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Step One > GI Pathology > Flashcards

GI Pathology Flashcards

1
Q

What is a pleophormic adenoma? How does it present? What is it composed of? Prognosis? What is a mucoepidermoid CA? What is it composed of? Presentation? What is a warthin tumor?

A

Benign mixed tumor of the salivary gland (most common)
Painless, mobile mass
Chondromyxoid stroma and epithelium
Recurs if incompletely excised or ruptured

Malignant tumor of salivary gland (most common)
mucinous and squamous components
painless, mobile mass

Benign cystic tumor with germinal centers

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2
Q

Describe the pathophys of achalasia. Presentation? Secondary causes? Diagnosis? Risks?

A

LES does not relax due to lack of myenteric plexus.
High LES resting pressure and uncoordinated peristalsis lead to progressive dysphagia of solids and liquids

Barium swallow-bird’s beak: dilated esophagus w/ an area of distal stenosis

Incr. risk of esophageal squamous cell CA

2nd=chagas, or malignancies

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3
Q

What is boerhaave syndrome? Cause? Treatment?

A

Transmural, distal esophageal with pneumomediastinum (air in mediastinum).

Violent retching

Surgical emergency

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4
Q

What is eosinophillic esophagitis? In which patients? Pathophys? Symptoms? Treatment?

A

Eosinophils in esophagus

Atopic patients

food allergens lead to dysphagia, heartburn, strictures

Unresponsive to GERD therapy

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5
Q

What are esophageal strictures associated with?

A

lye ingestion and acid reflux

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6
Q

What is esophagitis associated with? What is seen with candida, HSV 1 and CMV?

A

Infection in immunocompromised
Candida: white pseudomembrane
HSV-1=punched out ulcers
CMV=linear ulcers

Chemical ingestion

reflux

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7
Q

How does GERD usuallly present? Alternate pres? Pathophys?

A

Heartburn and regurgitation upon laying down

nocturnal cough, dyspnea, adult onset asthma

Decrease in LES tone

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8
Q

What is Mallory Weiss Syndrome? Symptoms? Epid?

A

mucosal lacerations at GE junction due to severe vomiting

hematemesis

Alcoholics and bulimics

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9
Q

What is plummer vinson syndrome? Incr. risk?

A

Dysphage, iron deficiency anemia, esophageal web, glossitis

esoph. squamous cell CA

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10
Q

What is sclerodermal esophageal dysmotility? Pathophys? symptoms?

A

Esoph. smooth muscle atrophy leads to decr. LES pressure and dysmotility leading to acid reflux and dysphagia leading to stricture, barretts, and aspiration

CREST

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11
Q

What is the pathophys of barretts esophagus? Associations? Risks?

A

Replacement of nonkeratinized sq. epith with nonciliated columnar with goblet cells in distal esophagus.

Due to GERD

Esophagitis, esophageal ulcers

Incr. risk of esophageal adenoCA

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12
Q

What are the two types esoph. cancer? Which is more common worldwide? In the U.S.? In which part of esoph. do they occur? What are some risk factors? Which are the risk factors associated with?

A

squamous: worldwide, upper 2/3
adenoCA: U.S., lower 1/3

AABCDEFFGH

Achalasia
alcohol-squamous
barretts-adeno
cigarettes-both
diverticula (zenkers)-squamous
esophageal web-squamous
familial
fat  (obesity)-adeno
GERD-adeno
Hot liquids -squam
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13
Q

What is acute or erosive gastritis? What are 3 pathophysiologies? Epid.?

A

Disruption of mucosal barrier leading to inflammation

Alcoholics and chronic nsaid takers

NSAIDS leads to decr. PGE2 leads to decr. gastric mucosa protection

Burns (curling ulcer-curling iron=burn) leads to decr. plasma volume which leads to sloughing of mucosa

Brain injury (cushing ulcer) leads to incr. vagal stimulation leading to incr. ACh leading to incr. H+ production

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14
Q

What are the two types of chornic gastritis (nonerosive)? What is the pathophys of each? Location of each?

A

Type A: Fundus/body; autoantibodies to parietal cells, pernicious anemia, and achlorhydria

Type B: Antrum; most common; H. pylori (MALT lympoma)

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15
Q

What is menetrier disease? pathophys? Risks?

