CM- GI-5- Viral Hepatitis

Question Answer
What are the five recognized hepatitis viruses A, B, C D, E&G
Does acute hepatitis only occur because of hepatitis virus infections no, CMV, EBV, HSV, Yellow Fever virus, Rubella all can cause acute hepatitis
What s/sx can help you differentiate cause of acute viral hepatitis between hepatitis viruses and other viral causes actually they present clinically in similar ways and the only way to differentiate them is Lab results
What clinicla features will patient with hepatitis present with anorexia, nausea, vomiting, right upper quadrant pain, elevated liver enzymes AST and ALT, headache, malaise, fever, Jaundice, dark urine, pale stool
What two hepatitis viruses are from fecal source A and E
what is the source of the majority of hep viruses Blood or body fluids
What hep viruses cause chronic infection those that are of blood or body fluid source B, C, and D
What are the best ways to avoid hep infection immunization and avoiding high risk behaviours
What will you likely see on lab eval of pt w/ viral hep WBC normal to low, Lymphocytes (large atypical), Mild protienuria, bilirubinuria (precedes jaundice), elecated AST/ALT early, then ALT/AST, acholic stool
What is the hallmark s/sx of viral hep Jaundice, usually develops late in infection
Hep called infectious hepatitis, incubation period 2-5 weeks, milder disease than hep B, asymptomatic infections are common especially in kids Hep A
What groupd is more likely to develop severe infectious hepatits from Hep A Adults especially pregnant women,
Is there a chronic form of Hep A no
What is the pathogenesis of HEP A viruses eneter via gut (fecal oral transmission), replicates in alimentary tract then spreads to infect liver hepatocytes, viremia is transient, virus is excreted in stools for 2 weeks preceding onset of s/sx
How do you dx Hep A culture of virus from in vitro material or HAV IgM in patients blood
How can you prevent Hep A infections passive immunization or active immunization(not in general use)
This hepatits has incubation period of 30-40 days acute self limiting hepatits no chronic carrier state and predominantly found in young adults 15-40yrs of age. (not hep A) Hep E
What is a major complication associated w/ Hep E Fulminant Hep in preganat women w/ high mortality rate up to 40%
What is the pathogenesis of Hep E replicates in gut then invades liver shed in stool prior to s/sx viremia is transient requires large inoculum to establish infection (very similar to Hep A)
How can you dx Hep E Specific IgM in serum though no routine lab tests are available
This Hepatitis has a incubation period of 1-6 months, insidious onset of s/sx, tend to cause more severe disease than Hep A asymptomatic infections occur frequently Hep B
How is Hep B transmitted sexually, parenterally, mucus membrane exposure,
What hep is associated with polyarteriitis nodosa (PAN) Hep B and C
Patient has an Ab against the surface (coat) protein of Hep B what antigen does it target HBsAG- produced as small spheres and tubules
What are HBcAg and HBeAg antigens of Hep B inner core protein (HBcAg) and secreted protein (HBeAg)
What is the first marker present in a pt w/ viral Hep B HBsAg
Will you find Hep B antigen HBcAg in the pts serum no it does not circulate
What is the HBV window period period during which HBsAg is not detectable and Anti HBs is not present but Anti HBc appears. Can last several weeks during this time a pt is likely to test negative but still be able to infect others
What is the pathogenesis of HBV infection from blood or body fluid exposure, virus replicates in liver, virus is shed into blood viremia is prolonged, blood is highly infectious of conatminated individual
What is the likely course of a HBV infection 90% self limited, 1-2% fulminant and 5-7% chronic carriers
What group is most likely to become a chronic carrier of HBV infants that get infected, immunocompromised pt, male>female
Can HBV be transmitted across the placenta yes 5-10% transmission rate
pt has failed to eliminate HBV and have a chronic infection what two ways could this chronic infection go Chronic Persistent- minimal liver damage or Chronic Active- aggressive destruction of liver tissue and rapid progression to cirrhosis or liver failure
What are chronic HBV patients at increased risk of developing Hepatocellular Carcinoma (HCC), 80% of pt w/ HCC are HBV carriers, have virus DNA in HCC cells
the following are high risk activities for what disease blood transfussions, serum product transfussion, sharing needles, razors, tattooing, acupuncture, renal dialysis, organ donation HBV, Hep C, HIV
What 2 hep antigens when found in the blood or serum indicate viral replication is taking place in the liver HBsAg and HGeAg
What ab indicates immunity following a hep infection it is detectable for life and is not found in chronic carriers Anti-HBs
When does the anti-HBe antibody become detectable when viral replication falls
What indicates pt has been exposed to HBV core IgM and core IgG antibodies against core protein
How can you prevent HBV infection active immunization with 3 doses of either serum derived or recombinant HBsAg vaccines both are eqully safe and effective
What liver condition can chronic viral hepatits B lead to macronodular cirrhosis
Your pt was working at a laundry and has never been vaccinated for HBV they got stuck by a needle left in someones clothes what should you order for them as a precaution (assume HIV isn't a problem) Hep B immune Globulin + vaccine if HBsAg negative. Newborns of Hep B mothers should get HBIG as well
Your patient is a chronic carrier of Hep B and just gave birth to a baby what should be done for the baby Give baby Hep B immune Globulin
This viral hep has an incubation period of 4-8 weeks cases are milder but more people infected develop chronic infection (50%) Hep C
What are major complications of Hep C Chronic liver disease and hepatocellular carcinoma
How is Hep C transmitted exposure to blood or body fluids of infected individual especially blood transfusion/products, organ donation, IV drug use, sex
How can you dx Hep C serology- HCV specific IgG indicates exposure not infectivity, PCR detects viral genome in pt serum, HCV RNA
What is chronic viral hepatitis >6months infection with either B,C, or D
What tx can you give for chronic HBV carrier interferon alpha 30% long term remission, or Lamivudine reduces HBV-DNA reduces ALT levels and 15-20% seroconvert
What tx can you give for chronic HCV Interferon alfa, 15% remit, Interferon/Ribavirin
If pt has inflammation extending beyond the portal areas into surrounding hepatic structures w/ extensive necrosis and fibrosis what are they suffering from chronic active hepatitis CAH
If pt has chronic inflammatory infiltration of portal areas with little or no fibrosis what are they suffering from chronic persistent hepatitis CPH
This hep virus requires comorbid infection with HBV Hep D uses the Hep B capsule so Hep D has HBsAg
What are the consequences of Hep D infection in pt increased severity of liver disease in hep B carriers.
pt is infected w/ a flavivirus, they present w/ glomerulonephritis, cryoglobulins, porphyria cutanea tarda (PCT), thrombocytopenia, neuropathy, thyroiditis sjorgren's syndrome or inflammatory arthritis name cause Hep G
What are the non viral causes of acute hepatitis Drugs, Alcohol, toxins, metabolic and autoimmune
What is the leading cuase of Acute Liver Failure in the US drug related hepatotoxicity
Pt has liver disease and is taking cascara, chaparral, comfrey, kava and ma-huang (they really like herbal meds) why could this be a problem compound liver disease
What drug is most common implication in alcoholic liver acetaminophen it has a syngergistic effect w/ alcohol
What are s/sx of alcoholic liver w/ acetaminophen nausea, vomiting, diarrhea abdominal pain and shock alt/ast
exposure to this drug can cause a Type I mild hepatitis which is typically benign or self limiting 20-30%, or can causea type II rxn w/ fever, jaundice and increased transaminases mortality of 50% Halothane and the fluranes
What effect can INH (isoniazid) have on the liver This drug causes a mild hepatitis toxicity in 20% of patients more men then female more in adults and cannot be distinguished clinically from viral heptatitis
This drug accumulate in hepatocytes and rarely causes clinical iver disease liver injury once done may continue for months you will see a transaminase elevation Amiodarone
Why do you see liver damage in HIV patients Anti-retroviral therapy has liver toxicity especially in HAART- highly active retroviral therapy
what is steatosis fatty liver
what is cirrhosis scarring and fibrosis of liver tissue
pt test positive for smooth mucle antibody they also have clinical signs of hepatitis what is the likely cause of their hepatitis autoimmune hepatitis AIH
What is Gilbert's sndrome glucoronyl transferase deficiency which is a benign chronic disorder w/ asymptomatic hereditary jaundice.

