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368 Cards in this Set
- Front
- Back
define odynophagia
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painful swallowing
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|
causes of esophageal chest pain
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GER, dysmotility, increased visceral sensitivity
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define dysphagia
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difficulty swallowing, food sticking
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what causes oropharyngeal dysphagia?
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inability to protect nasopharynx or larynx during swallowing
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what are symptoms of OP?
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nasal regurgitation, coughing, aspiration
|
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liquids or solids cuasing more problems in OP?
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liquids
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OP most commonly associated with which types of conditions?
|
cerebral or brainstem conditions (swallowing center), probs with striated muscle, imparment of UES opening
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dysphagia for liquids alone suggests:
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OP
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dysphagia for solids alone suggests:
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structural abnormality
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dysphagia for solids and liquids suggests:
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motility disorder
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long history of intermittent dysphagia for solids suggests:
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structural abnormality
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worsening of solid food dysphagia suggests:
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progressive narrowing due to stricture
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significant weight loss in dysphagic patients over 50 suggests:
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esophageal adenocarcinoma
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significant weight loss in dysphagic childred suggests:
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achalasia
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combination of chest pain and dysphagia suggests:
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diffuse esophageal spasm
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raynaud's phenomenon and dysphagia suggests:
|
scleroderma
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confirm esophageal motility disorder with
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manometry
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define reflux esophagitis
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macroscopic damage to the esophagus visible at endoscopy as erosions or ulcerations
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causes of GERD
|
abnormal LES (hypotonic LES, transient LES relaxations), hiatal hernia, defect in esophageal clearance mechanisms
|
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atypical reflux symptoms
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asthma, laryngitis, chronic cough, chest pain
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Diagnostic tests for GERD
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upper endoscopy, ambulatory pH monitoring
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complications from GERD
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stricture, Barrett's, ulcer
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where do strictures tend to occur?
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distal esophagus (greatest acid concentration)
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what is barrett's esophagus?
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when metaplastic columnar epithelium replaces normal squamous epithelium in distal esophagus
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what does barrett's look like?
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orange-red epithelium (vs. white/yellow for nl)
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How do you confirm a dx of Barrett's?
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mucus biopsies
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What type of monitoring should you do for patients with Barrett's?
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endoscopy/biopsy every 3 years
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What to do if patient is unresponsive to GERD medical treatment?
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laproscopic gastric fundoplication
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List structural lesions of the esophagus
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esophageal cancer, strictures, webs/rings, zenker's diverticulum
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difference between a web and a ring?
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ring is circumferential ring at squamocolumnar junction, web is semilunar and in mid to upper esophagus
|
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what is a Zenker's diverticulum?
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protrusion of the pharyngeal mucosa at pharyngoesophageal jxn through UES
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how do you treat Zenkers Diverticulum?
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surgical resection
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Causes of esophagitis not due to GER (3)
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pill induced, caustic injury, infectious esophagitis (in immcomp: candida, HSV, CMV)
|
|
List esophageal motility disorders (3)
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Achalasia, Diffuse Esophageal Spasm, scleroderma esophagus
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Pathophysio of Achalasia
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denervation of esophagus from loss of ganglion cells in Auerbach's plexus, lose peristalsis in smooth muscle and impaired LES relaxation
|
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Clinical findings in achalasia?
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gradual onset of dysphagia for solid and liquid, regurgitation and vomiting
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typical radiographic hallmark of Achalasia?
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bird's beak
|
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what is pseudo-achalasia?
|
a cancer that might resemble achalasia
|
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clinical findings in Diffuse Esophageal Spasm?
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intermittent, non-progressive dysphagia for solids and liquids, chest pain
|
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pathophysio of scleroderma esophagus
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atrophy and fibrosis of esophageal smooth muscle, hypotonic LES, severe reflux
|
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Esophageal location of esophageal squamous cell carcinoma
|
throughout esophagus
|
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esophageal location of esophageal adenocarcinoma
|
lower 1/3 of esophagus
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symptoms of esophageal carcinoma
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progressive solid food dysphagia, hoarseness, weight loss
|
|
list 5 causes of Dyspepsia
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PUD, GERD, gastric cancer, non-ulcer dyspepsia, meds
|
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what types of meds cause dyspepsia?
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alcohol, caffeine, iron, NSAIDS, antibiotics
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|
which symptoms suggest peptic ulcers?
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pain between meals or at night and releived by food or antacids
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four sources of afferent input into vomiting center
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Vagal/splanchnic from GI (visceral distention, peritonitis), vestibular system, higher CNS, CTZ
|
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where is the CTZ?
|
fourth ventricle
|
|
what stimulates the CTZ?
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drugs, chemotherapeutics, toxins
|
|
some CNS related causes of vomiting
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Increased ICP, Vestibular disorders, infections (encephalitis, meningitis)
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Define gastroparesis
|
decreased gastric motility
|
|
define Ileus
|
decreased intestinal motility
|
|
causes of peritoneal irritation (4)
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cholecystitis, acute pancreatitis, appendicitis, perforations
|
|
what is the common cause of acute vomiting without abdominal pain?