A

Gastric hyperplasia of mucosa
Hypertrophied rugae
Excess mucus production
Protein loss and parietal cell atrophy

Precancerous

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16
Q

What cancer occurs most commonly in the stomach? How is it characterized concerning spread? Presentation? What are the two types? What are they associated with? Location? Gross or micro hist? Describe 3 different metastases that often occur with stomach cancer.

A

Gastric adenoCA

Early aggressive local spread with liver/node metastases (presents late)

Intestinal=H. pylori, nitrosamines, smoking, achlorhydria, chronic gastritis
Lesser curvature
Ulcer with raised margins

Diffuse=not associated with H. pylori
Signet rings cells
Stomach wall thickened and leathery (linitis plastica)

Virchow node=left supraclavicular node

Krukenberg tumor=bilateral to ovaries

Sister mary joseph nodule=subQ periumbilical metastases.

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17
Q

Compare and contrast gastric and duodenal ulcers concerning pain, weight, association with h pylori, mechanism, causes, risk of CA, and biopsy

A

GASTRIC

pain greater with meals leading to weight loss

70% associated

Decr. mucosal protection against gastric acid

NSAIDS

Incr. risk of CA

Biopsy margins to rule out CA

DUODENAL

pain better with eating; weight gain

100%

Decr. mucosal prot. and incr. gastric acid secretion

ZE syndrome

Benign

Hypertrophy of brunners glands

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18
Q

Where do ulcer hemorrhages occur? From which arteries? Where do ulcer perforations occur? What might be seen on xray? Presentation?

A

Posterior stomach (left gastric) and duodenum (gastroduodenal)

Anterior duod.
Free air under diaphragm
referred pain to shoulder via phrenic nerve

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19
Q

What are some symptoms f malabsorption syndromes?

A

Diarrhea, steatorrhea, weight loss, weakness, vitamin and mineral defic

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20
Q

What is the pathophys of celiac disease? Symptoms? HLA associations? Other associations? Where does malabsorptions occur? Diagnosis? Microscopic Histology? Risks? Treatment?

A

Auto-immune mediated intolerance of gliadin (gluten protein)

Malabsorption and steatorrhea

HLA-2 and 8

Northern euro and dermatitis herpetiformis and decr. bone density

Anti-endomysial, anti tissue transglutaminase, anti-gliadin Abs

Blunting of villi, lymph in lamina propria

Incr. risk of malignancy

distal duod or prox. jej

Gluten free diet

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21
Q

What is lactase defic? microscopic hist? symptoms? What acquired thing can cause it? Explain a lactose tolerance test.

A

No lactase in brush border (on tips of villi, so can be knocked out due to injury-viral enteritis (self limited)).

Normal appearing villi

osmotic diarrhea

Positive for lactase defic. if it produces symptoms and serum glucose rises < 20mg/dL

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22
Q

How does pancreatic insufficiency lead to malabsorption? malabsorption of what? Lab findings? Causes? Explain how the D-xylose absorption test works.

A

Lack of enzymes—>malabsorptions of fat soluble vitamins, vit. b12, and fat

incr. neutral fat in stool

CF, cancer, and chronic pancr

Give d-xylose: If it ends up in urine, the problem is not with intestinal mucosa or bacterial overgrowht, much more likely due to panc. insuff (lack of enzymes)

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23
Q

What are the findings of tropical sprue? Treatment? Associations?

A

Similar to celiac

antibiotics

residency or travel to tropics

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24
Q

What is whipple disease? Micro histo? symptoms? Epid?

A

Infection with tropheryma whipplei (gram pos)

PAS positive foamy macrophages in intestinal lamina propria and mesenteric nodes

Cardiac, Arthralgias, and Neuro (CAN)

Older men

Foamy Whipped cream in a CAN

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25
Q

Compare and contrast crohn disease and UC concerning location, gross morphology, micro histo, complications? Intestinal manifestation, non intestinal manifestations, and treatment?

