal Abscesses
.
*Stomach (+ Duodenum) Diseases
NEUROLOGICAL GIT DISEASES
*Gastroparesis
Pathophysiology
loss of vagus (PNS) innervation to the stomach
paresis = paralysis of the stomach (circular, longitudinal, oblique) muscles to contract
food stays in stomach longer than normal
less gastric acid release (ACh)
Diagnosis
(GET) Gastric Emptying Test
Gold-standard test
fast night before & stop meds 4 days prior
fat free meal --> eggs and toast --> marked with radioisotope
2,4,6 hr. marks
4 hours --> normally should have > 60% gastric emptying
Upper GIT Barium imaging
Endoscopy
Signs & Symptoms
chronic nausea
emesis = vomiting
lack of appetite --> feel full
epigastric pain
malabsorption
GERD
Treatment
Metoclopramide
--> D2 receptor antagonist
Dopamine D2 receptors have
inhibitory effect on upper GIT
stimulation effect on lower
GIT (not sure details)
*Dyspepsia Differentials
Gastric / Duodenal *Ulcers
Treatment
Treat the Heart
Burn Symptoms
remember SAM ABCD and MS B
Neutralize gastric acid
Antacids
SAM with S/E ABCD
--> Sodium Bicarbonate
--> Aluminum Hydroxide
--> Magnesium Hydroxide
Mucosal Resistance
Protect Stomach from
excess acid without lower it
MS B
Bismuth Chelate
primarily increases bicarb and mucus
secondary H. pylori action
Sucraflate
sulphated sucrose
--> creates (-) charged sugar-gel coat
around epithelial layer
increases bicarb and mucus
Misoprostonol
PGE2 prostaglandin analogue
increases bicarb and mucus
Treat the Parietal part
of the Ulcer itself
PPIs
1st gen = omeprazole
2nd gen = esomeprazole
H2 Receptor Inhibitors
1st gen = cimetidin
2nd gen = ranitidine
3rd gen = famotidine
Treat Underlying reason for Ulcer
H. pylori or NSAID induced ulcer
Kill Underlying
H. Pylori Infection
Gram - bacili --> antibiotics
First Line Therapy
Macrolides
target 50s ribosomes
ACE
--> azythromycin
-->
clarithromycin
--> erythromycin
Penicilins
beta lactam ring prevent PBPs
from forming cross-links
-->
amocicilin
1 more item...
PPI
omeprazole
esomeprazole
2nd Line Therapy
3 more items...
NSAID induced ulcer
caused by inhibiting COX1
in the stomach and dudenum
Misoprostonol
PGE2 prostaglandin analogue
*PUD = Peptic Ulcer Disease
almost always H. Pylori
--> rarely can also be NSAIDs, alcohol, smoking
antrum of stomach/1st part of duodenum = Bulb of duodenum
Causes
Helicobacter Pylori (invade mucosa)
--> biggest factor
--> release toxins
autoimmune
--> antibodies to parietal cells
--> lower HCl- secretion and intrinsic factor
--> increased gastrin release = hypergastronemia
acute factors
--> same as acute above
H. Pylori vs. Autoimmune
corpus of stomach
low gastric acid production
--> since immune cells attacking them
high gastrin serum levels
lymphocytes and chronic immune cells involved
Auto-immunity to parietal cells
antrum of stomach/1st part of duodenum
higher gastric acid production
normal/low serum gastrin
neutrophils & acute leukocytes
Helicobacter Pylori
gram (-) rod
require neutral pH environment
--> need to invade mucosal cells to survive
urease +
--> can convert urea --> ammonia -->ammonium
--> increase local pH to survive
Duodenal Ulcer
~95% b/c of H. Pylori
from H. Pylori infecting the antrum of the stomach
--> lower portion of the stomach
In a PUD car crash ...
"AIR bags in the FRONT ... BLOOD in the BACK"
"AIR bags in the FRONT"
= perforation in anterior Duodenal bulb ulcers
"BLOOD in the BACK"
= ulcer bleeds happen in the posterior of the duodenal bulb
--> gastroduodenal artery
*Zollinger Ellison Syndrome
tumor in Islet cells of pancreas constantly secrete gastrin
--> increases gastric acid production in the stomach
--> constant duodenal ulcers and PUD
1 more item...
