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SFM4 > GI Pathophysiology > Flashcards

GI Pathophysiology Flashcards

1
Q

cranial nerve(s) for taste

A

back of tongue to front:
vagus (10)
glossopharyngeal (9)
facial (7) - chorda tympani

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2
Q

physiological role of taste buds

A

tongue: tasting food
airways: glucose, bacterial signalling molecules for ciliary function and immune response
GI tract: sweet and bitter, vomit, ciliary, immune

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3
Q

-guesia

A

taste problems
dysguesia - altered (such as more or less salty v sweet, which can lead to over-ingestion), medication effects (such as metallic or bitter taste)

hypo
aguesia - loss
can lead to undereating, eating spoiled foods

hyper

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4
Q

saliva regulation

A

PNS (most)

  • upregulated by food, smell, nausea
  • down regulated by dehydration, fear, sleep
  • ACh
  • M3 (muscarinic) on acinar and ductal cells

SNS (some)

  • leads to thicker saliva
  • T1 to T3 nerve root
  • norepinephrine
  • beta-adrenergic on acinar and ductal cells
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5
Q

xerostomia

A

dry mouth

d/t:

  • meds
  • Sjorgen’s, other AI
  • radiation
  • aging

c/q:

  • low appetite, dysguesia
  • impaired swallowing
  • dental problems
  • candidiasis
  • glossodynia (tongue pain)

tx:

  • switch or d/c offending meds if possible
  • otherwise, pilocarpine (muscarinic agonist, stimulates saliva) ± salivary substitutes
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6
Q

chewing regulation

A

trigeminal (5) nerve

initiation: voluntary
continuation: reflex

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7
Q

swallowing regulation

A

brainstem

initiation: voluntary
continuation: reflex

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8
Q

oropharyngeal dysphagia

A

difficulty swallowing

  • poor bolus formation
  • food retention in mouth
  • possible aspiration

d/t:

  • neuro
    • LOC
    • stroke
    • brainstem lesion or mass
  • myopathy/palsy
  • throat problems
    • oropharyngeal cancer
    • scarring
    • crichopharyngeal bar (hypertrophy)
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9
Q

foregut, midgut, hindgut

A

embryological structures

foregut = upper part of GI tract and accessory organs

  • esophagus
  • stomach
  • liver
  • biliary system
  • pancreas
  • upper duodenum

midgut –> middle part of GI tract

  • lower duodenum, jejunum and ileum (rest of SI)
  • most of colon

hindgut –> lower

  • distal colon
  • andus
  • rectum
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10
Q

GI neurocrines

A

ACh
NE
VIP (vasoactive intestinal peptide)
enkephalins

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11
Q

GI hormones

A

gastrin
CCK (cholecystokinin)
secretin

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12
Q

GI paracrines

A

histamine

somatostatin

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13
Q

Peyer’s patches

A

lamina of ilium
immune cells surrounded by single layer of epithelium
especially prominent in youths

  • M cells function somewhat similarly to T cells, communicate with lumen antigens for specific response
  • B cells, mostly IgA
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14
Q

Location in brain and receptors responsible for nausea

A 
Area postrema (in medulla)
Serotonin/5HT3, histamine, dopamine
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15
Q

Causes of nausea (general, not specific diseases)

A

Local factors

  • GI Rhythm disturbance/spasm
  • distention
  • blockage
  • chemical irritants

Central

  • increased intracranial pressure
  • psychological factors: stress, Pavlovian, smells, sights, thoughts, emotions

Circulating:

  • drugs, toxins, meds
  • uremia
  • acidosis
  • dehydration
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16
Q

Location in brain responsible for vomiting

A

Central pattern receptor in NTS (nucleus tractus solitarus)

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17
Q

Sequence of events vomiting

A

Autonomic discharge:

  • increased HR
  • sweating
  • nausea
  • salivation

Retching

  • gastric slow wave abolished
  • deep breath
  • closed glottis
  • ab and diaphragm contraction
  • lower esophageal sphincter relaxation