A

CROHN

Any portion, skip lesions, rectal sparing

transmural inflamm, cobblestone mucosa, creeping fat, bowel wall thickening, linear ulcers, fissures

Noncaseating granulomas and lymph aggregates (Th1)

Strictures, fistulas, perianal disease, malabsorption, nutritional depletion, CRC, gallstones

Diarrhea that may or may not be bloody

Migr. polyarthritis, erythema nodosum, ankyl spond, pyoderm gangren, apthous ulcers, uveitis, kidney stones

corticosteroids, azathioprine, antibiotics, infliximab, adalimumab

FAT GRANny and an old CRONE SKIPing down a COBBLESTONE road away from the WRECK (rectum)

UC

colon, continuous lesions, always with rectal involvement

mucosal and submuc inflammation, friable mucosal pseudopolyps with freely hanging mesentery. Loss of haustra (lead pipe on imaging)

Crypt abscesses and ulcers, bleeding, no granulomas (Th2)

Malnutrition, sclerosing cholangitis, toxic megacolon, CRC

blood diarrhea

erythema nodosum, ankyl spond, pyoderm gangren, apthous ulcers, uveitis, primary sclerosing cholangitis

5 aminosalicylic preparations, 6MP, infliximab, colectomy

ULCCCERS

Ulcers
large intest
Continuos
colorectal CA
crypt abscesses
extends prox.
red diarrhea
sclerosing cholangitis
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26
Q

What is IBS? Epid? symptoms? Treatment?

A

Recurrent abdominal pain with >= 2:

pain improves with pooping
change in stool frequency
change in appearance of stool

Middle aged women

chronic symptoms: diarrhea, constipation, or alternating

Treat symptoms

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27
Q

What is appendicitis? Cause in adults? Children? Presentation? Signs? Differential? Treatment?

A

acute inflammation of the appendix

children: lymphoid hyperplasia
adults: fecalith obstruction

Diffuse periumbilical pain migrates to mcburney point
Nausea
fever
peritonitis if it perforates

Psoas, obturator, rovsing sign
guarding and rebound tenderness

Diverticulitis (elderly), ectopic pregnancy

appendectomy

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28
Q

What is a diverticula? True? False? Where do false ones often occur?

A

Blind pouch protruding from alimentary tract that communicates w/ lumen

true: all 3 gut layers

False: only mucosa and submucosa

where vasa recta perforates the musc. externa

29
Q

What is diverticulosis? epid? pathophys? locations? Presentation? Complications?

A

many false divert. f the colon, often sigmoid

Very common in older people

Incr. intraluminal pressure and focal weakness in wall
Low fiber diets

asymptomatic or with vague discomfort
hematochezia

Diverticulitis, fistulas

30
Q

What is diverticulitis? Presentation? Complications? Treatment? Another name?

A

inflammation of diverticula

LLQ pain, fever, leukocytosis

May perforate leading to peritonitis, abscess formation, and bowel stenosis

Antibiotics

Colovesical fistula=pneumaturia

left sided appendicitis

31
Q

What is a zenker diverticulum? location? Presentation? Epid?

A

Pharyngeoesophageal false diverticulum

between thyropharyngeal and cricopharyngeal parts of the inferior pharyngeal constrictor

Dysphagia, obstruction, foul breath

Elderly males

32
Q

What is a meckel diverticulum? Symptoms? Micro histo? Diagnosis? five 2s?

A

True diverticulum; persistence of vitelline duct

Melena, RLQ pain, intussusception, volvulus, or obstr. near terminal ileum

pertechnate study for uptake by ectopic gastric mucosa

2 inches long
2 feet from ileocecal valve
2% of popul
first 2 years of life
2 types of ectopic tissue (gastric/pancr)
33
Q

What is malratation? Complications?

A

Anomaly of midgut rotation during fetal development leading to improper positioning of bowel, formation of fibrous bands (ladd bands).

volvulus, duod obstruction

34
Q

What is volvulus? Complications? Location in adults? Children?

A

Twisting of bowel around mesentary

obstruction/infarction

midgut: children

sigmoid; adults

35
Q

What is intussusception? Location? Presentation? Age? Diagnosis/treatment?

