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גסטרו Flashcards

1
Q

colonoscopy contraindications?

A 
risk/ benefit
no consent for non-urgent procedure 
acute diverticulitis 
fulminant colitis 
perforation (unless trying to close)
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2
Q

Colonoscopy Preparation?

A

3 days prior low fiber/ high liquid diet, 1 day before liquid only

Medications

  • anti coagulant/ anti platelets (?)
  • laxatives (2 days prior)
  • 1 day before special powder
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3
Q

Colonoscopy Risks?

A

Perforation (0.01 – 0.1%)

Bleeding (e.g. post-polypectomy)

Risks of sedation- cardiopulmonary

Miss rate - for large adenomas (=10 mm) 6% - 12%; for cancer - 5%.

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4
Q

Upper endoscopy Contraindications?

A

risk/ benefit

no consent for non-urgent procedure

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5
Q

Upper endoscopy Preparation?

A

fast

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6
Q

Upper endoscopy Risks?

A

Perforation of esophagus 0.03%
Sedation risks
Bleeding (therapeutic maneuvers)

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7
Q

EUS Indications?

A

Staging cancer
gastrointestinal wall abnormalities
suspected choledocholithiasis
pancreatic abnormalities

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8
Q

ERCP indications?

A

בעיקר צהבת חסימתית (טיפול)
CHOLANGITIS
ביופסיה

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9
Q

ERCP risks?

A

pancreatitis:

Hartmann fluids
Prophylactic pancreatic stenting
NSAIDs - נר

bleeding 0.1% - 2% (sphincterotomy)
Perforation <1%
infection
sedation risks

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10
Q

Dysphagia evaluations?

A
  1. fucking endoscopy!! (performed without stopping PPIs if needed)
  2. High resolution esophageal manometry
    - essential for diagnosis of achalasia
    - IRP(integrated relaxation pressure)
  3. Barium swallow
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11
Q

Eosinophilic esophagitis (EoE) characteristics?

A

Allergen/immune-mediated
dysphagia and food impaction
≥ 15 Eos/hpf of the esophageal mucosa

Often positive skin test to food allergens and family history of allergic diseases.

High response rates ( 40-50%) to PPI!!!

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12
Q

Pathogenesis of EoE?

A

food antigen activates immune system of a genetically susceptible individual

naive CD4‏ T cells differentiate into T-helper 2 (Th2) cells and secrete cytokines:
IL 5 eosinophil production, activation, and recruitment
IL4 and IL13 stimulate esophageal epithelial cells to produce eotaxin-3, an eosinophil chemoattractant

eosinophils release noxious eosinophil secretory products:
inflammation
fibrosis

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13
Q

EoE diagnosis?

A

biopsy only

also followup

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14
Q

EoE endoscopy?

A 
"טרכיאליזציה של הוושט"
edema
rings
exudates
furrows
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15
Q

Treatment of EOE?

A

Non pharmacologic

  • Elimination diet (single antigen? six foods elimination, elemental)
  • gradual Endoscopic dilatation in patients with fibrotic strictures
Pharmacologic
-Corticosteroids -topical budesonide
-Biologics 
less: 
PPI
Leukotriene inhibitors
Mast cell stabilizers
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16
Q

Six food elimination diet (SFED)?

A

dairy, wheat, eggs, soy, nuts, and seafood
gradual reintroduction
assessment of response is by histologic criteria( from mucosal biopsies)
Only 50% efficacy (elemental 91%)

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17
Q

topical steroids for EoE?

A

Budesonide 8-12 weeks (Orodispersable tablets)

20% deep clinical, histologic and endoscopic remission

15% esophageal candidiasis, mild

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18
Q

Mechanisms of Pain Originating in the Abdomen?

A 
Inflammation of the Parietal Peritoneum
Inflammation of abdominal viscera
Obstruction of Hollow Viscera
Vascular disturbances 
Abdominal Wall
Neurological
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19
Q

Inflammation of the Parietal Peritoneum pain etiology?

A

Infectious (e.g. appendicitis, pelvic inflammatory disease)

Chemical (e.g. intestinal perforation, bleeding)

Inflammatory (e.g. SLE, FMF)

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20
Q

Inflammation of the Parietal Peritoneum pain characteristics?

A

Steady & aching

its exact reference being possible (somatic nerves)

Intensity dependent on the type and amount of inducer (gastric acid, pancreatic juice&raquo_space; feces, bile, blood, urine )

Accentuated by pressure or changes in tension “quite patient”

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21
Q

Obstruction of Hollow Viscera: intestine, pain characteristics?

A

intermittent, or colicky (Labor like)

Poorly localized periumbilical

vomiting, constipation, partial obstruction can be accompanied by diarrhea

Previous abdominal surgery?
Crohn’s disease?

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22
Q

Obstruction of Hollow Viscera: Biliary tree, pain characteristics?

A

Suddendistention- steady rather than colicky
Chronic gradual- usually painless jaundice

Classically : RUQ pain with radiation to the right posterior region of the thorax

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23
Q

Obstruction of Hollow Viscera: Urinary track, pain characteristics?

A

urinary bladder- dull suprapubic pain
(an obtunded patient- restlessness)

ureter- flank, Severe pain, restless patient

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24
Q

abdominal Vascular disturbances?