Emesis

  • ab and duodenal contractions
  • increased intra-ab pressure
  • retrograde contraction thorough upper esophageal sphincter
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18
Q

esophageal mucosal tear

A
  • occurs usually d/t prolonged forceful vomiting + esophageal insult such as food poisoning, alcohol
  • initial emesis is non-bloody, then bloody
  • usually not an enormous amount of blood but can be
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19
Q

esophageal varices

A
  • end stage process of portal hypertension (typically cirrhosis-related)
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20
Q

ddx: forceful, non-bloody emesis followed by bloody emesis

A
  • classic finding for esophageal mucosal tear

- consider other causes of bleeding such as peptic ulcer disease, esophageal varices, etc if suggested by hx

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21
Q

when to start transfusion

A 
\+ hemorrhage + hypovolemic shock
Hgb 7
consider starting at higher Hgb if risk factors:
-- active MI
-- age
-- pre-existing CV disease

generally restrictive about transfusion d/t risks, supply/demand

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22
Q

labs to monitor when transfusing

A

** platelets - (1) with packed RBCs, you’re not transfusing platelets; (2) when they’re actively bleeding, they are losing platelets when they really need them

sodium - (1) whenever transfusing any fluids you’re messing with electrolytes; (2) they were probably hypER-Na to begin with and now you’re giving a bunch of things that are (somewhat) hypERosmotic

Hgb, CBCs - are you hitting goals?

iron (especially long term) - are you overloading?

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23
Q

chron’s vs uc clinical features

A

Chron’s:

  • anywhere in sb or colon
  • patchy
  • transmural
  • granulomatous
  • > 50% will require 1+ surgery
  • surgery is risky
  • pain ± diarrhea
  • obstructive sx/constipation

UC:

  • only in colon, always starting from rectum
  • continuous
  • mucosal
  • non-granulomatous
  • <50% require surgery, but surgery is curative
  • pain only accompanying diarrhea
  • diarrhea only, no constipation

both:

  • 15-30 typical onset
  • GI sx:
    • diarrhea ± blood
    • fecal urgency
    • abdominal pain
    • hyperactive bowel sounds
    • perianal disease
  • malnutrition sx
    • weight loss
    • anemia
    • in kids: impaired growth, delayed puberty
  • extraintestinal autoimmune sx
    • fever
    • tachycardia
    • joint pain
    • rashes
  • possible complication: primary sclerosing cholangitis
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24
Q

bowel/colon stricturing

A

stricture = very narrowed area
most common in Chron’s d/t inflammatory state

sx:

  • cramping after meals
  • hyperactive bowel sounds
  • bowel obstruction
  • vomiting
  • food avoidance
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25
Q

severe forms of UC

A

(uc = ulcerative colitis)

fulminant colitis
toxic megacolon

can be cured by surgery

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26
Q

ibd labs and tests

A

labs:

  • CRP for generalized inflammation
  • Fecal calprotectin from stool sample for inflammation in colon
  • CBC for anemia, leukocytosis
  • albumin low in severe disease
  • vitamin/nutrient/malnutrition panel
  • colonoscopy
    • Chron’s colitis / terminal ileitis
    • UC

small bowel imaging for Chron’s

    • CT, MRI
    • capsule endoscopy

UGD for upper GI Chron’s (less common)

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27
Q

tx severe ibd

A

surgery

hospitalization + strong immunosuppressants:

  • cyclosporine
  • anti-TNF (infliximab)
  • IV steroids
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28
Q

tx moderate ibd

A

outpatient tx w/ immunosuppressants

  • oral prednisone during *induction phase
  • thiopurines, methotrexate, other immunomodulators during *maintenance phase
  • biologics e.g. infliximab

general principle of achieving remission with induction agents (strong) and weaning to fewest drugs possible to maintain remission