A

telescoping of prox bowel segment into distal segment

ileocecal valve

intermittent abdom pain (blood compromise) and currant jelly stools

Children

Surgery

bulls eye apepearance on ultrasound

36
Q

What is hirschsprung disease pathophys? Mutation? Presentation? Treatment? Associations?

A

congenital megacolon

Neural crest cells don’t migrate s there are no nervous plexi in the rectum/distal colon

RET gene

bilious emesis
abdom distention
failure to pass meconium

DS

Transection

37
Q

What is acute mesenteric ischemia? Presentation? What is adhesion? What is angiodysplasia? Presentation? Location? epidem? What is duodenal atresia? Presentation? Association? What is ileus? Signs and symptoms? Causes? Treatment? What is ischemic colitis? Presentation? Location? epid? What is meconium ileus? What is necrotizing enterocolitis? Pathophys? Results?

A

critical blockage of intest. blood flow leading to necrosis
out of proportion abdom. pain; currant jelly stools

Fibrous band of scar tissue post surgery; obstruction and necrosis

tortous dilation of blood vessels=hematochezia
Cecum, terminal ileum asc. colon=older pts

Early bilious vomiting; double bubble; DS

Hypomotility w/o obstruction. Constipation and decr. flatus. Distended abdomen w/ decr. bowel sounds.
Abdom. durgeries, opiates, hypokalemia, sepsis
Bowel rest, electrolyte correction, cholinergic drugs

REduction in intest. blood flow.
pain after eating (weight loss)
watershed areas
Elderly

CF: meconium plugs obstructs intest, preventing stool passage

Premature, formula fed infants w/ immature immune system. necrosis of mucosa w/ possible perforation
Pneumomatosis intestinalis, free air in abdomen, portal venous gas

38
Q

What are colonic polyps? 3 kinds based on gross characteristics? Compare are contrast the 4 histologic types (hyperplastic, hamartomatous, adenomatous, and serrated) based on neoplastic abilillty, location, histologic nature, associated syndromes? Mutations? In adenomatous, what are the 3 types and what is their malignant potential?

A

small growths of tissue within colon. Neoplastic or not.
Gross: flat, sessile, or pedunculated

Histology:

HYPERPLASTIC
non-neo
smaller, rectosigmoid

HAMART
Non-neo. No significant risk of transform.
Normal colonic tissue with distorted arch
Peutz Jeghers and Juvenile Polyposis

ADENO
Neoplastic
Chromosome instability pathway via APC and KRAS mutations
Tubular: Least
tubulovillous: intermediate
Villous: most

SERRATED
Premalignant
CpG hypermethylation leading to microsatellite instability and mutations in BRAF.
Sawtooth pattern of crypts

39
Q

WHAT is FAP? Mutation? chromosome? progression to CRC? What is garDner syndrome? Turcot?

A

Thousands of polyps arise after puberty (pancolonic, always rectum).
Auto dominant mutation of APC tumor suppressor gene on chromosome 5q. 2 hit hypothesis
100% to CRC if not resected.

FAP and osseous and soft tissue tumors, cong. hypertrophy of retinal pigment epith, impacted/supernumery teeth

FAP and malignant CNS tumor (TURcot=TURban (head))

40
Q

What is peutz jeghers syndrome? Symptoms? Risks? What is juvenile polyposis syndrome? Symptoms? Risks?

A

auto dominant
numerous hamartomas in GI tract
hyperpigmentation of mouth, lips, hands, genitalia
Incr. risk of CRC, breast cancer, stomach, small bowle, and pancre. cancer

auto dom.
children under 5
numerous hamartomatous polyps in colon, stomach, and bowel
incr. risk of CRC

41
Q

CRC: Epid? Risk factors? Which locations are most common? How do they present in the ascending colon? Descending? How is the diagnosis made?

A

> 50; 25% have FH

adenomatous and serrated polyps, familial cancer syndromes, IBD, tobacco use, diet of processed meat with low fiber

rectosigmoid>ascending>descending

Asc: exophytic mass, iron defic. anemia, weight loss

Desc: infiltrating mass, partial obstruction, colicky pain, hematochezia

Iron defic. anemia in males and postmeno females
screen patients > 50
apple core lesion on barium enema x ray
CEA tumor marker: monitoring recurrence, not screening.