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food poisoning, infectious gastroenteritis, drugs
|
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acute onset of vomiting with severe pain suggests:
|
intestinal obstruction or peritonitis
|
|
chronic or recurrent vomiting suggests
|
obstruction of pylorus or small intestine, gastroparesis, or CNS and systemic disorders
|
|
define hematemesis
|
bright red emesis
|
|
define melena
|
jet black tarry fould smelling stool
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define hematochezia
|
bright red bloody bowel movements
|
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list 4 causes of UGI bleeding
|
PUD, portal hypertension, gastric neoplasms, and erosive gastritis, Mallory Weiss tears
|
|
Is initial hematocrit a good indicator of acute blood loss?
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not really, takes 24-72 hrs for equilibration
|
|
how much does one unit of blood raise hct?
|
3-4%
|
|
define erosions
|
single or multiple, small (<3mm) white linear breaks that don’t extend through the muscularis mucosa
|
|
define ulcers
|
mucosal breaks with obvous depth, white base, larger in size
|
|
most common sites of ulcers
|
duodenal bulb and gastric antrum
|
|
Causes of PUD
|
Hp, NSAIDs, Gastrinoma
|
|
How does Hp protect itself?
|
burrows into mucus layer by epithelial cells (pH 7) and uses urease to generate ammonia
|
|
how does Hp cause disease?
|
suppression of somatostatin
|
|
Mechanisms of NSAID induced injury
|
topical damage, PG inhibition thus loss of mucosal defense mechanisms, platelet inhibition so easier to bleed
|
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clinical findings in peptic ulcer disease
|
dyspepsia
|
|
complications from PUD
|
penetration or perforation, extensive bleeding, edema/scarring leading to obstruction
|
|
Who gets stress gastritis?
|
ICU patients: severe burns/trauma/sepsis etc
|
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Causes of gastroparesis (3)
|
neuropathic (enteric or extrinsic nerves), myopathic process (involving gastric smooth muscle), post-surgical probs (vagotomy, gastric resection)
|
|
symptoms of gastroparesis
|
nausea, vomiting, early satiety, bloating
|
|
when does vomiting occur with gastroparesis?
|
after a meal
|
|
definition of constipation
|
two or less bowel movements per week or excessive difficulty or straining on defacation
|
|
which pelvic floor muscles are responsible for continence?
|
pubococcygeus and puborectalis
|
|
common causes of constipation
|
poor dietary (to little fiber/fluids) or toilet habits, structural abnormalities (malignancy), systemic disease (myopathy, neuropathy, endocrine disorder, lyte imbalance, medication use)
|
|
first line treatment for constipation?
|
dietary fiber supplement
|
|
constipation lab tests available?
|
colonic transit study, defecography, anal manemtry
|
|
Major causes of lower GI bleeding (6)
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diverticulosis, vascular ectasias, neoplasms, IBD, ischemic colitis, anorectal disease
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describe lesions from Vascular Ectasias
|
small, multiple, painless, red flat submucosal blotch of vessels, looks like a fern
|
|
first thing to do w/ patient with acute GI bleed?
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assess volume status and rescucitate if necessary
|
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which acute GI bleed patients get colonoscopy?
|
anyone who is hospitalized due to bleeding
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|
evaluation tests for acute GI bleed?
|
anoscopy, sigmoidoscopy, colonoscopy, angiography, nuclear bleeding scan (99Tc RBC scan)
|
|
what is damaged in Celiac Sprue?
|
diffuse damage to proximal small intestinal mucosa = malabsorption
|
|
which genes are associated with celiac sprue?
|
HLA-DQ2 and HLA-DQ8
|
|
describe celiac sprue pathogenesis:
|
gluten sensitive T cells respond, Th1 reaction leading to inflammation and damage of intestinal mucosa
|
|
what 3 nutrients are absorbed in the proximal small intestine?
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calcium, iron, folate
|
|
impaired calcium absorption leads to:
|
osteoporosis
|
|
impaired iron absorption leads to:
|
iron deficiency anemia
|
|
impaired folate absorption leads to:
|
megaloblastic anemia
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Sprue in jejunum and ileum leads to:
|
carb malabsorption: flatulence, steatorrhea, weight loss, cramps
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clinical features of sprue in infancy:
|
failure to thrive, anorexia, irritability, abd pain, hypotnia, muscle wasting, abd distension, soft malodorous stool
|
|
clinical presentation of sprue in older children:
|
growth retardation, amenorrhea, rickets, osteoporosis, anemia
|
|
how to confirm diagnosis of sprue?
|
IgG and IgA against gliadin, foolow up + test with anti-tTG (tissue transglutaminase), if +, then sprue, confirm with bx
|
|
what disorder is associated with sprue?
|
dermatitis herpetiformis (pruritic papulovesicles over extremities and trunk), some px develop t-cell small bowel lymphoma (fatal)
|
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treatment of sprue?
|
gluten free diet, celiac support group
|
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3 main small bowel disorders
|
sprue, bacterial overgrowth, short bowel syndrome
|
|
causes of bacterial overgrowth (5)
|
gastric achlorydia, anatomic abnormalities leading to stasis, motility disorder that slows transit, fistula b/w colon and sm intestine, misc (elderly, AIDS)
|
|
how does bacterial overgrowth lead dz?