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29
Q

tx mild ibd

A

outpatient tx w/

  • elemental diet
  • rectally administered steroids e.g. budesonide
  • mesalamine, an NSAID specifically for ibd
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30
Q

histological signs of GERD

A
  • 6+ layers of basal cells in epithelium (normal is ~4)
  • extended vascular poles in epithelium
  • eosinophils in epithelium
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31
Q

(possible) disease progression of GERD

A

GERD –> barret’s esophagus –> esophageal cancer

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32
Q

layers of muscle throughout GI tract

A

2 in everything but stomach
- longitudinal + concentric = peristalsis

3 in stomach
- longitudinal + circular + oblique = churning

smooth muscle

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33
Q

tx bowel stenosis/strictures (a complication of IBD)

A

definitive: endo/coloscopic balloon dilation
ultra-definitive: surgical resection

m/w: npo, antiemetics, fluids, pain mgmt
± iv steroids

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34
Q

extraintestinal manifestations of IBD

A

ankylosing spondyliasis
SI joint dysfunction
rashes
others…

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35
Q

define zymogen

A

digestive enzyme released from pancreas

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36
Q

CCK produced by ___ and acts on ___
Secretin produced by ___ and acts on ___
Vagal ACh acts on ___

A

CCK produced by i cells and acts on acinar cells to produce zymogens

Secretin produced by S cells and acts on ductal cells to release Na+ and bicarb

Vagal ACh acts on both

some overlapping functions

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37
Q

cells of Cajal

A

colonic “pacemakers”
stimulate tonic contractions
determine speed of transit

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38
Q

diverticulosis vs diverticulitis

A

diverticulosis are outpouchings of mucosa and submucosa in the colon
common with aging (~60% by age 60)
usually asymptomatic

diverticulitis is inflammation or infection of these pouches and is a medical emergency

  • usually (not always) treat with abx
  • sometimes treat with surgery
  • constant pain, usually LLQ
  • ± constipation or diarrhea
  • ± fever
  • nonspecific labs
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39
Q

mutations in familial adenomatous polyposis (FAP)

A

APC

40
Q

mutations in HNPCC

A

DNA mismatch repair genes
several possible specific mutations
(hereditary non-polyposis colon cancer)

41
Q

hormone associated with carcinoid syndrome

A

serotonin/5-HT
metabolite 5-HIAA
this can be measured as a diagnostic

(this is a neuroendocrine colon cancer)

42
Q

GIST

A 
gastrointestinal stromal tumor
arises from cells of Cajal
most commonly in stomach
spindle-shaped
cKIT and DOG1+
tyrosine kinase KIT mutations
43
Q

toxic megacolon

A

sequela of IBD, c. diff
gross dilation of large ± small intestine
treat underlying condition

44
Q

toxic megacolon

A

sequela of IBD, c. diff
gross dilation of large ± small intestine
treat underlying condition

45
Q

mechanism of pain in IBS

A

visceral hypersensitivity

or undiagnosed

46
Q

causes of cholelithiasis

A
  • excess cholesterol in bile (by far the most common)
  • – mucin sludge + cholesterol microcrystals –> supersaturation
  • – impaired gallbladder motility
  • – lifestyle can help with prevention as it is linked to hypercholesterolemia, diabetes, and obesity; but there are also uncontrollable risk factors like F>M, genetics, Chron’s, rapid weight loss, octrenide meds, fasting
  • hemolysis= black pigment, radioopaque
  • infection= brown pigment, radiolucent
47
Q

hormone bile release

A

CCK

48
Q

biliary atresia

A
  • congenital or acquired biliary obstruction in newborns
  • bilirubinemia, pale stool, jaundice
  • a few weeks of life
  • dx w/ cholangiogram
  • requires surgery, good px after that
49
Q

biliary colic

A
  • uncomplicated biliary pain
  • dull RUQ/EG discomfort. w/ sudden on-off starting an hour or so after fatty meal
  • due to contraction against small stones
50
Q

acute cholecystitis

A
  • blockage of cystic duct by gallstone
  • urgent to emergent surgery
  • emergent IV fluids, pain control, abx (pip-tazo), admit
  • possible perforation
  • possible ileus (obstruction and fistula caused by large stone)

sx:

  • RUQ/EG pain ± fever ± WBCs ± nausea and vomiting
  • peritoneal signs and pain w/ movement
  • Murphy’s sign = pain w/ RUQ pressure + inhalation
  • 4-6 hours, steady

dx:

  • US
  • ± cholescintigraphy/HIDA (dye) scan
  • ± MRCP (magnetic resonance cholangiopancreatography)
51
Q

Murphy’s sign

A

acute cholecystitis

pain w/ RUQ pressure + inhalation

52
Q

choledocholecystitis

A
  • obstructive jaundice (common bile duct obstruction)
  • gallstone pancreatitis
  • common with age
53
Q

cholangitis

A
  • high mortality
  • most emergent
  • biliary tract obstruction
  • -> sepsis (often)
  • infection-related: bacteria from gut via:
    • choledocholithiasis (CBD obstruction)
    • malignancy
    • stricture
    • post-surgery or ERCP (endoscopic retrograde cholangiopancreatography)
    • ulcerative colitis

tx:

  • biliary drainage
  • abx (pip-tazo)
  • tx underlying condition
54
Q

complications of primary sclerosing cholangitis

A
  • sepsis
  • high mortality
  • cancer of gallbladder or bile duct
  • cirrhosis r/q liver tpx
55
Q

porcelain gallbladder

A

calcified wall d/t chronic inflammation

multiple stones

56
Q

sclerosing cholangitis

A
  • progressive inflammation –> bile duct obliteration
  • associated w/ IBD, UC>CD

sx:

  • pruritus (usually first sx)
  • jaundice
  • RUQ pain
57
Q

heme synthesis

A

TCA intermediate + one amino acid

early intermediates:

  • delta-aminolevulinic acid (∂-ALA)
  • porphobilinogen (PBG)

last step: chelation (Fe++)
– inhibited by Pb++

negative feedback to ALA synthase

58
Q

causes and effects of defective heme synthesis

A

cause:

  • genetic
  • Pb++ poisoning

effect:

  • anemia
  • etc
59
Q

acute intermittent porphyria

A
  • ∂-ALA and PBG accumulation d/t genetic defect
  • visceral pain
  • neurologic manifestations
60
Q

porphyria cutenea tarda

A
  • late-heme synthesis mutation resulting in buildup of porphyrins
  • blistering cutaneous photosensitivity
61
Q

Gilbert syndrome

A
  • benign
  • relatively low bilirubin-UGT levels
  • buildup of conjugated bilirubin, low uncongugated bilirubin
  • bilirubinemia
62
Q

Crigler-Najjar syndrome

A
  • more severe version of Gilbert syndrome
  • absent or complete defect bilirubin-UGT
  • buildup of conjugated bilirubin, no uncongugated bilirubin or bilirubin excretion
  • hyperbilirubinemia
63
Q

Dubin-Johnson syndrome and Rotor syndrome

A

buildup of conjugated bilirubin (unbound)

defect in transporters

64
Q

acute pancreatitis

A
  • severe, persistent epigastric pain radiating to back + nausea and vomiting
  • if mild, 3-5 day recovery (80% of cases)
  • if severe (20%), systemic complications, organ failure, and possible death

exam:

  • EG tenderness
  • Cullen’s sign = periumbilical bruising
  • Grey Turner sign = flank bruising
  • xanthomas (cholesterol-rich bumps on skin), if pancreatitis is caused by hypercholesterol

dx:

  • lipase, amylase > 3x normal
  • US to r/o other causes (e.g. biliary)
  • triglycerides possibly >1000
  • calcium
  • hepatic panel
  • CBC

causes:

  • usually gallstones or alcohol
  • also familial, autoimmune, infectious, spider and scorpion bites, idiopathic
65
Q