42
Q

Describe two different pathways that lead to CRC.

A

Microsatellite (lynch and sporadic): DNA mismatch repair gene mutations causing accumulated mutations

APC/beta catenin pathway (sporadic): AK-53
Loss of APC (colon at risk)
KRAS mutation (adenoma)
p53 or DCC mutation (CA)

43
Q

What is cirrhosis? Risks? What are some etiologies? Explain various symptoms and their pathophys.

A

Diffuse bridging fibrosis and nodular regeneration via stellate cells.

Incr. risk for HCC

Alcohol, chronic viral hep, biliary disease, genetic/metabolic disorders

Hepatic encephalopathy (decr. NH3 metabolism)
scleral icterus (jaundice)
fetor hepaticus (musky breath)
spider nevi (incr. estrogen)
gynecomastia (incr. estrogen)
jaundice
testicular atrophy
Asterixis (NH3)
Blleding tendency (decr. clotting factors, incr.  PT)
Anemia
Ankle edema
anorectal varices
esophageal varices (hematemesis)
peptic ulcer (melena)
splenomegaly
caput medusae
ascites
portal hypertensive gastropathy
44
Q

What is the major diagnostic use of ALP? AST and ALT? amylase, ceruloplasmin, Gamma glutamyl transpeptidase, lipase?

A

ALP: cholestatic and obstructive hepatobiliary disease, HCC, infiltrative disorders, bone disease

ALT > AST (viral hep, NAFLD)
AST > ALT (alcohol hep)

Amylase: acute pancr. and mumps

ceruloplasmin: decr. in wilsons

GGT: same as ALP except w/o bone (alcohol use)

Lipase: acute pancr (most specific)

45
Q

What are the symptoms of Reye Synddrome? Pathophys? Mechanism? Prevention?

A

Fatal childhood hepatic enceph

Mitoch. abnormalities
Fatty liver
hypoglycemia
vomiting
hepatomegaly
coma

Viral infectin (VZV or influenza B) plus aspirin

apirtin metabolites decr. beta oxidation

Avoid aspirin in children

46
Q

What is hepatic steatosis? Alcoholic hepatitis? Alcoholic cirrhosis?

A

Macrvesicular fatty change that may be reversible w/ alcohol cessation

Sustained, long term consumption;
swollen and necrotic hepatocytes w/ neutrophilic infiltratin
mallory bodies (intracytoplasm eosinophilic inclusions of damaged keratin filaments)
AST > ALT (toAST) 1.5

Final and irreversible form
Microodular, irregularly shrunken liver with hobnail appearance
Sclerosis in zone III (central vein)
Manifestations of chronic liver disease

47
Q

What is NAFLD? Pathophys? complications? lab values?

A

non alcoholic fatty liver disease
metabolic syndrome

fatty infiltrate of hepatocytes leading to cellular ballooning and necrosis

Cirrhosis and HCC

Nothing to do with alcohol

ALT>AST

48
Q

What is the pathophys/symptoms of hepatic encephalopathy? Treatment?

A

Cirrhosis leading to stunts leading to decr. metabolism of NH3 leading to neuropsych dysfunction

disorientatin/asterixis to difficult to arouse to coma

Lactulose and rifaximin

49
Q

What is HCC associated with? What might it lead to? Findings? Diagnosis?

A

HBV (with or without cirrhosis)

Cirrhosis (HCV, fatty liver disease, autoimmune disease, hemchrom, alpha 1 antitryp, wilson)

Specific carcinogens (aflatoxin from aspergillus)

Jaundice, tender hepatomegaly, ascites, polycythemia, anorexia. Spreads hematogenously

Budd Chiari syndrome

Incr. alpha fetoprotein, U/S, biopsy

50
Q

What is a cavernous hemangioma? Age? Management? Hepatic adenoma? Assocations? Prognosis? Angiosarcoma? Associations?

A

Common, benign
30-50 years
Don’t biopsy (hemorrhage)

benign
OCPs and anabolic steroids
Regress or spontaneously rupture (abdom. pain and shock)

Malignant, endothelial
Arsenic, vinyl chloride

51
Q

What is the pathophys of bdd chiari syndrome? Presentation/progression? Associations?