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bacteria deconjugate bile acids --> less micelle formation, direct damage to brush border, take up B12
|
|
resection of terminal ileum results in:
|
malabsorption of bile salts and B12
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|
how much small bowel resection do you need to cause steatorrhea?
|
>100cm of ileum resected --> bile salts arent taken up, steatorrhea, malabsorption of fat soluble vitamins
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four major bowel disorders
|
diverticulosis, polyps, neoplasms, appendicitis
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what are colonic diverticula?
|
mucosal protrusions that go through the muscular wall
|
|
what causes diverticula?
|
low fiber diet, high bowel intraluminal pressure lead to muscular hypertrophy, vasa recta penetrate to nourish, weaken wall, and pseudo-diverticula form
|
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which region of colon most involved in diverticula?
|
sigmoid: muscular contractions increase distally
|
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does rectum get diverticula?
|
no, no tenia coli
|
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complications of diverticula?
|
pain 2ndary to muscle spasm, perforation (diverticulosis), diverticular bleeding
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describe diverticular bleeding?
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abrupt onset, brisk output, red color, causes hemodynamic instability, 80% need transfusion
|
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two types of colon polyps
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adenomatous and non-adenomatous (hyperplastic, juvenile, hamartomas, inflammatory)
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describe hyperplastic polyps
|
common, small (usu <5mm), in rectosigmoid region, elongated crypts w/ papillary fronds w/ lots of epithelial cells, not malignant
|
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three types of adenomatous polyps
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tubular adenomas (lowest risk), tubluvillous adenomas, villous adenomas (highest risk)
|
|
underlying pathophys of appendicitis?
|
obstruction of tiny appendiceal lumen (fecalith, inflammation, tumor, muscle hypertrophy)
|
|
presentation of appendicitis?
|
abd pain, cramps, vomiting, nausea, sense of constipation, RLQ pain, mild fever, leukocytosis
|
|
4 bowel motility disorders
|
acute intestinal obstruction, acute small bowel ileus, acute colonic pseudo obstruction ("colonic ileus"), IBS
|
|
who gets ileus?
|
commonly seen in hospitalized patients
|
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when does IBS present?
|
early in life (first 2 decades)
|
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IBS clinical presentation:
|
chronic lower abd pain, crampy, intermittent, not at night, worse 1-2h after meals, relieved by defacation
|
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two causes of acute bowel ischemia
|
thrombotic SMA occlusion in px w/ atherosclerosis, embolic event in px w/ afib or LV thrombus
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pathophys of ischemic colitis?
|
transient episodes of low blood flow, esp in watershed areas fed by both SMA/IMA
|
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SMA-IMA watershed areas?
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splenic flexure and distal sigmoid colon
|
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clinical presentation of acute bowel ischemia?
|
bowel infarction, fever, tachy, hypoT, abd tenderness w/ guarding, leukocytosis, metabolic acidosis
|
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clinical presentation of ischemic colitis?
|
usu elderly, mild LLQ cramps, tenesmus, blood in stool
|
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diff b/w internal and external hemorrhoids?
|
internal: painless bleeding; external: no bleeding, but can get thromboses w/ pain/tenderness
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define diarrhea
|
>2 loose stools/day or increased liquidity
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define non-inflammatory diarrhea
|
leads to increased fecal fluid but does not disrupt the intestinal epithelium, characterized by watery, non-bloody and absence of fecal leukocytes
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define inflammatory diarrhea
|
caused by infections, agents, or events which disrupt intestinal mucosa, most infectious causes usu affect colon so volume is less, frequent smaller volume bowel movements and lower abd cramps, dysentery, + fecal leukocytes
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causes of acute diarrhea
|
infectious agents, bacterial toxins, medications, ingestion of non-absorbable osmotically active substances
|
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how to distinguish inflammatory from non-inflammatory diarrhea?
|
presence of fecal leukocytes
|
|
signs of dehydration:
|
dry mouth, decreased urination, weakness, lethargy, dry mucus membranes
|
|
signs of severe inflammatory diarrhea
|
fever >38.5, dysentery >8x/day, severe abd pain/tenderness, elderly, imunocompromised
|
|
Oral rehydration solution:
|
3.5g NaCl, 2.5g NaHCO3, 1.5g KCl, 20g Glucose in 1L of water
|
|
homemade oral rehydration solution
|
1/2 tsp salt, 1 tsp baking soda, 8 tsp sugar, 8 oz OJ, in 1L water
|
|
six physological categories of diarrheas:
|
osmotic, secretory, inflammatory, motility, chronic infection, malabsorption
|
|
how big of an osmotic gap for osmotic diarrhea?
