Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
100 Cards in this Set
- Front
- Back
|
Primary Biliary Cirrhosis
|
autoimmune disease, middle aged women
nonsuppurative, inflammatory destruction of medium sized intrahepatic bile ducts Test with AMA antibodies See xanthelasma |
|
|
What is the cause of death of primary biliary cirrhosis?
|
Liver Failure
after long progression of xanthomas, jaundice (delayed) pruritis, steatorrhea, osteomalacia (from malabsorption) portal HTN massive variceal hemorrhage, inercurrent infections |
|
|
Primary Sclerosing Cholangitis
|
Seen in middle aged MEN,fibrosing of the intra and extrahepatic bile ducts. see onion skinning, alternating dilation and stricture
high association with ulcerative colitis Charcot Triad: jaundice, fever, RUQ pain High ALP, progressive fatigue, jaundice, weight loss, pruritis, NEED liver transplant, increased risk for cholangiocarcinoma |
|
|
What is the difference between primary and secondary biliary cirrhosis?
|
pruritis
secondary is usually caused by a tumor at the head of the pancreas, gallstones, or malignancy of the biliary tree |
|
|
What are the layers of the gallbladder?
|
It lacks a muscularis mucosa and a submucosa.
1. has a mucosa lining (columnar) 2. fibromuscular layer 3. subserosal fat with arteries, lymph, nerves and paraganglia 4. peritoneal covering |
|
|
Charcot Triad
|
Fever, Jaundice and Right Upper Quandrant Pain
Seen in primary sclerosing cholangitis What else do you see with this? Often times ulcerative colitis |
|
|
How would you diagnose and treat Wilson's Disease?
|
DECREASED ceruplasmin levels, increased copper content
** serum copper is of no help treat with penicilliamine to chelate the free copper |
|
|
What is alpha 1 antitrypsin?
|
it is an important protease inhibitor (particularly needed to prevent breakdown of elastase, cathepsin G and proteinase 3) which are normally released from neutrophils at site of inflammation.
Deficiency of this, leads to emphysema, and cirrhosis (in the liver, where a1at is made, there is excess accumulation of the abnormally folded protein product, retained in the ER |
|
|
hepatocellular carcinoma
|
in the US where HBV is relatively low, cirrhosis is present between 80-95% of HCC; but HCC is on the rise in the US, due to the increase in HCV chronic hepatitis
repeated cycles of death and regeneration in chronic hep lead to the increased rate of HCC may lead to Budd Chiari Syndrome diagnosed by increased alpha fetoprotein |
|
|
What is required for a cholesterol gallstone to occur?
|
supersaturation of bile with CHOLESTEROL
gallbladder hypomotility promotes nucleation (cholesterol is no longer dispersed, and collects into solid choleserol monohydrate crystals) Cholesterol nucleation is accelerated Mucus hypersecretion is the gallbladder traps the crystals, permitting their aggregation into stones |
|
|
What is required for pigment gallstones to occur?
|
black: sterile gallbladder bile
oxidized polymers of Ca salts of unconjugated bilirubin along with CaCO3, CaPO3, and mucin glycoprotein-- calcim makes them radiopaque inverse relationship bewteen size and number of black stones brown: infected intra or extrahepatic ducts, greasy |
|
|
Cetuximab (Erbitux)
|
antibody to EGFR-1 to treat colon and head &neck cancer, it only works in K-ras wild types. If Kras is mutated, EGFR1 won't affect Kras at all
IMC-225 |
|
|
With stage IV disease, how would you treat colon and rectal cancer?
|
The exact same. Stage four means there are distant mets, if you can keep 30% of the liver, you can remove as many mets as you need to.