CM- GI-7- Biliary Disease

Question Answer
What is cholelithiasis presence of stones in the gall bladder
Who is most likely to suffer from cholelithiasis female, pregnancy, pt > 40yrs, or w/ family history
What factors can predispose you to developing cholelithiasis obesity, oral contraceptives, diabetes, rapid weight loss, estrogen replacement tx, ileal disease, decreased physical activity
What ethnicities are more prone to suffer from cholelithiasis Hispanics, northern European and pima Indians, less common in African Americans except with sickle cell disease
If you have a pt on total parenteral nutrition what complication are they more prone to develop cholelithiasis
What test can you order to dx cholelithiasis oral cholecystography and Gallbladder ultrasound
This visualization technique is used to examine biliary tree (gallbladder, bile and pancreatic ducts) by combining x-ray and endoscopy useful for id of strictures and biopsy of lesions and gallstones Endoscopic Retrograde cholangiopancreatography ERCP
What visualization technique of the gallbladder uses radioisotopes Cholescintigraphy- HIDA scan hydroxy iminodiacetic acid scan
What does a HIDA scan show shows gallbladder activity not especially useful for seeing stones though
what is cholecystogram x-ray used to evaluate gallbladder
Who is more effected by cholecystitis Men are more affected than women though women get gallstones more than men
What are the s/sx of cholelithiasis 80% asymptomatic, upper right quadrant pain of constant boring quality, can also have referred pain to scapular or supracervical region. Onset starts within hours of eating
What will you see on physical exam of pt with cholelithiasis normal unless having biliary colic then +murphy sign, severe intermittent cramping pain RUQ, occurs mostly at night, lasts from a few minutes to hours
What is the tx if pt develops acute cholecystitis IV fluids, antibiotics, and analgesics then cholecystectomy should be done within 72hrs
When wouldn't you want to perform a cholecystectomy with acute cholecystitis pt has diffuse peritonitis, acute gallbladder perforation, systemic sepsis, diabetes, patient develops acalculous acute cholecystitis in ICU, or emphysematous cholecystitis
When would you do an open cholecystectomy over laparoscopy if gallbladder is extremely inflamed, infected or has large gallstones
your pt can't be put under general anesthesia and is having acute cholecystitis what can be done for them put in a percutaneous cholecystostomy tube under local anesthesia. Tube can be removed in 6 weeks if it is acalculous
What are gallstones made of cholesterol, bilirubin, calcium, other organic material only 10% are pure cholesterol
What will you see on labs if pt has cholelithiasis normal labs unless obstruction then you get increased alk phos an bilirubin
When would you prefer to use MRCP (magnetic resonance cholangiopancreatography) over ERCP (endoscopic retrograde cholangiopancreatography) Pediatric or Elderly pt, pt with co morbidity, acute pancreatitis, cholangitis. But it may miss low grade strictures and you can get false positives
What are some complications that can arise w/ cholecystitis infection of gallbladder, mirizzi's syndrome (impacted gallbladder stone in cystic duct or neck of g.b.), cholecystoenteric fistula (erosion of stone through g.b wall, acute cholangitis
What treatment can be given to get rid of gall stones without removing gallbladder direct solvent dissolution (methyl tertiary butyl ether), extracorporeal shock wabe lithotripsy (used on big stones >3cm), oral bile salts (ursodiol/chenodial for poor surgical candidates)
This is inflammation of Gallbladder w/o detectable stones and s/sx of biliary colic. Pt presents w/ fever and elevated amylase occurs with trauma, burn patients or immunosuppressed Acalculous Cholecystitis
Who are at increased risk for developing acalculous cholecystitis burn patients on ventilators, immunosuppressed, trauma pt on ventilators
Why is acalculous cholecystitis concerning high mortality rate of 10-50% can be dx with HIDA scan that show gallbladder dyskinesia,
What is the most common cause of acute pancreatitis world wide choledocholithiasis- bile duct stones that have migrated from gallbladder to common bile duct
What is recommended tx for choledocholithiasis stone passes spontaneously in mild cases but cholecystectomy is recommended
This is associated with biliary obstruction and then infection of biliary tree 6-9% of pts with gallstones develop this acute cholangitis
What is Charcot's triad of cholangitis pain, fever, jaundice
What is Reynolds pentad a combination of Charcot's triad w/ two more concerning signs indicating an emergency cholangitis Pain, Fever, Jaundice (Charcot's triad), w/ hypotension and mental confusion
What will you likely see on labs in cholangitis increased serum total bilirubin >2mg , CBC shows leukocytosis, LFT shows elevated AST, cultures may show aerobic and anaerobic gram neg bacteria
What is the tx for cholangitis antibiotic therapy and ERCP with sphincterotomy
What are the common biliary tract neoplasms gallbladder carcinoma, cholangiocarcinoma, adenocarcinoma of ampulla of vater.
what is the tx for neoplasms of gallbladder and biliary tract surgical excision increases 5yr survival rate