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>50 mosm/Kg
|
|
when does osmotic diarrhea resolve?
|
when patients are fasting, because no longer ingesting osmotically active substance
|
|
common causes of osmotic diarrhea?
|
carb malabsorption (lactose, sorbitol), inorganic ion digestion (laxatives)
|
|
cause of fictitious diarrhea?
|
laxative abuse: consider in young women w/ eating disorder, px with psychiatric problems
|
|
pathophys of secretory diarrhea
|
increased intestinal secretion of lytes and water or decreased absorption, has normal osmotic gap
|
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does secretory diarrhea resolve with fasting?
|
no, not due to an osmotically active substance
|
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causes of secretory diarrhea
|
certain laxatives, endocrine tumors (VIPoma, calcitonin tumor), malabsorption of bile acids
|
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causes of inflammatory diarrheas:
|
UC, Crohn's, infections
|
|
motility disorders causing diarrhea
|
rapid intestinal transit (irritable bowel syndrome), stasis leading to bacterial overgrowth (vagotomy, anatomic abnormalities)
|
|
causes of diarrhea due to malabsorption
|
impaired intraluminal digestion (pancreatic insufficiency, bile salt deficiency, gastrectomy), inadequate epithelial absorption (reduced surface area, small intestinal mucosal disorders), defective absorption via lymphatics
|
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causes of pancreatic insufficiency
|
chronic pancreatitis, cystic fibrosis, surgical removal
|
|
causes of bile salt depletion:
|
bacterial overgrowth (bile salt deconjugation), disease or removal of terminal ileum, chronic liver disease, bile duct obstruction
|
|
causes of poor intestinal epithelial absorption
|
reduced surface area (resection), mucosal disorders (celiac sprue, tropical sprue, whipple's disease, crohn's disease)
|
|
malabsorbed nutrient in: megaloblastic anemia
|
B12
|
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malabsorbed nutrient in: tetany, paresthesias
|
calcium, vitamin D
|
|
malabsorbed nutrient in: night blindness
|
vitamin A
|
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uncomplicated diarrhea resolves with fasting suggests:
|
osmotic process
|
|
profuse water diarrhea with dehydration suggests:
|
secretory diarrhea
|
|
dysentery suggests:
|
inflammatory diarrhea
|
|
voluminous gas suggests:
|
carb malabsorption
|
|
useful stool analysis tests (6)
|
fecal fat, fecal weight, stool osm and lytes, fecal leukocytes, lax screen, screen for ova/parasites
|
|
What does fecal fat quantity tell you?
|
>10g is significant, >20g suggest pancreatic insufficiency
|
|
describe d-xylose test
|
d-xylose is pentose sugar, passively absorbed across from lumen if normal intestinal mucosa and thus abnormality from pancreatic insufficiency
|
|
how to test for bacterial overgrowth in small bowel
|
aspirate small bowel fluid for culture, breath hydrogen analysis after oral carb administration
|
|
What does schilling test do?
|
tests if B12 deficiency due to pernicious anemia, terminal ileum disease, or bacterial overgrowth
|
|
Two types of gallstones
|
cholesterol stones and pigmented stones (calcium salts of bilirubin, carbonate, phosphate, palmitate)
|
|
three stages of cholesterol stone formation
|
formation of saturated bile, nucleation, growth of stone
|
|
two types of nucleation
|
homogenous and heterogenous
|
|
what is homogenous stone nucleation?
|
coalescence of cholesterol moolecules to precipitate
|
|
what is heterogenous stone nucleation?
|
some particle other than that of pure cholesterol acts as the nidus of nucleation
|
|
conditions associated with stone formation?
|
obesity, diet (high calorie, fasting), increased serum triglyceride, decreased serum HDL, clofibrate, cholestyramine, malabsorptive disorders, estrogen, pregnancy, Pima Indian
|
|
how does clofibrate predispose to stones?
|
raises cholesterol saturation of bile
|
|
how does cholestyramine predispose to gallstones?
|
prevents reabsorption of bile acids
|
|
list gallstone related diseases (5)
|
asymptomatic gallstones, symptomatic cholelithiasis and chronic cholecystitis, acute calculous cholecystitis, choledocholithiasis, bacterial cholangitis
|
|
most common presentation of gallstone disease?
|
biliary colic, caused by transient gallstone obstruction of biliary tract
|
|
describe biliary colic pain
|
abrupt onset, gradually subsides, minutes to hours, RUQ and epigastrium, w/ nausea/vomiting
|
|
cause of cholecystitis
|
repeated minor episodes of cystic duct obstruction, leads to chronic inflammation and scarring
|
|
chronic cholecystitis predisposes to:
|
gallbladder adenocarcinoma
|
|
most sensitive test for gallstones?
|
US
|
|
treatment of cholelithiasis and cholecystitis?
|
cholecystectomy
|
|
what is acute calculous cholecystitis?
|
gallstone impacts and obstructs cystic duct
|
|
causes of gallbladder inflammation on acute calculous cholecystitis
|
release of phospholipase from gallbladder mucosal cells and its conversion to toxic substances
|
|
signs and symptoms of acute calculous cholecystitis?
|
RUQ pain, tender, fever, leukocytosis, murphy's sign
|
|
what is murphy's sign?
|
instruct patient to breath deeply during palpation in right subcostal area, sudden increase in pain and sudden termination of inspiration
|
|
complications of acute cholecystitis?
