Professional Documents
Culture Documents
*Palmar
Erythema
*Clubbing
*Caput Medusa
-back up of
blood flow
*Gynecomastia
*Ascites
Asterixis (during
Encephalopathy
)
*BUT AST/ALT does not provide PROGNOSTIC INFO on someones outcome in liver
disease
Hyperbilirubine Unconjugated hyperbilirubinemia not taking bilirubin into the liver and
mia with Normal excreting it SO the bilirubin just builds up in the blood.
Liver Tests Gilberts mild elevation, worst when fasting or sick
Crigler-Najjar complete deficiency of glucuronyl transferase,
incompatable with life liver transplant
Hemolysis and ineffective erythropoiesis
Conjugated hyperbilirubinemia
Dubin-Johnson syndrome
Rotors syndrome
Cholestasis of pregnancy
Diagnostic features
Transferrin saturation > 45% (Serum Iron / TIBS) 1st test
Ferritin > 400
HFE gene studies
C282Y/C282Y
Remember, only 90% of clinical hemochromatosis
patients will be homozygous C282Y
C282Y/H63D heterozygote (5% clinical expression)
Hepatic iron concentration > 20,000 mcg/g dry weight
Hepatic iron index > 1.9
Hepatitis may occur with limited or no symptoms, but often leads to jaundice,
anorexia (poor appetite) and malaise. Hepatitis is acute when it lasts less than six
months and chronic when it persists longer. A group of viruses known as the
hepatitis viruses cause most cases of hepatitis worldwide, but hepatitis can also be
caused by toxic substances (notably alcohol, certain medications, some industrial
organic solvents and plants), other infections and autoimmune diseases
Hepatitis A Hepatitis A
RNA virus (picornavirus)
Short incubation
*15 to 50 days
Transmission
*Fecal-oral (day care centers,
travelers, gays)
*Cases may be sporadic or common
source
TRAVEL?
Illness is typically mild and may not be recognized as viral hepatitis
May have clinical and biochemical relapse during recovery
Hepatitis B Hepatitis B
DNA virus (hepadnavirus family)
Longer incubation period
30 to 180 days
Transmission
Sexual (blood is the main way
spread high incidence previously
assoc. blood trans)
Parenteral
Vertical especially E. Asia,
can smolder for decades and
present in 20-30s
Clinically more severe illness in
acute infection
Carrier rate is 5 to 10%
Treat with IFN-
Pre-exposure prophylaxis
HBV vaccine
Post-exposure prophylaxis
Hyperimmune B immunoglobulin
(HBIG)
Hepatitis C Hepatitis C Virus
Virus RNA virus
Long incubation period
15 to 180 days
Transmission
Parenteral IVDU, tattoos, inhaled
cocaine
Inapparent parenteral (blood
transfusions)
Typically a mild clinical acute illness
Once infected, the carrier rate > 65%
*NODULES are liver tissue that is trying to survive lost orientation are in
random orientations
Causes of Cirrhosis
Ascites Severe acute liver injury such as fulminant hepatitis
Peritoneal disease such as tuberculosis, mesothelioma, or metastases
Ovarian tumors (Meigs syndrome)
Hepatic vein occlusion (Budd-Chiari)
Veno-occlusive disease
CAUSES Liver, lover, tumor, tuber(culosis) (also the kidneys, note lover =
heart)
*do paracentesis on ALL patients with ascites (do cell count, albumin, gm stiain)
Hepatorenal Definition
Syndrome Progressive oliguria and progressive azotemia in a patient with
advanced liver disease, either acute or chronic
Precipitating events
Gastrointestinal bleeding, sepsis
Large volume paracentesis, vigorous diuresis
Hyponatremia
*kidney get confused by the elevated VASOACTIVE substances getting released
the kidney responds to the low BP via +RAS which puts the kidneys in a
profound state of HYPOPERFUSION
Alcoholic Fatty Most common histologic abnormality
Liver Symptoms/signs may be absent or minimal
RUQ abdominal pain
(AST Hepatomegaly
ELEVATED!!) Ultrasound may suggest fatty change
Aminotransferases normal to slightly increased
Therapy is abstinence from ethanol
Hepatocellular Associations
Carcinoma Hemochromatosis
All forms of cirrhosis esp. Hep C
Less common in Wilsons disease and PBC
HBV with or without cirrhosis and HCV with cirrhosis
A1AT deficiency and tyrosinemia
Drugs and toxins (e.g. anabolic steroids), IVC webs
**recall see inc. -Fetal Protein
Cholangiocarcin Associations
oma Sclerosing cholangitis
Choledochal cyst
Carolis disease
Biliary atresia
Toxins
Thorium, arsenicals,
vinyl chloride
Liver flukes
*KUPFFER CELLS
macrophages, clean up
depris, apotosis, CD68+
(endothelial cells CD34+)
See clinically?