A

Thrombosis of hepatic veins with centrilobular congestion and necrosis leading to congestive liver disease. Maybe nutmeg liver.

Hepatomegaly, varices, abdom pain, liver failure

Hypercoag states, PV, postpartum state, HCC

52
Q

What is the pathophys of alpha 1 antitrypsin defic. in liver and lung? lab/histo findings in liver?

A

misfolded gene product protein aggregates in hepatocellular ER leading to cirrhosis with PAS pos. globules in liver.

In lungs, decr. alpha 1 antitryp leads to more elastase in alveoli leading to decr. elastic tissue leading to panacinar emphysema

53
Q

What is jaundice? At what levels does it occur? What are some causes of direct? indirect? Mixed?

A

Abnormal yellowing of skin/sclera due to bilirubin
>2.5mg/dL in blood

Indirect: hemolytic, physiologic, crigler najjar, gilbert

Direct: biliary tract obstruction (gallstones, cholangiosarcoma, panc. or liver cancer, liver fluke), biliary tract disease (primary sclerosing cholangitis, primary biliary cirrhosis), excretion defect (dubin johson, rotor)

Mixed: hepatitis, cirrhosis

54
Q

What is the pathophys of phsiologic neonatal jaundice? Treatment?

A

Immature UDP-glucoronosyltransferase leads to indir. hyperbili leading t jaundice and kernicterus (bili in basal ganglia)

Phototherapy

55
Q

Pathophys of gilbert? Symptoms? crigler-najjar syndrome type I? Treatment? Dubin Johnson? Rotor syndrome?

A

Mildly decr. UDP glucronyltransferase conjugation and impaired uptake.
Asymptomatic or mild jaundice
Bili incr. with fasting and stress

Absent UDP GT
Early in life
Patinets die within a few years
Jaundice, kernicterus
Plasmapheresis and phototherapy

Direct hyperbili due to defective excretion.
grossly black liver
benign

similar to dubin johnson but milder and w/o black liver

56
Q

What is the pathophys of wilsons disease? Symptoms? genetics? chrom? treatment?

A

A hepatocyte copper transporter ATPase (ATP7B gene) isn’t functioning well.
Hepatic copper is not excreted into bile and doens’t enter circ. as ceruloplasmin

Auto recessive (chromosome 13)

CCCCCopper is Hella BADDD

ceruloplasmin decr. 
cirrhosis
Corneal deposits (kayser fleischer rings)
copper accumulation
Carcinoma (HCC)

Hemolytic anemia

Basal anglia degen
Asterixis
Dementia
Dyskinesia, dysarthria

Chelation=pencillamine, trientine (oral zinc)

57
Q

What is the pathophys of hemochromatosis? Causes? Lab findings? Micro histo? Mutation? HLA type? Treatment?

A

Deposition of hemosiderin (stains blue)

BRONZE DIABETES
Micronodular cirrhosis
diabetes mellitus
skin pigmentation

HF
Test. atrophy
Incr. risk of HCC

Auto recessive (C282Y or H63 on HFE gene)-HLA A3
Secondary to chronic transfusion therapy

Incr. ferritin, incr. iron, decr. TIBC, incr. transferrin sat.

Prussian blue stain

Phlebotomy, chelation w/ diferasirox, deferoxamine, deferiprone

58
Q

How does biliary tract disease present? Lab findings

A

pruritus, jaundice, dark urine, light colored stool, HSM

incr. conjugated bili, incr. cholesterol, incr. ALP

59
Q

What is the pathphys of secondary biliary cirrhosis? Epid? Complications?

A

Extrahepatic biliary obstruction leads to pressure in intrahepatic ducts leading to injury/fibrsis and bile stasis

Pts. with known obstructive lesions (gallstones, biliary strictures, pancr. CA

Ascending cholangitis

60
Q

Pathophys of primary biliary cirrhosis? Epid? Assocations? Antibody?

A

autoimmune reaction leading to lymphocytic infiltrate + granulomas leading to destructin of intralobular bile ducts

middle aged women

other autoimmune conditions

Antimitochondrial antibody

61
Q

Pathophys of primary sclerosing cholangitis? epid? Associations? Complicatins? Lab findings?