CM- GI-6- EtOH hepatitis

Question Answer
What is the major site of drug metabolism in the body Liver
What are the main functions of the liver involved in metabolic functions of glucose, proteins, fats, bile, cholesterol, hormones and drug metabolism
what do the hexagonal shaped liver lobules form they are the structural and functional units of the liver made of hepatocytes with portal triads found at each of the six corners of each lobule
what do the portal triads consist of bile duct, hepatic artery, hepatic portal vein
what function do the hepatocytes carry out production of bile, process blood borne nutrients, store fat soluble vitamins and detoxification
This condition occurs w// macro vesicular infiltration of liver cells w/ triglycerides then neutrophilic infiltration leading to hepatocyte death Alcoholic Steatosis
How much alcohol needs to be consumed to cause liver disease 4-8 drinks daily for 10 yrs
What will your liver enzyme profile typically be in alcoholic hepatitis AST>ALT
What is the progression of s/sx w/ alcoholic hepatitis liver cell death, jaundice, loss of liver function and potentially development of Acute Liver Failure (ALF). If patient doesn't stop drinking after developing steatosis (fatty liver) they can progress to cirrhosis rapidly
What are contributing factors for developing alcoholic liver disease Women>Men, Poor diet/nutrition, Obesity, concurrent hepatitis C or B infection
what are the s/sx of alcoholic liver disease pruritis, nausea, vomiting, anorexia, fever, abdominal pain, agitation/anxiety due to ETOH withdrawal, confusion
What will you see in ACUTE alcoholic hepatitis s/sx Jaundice, Fever, Encephalopathy (severe Cases), seizures/tremors, tender hepatomegaly, splenomegaly
if pt has spider nevi, facial telangectasia, collateral veins on abdominal walls (caput medusa), portal venous bruits, esophageal varices, ascites, gynecomastia, testicular atrophy, palmer erythema, paroitd hypertrophy what do these s/sx corrolate with signs of advanced liver disease
How can you differentiate between alcoholic hep and viral hep ALT is preferentially increased in active hep C, biopsy will reveal cause, serology
What will help you differentiate between toxic/drug induced hep and ETOH hep history of exposure, abnormal LFTs, drugs can compound ETOH induced hepatitis such as acetaminophen
What is nonalcoholic steatohepatitis fat liver and inflammation w/ no hx of ETOH, important cause of cirrhosis and liver failure
What will you likely see on liver function test in nonETOH steatohepatitis ALT>AST, bilirubin normal, elevated serum ferritin,
What is nonalcoholic steatohepatitis associated with associated with noninsulin dependent diabetes, and hyperlipidemia
How can you tell hemochromatosis from other causes of hepatitis especially nonalcoholic steatohepatitis both have elevated serum ferritin, but NASH has more elevated ALT>AST than hemochromatosis, biopsy will have increased iron staining in hemochromatosis
What are s/sx of acute ETOH withdrawal tremor, nausea, sweating, irritability, auditory and visual hallucinations
What is Wernicke Korsakoff syndrome memory loss, confabulation, wide base gait, past pointing, opthalmoplegia, nystagmus, peripheral neuropathy (from malnutrition) and is associated with alcoholic hepatitis
What is fulminant hepatic failure pt develops impaired brain function within 8 weeks from increased intracranial pressure in previously healthy patient or one with unrecognized or stable liver dysfunction
Apart from affecting the liver what other areas of the body does ETOH abuse affect Can cause spontaneous bacterial peritonitis, malabsorption, pancreatitis, esophageal varices, endocrine problems- hypogonadism, impotence, gynecomastia, pseudo Cushing's, hypoglycemia, HTN, anemia
How does ETOH abuse cause spontaneous bacterial peritonitis poor nutrition plus direct effects of alcohol impairs mucosal barrier
If AST:ALT ratio is 2-3 what is the likely cause alcoholic hepatitis
Apart from liver disease what else can cause an elevation of AST that actually is false disorder of Cardiac, skeletal muscle, kidney, or hemolysis of specimen
What lab tests will you want to evaluate in liver disease AST:ALT, Bilirubin, Albumin, PT, glucose, sodium, CBC, Ammonia, liver biopsy (if called for), Abdominal ultrasound,
Why do you want to look at albumin when evaluating liver decreased albumin shows low protein synthesis of liver caused by inadequate nutrition or loss (common in ETOH liver problems)
Why would abdominal ultrasound be helpful in ETOH hep can show enlarged/small liver, fatty liver, decreased protal vein flow, cirrhosis, splenomegaly, and masses and cysts
What is the tx for ETOH liver disease ABSTINENCE, rehab, counseling, aggressive nutrition, folic acid, thiamine w/ glucose (to avoid Wernicke Korsakoff syndrome)
Pt has ETOH liver disease and encephalopathy, prolonged PT time and elevated bilirubin what tx are you going to order for them prednisolone, lactulose (inpatient), antibiotics if sepsis is present
What can you give to help with ETOH withdrawal Benzodiazepines
Pt has severe ascites as a complication of their ETOH liver disease what treatment would you order paracentesis
Pt has esophageal varices that are bleeding what tx would you order balloon tamponade or transjugular intrahepatic portosystemic shunt if they don’t respond to tx
What does pentoxifylline do for ETOH liver disease inhibits TNF Alpha, decreases mortality and hepatorenal failure
What is the prognosis for your pt if their PT test is >3 seconds above control limits w/ acute ETOH liver disease their mortality rate rises 20%, if PT test prohibits biopsy mortality rate is >40% at one year
What is the mortality rate for severe acute ETOH hepatitis mortality rate of 50% at one month
When should you refer pt for live transplant very high bilirubin, elevated creatinine, increased INR and ascites or encephalopathy (have short term prognosis), hepatic failure
Why is ETOH abstinence so important after a pt has had an episode of mild to moderate ETOH hepatitis if they continue to drink 50% will develop cirrhosis and 40% of them will die within 5 yrs
What are common causes of liver cirrhosis ETOH liver disease, Viral Hep, fatty liver w/ obesity and NASH, hepatic congestion drugs- methotrexate, methyldopa, hemachromatosis, primary biliary cirrhosis, Wilson's disease, cystic fibrosis, shisto,
What are some genetic causes of liver cirrhosis Hemachromatosis, Wilson's disease, Alpha -1 antitrypsin deficiency
What is cirrhosis fibrosis and nodular regeneration of liver after hepatocellular injury
What are common s/sx of cirrhosis most are asymptomatic until can't compensate further, will show anorexia, nausea, vomiting, diarrhea, fatigue, weakness, fever, jaundiced, pruritis, pale stools, dark urine
What s/sx of the skin and nails would you look for indicating possible cirrhosis these s/sx are variable jaundice, palmar erythema, spider telangiectasias, ecchymosis, caput medusa, xanthomas, clubbing
What abdominal signs point toward cirrhosis of liver ascites, venous hum over periumbilical veins, hypogonadism, enlarged or small nodular liver, tender hepatomegaly, palpable spleen (portal hypertension)
What neurologic signs indicate possible cirrhosis tremor of asterixis, choreoathetosis, dysarthria (Wilson's disease)
what are Dupuytren's contractures fibrous change of palmar fascia affects ring fingers possible sign of cirrhosis of liver
What is the tx for cirrhosis dc ETOH, aggressive nutrition, sodium restriction, vitamin supplementation and mostly treat complications, portal hypertension, ascites, Wilson's disease, encephalopathy
What is hepatopulmonary syndrome liver doesn't clear circulation pulmonary vasodilators so you get intrapulmonary vascular dilation leading to dyspnea, and decreased oxygen saturation, Tx is liver transplant
When is liver transplant indicated irreversible progressive chronic liver disease, acute hepatic failure and metabolic diseases of the liver survival rate is 80% 5 yr