Jaundice
Hypoalbuminemia
Hyperammonemia one of the most damaging consequences =
encephalopathy
Fetor hepaticus- musty sweet & sour
Impaired estrogen metabolism-palmar erythema, spider angiomas and
gynecomastia
Coagulopathy-(II, VII, IX & X)
Hepatic encephalopathy due to hyperammonemia
Cirrhosis Bridging fibrous septa-from portal area to portal area and/ central vein
Regenerating parenchymal nodules regenerative nodules in areas of
hepatocellular necrosis but dont form the proper connections
Disruption of the architecture of the entire liver increase in pressure in
portal hypertension, vascular architecture is reorganized
*normal liver = 1400 grams if an alcoholic ~ = 2400 g with most of the weight
as FAT with slow progression of fibrosis
*eventually alcohol taste bad the liver begins to shrink
Portal Increased resistance to portal flow at the level of the sinusoids and
hypertension compression of central veins by perivenular fibrosis
Ascites-excess fluid in the peritoneal cavity
Sinusoidal hypertension
Increased lymphatic flow-up to 20L/day
Intestinal fluid leakage
Renal retention of sodium and water due to 2 hyperaldosteronism
Porto-systemic shunts
Splenomegly
Viral hepatitis A Infectious hepatitis-no chronic hepatitis form CLEAR THE DISEASE
*acute SELF Low fatality rate
LIMITED Single stranded RNA picornavirus
(wimpiest form) Fecal-oral spread flies
IgM antibody against HAV-present at time of symptoms
IgG antibody persists for years providing protective immunity
Hep A incubation period 2 weeks 3 months
-most have symptoms malaise most common
by the time jaundice develops ususally
cleared the virus
Hepatitis B Acute hepatitis, non progressive chronic hepatitis, progressive hepatitis,
(serum) fulminant hepatitis
hepatitis * I.E. has both ACUTE and CHRONIC PHASES (incorporates into our genome
= persistent hepatitis), was frequently associated with blood transfusions
DNA virus
Nucleocapsid core proteins(HBcAg) and HBeAg
Envelope glycoprotein(HbsAg)-hepatocytes can synthesize massive
quantities of this protein
A DNA polymerase (reverse transcriptase activity)
A protein from the X region (HBX)-necessary for viral replication
Proliferative phase-HBV DNA is present in episomal form-complete virions
Leads to activation of cytotoxic CD8+T lymphocytes and hepatocyte
destruction.
Integrative phase-viral DNA is incorporated into the host genome in
hepatocytes not destroyed
CREATES IMMUNE COMPLEXES polyarteritis nordosa
HBV serologic diagnosis
Long asymptomatic 4 to 26 week incubation
HBsAg appears before the onset of symptoms
HBeAg, HBV- DNA and DNA polymerase-signify active viral replication
IgM anti-HBs-detectable just before symptoms
Anti-Hbe-detectable shortly after the disappearance of HBeAg-meaning
infection has peaked
IgG anti-HBs comes months after disappearance of HBsAg
Primary VS
Secondary
BILIARY
CIRRHOSIS
Primary Inflammation, obliteraive fibrosis and segmental
sclerosing constriction of the intrahepatic and extrahepatic bile
cholangitis ducts
Seen in association with inflammatory bowel disease
Males(2:1) 3 -5 decades, Onion-skin fibrosis,
Autoantibodies in less than 10% of cases
*outflow obstruction =
BUDD-CHIARI
SYNDROME
Peliosis hepatis Sinusoidal dilation, Associated with anabolic steroids,In HIV patients seen
mostly with infection by Bartonella henselae
Neoplasms
Hepatic Drug toxicity after Bone Marrow transplantation can have a lot of post-
complications of transplant LIVER probs
Organ or Bone Quite common- up to 50%
Marrow Tender hepatomegaly, hyperbilirubinemaia, centrilobular necrosis and
Transplantatio inflammation
n May get a veno-occlusive process
Liver Transplant Acute-within 2 weeks-mixed inflammatory cell infiltrate in portal tracts and in
pathology the endothelial layer of portal and hepatic vein branches
Chronic-cell mediated destruction of intrahepatic bile ducts(vanishing bile
ducts) and occlusion of hepatic arteries
Pathology of the Large Bowel
Infectious Viral - usually mild to moderate gastroenteritis with diarrhea and vomiting
Enterocolitis Rotavirus - 6 to 25 months old
Norwalk virus - older, adults, epidemic outbreaks (cruise ships)
Adenovirus - 2nd most common in children
Bacterial Mechanisms
Preformed toxin ingested in contaminated food - Staph
Infection by toxigenic organism which grow in gut and produce toxin-
E.coli
Infection by enteroinvasive organism which invades epithelial cells
-Shigella
Staph Aureus
Enterotoxin present in food
Symptoms come and go quickly
Antibiotic- *when giving broad spectrum antibiotics, frequently you wipe out the NORMAL
Associated FLORA but not the C. DIFFICILE = and therefore unchecked the C. diff OVERGROWS
Colitis (unopposed by the normal flora)
C. difficile
Known as pseudomembranous colitis
Psuedo Membrane forms on the surface of the colon usually from
the rectum to some point proximally
Idiopathic Spectrum from Ulcerative colitis to
Inflammatory Crohn disease
Bowel Disease Chronic relapsing inflammatory
disorders of obscure origin
Genetic predisposition: HLA
Dr1/DR1/DQws in 27% of white pts
with CD
HLA-DR2 is increased in pts with UC
Infectious causes - mycobacterium?
