PMED(M3)- GASTROINTESTINAL DISEASES

hepatitis A

highly contagious and is spread largely by the fecal–oral

route, especially when sanitary conditions are poor

hepatitis A

occur in sporadic as well as epidemic forms

hepatitis A

Groups at high risk for acquiring hepatitis A include

travelers to developing areas of the world, children in

day care centers, men who have sex with men, injection

drug users,

hepatitis A

particularly in older adults and in patients with

preexisting chronic liver disease

hepatitis A

the most common cause of relapsing cholestatic

hepatitis

Jaundice

occurs in 70% of adults infected with

HAV

IgM specific anti HAV

rises early in the disease and persists

for only 4 to 12 months

HAV vaccine

recommended for all patients with

chronic liver disease and

recipients of pooled plasma

products

hepatitis D

linked to hepatitis B, and consequently its epidemiology is

similar

hepatitis D

can be spread by the parenteral route and through sexual

contact

hepatitis D

more severe than hepatitis B

hepatitis D

cause

severe chronic hepatitis and ultimately cirrhosis

hepatitis D

occurs in two clinical patterns termed coinfection and

superinfection

Delta coinfection

simultaneous occurrence of

acute HDV and acute HBV infections

Delta coinfection

resembles acute hepatitis B but may

manifest a second elevation in

aminotransferase levels

Acute delta superinfection

clinical features of acute

hepatitis who has HBsAg and

anti-HDV but no IgM anti-HBc in

serum

Acute delta superinfection

is more frequent than coinfection

hepatitis E

responsible for epidemic and endemic forms of non-A,

non-B hepatitis

hepatitis E

occur in less developed areas of the world: India, Pakistan,

China, northern and central Africa, and Central America

hepatitis E

spread by the fecal–oral route and most cases can be traced to exposure to contaminated water

under poor hygienic conditions

hepatitis E

less contagious than hepatitis A,

hepatitis E

more severe than other forms

of epidemic jaundice

15-60 days

incubation period of hepa E

Hepatitis E virus

small nonenveloped,

single-stranded RNA virus that is currently unclassified

HEV virions and antigen

can be detected in stool and

liver during the incubation

period and early

symptomatic phase,

hepatitis non a-e

viral in etiology but

cannot be attributed to any known virus

hepatitis non a-e

clinical features are

similar to those of recognized forms of acute

hepatitis.

hepatitis non a-e

no clear

source of exposure can be identified

hepatitis non a-e

Rare cases have been reported after blood

transfusion

hepatitis non a-e

associated with the

complications of acute liver failure and

aplastic anemia

hepatitis non a-e

more common cause of fulminant hepatic

failure

Chronic hepatitis

develops in approximately one third

of patients with non–A-E hepatitis

Acetyl aldehyde

the metabolite of alcohol

Cytokines

directly and indirectly damage liver

hepatocytes

Lipopolysaccharides

can activate Kupffer cells, leading to

enhanced chemokine release

anemia, purpura, ecchymoses, gingival bleeding,

palmar erythema, nail changes

Less specific signs of alcoholic liver

Fatty liver

earliest change seen in alcoholic

liver disease

Fatty liver

characterized by presence of a fatty

infiltrate

Fatty liver

may emerge after only

moderate usage of alcohol

Alcoholic hepatitis

second and more serious form of

alcoholic liver

Alcoholic hepatitis

characterized by destructive cellular

changes that can lead to necrosis

Nutritional factors

may

play a significant role in the

progression of alcoholic hepatitis

Cirrhosis

sequela of alcohol abuse and the

10th leading cause of death

Cirrhosis

third and most serious form of

alcoholic liver disease

Cirrhosis

an irreversible condition

characterized by progressive

fibrosis and abnormal regeneration

of liver architecture

Cirrhosis

results in the progressive

deterioration of the metabolic and

excretory functions of the liver,

Thrombocytopenia

caused by the

combination of

hemorrhagic

tendencies and

severe portal

hypertension

Thrombocytopenia

consequence of

sequestration of

platelets in the

spleen

esophagitis, gastritiis, pancreatitis

myriad of health

problems;