Chapter 1

Question Answer
smallest unit of an element of matter atom
smallest living unit cell
an association of cells with the same general structure and function tissue
an association of several tissue types that carry out a specific function organ
a single individual of a particular life form organism
Anatomy deals with the structure (morphology) of the body and its parts

Vocab of whole chapter

Question Answer
States of Matter Physical forms of matter; solid, liquid, and gas.
Solid State of matter in which the volume and shape of a substance are fixed
Liquid The state of matter that has a definite volume but not a definite shape.
Viscosity The resistance to flow
Gas A form of matter that doesn’t have a definite volume of shape.
Surface Tension The force that acts on the surface of a liquid and that tends to minimize the area of the surface
Temperature A measure of how hot or cold something is (a measure of the movement of particles)
Volume A measure of the size of a body or region in 3D space.
Pressure The amount of force exerted per unit area of a surface.
Boyle’s Law The law that the volume of a gas is inversely proportional to the pressure of a gas when temperature is constant.
Charles’s Law The law that states that the volume of a gas is directly proportional to the temperature of a gas when pressure is constant.
Melting The change of state in which a solid becomes a liquid by adding energy.
Evaporation The change of a substance from liquid to gas
Boiling The conversion of a liquid to a vapor when the vapor pressure of the liquid equals the atmospheric pressure.
Condensation The change of state from a gas to a liquid.
Sublimation The process in which a solid changes directly into a gas.

Unit 4

Question Answer
Vibration a back and forth motion that repeats itself.
Waves the disturbance made by the vibration
can be many mediums for travel
water
solids
air
longitudinal wave
transverse wave

LONGITUDINAL WAVE disturbance that causes particles to move closer together or farther apart in the same direction that the wave is moving.
TRANSVERSE WAVE disturbance that causes motion that is perpendicular to the direction that the wave is moving.
AMPLITUDE displacement from rest to the crest or from rest to the trough.
PERIOD (T) time for the wave to repeat itself.
WAVELENGTH (cm or meters) is length in which wave repeats itself.
CREST maximum disturbance from rest
TROUGH maximum disturbance in the opposite direction from rest.
electromagnetic spectrum waves with both electric and magnetic properties.
are produced by accelerating electric charges, such as an electron oscillating in harmonic motion.
What does the electromagnetic spectrum include? The spectrum contains visible light
Lower frequencies
radio waves (low frequency) (TV)
ex: infrared waves (heat food)
Higher frequencies (more energy)
ultraviolet waves (burn your skin!)
high frequency X rays (medical uses)
gamma rays
How do the waves differ? The wavelengths visible to our eyes constitute only a thin portion of the electromagnetic spectrum.
49% of sun’s radiant energy is visible
46% is infrared
rest is ultraviolet.
radiant energy comes from the sun as photons
How does light relate to energy? When light hits an object:
some energy is absorbed
some energy is reflected
Atoms can absorb only those waves whose energy would move them to a possible energy state for the atoms.
What is visible light? Visible light is only a tiny portion of the EM spectrum.
ranges from 400 – 750 nanometers
red, orange, yellow, green, blue, indigo, violet
[red, yellow, green, cyan, blue & magenta]
can be bent…reflected, refracted, transmitted and absorbed
How does light produce color? Each element has a different set of wavelengths it can absorb
Clear transparent objects don’t have the right wave lengths for any visible light of any color
Color is a function of the photons the object does not absorb
It may transmit or reflect photon
What are photons? the energy in a light wave of a given frequency is a specific amount of energy.
each photon has an energy (E) that is related to the frequency of light.
connects both the light wave/light particle theories.
light is a stream of moving photons.
What is reflection? light travels in a straight line from its source until it encounters some object or particles of matter
rays reflected from a perfectly smooth surface are parallel to each other
rays reflected from a rough surface causes rays to travel in random directi
How does reflection happen? can think of light as “bouncing” off a surface.
it actually is more complex.
think in terms of light rays, so we can use the Law of Reflection.
“The angle of incident is equal to the angle of reflection” when in the same plane.
Is there one ray from each object? only three lines are usually shown.
The incident ray
The reflected ray
And a line called “normal”
What is refraction? a change in direction of a light ray when it moves through different transparent materials.
results from a change in speed when light passes from one transparent material to the next.
What is light absorption? Materials can be classified as to how much of the light falling on them is reflected
Opaque objects reflect light, absorb light or do a combination
Absorbed light gives up its energy to the material,may be remitted at a different wavelength or temperatu
What is diffraction? the bending of light around the edge of an opaque object.
the determining factor is the size of the opening (or obstacle) compared to the wavelength.
White light a mixture of all visible frequencies. (just need red, green, blue)
Primary (additive) colors red, green and blue.
Complementary colors (mixture of additive primaries) are cyan (turquoise), yellow, and magenta (purplish red).
yellow red + green
cyan green + blue
magenta blue + red
What is subtractive mixing? Subtractive refers to situations where the mixture is made from light absorbing pigments (paint or computer printer).
Primary subtractive pigments are cyan, magenta, and yellow (check your printer).
Paint stores call these blue (cyan), red and yellow.
subtractive colors Cyan, Magenta and Yellow