Measles virus, need bacteria
Abnormal Host Immunoreactivity-
abnormal T-cell responses -- too
much T-cell activation and too little
control by regulatory T-cells
P-ANCA is positive in 75% of UC
(but only 11% of those with CD)
Inflammation of the GI tract
Simmering chronic inflammation
Bouts of acute inflammation = activity (neutrophils in crypts)
*model of IBD Pathogenesis 1.) driven by bacteria 2.) T-cell activation excessive
activation
Crohn Disease
Sharply
Crohns is to delimited and
the CORE transmural- full
(extends thickness- skip
deeply) lesions can
get random
lesions with
normal bowel in-
between
Noncaseating
granulomata
Fissuring (narrow
ulcers) with
fistulas can
cause loops of
bowel to stick
together
Anywhere in the gut- but most common in terminal ilium
3/100,000 - smoking a risk factor
Intestinal wall thick, edematous
Creeping fat
Linear ulcers, cobblestone pattern
Inflammation through wall
Granulomata
Aphthous ulcers
Microsatelite
instabilty/HNPC
C
Colon if invasion into the lamina still considered in situ if it breeches past the
basement membrane = invasive carcinoma
PMP is not a 1. Low grade Largely pools of mucin with scattered benign
single entity appearing mucosa
a. Arises from low grade process in appendix single
layer
Peritonitis
Infectious
Sterile chemical (bile or pancreatic enzymes)
Sclerosing retroperitonitis
Tumors (Metastatic vs. primary)
Non-tumoral conditions (e.g. endometriosis)
Adhesions Adhesions
Fibrous bands which connect loops of bowel to one another,
surrounding organs or abdominal wall
Secondary to:
Surgery, Infection, Endometriosis
Intussusception Intussusception
One segment of bowel
telescopes into the immediately
distal segment
Children
Otherwise healthy
No point of traction
Adults
Results from some mass
or tumor acting as a point
of traction
Volvulus Volvulus
Twisting of a loop of bowel around its mesenteric base
Most often occurs in sigmoid colon
Occurs rarely
Ischemic bowel Arterial thrombosis-ASVD,
disease systemic vasculitis
Dissecting aneurysm,
etc.
Arterial embolism-
vegetations, angiographic
procedures
ASVD
Venous thrombosis-hypercoagulable states, oral contraceptives
Non-oclusive ischemia-cardiac failure, vasoconstrictive drugs
Miscellaneous-radiation
Complications if transmural
Perforation
Vascular collapse and shock
50-75% death rate
Mucosal and Mural
Nonspecific abdominal complaints, Bloody diarrhea
All types are easy to confuse with other entities
Small bowel Rare overall with tumors in the small bowel when compared to stomach and
malignancies colon
75% of the length of the GI tract but 3-6% of tumors
Benign tumors
Adenomas and mesenchymal tumors
Malignant tumors
1% of GI malignancies
Adenocarcinoma and carcinoid
Lymphoma
*How to diagnose? - Place a ORAL GASTRIC TUBE and it stops MID THORAX and on
XR see AIR IN STOMACH = DISTAL TEF (only cause for air to be in stomach)
H-typed TEF These are diagnosed later in life with recurrent pneumonia or
(no esophageal persistent cough
atresia) *baby can swallow but reflux secretions will go into lungs will
eventually cause pheumonia note the angle, so will be minimal
flow but eventually becomes symptomatic
OSMOTIC
improves with fasting
lactose intolerance, CHO malabsorption, fructose intolerance, Mg+ laxatives,
lactulose, PEG
increased solute gap
Simplified 5- 1. Does the patient really have diarrhea? Beware of fecal incontinence
Step Approach and impaction.
to Diarrhea 2. Rule out medications as a cause of diarrhea (drug-induced diarrhea).