Alcoholic steatohepatitis

characterized by the sudden

development of tender

hepatomegaly, jaundice, and fever in

a person who has been drinking

heavily

Alcoholic steatohepatitis

associated with a flu like

prodrome

Alcoholic steatohepatitis

associated conditions such as alcohol

withdrawal syndrome, GI bleeding,

infection, or pancreatitis

Bleeding tendencies

significant feature in advanced

liver disease

portal hypertension

development of ascites and esophageal varices

Alcohol amnestic disorder

in which the patient is

unable to learn new

material or to recall known

material

Alcohol amnestic disorder

alcoholic blackouts also

may be a feature

Identification and intervention and management of central nervous system

tx of patients with alcoholism

Identification and intervention

the first and second step of tx of pt with alcoholism

Identification and intervention

during this phase, the patient may

refuse to accept the diagnosis and

often will deny that a problem exists

Manage the central nervous

system

third step

Disulfiram

used for some

patients during

alcohol

rehabilitation

Naltrexone and

Acamprosate

used to

decrease the

amount of alcohol

consumed or

shorten the period

during which

alcohol is used in

cases of relapse

Naltrexone

opioid

antagonist

Acamprosate

an ihibitor

PEPTIC ULCER DISEASE

well-defined break in the GI mucosa (at least 0.5 mm)

PEPTIC ULCER DISEASE

results from chronic acid or pepsin secretions and the

destructive effects of and host response to Helicobacter pylori

PEPTIC ULCER DISEASE

result when the balance between aggressive factors and defensive factors is disturbed

First portion of duodenum

the location of most

PUD in Western populations

Gastric ulcers

more frequent PUD in asia

upper jejunum

rarely involved PUD

helicobacter pylori

formerly Campylobacter pylori

helicobacter pylori

the primary aggressive factor

helicobacter pylori

a microaerophilic, gram-negative, spiral-

shaped motile bacillus with four to six flagella

helicobacter pylori

resides at the interface between

the surface of the gastric epithelium and the mucous gel

helicobacter pylori

produces a potent urease

urease

hydrolyzes

urea to ammonia and carbon dioxide

urease

may protect bacteria from

the immediate acidic

environment

Ammonia

yung

nagccause ng

ulcerations

helicobacter pylori

may serve as a reservoir of infection and

reinfection along the alimentary tract

NSAIDS

the second most common cause of PUD

NSAIDS

directly damage mucosa, reduce

mucosal prostaglandin production, and inhibit

mucus secretion

stomach

ulcers caused by NSAIDs are located more

often in the ___ than in the duodenum

NSAIDS

Nitrogen-containing

bisphosphonate drugs

for the treatment of

osteoporosis

Nitrogen-containing

bisphosphonate drugs

associated with

development of esophageal

and gastric ulcers

Cystic fibrosis

predisposes to ulcers because it reduces

bicarbonate secretion

Cytomegalovirus infection

a rare cause of PUD in human

immunodeficiency virus (HIV)–infected

persons

Epigastric pain

most common s/s of PUD

Epigastric pain

long-standing (several

hours), sharply localized,

and recurrent pain

Epigastric pain

the pain is described as

“burning” or “gnawing” but

may be “ill-defined” or

“aching.”

Epigastric pain

ingestion of food, milk, or

antacids provides rapid relief

in most cases

Gastric ulcer

are unpredictable in their

response to food;

Gastric ulcer

epigastric tenderness

often accompanies the

condition

protracted vomiting

sign of gastric outlet (pyloric) obstruction

Melena

blood loss due to GI hemorrhage

Triple therapy

a conventional regimen for

antisecretory drugs

Antisecretory

drugs

provide

rapid

relief of

pain and

accelerate

healing, for ot with PUD

Antisecretory

drugs

their use

in

combinati

on with at

least two

antibiotic

s is

effective in

eradicatin

g H. pylori

Antisecretory

drugs

these

drugs

alone do

not

eradicate

H. pylori

Quadruple therapy

used in areas where high

prevalence of antimicrobial

resistance occurs