summary Q

Question Answer
better growth on SBA than MAC Oxidase +, TSI (K/K) Suspect a NF
found where moisture accumulates, all have pyoverdin Pseudomonads
Cystic fibrosos, Jacuzzi/hot tub syndrome, swimmers ear P.Growth on SBA, MAC, CHOC(green/yellow colonies), 47 days aeruginosa
Virulence factors: attachment, invasion, toxins P. aeruginosa
lab ID: lg colonies, pyocyanin, “grape-like odor”, Oxi +, TSA +(green slant), growth at 42 C, Glucose +, Citrate + P. aeruginosa
needs 2x grug therapy P. aeruginosa
differentiated by gelatin hydrolysis P. flurescens +, P. putida (nasty odor) =
soil denitifier P. stutzeri
used to belong to Pseudomonas Burkholderia
onion bulb rot (plant pathogen), found in IV fluids, detergents, disinfectants Burkholderia cepacia
Growth on SBA, MAC, CHOC(green/yellow colonies), 47 days Burkholderia cepacia
motile+, lysine/ornathine+, glucose/maltose/lactose/mannitol+ Burkholderia cepacia
“glanders”(respiratory disease in animals), NON-MOTILE B. mallei
meliodosis (aggressive granelomatous pulmonary disease) B. psuedomallei
3rd most NF in nosocomial infections, aerobic, motile by flagella, implants self in medical devices Stenotrophomonas maltophilia
-“ammonia odor” , Oxi/Cat + , Esculin +, Maltose+++++(strong) Stenotrophomonas maltophilia
MAC growth (purple), Oxi=, Cat + , Nonmotile nonmotile Acinetobacter
seen in nosocomial infectons: ICU Acinetobacter
contamination, nonsaccharolytic A.iwoffii
saccharolytic (glucose +) A. Baumannii
live in seawater thus Halophilic except V. chorela Vibrio
Oxi+, MAC growth, comma-shaped/curved rods Vibrio
cause CHOLERA a water borne illness (severe gastroenteritis) found in plankton, fresh, blackish, and salt water V. cholera
cholera toxin/Choleragen; “rice water stool” V. cholera
non hemolytic, VP= : classic V. cholera 01 beta-hemolytic, VP+ : el tor V. cholera 01 yellow on TCBS, sucrose+ V. cholera
growth 1-2% NCl, gastroenteritis from seafood(shell fish/ousters), TCBS green(sucrose=) V. parahemolyticus
wound infections then septicemia from raw shellfish/oysters, lactose+: V. vulificus
Oxi+, glucose+, found in flesh water, warm/cold blooded animal disease, motile by 1 flagella, grow 0-42 C Aeromonas
MAC/SBA(beta) growth, Oxi/Ind+ aerolysin (cytotoxic enterotoxin) A. hydrophilia
found in fresh water, growth SBA/MAC, motile Plasiomonas
cause gastritis from cold blooded animals P. shigelloides
-“darting motility”,curved/S shaped, “seagull shape” most common cause of diarrhea Capylobacter jejuni
microphilic, Cat/Oxi+, NLF, growth 42 C, Hippurate hydrolysis +, Campy-blood agar(sodium bisulfide) Capylobacter jejuni
curved, microaerophilic, high humidity Cat/Oxi/Urease+; EIA, urease test on biopsy, direct stain, stool antigen test Helibacter pylori
ulcers, gastric cancers Helibacter pylori
motile, Oxi + , growth MAC NLF, Nitrite to gas Alcaligenes faecalis
feather edge, “fruity” odor, groth in 6.5% NaCL Alcaligenes faecalis
-motile respiratory pathogens Bordetella bronchiseptica
non-motile respiratory pathogens Bordetella pertussis/parapertussis
pertussin toxin, tracheal cytotoxin, hemoaggutination Bordetella
catarrhal/paradxysmal/convalescent stage pertussis toxin
-temporal vaccine available -DFA/culture from nasal specimen Bordetella
Bordet-Genou/Regan-Lowe Bordetella
milder pertussis, nontoxigenic strain, Cat+Oxi=Urea+(24 hrs) B. parapertussis
Kennel cough in dogs, growth SBA/MAC, Cat/Oxi+Urea+(4 hrs): B. bronchiseptica
Cat/Oxi +, 20-43 C temp. range L. pneumophilia
-Cysteine/iron, BCYE -found in water ex. Lakes/air conditioners, lives/multiply in protozoa/bronchial macrophages Legionella
-get from breathing in: Legionnaires disease(pneumonia)/ Pontiac fever -urine test detects antigen, DFA, serological Legionella
zoonotic disease Brucella
(most virulent) from sheep/goat B. melitensis
Cat/Oxi +, no carb., Brucella agar (5% horse/rabbit serum), “fine grains of sand” on gram stain Brucella
-survives RES system -Brucellosis, Undulant, Mediterranean, Malta fever Brucella
-get from dairy products, contact from animal -serology is the gold standard Brucella
-growth on SBA/CHOC, no MAC -Oxi/Cat/Ind +; Urea =;“sick TSI” Pasteurella multocida
-“musty” “mushroom” odor -get from animal contact esp. cat/dog bite (Cellulitis), respiratory tract/eye infect Pasteurella
-leading cause of endocarditic within genus -Cat/Oxi =, Nitrate +, glucose/lactose fermented Hemophilus aphrophilus
-dental infections; Cat + Oxi = -poor growth on SBA/CHOC, adhere to agar, “pointed star” Actinobacillus actinomycetemconitans
-associated exclusively with endocarditis -rosettes on gram stain -Oxi/Ind + ; cat/Nit = Cardiobacterium hominis
-fist fight/bite “clenched fist wound” -pits agar, “bleach odor” -Oxi/Nit + ; non motile ; non saccharolytic Eikenella corrodens
–plumb rods in chains; Oxi + Cat = ; ferment glucose -flora of pharynx in young children; Remel Rapid NH Kingella spp. denitrificans/kingae
better growth on SBA than MAC Oxidase +, TSI (K/K) Suspect a NF
found where moisture accumulates, all have pyoverdin Pseudomonads
Cystic fibrosos, Jacuzzi/hot tub syndrome, swimmers ear P.Growth on SBA, MAC, CHOC(green/yellow colonies), 47 days aeruginosa
Virulence factors: attachment, invasion, toxins P. aeruginosa
lab ID: lg colonies, pyocyanin, “grape-like odor”, Oxi +, TSA +(green slant), growth at 42 C, Glucose +, Citrate + P. aeruginosa
needs 2x grug therapy P. aeruginosa
differentiated by gelatin hydrolysis P. flurescens +, P. putida (nasty odor) =
soil denitifier P. stutzeri
used to belong to Pseudomonas Burkholderia
onion bulb rot (plant pathogen), found in IV fluids, detergents, disinfectants Burkholderia cepacia
Growth on SBA, MAC, CHOC(green/yellow colonies), 47 days Burkholderia cepacia
motile+, lysine/ornathine+, glucose/maltose/lactose/mannitol+ Burkholderia cepacia
“glanders”(respiratory disease in animals), NON-MOTILE B. mallei
meliodosis (aggressive granelomatous pulmonary disease) B. psuedomallei