A

concentric onion skin bile duct fibrosis leading to alternating strictures and dilation with beading of intra and extra hepatic bile ducts on ERCP and MRCP

young men with IBD

Hypergammaglobulinemia (IgM
MPO-ANCA/p-anca

Ulc. colitis

SEcondary biliary cirrhosis
CholangioCA

62
Q

What are some causes of bile stones? What are some risk factors? Symptoms?

A

Incr. cholesterol and/or bilirubin
Decr. bile salts
Gallbladder stasis

Female, forty, fat, fertile (pregnant)

Jaundice
fever
RUQ pain

63
Q

compare and contrast the two types of gallstones concerning radiofeatures, make up, and associations.

A

Cholesterol (radiolucent): 80% of stones
Obesity, crohns, advanced age, clofibrate, estrogen therapy, multiparity, rapid weight loss, Native american

Pigment stones (black=radioopaque: calcium, bilirubinate, hemolysis; brown=radiolucent: infection)
Chronic hemolysis, alcoholic cirrhosis, advanced age, biliiary infections, TPN
64
Q

What do gallstones most often cause? What else? What is biliary colic? Pathophys of gallstone ileus? Diagnosis? Treatment?

A

Cholecystitis; also cholangitis, acute pancr, bile stasis

Biliary colic: neurohormonal activation (by CCK after a fatty meal) leasd to contraction of gallbladder. Stone enters the cystic duct, usually causes pain.

Gallstone ileus: fistula between gallbladder and small intestine, leading to air in biliary tree and allowing passage of gallstones into intestinal tract which may obstruct ileocecal valve.

Ultrasound

Cholecystectomy

65
Q

What is cholecystitis? Usual cause? Pathophys? Signs? Lab findings? Diagnosis?

A

Acute or chronic inflammation of gallbladder

cholelithiasis blocking cystic duct leading to secondary infection
Rarely ischemia or primary infection

Murphy sign: inspiratory arrest n RUQ palpation due to pain

Incr. ALP if bile duct becomes involved.

HIDA or U/S

66
Q

What is a porcelain gallbladder? Cause? Treatment? Risks?

A

Calcified gallbladder due to chronic cholecystitis
Incidental finding on imaging
Prophylactic cholecystectomy
high rates of gallbladder CA

67
Q

What are some causes of acute pancreatitis? Presentation? Lab findings? What can it lead to? Complications?

A

GET SMASHED

Gallstones
Ethanlol
Trauma
Steroids
Mumps
Autoimmune disease
Scorpion sting
Hypercalcemia/hypertriglyc
ERCP
Drugs

Epigastric abdom pain radiating to back
anorexia
nausea

Incr. amylase, lipase (specific)

DIC, ARDS, diffuse fat necrosis, hypocalcemia, pseudocyst formation, hemorrhage, infection, multiorgan failure

Pancreatic pseudocyst: cyst of pancreatic enzymes lined by granulation tissue, not epithelium, can rupture and hemorrhage

68
Q

Describe chronic pancreatitis. Causes? What can it lead to? Lab findings?

A

chronic inflammation, atrophy, calcification of the pancreas

Alcohol abuse and idiopathic

CF leads to chronic pancreatic insufficiency

Can lead to pancreatic insufficiency leading to steatorrhea, fat soluble vitamin deficiency, diabetes mellitus

Amylase and lipase may or may not be elevated

69
Q

Average survival of pancreatic AdenoCA? Histo? Composition? Location? Tumor marker? Risk factors? Presentation? Treatment?

A

1 year; very aggressive tumor; metastasized at presentation

pancreatic ducts (disorganized glandular structure with cellular infiltratin

Pancreatic head

CA 19-9

Tobacco use
Chronic pancreatitis
Diabetes
Age > 50
Jewish and afr american males
Abdom pain radiating to back
Weight loss (malabsorption and anorexia)
Migratory thrombophlebitis (trousseau syndrome): redness and tenderness on palpation of extremities
Obstructive jaundice w/ palpable non tender gallbladder

Whipple procedure, chemotherapy, radiation therapy

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