|
gallbladder empyema, sepsis, perforation
|
|
diagnosis of acute cholecystitis
|
US shows thickened wall, fluid surrounding wall
|
|
treatment of cholecystitis
|
IV hydration, IV abx, cholecystectomy
|
|
what is choledocholithiasis?
|
stones IN the bile duct
|
|
signs and symptoms of choledocholithiasis?
|
same as acute calculous cholecystitis
|
|
diagnosis of choledocholithiasis?
|
US shows dilated bile ducts, endoscopic ultrasound, cholangiography
|
|
treatment of choledocholithasis?
|
must be removed, even if asymptomatic
|
|
what is charcot's triad?
|
biliary colic, juandice, fever
|
|
symptoms of bacterial cholangitis
|
charcot's triad
|
|
treatment of bacterial cholangitis?
|
IV abx
|
|
who gets acalculous cholecystits?
|
patients hospitalized with serious illness
|
|
what is Primary sclerosing cholangitis?
|
idiopathic inflammaotry and fibrosing dz of biliary tree, immune mediated, progressive, cirrhosis and death
|
|
symptoms of PSC
|
often asyx, eventual elevation of alkaline phosphatase, pruritus, juandice, RUQ pain
|
|
Dx of PSC?
|
cholangiogram
|
|
Sphincter of Oddi Dysfunction and Papillary Stenosis causes?
|
biliary type pain
|
|
causes of acute pancreatitis
|
alcohol and gallstones most common, then drug induced and idiopathic
|
|
presentation of pancreatitis
|
begins abruptly, often after meal, severe epigastric pain, nausea, vomiting, more severe when supine, tachy, dehydration, leukocytosis, hemoconcentration
|
|
diagnosis of acute pancreatitis
|
elevated serum amylase, elevated serum pancreatic lipase, US and CT
|
|
serum amylase and gallstone or alcohol causes of acute pancreatitis?
|
in EtOH related, elevation persists for days and slowly drops, in gallstone related, amylase falls abruptly w/in 24-48 hrs
|
|
systemic complications of acute pancreatitis?
|
vascular instability, shock, DIC, renal insufficiency
|
|
local complications of acute pancreatitis?
|
pancreatic hemorrhage, hemosuccus pancreaticus, acute pancreatic fluid collections, pancreatic pseudocyst, necrosis
|
|
risk assessment of acute pancreatitis?
|
use Ranson's Criteria, the more criteria fulfilled, the worst outcome
|
|
treatment of acute pancreatitis?
|
supportive, limit systemic complications, prevent necrosis, prevent infection, lots of fluid resuscitation
|
|
leading cause of chronic pancreatitis?
|
alcohol, NOT gallstones
|
|
how does chronic pancreatitis manifest?
|
abd pain, impaired pancreatic excretions, chronic inflammation, fibrosis, atrophy, calicifications
|
|
complications of chronic pancreatitis
|
pancreatic pseudocyst, ascites, splenic vein thrombosis, biliary stricture
|
|
how to treat pancreatis pseudocyst?
|
surgical drainage
|
|
how to diagnose chronic pancreatitis?
|
fecal fat, CT, ERCP
|
|
treatment of chronic pancreatitis?
|
sx management
|
|
predisposing factors to pancreatic cancer?
|
cigs, EtOH, gallstones, animal rich diet, DM, chronic pancreatitis
|
|
sx of pancreatic cancer?
|
compression and invasion of adjacent structures, pruritus, enlarged liver
|
|
List 4 inflammatory bowel diseases
|
UC, Crohn's, microscopic colitis, collagenous colitis
|
|
central pathophys in IBD?
|
immune dysregulation, too much Th1, not enough Th2/3
|
|
CD genetic predisposition gene?
|
NOD2
|
|
what does NOD2 do?
|
activated NFkB in response to bacterial LPS, key in innate response to gut bacteria
|
|
typical initial lesion in Crohn's?
|
Apthous ulcer of mucosa (small shallow ulceration, white base)
|
|
Pathology of Crohn's
|
extending through all layers of intestinal wall, skip lesions, ulcers enlarge and deepen to form linear ulcerations, cobblestone appearance, perfs and abscesses, stricture and granulomas
|
|
List the three patterns of Crohn's
|
Inflammatory, Perforating, Fibrostenotic
|
|
highlight of inflammatory crohn's?
|
mucosal inflammation with erosion and ulceration predominating
|
|
highlight of perforating CD?
|
transmural inflammation, perf of bowel, formation of fistula and contained abscesses
|
|
sx of CD?
|
constitutional (fever, fatigue, weight loss), Diarrhea (multifactorial origin), abd pain, malnutrition, mild leukocytosis, anemia, fistula
|
|
rectal exam in CD reveals?
|
often, fistual-in-ano and anal fissures
|
|
Imaging studies for CD?
|
barium enema, CT, Colonoscopy
|
|
DDx of CD?
|
acute appendicitis, intestinal TB, fungal infxn, malignancy, vasculitis of intestinal vessels, UC
|
|
what is UC?
|
chronic inflammatory dz of colonic mucosa
|
|
do you get transmural inflammation in UC?
|
No, only in CD
|
|
UC progression?