24-30 month survival |
|
|
You have a 54 year old adenocarcinoma of the rectum. Endorectal ultrasound suggest T2N1 stage III diease. What do you do?
|
Stage 2 and 3 rectal cancer require neoadjuvant chemo and radiation therapy, which will decrease the need for a colostomy, decrease the size of the tumor before resection.
|
|
|
you have a 50 year old man had colon cancer, without adjuvant therapy. Ct scan showed two mets to the liver. What do you do?
|
you could resect the liver mets, you could do some agressive chemo and biologics, you could do some radiofrequency ablation of the liver, before resecting
|
|
|
How do you treat anal squamous cell carcinoma?
|
5-FU/Mitomycin and Radiation Therapy
|
|
|
what should you test for in a patient you suspect to have celiac sprue?
|
IgA anti-endomysial antibody
TTG assay |
|
|
Canker Sore
|
Apthous Ulcer; NOT herpes
peripheral red halo; pain out of proportion to the size |
|
|
Cold Sore
|
Herpes Labialis; herpes simplex (usually HSV-1)
flu like symptoms, oral, perioral lesions, red enlarged painful gingiva |
|
|
Actinic Chelietis
|
white, cracking hyperkeratoticplaques, usually on the lower lip, may progress to SCC; malignant transformation 6-10% of the time
|
|
|
What is the most common soft tissue lesion of the oral cavity?
|
Irritation Fibroma; benign proliferation following trauma
|
|
|
what is the presentation of oral SCCC?
|
Cervical Lymphadenopathy
Leukoplakia, or Erythroplakia Ulcerated lesion that won't go away History of smoking, drinking (possible role of HPV) exophytic mass, wart |
|
|
Behcet's Disease
|
Vasculitis, must see apthous ulcers, and other constellation of symptoms, like arthritis, uveitis, cardiovascular probs
Common in the Middle East |
|
|
Apthous Ulcers
|
idiopathic, local T cell immune dysfunction
Small proportion of canker sores may be associated with systemic illnesses (HIV, Behcet's Disease, Malabsorption syndromes (celiac, crohn's) Reiter's syndrome |
|
|
Oral Squamous Cell Carcinoma
|
Most common site is on the tongue
Risk factors: smoking, especially when drinker too hard and firm, but not painful |
|
|
Inflammatory Odontogenic Cysts
|
Periapical granuloma (not a true cyst)
this may progress into a cyst Periapical (radicular) cyst-- this is the most common jaw cyst, most common odontogenic cyst |
|
|
Periapical Cyst
|
non keratinized, epithelial lining due to chronic inflammation
it's asymptomatic, unless secondarily infected |
|
|
Periapical Granuloma
|
This is a precursor to a periapical cyst; it's chronically inflammad granuloma. Very common
|
|
|
Dentigerous Cysts
|
Crown of impacted tooth, generally in the wisdom teeth
Occurs in teens or twenties |
|
|
Odontogenic Keratocyst
|
this is agressive, associated with NBCCS, found especially in the posterior mandible
palisading basal cell layer |
|
|
Ameloblastoma
|
epithelial tumor arising from the precursor cells of enamel origin (reverse polarization)
recurrences are common, so you need long term follow up it's agressive, but beningn, usually occuring on the posterior mandible |
|
|
Odontoma
|
hamartoma, not a neoplasm
compound:recognizable tooth (anterior maxilla) complex: hapharzard tooth product (posterior jaws) |
|
|
Vit B1 deficiency
|
Beriberi (thiamine deficiency)
In the US mostly due to chronic alcholism Dry: polyneuropathy Wet: Dilated Cardiomyopathy Wernicke-Korsakoff Syndrome: atrophy of the mamillary bodies, causing visual changes, ataxia, confusion, anisocoria |
|
|
Wernicke Korsakoff Syndrome
|
Vit B1 Thiamine, deficiency
atrophy of the mamillary bodies |
|
|
Functions of Thiamine
|
Regulates the oxidative decarboxylation of alpha ketoacids
Cofactor for the ketolase in the PPP Maintains neural membranes and normal neural conduction |
|
|
Riboflavin Deficiency
|
Glossitis, Chelitis, Interstitial keratosis, Dermatitis
seen in alcholics |
|
|
Niacin Deficiency
|
See the 4 D's-- this is Pellagra
Dermatitis, Diarrhea, Dementia and Death Niacin is incorporated into NAD and NADP |
|
|
Vitamin C deficiency
|
Scurvy: bleeding gums
Supress the rate of synthesis of collagen peptides, Weak walls of vessels lead to hemorrhages, interferes with bone growth |
|
|
Folate (b12) Deficiency
|
Megaloblastic anemia and neural tube defects
Folate is needed for nucleic acid synthesis Folate is heat labile, so it's depleted in cooked foods |
|
|
Hallmark of reflux esophagitis?