3rd most NF in nosocomial infections, aerobic, motile by flagella, implants self in medical devices Stenotrophomonas maltophilia
-“ammonia odor” , Oxi/Cat + , Esculin +, Maltose+++++(strong) Stenotrophomonas maltophilia
MAC growth (purple), Oxi=, Cat + , Nonmotile nonmotile Acinetobacter
seen in nosocomial infectons: ICU Acinetobacter
contamination, nonsaccharolytic A.iwoffii
saccharolytic (glucose +) A. Baumannii
live in seawater thus Halophilic except V. chorela Vibrio
Oxi+, MAC growth, comma-shaped/curved rods Vibrio
cause CHOLERA a water borne illness (severe gastroenteritis) found in plankton, fresh, blackish, and salt water V. cholera
cholera toxin/Choleragen; “rice water stool” V. cholera
non hemolytic, VP= : classic V. cholera 01 beta-hemolytic, VP+ : el tor V. cholera 01 yellow on TCBS, sucrose+ V. cholera
growth 1-2% NCl, gastroenteritis from seafood(shell fish/ousters), TCBS green(sucrose=) V. parahemolyticus
wound infections then septicemia from raw shellfish/oysters, lactose+: V. vulificus
Oxi+, glucose+, found in flesh water, warm/cold blooded animal disease, motile by 1 flagella, grow 0-42 C Aeromonas
MAC/SBA(beta) growth, Oxi/Ind+ aerolysin (cytotoxic enterotoxin) A. hydrophilia
found in fresh water, growth SBA/MAC, motile Plasiomonas
cause gastritis from cold blooded animals P. shigelloides
-“darting motility”,curved/S shaped, “seagull shape” most common cause of diarrhea Capylobacter jejuni
microphilic, Cat/Oxi+, NLF, growth 42 C, Hippurate hydrolysis +, Campy-blood agar(sodium bisulfide) Capylobacter jejuni
curved, microaerophilic, high humidity Cat/Oxi/Urease+; EIA, urease test on biopsy, direct stain, stool antigen test Helibacter pylori
ulcers, gastric cancers Helibacter pylori
motile, Oxi + , growth MAC NLF, Nitrite to gas Alcaligenes faecalis
feather edge, “fruity” odor, groth in 6.5% NaCL Alcaligenes faecalis
-motile respiratory pathogens Bordetella bronchiseptica
non-motile respiratory pathogens Bordetella pertussis/parapertussis
pertussin toxin, tracheal cytotoxin, hemoaggutination Bordetella
catarrhal/paradxysmal/convalescent stage pertussis toxin
-temporal vaccine available -DFA/culture from nasal specimen Bordetella
Bordet-Genou/Regan-Lowe Bordetella
milder pertussis, nontoxigenic strain, Cat+Oxi=Urea+(24 hrs) B. parapertussis
Kennel cough in dogs, growth SBA/MAC, Cat/Oxi+Urea+(4 hrs): B. bronchiseptica
Cat/Oxi +, 20-43 C temp. range L. pneumophilia
-Cysteine/iron, BCYE -found in water ex. Lakes/air conditioners, lives/multiply in protozoa/bronchial macrophages Legionella
-get from breathing in: Legionnaires disease(pneumonia)/ Pontiac fever -urine test detects antigen, DFA, serological Legionella
zoonotic disease Brucella
(most virulent) from sheep/goat B. melitensis
Cat/Oxi +, no carb., Brucella agar (5% horse/rabbit serum), “fine grains of sand” on gram stain Brucella
-survives RES system -Brucellosis, Undulant, Mediterranean, Malta fever Brucella
-get from dairy products, contact from animal -serology is the gold standard Brucella
-growth on SBA/CHOC, no MAC -Oxi/Cat/Ind +; Urea =;“sick TSI” Pasteurella multocida
-“musty” “mushroom” odor -get from animal contact esp. cat/dog bite (Cellulitis), respiratory tract/eye infect Pasteurella
-leading cause of endocarditic within genus -Cat/Oxi =, Nitrate +, glucose/lactose fermented Hemophilus aphrophilus
-dental infections; Cat + Oxi = -poor growth on SBA/CHOC, adhere to agar, “pointed star” Actinobacillus actinomycetemconitans
-associated exclusively with endocarditis -rosettes on gram stain -Oxi/Ind + ; cat/Nit = Cardiobacterium hominis
-fist fight/bite “clenched fist wound” -pits agar, “bleach odor” -Oxi/Nit + ; non motile ; non saccharolytic Eikenella corrodens
-plumb rods in chains; Oxi + Cat = ; ferment glucose -flora of pharynx in young children; Remel Rapid NH Kingella spp. denitrificans/kingae
-tularemia(get from animal carcasses, biting ticks),use safety BSC III Francisella tulrensis
-BCYE (cystine/iron), CHOC+, slow growth (25 days) -sm green drop like colonies -Cat + , ELISA, PCR Francisella tulrensis
-most normal flora of upper respiratory tract -DO NOT refrigerate,“blood lover”, Oxi/Cat + Haemophilus
-tiny, nonmotile gram neg. coccobacilli – X (hemin), V (NAD): CHOC provides both Haemophilus
-affects children spread by droplets and close contact -needs X & V H. influenza
-virulent factors:polysaccharide capsule, capsule type B , IgA proteases -non-encapsulated strain: adherence, lipoliosaccharide (LOS) H. influenza
satellites around S. aureus on SBA (sm translucent colonies) H. influenza
– “pink eye”(conjunctivitis) -Brazilian purpuric fever -needs X & Y -Remel Rapid NH ID (4 hrs) H. aegyptius
-STD: genital ulcers/chancres/chancroid -X factor only -plate immediately, high humidity, growth 2-14 days, “school of fish”, Cat = , Oxi + H. ducreyi
V only H. parainfluenzae
-X & V -Beta hemolysis in rabbit/horse BA H. haemolyticus
gram neg. diplococcic ”kidney shaped” Oxi/Cat +, CHOC for isolation Neisseria
sexually transmitted N. gonorrhaeae
-males asymptomatic – PID (pelvic inflammatory disease) N. gonorrhaeae
-virulence: pili, IgA protease, capsule -specimen: genital sites, use Dacon/Rayon swab, plate immediately onto CO2 generators & bags N. gonorrhaeae
-MTM (Modified Thayer Martin)-antibiotics inhibits other bacteria -ID: gram neg. diplococcic, CHOC growth, not SBA, Cat/Oxi + N. gonorrhaeae
-affects adolescents(college dorms) -vaccine -community acquired meningitis N. Meningitidis
-strains: A,B,C,Y, W135 -virulence: pili, capsule, endotoxins, IgA protease -specimen: CSF, blood, skin scrapings N. Meningitidis
-ID: growth CHOC/SBA/MTM, Cat/Oxi + CTA (cystine trypticase soy)-red + -BBL crystal NH ID -DNA prove N. Meningitidis
-normal in respiratory tract, pathogenic if found in sterile site N. lactamica, N. sicca, N. subflava
-gram neg. diplococci -growth in SBA, no MAC -normal respiratory flora -Oxi/Cat + -Nitrate reduction + -Asacchrolytic Moraxella catarrhalis
causes abortion/sterility in animals Campylobacter jejuni
causes whooping cough Bordetella perussis