|
from mild edema to ulcerations, fibrosis of colon, pseudopolyps (regenerating mucosa), crypts get messed up
|
|
Crypt damage in UC
|
crypt abscesses, distortion of crypts with shortening and branching
|
|
UC distribution
|
continuous, begins in columnar mucosa of anorecal junction, works proximally, no rectal sparing
|
|
what do you call UC if limited to rectum?
|
ulcerative proctitis
|
|
what do you call UC if limited to sigmoid?
|
limited UC
|
|
what do you call UC if extends throughout colon?
|
pancolitis
|
|
clinical presentation of UC
|
bloody diarrhea, tenesmus, cramps, fever, weight loss
|
|
dx of UC?
|
biopsy
|
|
DDx of UC?
|
infectious colitis, acute (shig, salm, campy, ecoli), radiation induced colitis, ischemic colitis
|
|
treatment of UC
|
surgical resection, but use Crohn's drugs too
|
|
extra-intestinal manifestations of IBD
|
joints, skin, eyes, liver
|
|
joint manifestations of IBD
|
peripheral arthritis, ankylosing spondylitis, sacroileitis
|
|
skin manifestations of IBD
|
erythema nodosum, pyoderma gangrenosum
|
|
ocular manifestations of IBD
|
conjuctivitis, scleritis, uveitis
|
|
liver manifestations of IBD
|
PSC
|
|
patients younger than 30 likely to have (liver dz)?
|
parenchymal disease
|
|
patients older than 65 likely to have (liver dz)
|
gallstones and malignancies
|
|
patients between 30-50 likely to have (liver dz)
|
chronic liver disease
|
|
children and young adults likely to have (liver dz)
|
viral hepatitis
|
|
at what bilirubin level is juandice apparent?
|
> 3 mg/mL
|
|
stigmata of chronic liver disease
|
cachexia, muscle wasting, spider nevi, palmer erythema, dupuytren's contracture, leuconychia, parotid enlargement, skin pigmentation, gynecomastia, loss of secondary sexual hair
|
|
small nodular liver suggests:
|
cirrhosis
|
|
large nodular liver suggests:
|
malignancy
|
|
ascites in presence of juandice suggests:
|
cirrhosis
|
|
Define AST/SGOT
|
aspartate aminotransferase, from cytosol and mito and found in liver and lots of other cells
|
|
define ALT/SGPT
|
alanine aminotransferase, from cytosol only and only in liver
|
|
what to AST/ALT signify?
|
liver cell injury, ALT more specific than AST
|
|
define AP
|
widely distributed enzyme, usu from liver/bone
|
|
what does elevated liver AP signify?
|
increased synthesis due to obstruction of bile flow
|
|
AST/ALT levels above 1000 signifiy?
|
severe acute hepatitis, drug associated injury, or prolonged hypoT
|
|
define cholestasis
|
physiological and clinical manifestations result from impaired bile flow
|
|
What is the most sensitive marker of cholestasis?
|
elevated AP
|
|
predominant hepatocellular injury signified by which lab results?
|
elevated AST/ALT relative to AP and elevated bilirubin relative to AST/ALT
|
|
what type of bilirubin is elevated in cholestasis?
|
conjugated
|
|
causes of unconjugated bilirubinemia
|
overproduction of BR due to hemolysis or ineffective erythropoiesis, inheretied (UGT-1A1)
|
|
what is Gilbert's Syndrome?
|
UGT activity reduced to 25%, unconjugated Bremia
|
|
what is UGT?
|
uridine diphosphate glucuronosyltransferase
|
|
how to diagnose Gilbert's Syndrome?
|
elevated unconjugated BR in absence of overt hemolysis in an otherwise healthy person
|
|
treatment of Gilbert's Syndrome?
|
none…benign
|
|
what is Crigler Najjar Syndrome?
|
rare, severe UGT deficiency, results in brain injury from high unconjugated BR levels
|
|
Causes of conjugated bilirubinemia?
|
Rotor Syndrome, Dubin-Johnson Syndrome
|
|
total bilirubin levels in Rotor syndrome
|
2 to 5
|
|
pathophys of dubin-johnson syndrome
|
impaired ATP mediated transport of bilirubin diglucuronide
|
|
liver histology of dubin-johnson?
|
black liver!
|
|
how to determine between clotting factor sythesis disorder or vit K deficiency?
|
give Vitamin K to see if they improve
|
|
which hepatitis viruses can cause acute hepatits?
|
All
|
|
which hepatitis viruses cause chronic hepatitis?
|
B,C,D
|
|
non hepatitis viruses that can cause hepatits?
|
CMV, EBV, HSV, leptospirosis
|
|
whats the most common cause of end stage liver disease?
|
Alcoholic Liver Disease
|
|
list the various types of ALD
|
Alcoholic Steatosis, Alcoholic Hepatitis, Alcoholic Cirrhosis
|
|
histological manifestation of alcoholic steatosis?
|
hepatocytes containing large vesicles filled with triglyceride
|
|
is alcoholic steatosis reversible?
|
yes
|
|
histological manifestation of alcoholic hepatitis?
|
lobular predominant polys, Mallory Bodies, steatosis, bile duct proliferationpericellular fibrosis
|
|
clinical features of alcoholic hepatitis?