Cullen’s sign

A

periumbilical bruising

acute pancreatitis

66
Q

Grey Turner sign

A

flank bruising

acute pancreatitis

67
Q

pancreatic pseudocysts

A
  • not “true” cyst d/t no epithelial lining, but significant buildup of serous fluid
  • dx CT, US
  • sx: pain, distension, anorexia, infection/abscess
68
Q

chronic pancreatitis

A
  • inflammation, scarring, fibrosis, eventual irreversible loss of function of pancreas
  • moderate to severe chronic pain

sx:

  • EG pain –> back
  • after meal, lying down
  • intermittent or constant
  • steatorrhea (fatty stool) d/t (~90%) loss of exocrine function
  • pain ≠ imaging severity

dx

  • lipase and amylase either elevated or low d/t exhausted reserves
  • tBili and alkaline phosphatase if bili is involved
  • low vit D, other fat-soluble vitamins
  • elevated tri >1000, intermittent or constant
  • fecal elastase
  • IgG4 if autoimmune

dx:

  • pancreatic stim test
  • imaging

causes:

  • alcohol
  • smoking
  • hyper-triglycerides
  • autoimmune
  • obstruction
  • hereditary
  • idiopathic

complications:

  • osteopenia
  • type I-ish diabetes (LOF but not autoimmune)

tx:

  • enzyme supplementation
  • celiac plexus block for pain
69
Q

ductal adenocarcinoma

A
  • main pancreatic cancer

sx:

  • low energy
  • weight loss
  • jaundice and hepatomegaly
  • palpable RUQ mass
  • anorexia
  • cachexia
  • abdominal pain
  • dark urine
  • Corvoisier’s sign (tender, palpable gallbladder)

Rfx:

  • smoking
  • chronic pancreatitis
  • diabetes
  • age

dx:
- imaging

tx:
~ 15% surgical - Whipple
~ 60% metastasis - chemo

px:

  • poor
  • once metastasized usually <1 year despite chemo
70
Q

aspartate aminotransferase

A
  • AST
  • released with hepatocyte, myocardial, or skeletal muscle damage
  • part of liver function tests
71
Q

alanine aminotransferase

A
  • ALT
  • most specific LFT for liver damage
  • found in hepatocyte mitochondria
72
Q

alkaline phosphatase

A
  • ALP
  • produced by bile duct, bone, placenta, intestinal damage
  • part of LFTs
73
Q

gamma glutamyltranspeptidase

A
  • GGT
  • hepatocytes and biliary tract
  • nonspecific
  • not in bone
74
Q

LFTs

A 
* ALT (liver, sp)
albumin
AST (liver, nsp)
ALP (bile, nsp)
* bilirubin (liver and bile, sp)
GGT (liver and bile, nsp)
prothrombin
INR
75
Q

chronic liver disease vs acute sx

A

chronic

  • may be asymptomatic
  • fatigue
  • malaise
  • poor appetite
  • itching
  • weight loss

acute or end-stage

  • jaundice and icterus (jaundice of eyes)
  • dark urine
  • abd pain
76
Q

diagnosing and staging liver diseases

A
  • biopsy, percutaneous or transjugular
  • US
  • MRI
  • transient elastography: specialized US for fibrosis

early stages may be reversible
all paths lead to cirrhosis

77
Q

liver failure sx

A
  • small, nodular, cirrhosed liver
  • jaundice, icterus, ^bili
  • sex hormone dysfunction sx: testicular atrophy, gynecomastia, spider angioma, palmar erythema
  • portal HTN: splenomegaly, ascites
  • impaired detox –> neuro decline, asterixis (loss of motor control), and hepatic encephalopathy (swelling)
  • esophageal and gastric varices as shown by EGD
78
Q

liver failure lab findings

A

LOW:

  • albumin
  • thrombocytes
  • clotting ability (i.e. increased INR)

HIGH:

  • bilirubin
  • INR

VARIABLE (dep on disease state):