EXAM 3. Distinguish acute from chronic diarrhea.
4. Categorize the diarrhea as inflammatory (BLOODY), fatty (OIL
DROPLETS), or watery.
5. Consider factitious diarrhea (LAXITIVES)
Red flag Recent onset of constipation in older age (> 50 years) = Obstruction?
features in Rectal bleeding, Weight loss
chronic Family history of colon cancer
constipation Iron deficiency anaemia
Haem positive stool
Pooping
*SYNDROME exists bc the patient decided to go to the doc = IBS (i.e. lots of
people have GI probs)
*IBS patients just see the doc more frequently, the controls had the same incidence
of probs
*WHY are some people hyper vigilant in seeing the doc? SEXUAL ABUSE,
TRAUMATIC EXPERIENCES (KOSOVO WAR), PSYCHOSOCIAL COMPONENTS = IBS
*SPRUE is increasing in incidence, check with the ANTIBODY TEST (much
better than biopsy)
How do you Psychotherapy - Interpersonal
treat IBS? Treatment
PSYCHOTHERAP One well-designed study using
Y!! psychotherapy (interpersonal
treatment) was able to show that
the active therapy was superior to
medical treatment in reducing
diarrhea, abdominal pain,
physician visits and symptoms of
anxiety and depression. The
improvement in bowel symptoms
paralleled the psychological
treatment. Since no physiological
studies were done, it is not known
whether the psychotherapy improved bowel physiology or just the cognitive
interpretation or degree of coping with the symptoms.
Mechanisms of Luminal
Malabsorption Pancreatic insufficiency
chronic pancreatitis
Improper mixing, rapid transit, bacterial overgrowth, ZE
Bile salt deficiency
Bacterial overgrowth
Increased losses (terminal ileum)
Reduced synthesis, secretion (liver disease)
Mucosal
Diffuse disease (sprue)
Resection
Transport
Lymphatic conditions
Nutrition
Diets Atkins 4.7 kg low at 1 year also better BP, HDL, TG BUT the type of diet
doesnt matter its about # CALORIES in
redistribution of bodys
protein content
depletion of skeletal muscle
increased synthesis of
acute-phase proteins i.e.
part of the STRESS RESPONSE
increased Basal Energy
Expenditure
hypercaloric feeding doesnt
reverse loss of lean mass
Energy-intensive
High rates of hepatic protein
synthesis require large quantities of essential AAs
Need for AAs drives loss of skeletal muscle
Adaptive over the short term (muscle replaced rapidly after recovery)
Nutritional *the best is SUBJECTIVE GLOBAL ASSESSMENT i.e. the basic H&P
Assessment
Go to Jejunal
feedings if
worried about
gastroparesis,
and reflux
REFEEDING *As you start refeeding patients
SYNDROME and if it occurs TOO FAST the
EXAM following are possible, all leading to
CARDIORESPIRATORY FAILURE
Drugs for the Peptic Ulcer: lesion of gastric or duodenal mucosa occurring at a site where the
Treatment of mucosal epithelium is exposed to acid and pepsin. (generally NOT a disease of
Peptic Ulcers EXCESSIVE ACID but a disease of loss of STOMACH DEFENSE MUCOSAL BARRIER
is disrupted)
GOAL #1 is to reduce the PAIN, can promote HEALING by treating the cause = H.
Pylori
*Have ANTIACIDS
(bismuth simple bases
that chelate acids in the
lumen)
Cimetidine (Tagamet) first one developed, should not be used, INHIBITS P450s
therefore has significant D-D INTERACTIONS, and has ANTIANDROGENIC EFFECTS
Ranitidine (Zantac)
Famotidine (Pepsid)
Nizatidine (Axid)
*best to take drugs PRIOR to BEDTIME leads to the greatest change in ULCER
HEALING
Gastric Proton Pump Inhibitors are PRO drugs that undergo bioacitvation occurs AT
Antisecretory THE SITE OF ACTION they are all WEAK BASES and therefore PROTINATED in the
Drugs stomach = +activated and bind to and PERMINATELY INHIBIT the pump.