|
fever, RUQ pain, juandice, high WBC, increased PT, AST > ALT (2:1), increased uric acid, increased lactase
|
|
how to determine prognosis in alcoholic hepatitis?
|
MDF: maddrey determinant function
|
|
how much alcohol intake for alcoholic cirrhosis to develop?
|
30-60g/d for 15-20 years
|
|
mechanisms of alcohol injury?
|
EtOH induces CYP2E1: increases ROS, stims lipogenesis so increased serum free fatty acids, decreased VLDL, steatosis, lipid peroxidation, inflammation, cytokines
|
|
histological characterization of NAFL
|
soley hepatocytes containing large fat vesicles
|
|
histological characterization of NASH
|
macrovesicular steatosis with added liver cell necrosis and inflammation
|
|
when is NAFLD suspected?
|
elevated liver enzymes (ALT>AST)
|
|
how to confirm diagnosis of NAFLD?
|
biopsy
|
|
what hints at likelihood of disease progression in NAFLD?
|
hepatocyte necrosis and fibrosis
|
|
metabolic hallmark of NAFLD?
|
hepatic insulin resistance
|
|
what mediates hepatic insulin resistance in NAFLD?
|
altered hepatocyte insulin signaling
|
|
what are the "Two Hits" in NAFLD?
|
shift in fatty acid metabolism to net lipogenesis from lipolysis and oxidant stress and cytokine injury leading to fibrosis
|
|
how to treat NASH?
|
none
|
|
List the AutoImmune Hepatitises
|
autoimmune hepatitis, PBB, PSC
|
|
describe Autoimmune Hepatitis?
|
chronic inflammatory dz, gradual progression to cirrhosis
|
|
which gender gets AIH more often?
|
women
|
|
what are the charateristics of AIH?
|
serum autoantibodies, hyperglobulinemia, periportan hepatitis
|
|
clinical findings in AIH?
|
from nothing to fatigue, anorexia, nausea, abd pain, cirrhosis, acute liver failure, acne, amenorrhea
|
|
extrahepatic manifestations of AIH?
|
arthralgias, hemolytic anemia, TPP, DM, thyroiditis, UC
|
|
Type 1 AIH characterized by?
|
ANA and ASMA (anti smooth muscle antibodies), responds to corticosteroids
|
|
Type 2 AIH characterized by?
|
antibodies to liver/kidney microsomes (LKM)
|
|
Type 3 AIH characterized by?
|
antibodies to soluble liver antigen (SLA)
|
|
histopathological features of AIH?
|
portal mononuclear and plasma cell infiltrate into hepatic parenchyma, normal bile ducts
|
|
age peaks when AIH occurs?
|
under 30 and 50-60
|
|
how to treat AIH?
|
prednisone
|
|
what is PBC?
|
chronic, non-suppurative cholangitis characterized by injury to duct
|
|
histo features of PBC?
|
lymphoid aggregates, epithelial injury
|
|
which gene predisposes to PBC?
|
HLA-DRW8
|
|
Which gender gets PBC more?
|
95% women
|
|
lab results with PBC?
|
increased AP, + anti-mitochondial antibody, increased IgM, hypercholesterolemia
|
|
treatment of PBC?
|
symptomatic and supportive and ursodeoxycholic acid, finally transplant
|
|
histo features of PSC?
|
progressive fibrosing inflammation, disappearance of intra and extrahepatic bile ducts
|
|
chilnical picture of PSC?
|
intermittent cholangitis, labs reflect cholestasis
|
|
how to diagnose PSC?
|
visualize biliary tree w/ cholangiography
|
|
treatment of PSC?
|
endoscopic therapy to maintain patency, early liver transplant preferred
|
|
mechanisms of drug related liver toxicity
|
metabolized to more toxic product, ROS generation, Cyt450 induction
|
|
how much acetominophen ingested for toxicity?
|
over 10g
|
|
mechs of NAPQI toxicity?
|
conjugated to GSH decreasing GSH availability, react with protein sulfhydryls, interfere with cellular Ca2+ transport/balance, Redox cylcing generating ROS
|
|
chronology of acetominophen toxicity
|
24-48 hrs: nausea/vomiting, liver disease after 72h
|
|
how to treat acetominophen tox?
|
N-acetylcysteine given immediately, eventual liver transplant
|
|
whats Hereditay Hemochromatosis?
|
defect/dysregulation in Divalent Metal Transporter, too much Fe uptake from intestine
|
|
mutations in which gene lead to HH?
|
HFE
|
|
pathophys of HH?
|
HFE mutation = inability of intestinal crypt cells to sense systemic iron stores through interaction with transferrin, overexpresses DMT
|
|
manifestations of HH?
|
chronic liver disease, endocrine dysfunction, heart failure, arthritis
|
|
treatment of HH?
|
Fe depletion through repeated phlebotomy
|
|
what is wilson's dz?
|
hereditary disorder of cellular copper export, leading to marked decrease in billiary copper excretion
|
|
clinical presentation of Wilson's
|
AST/ALT elevation, chronic hepatitis, hepatic steatosis, cirrhosis, acute liver failure
|
|
where does copper accumulate in wilsons?