  • AST
  • ALT
  • ALP
  • GGT
79
Q

portal vein htn causes and effects

A

blood backs up into portal vein branches d/t

  • cirrhosis*, sarcoidosis, schisto (intrahepatic)
  • portal vein obstruction (prehepatic)
  • hepatic vein obstruction, right HF, pericarditis (posthepatic)

branches:

  • right and left gastric veins –> gastric and esophageal varices
  • paraumbilical vein –> caput medusae (varices around umbilicus)
  • splenic vein –> splenomegaly –> platelet consumption
  • inferior mesenteric vein –> rectal anastomoses and varices
  • superior mesenteric vein

other consequences:

  • ascites from high intravascular pressure (blood backup) + low oncotic pressure (low albumin d/t liver disease) + Na+ and H2O retention d/t kidney effects
  • -> liver disease
  • intrahepatic = cause
  • prehepatic = effect; insufficient blood supply to liver
  • posthepatic = effect; intrahepatic htn

complications:
- spontaneous bacterial peritonitis = infection of ascites fluid typically d/t gut damage –> leakage of gut bacteria

80
Q

spontaneous bacterial peritonitis

A
  • infection of ascites fluid
  • typically d/t gut damage –> leakage of gut bacteria; other sources of infection also possible

tx:

  • usually single bacterial species
  • start with 3rd gen ceph e.g. cephtriaxone, as this covers most of the common offenders
  • abx prophylaxis can be used in high risk

sx:

  • fever
  • abd pain
  • altered mental status
  • neutrophilic ascites (> 250 PMN/mm3)

complications:
- hepatorenal syndrome (kidney failure w/ hypER-K, etc.)

81
Q

tx cirrhotic portal htn

A
  • tx underlying cause
  • definitive: liver tpx

for ascites:

  • diuretics e.g. furosemide and spironolactone
  • salt restriction
  • paracentesis (remove fluid via big needle)

for varices:

  • non selective beta blockers e.g. propranolol to reduce pressure
  • variceal ligation and obliteration
  • TIPS (transjugular intrahepatic portosystemic shunt)
82
Q

hepatic encephalopathy

A
  • altered mental status d/t toxic buildup
  • ranges from mild confusion to coma

dx:

  • clinical presentation
  • possible elevated ammonia (nsp.)

risk fc:

  • infection
  • constipation
  • GI bleed
  • renal failure

tx:

  • underlying cause
  • tx constipation: 3 soft stools/day w/ lactulose
  • rifaximin $$ = chronic non-absorbable abx
83
Q

end stage liver disease

A

decompensated cirrhosis:

  • bleeding varices
  • hepatic encephalopathy
  • ascites
  • jaundice
  • LFTs very poor

dx:
- MELD score based on clinical criteria and labs (INR, bili, sCr)

tx:
- transplant: 1 yr survival = 92%, but few donors

84
Q

acetaminophen-induced fulminant hepatic failure

A

~50% of all FHF

hyperacute: cerebral edema
subacute: renal failure, portal htn
(usually)

dx:
- clinical presentation
- hx of acetaminophen use
- - >12 g/24 h, 1-4 g per dose
- INR > 1.5 (slow clotting)
- elevated ALT/AST (>3500)
- low bilirubin
- no preexisting liver conditions

tx:

  • NAC (n-acetyl cysteine) ~70% success
  • rest need tpx ~70% success
  • so overall ~90% survival
85
Q

non-acetaminophen fulminant hepatic failure

A

d/t:

  • viral hepatitis
  • ischemic hepatitis
  • Wilson’s disease
  • drug or supplement
  • idiosyncratic

as with acetaminophen induced:

  • INR > 1.5
  • elevated ALT/AST >3500
  • low bili
  • no preexisting liver conditions

worse outlook than acetaminophen induced
~30% survival

86
Q

alcoholic hepatitis

A
  • hepatic steatosis (fatty liver)
  • initially reversible
  • if severe, poor short term mortality
  • seen in 10-20% of alcoholics

dx:

  • clinical
  • AST/ALT > 1 (usually)

tx:

  • prednisone
  • supportive
  • alcohol abstinence
87
Q

hemochromatosis

A
  • genetic: HFE gene
  • high iron absorption w/o compensatory excretion
  • -> oxidative stress, fibrosis
  • sx don’t usually develop until 40/60 y/o when iron has built up sufficiently
  • can also be secondary to chronic transfusion

dx:

  • high iron/transferrin
  • high ferritin
  • genetic testing
  • biopsy

tx:

  • serial phlebotomy
  • iron chelation
88
Q

Wilson’s disease

A
  • genetic: ATP7B copper transport gene
  • copper gets stuck in hepatocyte (can’t leave via transport gene)
  • -> hepatocyte death and release of copper (so overall elevated Cu in liver, brain, cornea–ring around eyes, kidneys
  • presents in teens/20s when copper has built up sufficiently and symptoms have progressed sufficiently
  • sx usually subclinical prior to that

dx:

  • ring around iris (Kayser-Fleischer rings)
  • high urinary and serum copper
  • low serum ceruloplasmin (copper-containing protein)

sx:

  • neuro: movement disorders, dementia, psych sx
  • Kayser-Fleischer rings
  • hepatitis, acute or cirrhotic
  • hemolytic anemia
  • kidney disease

tx:

  • chelation w/ *penicillamine
  • liver tpx curative
89
Q

alpha-1 antitrypsin deficiency

A
  • genetic: infant, ped, and adult
  • alpha-1AT buildup in hepatocytes
  • fibrosis/cirrhosis
  • high HCC risk
  • requires tpx
  • also lungs (panacinar emphysema, IPF w/o smoking hx)
90
Q

primary biliary cholangitis (cirrhosis)

A
  • T cell destruction of interlobular biliary epithelium
  • -> cholestasis
  • -> cirrhosis
  • mostly middle-aged women
  • often comorbid with other autoimmune
  • especially UC>CD IBD
  • environmental triggers such as infections and chemicals, including cosmetics

sx:

  • fatigue
  • pruritus

dx:

  • anti-mitochondrial Ab
  • ALP >1.5x normal
  • ANA+
  • hyperlipidemia

tx:

  • ursodeoxycholic acid (slows)
  • liver tpx
91
Q

autoimmune hepatitis

A
  • immune destruction of hepatocytes
  • hepatocellular damage pattern
  • -> cirrhosis
  • mostly women, any age
  • often comorbid with other autoimmune
  • environmental triggers e.g. infections, chemicals incl cosmetics

dx:

  • IgG elevated
  • anti-smooth muscle Ab
  • anti-liver-kidney microsomal Ab
  • AST/ALT elevated

tx:

  • prednisone
  • other immunosuppressants
92
Q

hepatic adenoma

A
  • rare, benign liver tumor but carries bleeding risk
  • F 30-50 d/t OCP hormone use
  • resect if symptomatic
  • otherwise just stop hormones
93
Q

focal nodular hyperplasia

A
  • common, benign, asymptomatic
  • F 30-50
  • “stellate scar” from abnormal blood vessel
  • no intervention needed
94
Q

hepatic hemangioma

A
  • very common, benign
  • usually asymptomatic, incidental finding on imaging
  • don’t biopsy as it is a vascular lesion
  • F>M 30-50
  • no intervention needed
95
Q

hepatocellular carcinoma

A
  • among most common causes of cancer death
  • may be multiple synchronous tumors

sx:

  • incidental from imaging
  • abnormal LFTs
  • weight loss
  • anorexia
  • jaundice
  • decomp of stable cirrhosis
  • new onset hepatic vein thrombosis (Budd Chiari syx)

causes:

  • hep B
  • cirrhosis
  • afloxatin exposure
  • at-risk should screen w/ US and serum alpha-fetoprotein (AFP) every 6 mo

tx:

  • portal vein embolization
  • transarterial chemoembolization
  • radio frequency ablation
  • surgery
  • tpx if small lesions, not metastasized

SFM4 (10 decks)

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