|
eosinophilic infiltrates, basal cells hyperplasia and elongation of papilla with congestion
10% will progress to Barrett's |
|
|
What do you see with barret's esophagitis?
|
intestinal metaplasia, glands with the presence of goblet cells
40X higher risk of developing adenocarcinoma |
|
|
In whom will you see pyloric stenosis most frequently?
|
Trisomy 18 and Turner's Syndrome
|
|
|
What are the hypertrophic gastropathies?
|
Menetrier's: hyperplasia of the gastric rugae and mucous cells along with hypochlorhydria due to fundic gland atrophy
Zollinger Ellison Syndrome: |
|
|
What is the progression from esophagitis to adenocarcinoma
|
3-4% of the US have GERD
6-12% of GERD pts. develop Barret's 3-5% of BE develop adenocarcinoma (which is proportional to the amount of dysplasia) |
|
|
Acute Gastritis
|
neutrophils
occurs by NSAIDS, smoking and drinking |
|
|
Chronic Gastritis
|
INCREASED acid secretion (seen with H. Pylori) the most common cause, with CagA+ strain being worse
DECREASED gastric acid: Autoimmune mediated against the parietal glands (or IF) see lymphocytes and plasma cells, which leads to glandular atrophy, and G cells hypertrophy (due to the decreased H+ secretion) See lymphocytes and mast cells, atrophy of mucosal glands |
|
|
H. Pylori is associated with what disease states?
|
Peptic Ulcers (gastric and duodenal)
Gastric Carcinoma (adenocarcinoma, see signet rings..) Gastric MALT lymphoma |
|
|
gastric carcinoma
|
Signet rings
Kruckenburg Tumor (hematogenous spread to ovaries) Virchow's node (left supraclavicular node drains the abdomen) Lesser Curvature or prepyloric region (rarely the fundus) H. pylori is highly implicated in the intestinal type gastric carcinoma-- fungating mass (Diffuse type gastric carcinoma has no association to h. pylori, but has the linitis plastica-- and will spread..) |
|
|
gastric MALT lymphoma
|
associated with h. pylori, and t(11;18) of c-myc
better prognosis than gastric carcinoma |
|
|
GIST
|
c-kit, CD-117
Derived from the Interstitial Cells of Cajal Treat with GLEEVEC! |
|
|
Autoimmune Gastritis
|
Ab to parietal cells, decreased IF, may lead to pernicious anemia, and associated with other autoimmune diseases (hashimotos, Addisons)
|
|
|
Councilman Bodies
|
eosinophilic contractions of apoptotic hepatocytes without nuclei (this is also seen in yellow fever)
|
|
|
Ground glass hepatocytes
|
Seen in Hep B
|
|
|
Hepatitis B
|
DNA virus, the virion is called a Dane particle, needing the X protein for infectivity, the hepatocytes take on a ground glass appearance, can be transmitted by any bodily fluid
|
|
|
Tell me about acute viral hepatitis
|
Dx with super high ALT and AST, ALT usually higher (20 fold)
flu like sx, altered taste, dark urine, pale stools, pruritis, Joint point in HepB 3 phases Incubation: PEAK infectivity Pre-icteric: constitutional, non specific sx Icteric (occurs 50% of the time) |
|
|
Chronic Viral Hepatitis
|
seen in Hep B, C & D
piecemeal necrosis, lymphocytes spill over into the next plate, bridging fibrosis and macronodular cirrhosis Tx: IFN alpha + lamuvidine for Hep B IFN alpha + ribavirin for HepC |
|
|
What other systems are affected with chronic viral hepatitis?
|
Kidney: focal segmental glomerulonephritis
Vasculitis: PAN in HepB Cryoglobulinemia |
|
|
Hepatitis C
|
Increased rate of progression to Chronic Hepatitis
will not turn into fulminant |
|
|
Peptic Ulcer Disease
|
most common in the pylorus and antrum, near the lesser curvature
usually single, if multiple should investigate ZE; clean punched out ulcer, that invades the submucosa NOT a precursor to carcinoma associated with chronic gastritis (which may be a precursor to gastric adenocarcinoma) Clinical: epigastric pain lasting 1-3 hours; gastric ulcer is greater with meals; duodenal ulcer decreased pain with meals |
|
|
How could you distinguish what type of dysphagia has depending on the presentation?