Antrum of Stomach Ulcer
come from H Puylori invade the corpus = body of the stomach
--> as opposed to the more common antrum
rarer to have stomach corpus ulcers
--> but are more dangerous since can lead to gastric lymphomas and adenocarcinoma of the stomach
~70% of these are b/c of H. Pylori
"LESSER is LEFTER"
--> gastric lesser curve ulcers hit the left gastric artery
Acute
Risk Factors
alcohol
stress
NSAIDS (particularly COX1) --> aspirin, Ibuprofen
Pathophysiology
loss of protective mucus barrier to gastric acid
less mucin from Goblet cells
NSAIDs stop PGE2 from inhibiting parietal cells also
--> NSAIDs increase gastric acid
.
Mouth/Oral Cavity Diseases
normal cell type = stratified squamous
Pathogen Infections
Herpes Simplex Virus
HSV1
HSV2
Candidiasis/Oral Thrush
normal microbiota
Inflammatory Diseases
2M : F
smoking
Leukoplakia
means "white plaques"
lower (5-20%) risk for malignancy
Erythroplakia
means "red plaques"
higher risk for malignancy
Mouth Ulcers
Oral Cancer
95% are squamous cell carcinoma
Pharynx
Tonsilitis
bacteria --> streptococcus (mostly)
Tumours
Pharangitis
Viruses --> adeno- and rhinovirus.
bacteria --> streptococcus (mostly)
Salivary Glands
3 salivary glands
submmandibular (mix)
sublingual (amylase high, low fluid)
Parotid (fluid moslty)
Xerostomia
produce little to no saliva
Infections
Viral --> mumps (cheeks swell up)
bacteria --> staph. aureus, streptococcal
Tumors
larger the gland --> more # of tumors, but less malignant
--> ex: 60-80% of tumors are parotid salivary gland tumors
smaller the gland --> less # of tumor, but less malignant
LIVER ASCITES
Treatment
Diarrhea
Treatment
Constipation
Treatment
Differentials: Crampy Abdo. Pain +/- blood in stools
Ischemic Bowel Disease
case example:
Notes
:
Ischemic colitis is extremely common in the elderly and must be ruled out whenever there is the following:
--> IBS like crampy-abdo. pain on passing bowel movements and
--> blood in the stool in the
--> elderly with cardiac problems
Difficulty Swallowing Pathologies
Achalasia
achalasia = "does not relax"
Notes
:
Achalsia leads to inflammation and neuronal degeneration in the esophageal wall
Case presentation:
Positive Findings
Rectal Bleeding
Bleeding types
VISIBLE blood
"coffee ground" or black
at or proximal to the cecum
brighter red
at or distal to the cecum
OCCULT blood = Non-visible blood
(Soft) Excluded Differentials:
IBS
Chron's Disease (bleeding less common)
Differentials:
Ulcerative Colitis
tumour/large polyp
cancer
*Swallowing and Esophageal disorders
achalasia
--> loss of inhibitory neurons in the esophagus
--> especially at the LES where it is unable to relax
scleroderma of the esophagus
--> LES has NO tone and cannot close
--> highly related to GERD
Esophageal spasm
Cricopharyngus dysfunction
--> the chrico is needed to contract behind the food bolus
--> this is needed to start peristalsis in the throat
*Perforated Viscus
viscus = visceral organ
air gets into the peritoneum and rises to the diaphram
air under diaphragm see on CXR
*Polyps disorders
Gastric Tumors
90% are Adenocarcinoma
--> makes sense as most of stomach is glandular,
not squamous
diffuse vs. intestinal
Diffuse = signet ring cells
*Peutz-Jehgers Syndrome
GIT hamartoma polyps in the GIT
petechiae surrounding the mouth is key
this is a benign condition with benign polyps in the GIT
--> but they have an increased risk for colonic CA
note they present as young teens or adults
--> present ages 10-30
--> with mild abdominal discomfort and petechiae around the mouth
hyperpigmented macules on the lips and oral mucosa (
melanosis
)