CM- GI-8- Pancreatitis

Question Answer
What is pancreatitis and what are the common causes of it inflammation of the pancrease can be caused by auto digestion of pancres (necrotizing) or more commonly (80%) of cases are due to obstructive gallstones or heavy ETOH use (interstitial)
what are some unsual causes of pancreatitis hereditary (cystic fibrosis), Medications (thiazide, furosemide, tetracycline, azothiaprine, nitrofurantoin, oral contraceptives) Chemical Exposure, pregnancy, blunt trauma
What is a complication of pancreatitis that is alarming because it can result in death in 10-15% of cases and can recurr if you don't treat precipitating factors Necrotizing Pancreatitis
What is ranson's criteria for assesing how severe a pts acute pancreatitis is based on patient being either alcoholic or nonacoholic and certain criteria in the first 48hrs. If pt meets 3 criteria they need team management
If patient meets 3 Ranson's criteria for acute pancreatitis what do they need? team management with intensivist, surgeon and gastroenteroligist, monitored in ICU they have a predicted mortality of 15%
What is the predicted mortality if a patient meets 7-8 Ranson's criteria for acute pancreatitis 100%
what are the sx of acute pancreatitis diffuse severe upper abd pain, that radiates straight through the back unaffected by postion, may improve leaning forward. Pain escalates in intesity at peaks in 10-20min, N/V, dyspnea, narcotics don't help pain
What are some signs of acute pancreatitis pallor, diaphoresis, tender upper abdomen, fever 101-103, abdominal distention, ileus, initial hypertension
If patient has severe acute pancreatitis what signs are you possibly going to see guarding, tenderness w/ motion and percussion, Grey-Turner's sign (flank ecchymosis) Cullen's (periumbilical ecchymosis), increased heart rate, hypotension,
What would you expect to see on following lab work up values if pt has acute pancreatitis, CBC, HCT, Serum Amylase, Urine Amylase, Serum Lipase, Serum Calcium, Serum glucose, LFT's, C-reactive protein CBC- looking ofr infection, HCT >47%, Serum amylase- sig if 3x normal, Urine amylase-confirms serum amylase, Serum lipase- sig if 3x normal, Serum glucose- hyperglycemia due to interference w/ insulin production,
What procedure would you order that is diagnostic, prognostic and therapeutic value for acute pancreatitis CT/MRI
How do you manage acute pancreatitis NPO (nothing by mouth), Give IV fluid replacement, bed rest, nasogastric suction, meperidine (demerol) analgesic drug of choice. If pt becomes pain free and bowel sounds are present start clear liquids, IF not start enteral/parenteral nutrition
How do the following relate to pancreatitis: azotemia, pancreatic necrosis, internal pancreatic fistula, pseudoanuerysm, ARDS, pancreatic abcess, pseudocyst, diabets, steatorhea, intestinal obstruction All are possible complications of pancreatitis
What is the prognosis of patient with acute pancreatitis 80% will have mild episode that subsides in 7 days 3% will progres to severe and develop complication
What is chronic pancreatitis recurrent persistent inflammation of the pancrease w/ pancreatic exocrine and endocrine insufficiency makred by strictures, calculi and dilation of pancreatic duct
What are the irreversible pancreatic changes that characterize chronic pancreatitis Strictures, Calculi, dilation of pancreatic duct
what is the etiology of chronic pancreatitis male>female, chronic alcoholism, obstruction, annular pancreas, herediatry pancreatitis, untreated hyperparathyroidism
What pancreatitis is marked by infrequent attacks of abdominal pain, irregular narrowing of pancreatic duct, swelling of pancreatic parenchyma, high levels of immunoglobulin IgG4 Sclerosing Pancreatitis
What do you want to focus your history on in suspected pancreatitis EtOH use, lab tests, diagnositc imaging
What labs do you want to test for chronic pancreatitis serum amylase and lipase, hyperglycemia, glycosuria, hyperbilirubinemia, increased alkaline phosphatase. 72hour fecal fat determination, bentiromide (confirms pancreatic insufficeincy) elevated serum IgG4
What imaging studies do you want to order looking for acute pancreatitis plain abdominal x-ray(look for calcification), Ultrasound, endoscopic ultrasonography, CT scan, and ERCP
If the chronic pancreatitis is autoimmune related how do you want to manage it glucocroticoids, aboid EtOH, frequent small vol low fat meals, avoid narcotics, enzyme supplements, octreotide, nerve block, treat complications
What surgical options are available for treating chronic pancreatitis pancreatectomy, ERCP with sphincterectomy, stone extraction, psedocyst drainage, transduodenal sphincteroplasty, pancreaticojejunosotomy.