|
Mechanical: can't swallow solids, but has no trouble with liquids
Motility: can't swallow liquids either (achalasia) |
|
|
Infectious Esophagitis
|
Caused by CMV, HSV and Candida Albicans
|
|
|
What are some possible causes of odynophagia?
|
painful swallowing
may be caused by ulcerated esophagus, or infectious esophagitis |
|
|
Extraesophageal manifestations of GERD?
|
Nocturnal Cough
Frequent Sore Throat Horseness, Laryngitis Asthma Exacerbations |
|
|
What is the standard treatment of GERD absent of any alarm symptoms? With alarm sx?
|
Tx PPI for 4 weeks, if not healed up, check for H. Pylori
If alarm sx are present: (odynophagia, weight loss, recurrent vomitting) do an Upper endoscopy |
|
|
abetalipoproteinemia
|
lack of apoprotein B results in an inability to transport chylomicrons out of the intestinal cell, resulting in abetalipoproteinemia
|
|
|
How are lipids absorbed?
|
Salivary and pancreatic lipases (+phospholipase A2+ cholesterol ester hydrolase) break down lipids into cholesterol, fatty acids, monoglycerides and lysolecithin. These hydrophobic lipid components are solubilized by bile acids into micelles, which bring the products into contact with the villi. FA, monoglycerides, and cholesterol diffuse across the enterocyte membrane. Glycerol is hydrophilic, and isn't contained in the micelles. Once inside the enterocyte, the lipid products are re-esterified into trigylcerides, cholesterol ester and phospolipids, and along with apoproteins, form CHYLOMICRONS. These chylomicrons are transported out of the cell via exocytosis, and into the lymph vessles.
|
|
|
Cholestasis
|
biliary obstruction, either intrahepatic or extrahepatic.
develop pruritis, skin xanthomas, elevated ALP |
|
|
What are the three morphological signs of cirrhosis?
|
Bridging fibrosis (portal triad to central vein)
Nodularity of the liver that reorganizes the vasculature Regeneration nodules |
|
|
What are the three most common causes of cirrhosis in the US?
|
60-70% alcohol
10% Viral Hepatitis 5-10% Biliary Disease |
|
|
What are the effects of portal hypertension?
|
esophageal varices, caput medusa, ascites, rectal varices, splenomegaly
|
|
|
What are the effects of hepatic cell failure?
|
Jaundice, Bleeding tendencies, Estrogen Metabolism (spider nevi, gynecomastia, and testicular atrophy/loss of hair) Iron Deficiciency (macrocytic anemia), Astertistic, Encephalopathy
|
|
|
What are the morphologic signs of Chronic Hepatitis?
|
Piecemeal Necrosis
Inflammation in portal triads (see lymphocytes) Bridging fibrosis and regenerative nodule formation |
|
|
What does fulminant hepatitis look like grossly?
|
Acute, yellow atrophy
Rapid onset of hepatic insuffiency within 2 weeks, with viral hepatitis causing 50-60% of the cases Drugs and Chemical Toxicity: Acetominophen, Isonizid, Halothane, Anti-depressants... |
|
|
What is the difference between primary and secondary biliary cirrhosis?
|
Primary, the bile ducts are virtually destroyed, you won't see any regenerative nodules, the basic architecture is maintained-- see poorly formed granulomas in the bile duct
Secondary, you see a dilation and proliferation of the bile ducts You'll see periportal fibrosis in both |
|
|
What is primary sclerosing cholangitis?
|
Seen in older men, often times iwth an inflammatory bowel disease; see onion skinning, and the Charcot Triad of fever, RUQ pain and jaundice
There is an increased risk for cholangiocarcinoma ERCP shows beading from the alteration of stenosis and dilation |
|
|
Von Meyenburg Complexes
|
Hamartomas of the bile duct, these are benign
|
|
|
Caroli Disease
|
larger ducts of the intrahepatic biliary tree are segmentally dilated
|
|
|
Anchovy paste in the liver?