*best to take IN THE MORNING PRIOR TO MEAL get large premeal acid rush
and the acid pump is inhibited
*are not useful for immediate relief takes several days for the pumps to be
inhibited- once active they inhibit 90-100% of H+ PUMPS are highly efficacious,
with limited adverse effects
*raise the pH BUT why do we have acid what is the LONG TERM effect of PPI?
no evidence of tumor formation, BUT have seen reduce defenses against
bacterial infections, Ca+2 absorption is reduced (higher fractures),
hypomagnesiuma.
METOCLOPRAMIDE = DA is an
Ach ANTAGONISTS therefore by inhibiting DA then get an increase in the release
of Ach = INC. GUT MOTILITY
*may be used in nausea/vomiting i.e. as an antiemetic
*SEs can cross the BBB and block D2 receptors in the brain can cause
tardive dyskinesia
Antidiarrheal Opioid Agonists:
Drugs Codeine only need low doses to achieve
- antidiarrheal effect
Morphine
Loperamide (Imodium) does not cross the BBB
less efficacious
Diphenoxylate semiperminant in the BBB is combined with ATROPINE = slows
motility but is combined to limit its abuse potential b/c get atopine SEs at high
concentrations blurry vision, inability to poop etc.
Bismuth Subsalicylate i.e. is Pepto BIsmal not absorbed orally therefore can
create a BLACK STOOL
Gastrointestinal Bleeding
Gastric Cancer
Mallory-Weiss *excessive wretching
Initial *RESUSCITATION refers to the infusion of IV fluids and blood transfusion. Goal is
Resuscitation to prevent hypovolemaia and subsequent shock from occurring.
and Medical
Management Clinical Assessment
Hx (what is the source?)
PE vital signs (is the patient hypotensive due to blood loss?)
NGT aspirate
Admission to ICU or monitored bed
Resuscitation- doesnt matter what you use initially based on initial Hgb if
<7 then do blood transfusion
IVF
Transfusion of blood products (PRBC)
Endotracheal intubation
Ongoing hematemesis or altered MS
Correction of coagulopathy
Evaluation of Esophagogastroduodenoscopy (EGD)
UGI Tagged RBC scanning CTe, CTA, MRA noninvasive ways to look for
Hemorrhage bleeding
Arteriography
Surgery
Two Strikes Rule 2 x that you failed time to look at open surgery
Natural History *far left are large varices treat with successive banding
of Varices
Management of Varicele
Acute Variceal Resuscitation give blood, fluids
Bleeding Octreotide infusion decreases bleeding (mimics
somatostatin - +vasoconstriction and therefore
reduces portal vessel pressures in bleeding varices).
Antibiotics (quinolones)
Endoscopic Rx
Sclerotherapy
Band ligation
Balloon Tamponade extended in the esophagus, rarely used
Transjugular intrahepatic portosystemic shunt (TIPS) (see pic)
Beta-blockers when stable as primary or secondary prophylaxis
Lower GI bleeding
Lower GI Diverticulosis
Bleeding Ischemic colitis
DIFFERENTIAL Colon polyp
Angiomas
Cancer
Hemorrhoids
Inflammatory bowel disease
Diverticular Brisk, abrupt onset, intermittent LGI bleeding
Bleeding Most common cause of severe hematochezia
Most frequently originates in right colon (70%)
Scinitigraphy = Bleeding rate > 0.1/cc/min (just tells you if there is bleeding not where it is
TAGGED RED from)
CELL SCAN Technetium-tagged RBC scan
Nonspecific localization and lack of etiologic diagnosis
Follow up with confirmatory angiography and/or endoscopy
Small Bowel EXAM MOST bleeding will be DIAGNOSED with UPPER or LOWER ENDOSCOPY
Bleeding but 3-5% in the small bowel
Proximal jejunum angioectasia (PROXIMAL J most common bleeding source)
Similar to right colon AVMs
Capsule endoscopy
Balloon assisted enteroscopy
Double balloon endoscopy
Single balloon enteroscopy
Intraoperative enteroscopy
Somatic Pain T6-12 = INTERCOSTAL NERVES they innervate the abdominal wall
Elderly Male with severe epigastirc pain to back mass in chest = LEAKING
ABDOIMINAL ANEURYSM
GI HISTOPATHOLOGY LAB
Ulcerative *involves the entire colon mucosa and submucosa only vary shallow
Colitis
Barretts *GOBLET CELLS intestinal metaplasia
Esophagus 30-40 x increase in ADENOCARCINOMA RISK
ILEUM *cannot distinguish exact transiton point from the jejunum but generally see the
presence of PAYERS PATCHES lymphoid aggregates (M cells)
COLON *NO villi are projecting from the surface have TENAE COLI
*high # of GOBLET CELLS (gotta lube the POO!)