What is the prognosis for patients with chronic pancreatitis long term survival is poor better if they have recurrent acute pancreatitis from cholelithiasis, hyperparathyroidism or stenosis of sphincter of oddi
what type of cancer is pancreatic cancer and what is the survival rate pancreatic cancer is an adenocarcinoma of the epithelium of the pancreatic duct 5 year survival is 3%
When are you most likely going to see a patient with pancreatic cancer male>female, in old age, AA>caucasian>asian/hispanics, 7% have family hx
what are the risk factors for pancreatic cancer age, obesity, tobacco, chronic pancreatitis, industrial carcinogens, DDT, radiation, gasoline derivatives, hereditary, tropical pancreatitis, gastrectomy, diabetes, cytotoxic agents
How do the following relate to pancreatic cancer multiple endocrine neoplasias, breast cancer BRCA2 mutation, peutz jegher's syndrome, neurofibramatosis, ataxia telangectasia, gardner's syndrome all hereditary syndromes that increase risk of developing pancreatic cancer
what are the s/sx of pancreatic cancer persistent/recurrent epigastric pain, LUQ pain, pain referall to upper left lumbar region, anorexia, N/V, jaundice, GI bleed, excoriations on skin, constipation, flatulence, weight loss and cachexia, mild guarding, ileus, steatorrhea late in course
When working up pancreatic cancer what labs would ou order serum lipase/amylase, LFT's, stool for occult blood, glucose, CBC, cancer antigen
What imaging studies would you order for pancreatic cancer endoscopic ultrasound, CT of abdomen and pelivis, Chest x-ray, ERCP (90% sensitvie)
What is the diagnostic procedure of choice for pancreatic cancer Percutaneous needle biopsy using ct guided or ultrasound guided. Sensitivity is 90% and specificty is 100%
What are the tx options for pancreatic cancer surgery (either curative or palliative) Chemotherapy (streptozocin, mitromycin C, 5FU 19wk median survival), or combine chemo with radiation (mean survival is 11 months)

Review Game for Unit Test on Matter – 3 points EC

Question Answer
Matter anything that takes up space and has a mass or volume
Element the simplest kind of substance usually
Molecule a particle that contains more the one atom joined together
atom the smallest particle of an element that has all the same properties of the element
Nonmetal an element that is a poor conductor of heat and electricty
Metal A substance that conducts heat and electricty well
Metalloid one of a group of elements that has properties of both metals and nonmetals and is on the "staircase".
Mixture a combination of two ore more substances that keep their properties
Suspension a mixture in which the particles settle and seperate over time
Solution A misture that stays mixed over time and you can see through clearly.
Solvent the part of the solution that does the dissolving
Solute the part of the solution that gets dissolved
filtering a way of seperating particles of different sizes
chemical change a change in matter that produces a new substance with new properties
compound a substance that is formed with 2 or momre substances are combines and a chemical change takes place.
Density a measure of how tightly matter is packed in an object.

This is to help me study

Question Answer
Main control center of nervous system? Brain
Vertebrae encloses the _______? Spinal Cord
Part of the brain that looks like a mushroom that controls voluntary movements? Cerebrum
___ controls involuntary process of the body? Medulla
All parts of nervouse systeem except for brain and spinal cord? Peripheral Nervous System
Brain and spinal cord only makeup? Central Nervous System
__ nerve cell transfer messages? Neuron
___ collects all parts of senses? Receptors
Fluid filled organ in inner ear? Cochlea
____ collection of glands that secretes hormones? Endocrine System
Male and Female sex cells? M- sperm: Fertilizes the egg.F- egg: Fertilized by the sperm.
2 reproductions? Sexual: 2 organismsAsexual: 1 organisms
Humans are ____ mammals? Placental Mammals
Frogs practice___ fertilization? External Fertilization
2 tubes the sperm travels through? Vas Deferens and Uretha
Part of the reproductive where egg is fertilized by the sperm? Fallopian Tube
STD that affects immune system? HIV/AIDS
STD affects liver? Hepititas B
Inability to reproduce? Infertility
Connects the embryo to placenta? Umbilical Cord
Female reproductive system houses the baby? Uterus
Progression of growth that is after embryo but before birth? Fetus
Progression of growth that is before adulthood but after infancy and childhood? Adolescence
1st step in growth and development? Fertilization
2 way exchange organ in uterus? Placenta