|
Entamoeba Histolytica amebic abscess
|
|
|
angiosarcoma of the liver
|
the endothelial cells are malignant, this is very rare
occurs by vinyl chloride toxicity |
|
|
Focal nodular Hyperplasia
|
occurs in young women, it's a well-demarcated nodule, witha central white gray stellate scar
Adenomas are similar, in that they occur in young women on birth control, but are generally multiple, and will regress on discontinuance of use |
|
|
What is the most common salivary gland tumor and how does it present?
|
Pleomorphic Adenoma.
Painless, movable, has a high rate of recurrence Often in the parotid gland |
|
|
What is the most common malignant tumor of salivary glands?
|
Mucoepidermoid Carcinoma
it may mimic a mucocele, which presents as a smooth mass on the lower lip, due to a severed salivary duct with mucous extravasation |
|
|
What is Warthin's Tumor?
|
Benign, also called a papillary cystadenoma lympomatosum, occuring only in the parotid, 10% are bilateral
|
|
|
Scleroderma patient develops odynophagia. Barium swallow reveals enlarged esophagus just above the GE junction. What is your dx and main concern?
|
Esophageal dysmotility with low pressure distal to the LES, causes achalasia
Worrisome because there is an increased risk for esophageal carcinoma (adenocarcinoma) |
|
|
What is the primary problem in Hereditary hemachromatosis?
|
Defective in the HFE, which helps the intestine uptake the plasma transferrin. Without this uptake, iron accumulates in the liver, joints, skin, pituitary, heart
Women will often not present with symptoms until they are post-menopausal and are not losing Iron Sx: Cirrhosis, Bronzed Diabetes |
|
|
patient sets off airport metal detectors... naked.
|
hereditary hemochromatosis, total body iron may reach up to 50 grams
Increased transferrin saturation, increased ferritin, increased total iron, and decreased TIBC Hemochromatosis Can Cause Deposits CHF, Cirrhosis, (bronzed) Diabetes |
|
|
In what salivary glands will you find the most malignant turmors?
|
Sublingual 80% are malignant
|
|
|
Which hepatitis has the highest tendency for a carrier state?
|
Hep C, it's a flavivirus
>65% of HepC patients will have a carrier state |
|
|
What are the current guidelines for colon screening?
|
Everyone 50 or older
Fecal Occult Blood Test: every year Flex Sig: every 5 years Double Contrast Barium Enema: every 5-10 years Colonoscopy: every 10 years |
|
|
What causes the majority of GI bleeds?
|
Upper GI ulcerations
75% of GI bleeds are upper, of those, most are from ulcerations |
|
|
What malignant salivary tumor is most common in non-parotid glands, with a propensity for perineural invasion?
|
adenoid cystic carcinoma
|
|
|
What are the most common causes for obstruction in the small bowel?
|
Adhesions (prior surgery)
Hernia Neoplasms |
|
|
What solute gap is consistent with osmotic diarrhea?
|
60
solute gap: stool osm- 2x(stool Na + K) |
|
|
What is the Solute Gap used for?
|
To determine secretory from osmotic diarrhea
need stool electrolytes and osmoles solute gap more than 60 indicates osmotic diarrhea |
|
|
Collagenous Colitis
|
now called microscopic colitis
watery diarrhea, no bleeding, predominantly older women (40's)with a normal endoscopy |
|
|
what is metabolic syndrome?
|
HTN
Insulin Resistance Hyperuricemia Dyslipoproteinemia High Waist to Hip Ratio Men: greater than 1 Women greater than 0.6 |
|
|
What BMI is classified as overweight? obese?
|
<25 is overweight
<30 is obese |
|
|
At what point are you qualified for bariatric surgery?
|
a BMI more than 40, or more than 35 plus obesity related diseases
|
|
|
What would you see on exam of a patient who is bulimic?
|
Parotid Gland enlargment
Elevated amylase levels Generally have normal to high BMIs |
|
|
Cachexia
|
depleted skeletal muscle
increased synthesis of the acute phase proteins increased basal energy expenditure hypercaloric feeding doesn't help |