|
liver, kidney, basal ganglia, corneas
|
|
what are kayser-fleisher rings?
|
green rings at periphery of cornea in px with Wilson's Dz
|
|
how to diagnose Wilson's Disease?
|
low serum ceruloplasmin, increased renal excretion during 24h collection, elevated liver tissue [Cu]
|
|
how to treat Wilson's?
|
low copper diet, chelators, transplant
|
|
what is Alpha-1-Antitrypsin deficiency?
|
inherited deficiency, disease in lungs and liver
|
|
whats A1AT?
|
protease inhibitor synthesized in hepatocytes, acts in lungs to protect from proteases released from neutrophils
|
|
how does A1AT cause disease in liver?
|
accumulated unsecreted abnormal protein, manifest as intracellular globules
|
|
main causes of acute liver failure?
|
acetominophen, drug rxns, Hep A/B
|
|
List 5 liver diseases common in pregnancy
|
Hyperemesis Gravidarum, intrahepatic cholestasis of pregnancy, AFLP, Pre-eclampsia, HELLP
|
|
what is hyperemesis gravidarum?
|
intractable nausea/vomiting in first trimester
|
|
whats ICP?
|
intrahepatic cholestasis of pregrancy
|
|
hallmark of ICP?
|
intense pruritus, usually in third trimester
|
|
what suggests ICP?
|
increased total serum bile acids (up to 100x) w/ pruritus
|
|
what is pre-eclampsia?
|
multisystem disorder associated with proteinuria, HTN, peripheral edema, hyperreflexia, massive aminostransferase increase
|
|
what is HELLP?
|
hemolysis, elevated liver enzymes, low platelet count
|
|
cirrhosis results from what pathophys change?
|
fibrous associated structural changes in intrahepatic sinusoidal channels ana altered vasomotor tone
|
|
results of portal hypertension?
|
variceal hemorrhage, ascites, hepatic encephalopathy, prominent abd cuteaneous veins, splenomegaly
|
|
lab manifestation of splenomegaly?
|
thrombocytopenia
|
|
how to measure portal blood pressure
|
directly during surgery, percutaneously, or with balloon wedge pressure
|
|
what is portal hypertensive gastropathy?
|
pressure related increase in gastric mucosal blood flow and vessel caliber, causes bleeding
|
|
how high of a portal blood pressure is required for esophagela vericeal rupture?
|
> 12mm Hg
|
|
endoscopic signs of varices
|
red wale sign and cherry red spot
|
|
management of variceal bleeding
|
hospital, large bore IV, fluid rescucistion, ocreotide to lower pressure, band ligation, variceal ligation, TIPS
|
|
define ascites
|
presence of free fluid in the periotneal cavity
|
|
mechanism of ascites?
|
change in hepatic structure, sequestration of larger than normal fraction of blood, decreased peripheral arterial resistance, increased renal retention of Na/H2O
|
|
what is hepatic hydrothorax?
|
when ascited fluid gains access to thoracic cavity
|
|
how to evaluate ascites?
|
paracentesis, Serum-Ascites Albumin Gradien (SAAG), send for culture/white count
|
|
management of cirrhotic ascites?
|
restrict dietary sodium, use diuretic, large volume paracentesis, TIPS
|
|
pathophys of Spontaneous Bacterial Peritonitis
|
SBP: infection of ascitic fluid in absence of intra-abdominal cause, most often in px with ALD
|
|
two factors to predispose to SBP
|
portal HTN increases translocation of bacteria from GI, low ascites protein concentration leads to lower opsonization
|
|
clinical presentation of SBP
|
fever, abd pain/tenderness, altered mental status
|
|
dx of SBP?
|
complete analytic paracentesis, high poly count
|
|
typical bacterial causes of SBP?
|
E. Coli, s pneumo, klebsiella, usually monobacterial
|
|
management of SPB?
|
systemic antibiotics
|
|
pathphys of hepatic encephalopathy?
|
decreased clearance of toxins in portal blood that alter brain metabolism and function
|
|
precipitating factors for hepatic encephalopathy?
|
increased nitrogen load, deteriorating liver fxn, hypovolemia, acid/base or lyte imbalance, incrase portal/systemic shunting
|
|
management of HE?
|
correct precipitating factors, laculose, acidify luminal contents
|
|
complications of cholestasis
|
pruritus, hepatic osteodystrophy, fat soluble vitamin deficiency
|
|
treatment of pruritus?
|
topical moisturizing soap, anion exchange resin, vile salets, doxepin, opioid antagonists (naloxone)
|
|
what is hepatic osteodystrophy?
|
bone disease in px with chronic liver disease, osteoporosis and osteomalacia
|
|
how to detect osteodystrophy?
|
dual energy xray absorptiometry (DEXA)
|
|
end stage liver disease presentaiton?
|
GI hemorrhage, juandice, HE, coagulopathy, thrombocytopenia, ascites, renal failure, liver dysfunction
|
|
how to determine liver disease prognosis?
|
MELD: model fo end stage liver disease; predicts 3 month mortality
|