A

intestinal ischemia:
Acute mesenteric ischemia
Non-occlusive mesenteric ischemia (NOMI):
Abdominal angina

Vascular rapture (AAA)

Ovarian/testicular torsion

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25
Q

Acute mesenteric ischemia pain characteristics?

A

Acute obstruction (AF emboli?)

After few hours of ischemia -mucosal infarction and necrosis - peritoneal findings.

Pain typically poorly localized and visceral, without tenderness

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26
Q

Non-occlusive mesenteric ischemia (NOMI) pain characteristics?

A

Chronic partial obstruction

low-flow states pain (e.g. shock, hemodyalysis)

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27
Q

Abdominal angina pain characteristics?

A

Post-prandial pain (increased blood flow to the stomach, decreased flow to the intestine)

stenosis of at least 2 out of 3 major arteries (celiac trunk / SMA / IMA) is usually required to produce symptoms

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28
Q

Abdominal Wall pain characteristics?

A

constant and aching

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29
Q

abdominal neurological pain?

A

related to defecation
change of stool frequency
change in stool form

at least once a week for 3 months

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30
Q

important DD for abdominal pain?

A

inferior wall MI- epigastric pain

torsion of testis- lower abdomen

metabolic- diabetes (keto bodies irritate peritoneum)

neurologic- herps zoster, intense pain with dermomyotome distribution which can precede rash

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31
Q

Approach to PAIN – lab tests?

A

ECG (especially if epigastric pain)

Inflammatory markers: CBC, CRP, ESR

Chemistry: 
Electrolytes, creatinine, BUN
Amylase (elevates in pancreatitis, bowel wall damage), lipase (amylase in vommiting is from saliva glands)
Liver enzymes, bilirubin
Lactate (Ischemia)
blood gases (metabolic acidosis)
Glucose (DKA)
Urinalysis (ketones, infection, signs of dehydration)

Pregnancy test (ectopic?)

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32
Q

Approach to PAIN – radiology tests?

A
  1. Abdominal X-ray
    intestinal obstruction, perforated ulcer, Some kidney stones
  2. Chest X-ray: free air
  3. US
    1st choise in appendicitis- in skinny patients
    gallbladder, liver, biliary tree vascular and kidney disease
    IBD
  4. CT- very useful but radiation
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33
Q

polyp definition?

A

a grossly visible protrusion from the mucosal surface

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34
Q

Pathological classification of polyps?

A

Nonneoplastic hamartoma- congenital

cancerous potential (<1% become malignant):

Serrated (hyperplastic) polyp- BRAF, right colon

Adenomatous polyp- clearly premalignant, contain dysplastic tissue

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35
Q

Clinical factors to determine the probability of an adenoma becoming a cancer?

A

gross appearance:
Pedunculated (stalked) < sessile

Histology:
Tubular < villous, tubulovillous

Size:
negligible (<2%) in lesions <1.5 cm
intermediate (2–10%) in lesions 1.5–2.5 cm
substantial (10%) in lesions >2.5 cm

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36
Q

advanced adenoma criteria?

A

Adenoma >= 1 cm

Adenoma with high grade dysplasia

Adenoma with villous/tubulovillous histology

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37
Q

CRC screening Available tests?

A

Stool tests:
Fecal Occult Blood
exfoliated DNA- very limited today

Structural exams
Flexible sigmoidoscopy (FSIG)- canada only
Colonoscopy
Computed tomographic colonography (CTC)

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38
Q

Fecal Occult Blood test (FOBT) types?

A 
Guaiac-
only one with Solid evidence (3 RCT’s)
specimens from 3 bowel movements
influenced by foods  and medications (anticoagulants, NSAIDS,red wine)
not specific

Fecal Immunochemical Tests (FIT)-
human blood and only for lower GI bleeding
only 1 or 2 stool specimens
not influenced by foods or medications

WILL BE USED ONLY FOR SCREENING, NO USE IN IDA

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39
Q

exfoliated DNA test?

A

cancer cells contain abnormal DNA
Colon cells are shed continuously (blood not)
3 year testing interval
positive tests must be evaluated by colonoscopy (no solution if negative)

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40
Q

stool tests Limitations?

A

Limited sensitivity for adenomas
Lower sensitivity for Rt. colon cancer
Old versions of FOBT are not sensitive enough

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41
Q

CRC screening guidelines?

A

50-75 (USA), In israel still 45 cause no evidence for change in prevalence

FOBT or FIT- every year, TEST OF CHOISE IN ISRAEL
colonoscopy- every 10 years
CTC- every 5 years
flexible sigmoidoscopy every 10 years+ annual FIT (not in use)
capsule- not recommended

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42
Q

Colonoscopic surveillance (if was) guidelines?

A 
repeat every 3 years:
5-10 tubular adenoma< 10mm
adenoma>= 10mm
ademnoma <10mm, low grade dysplasia, tubo/villous
adenoma high frage dysplasia

10 adenoma on single exam- repeat annually, and genetic testing

Partial resection of adenoma / SSP <20mm- repreat every 6mo

less than 20 HPserrated< 10mm up to proximal to sigmoid colon- every 10 years

family history- begin at 40 and repeat every 5-10y

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43
Q

Prevention of CRC?

A

FOLATE (B9)

Calcium binds bile and fatty acids, which cause proliferation of colonic epithelium.

Asperin-
reduces the risk of colon adenomas and carcinomas as well as death

NSAID-
prevent adenoma formation or cause regression
cannot be taken routinely obviously

Estrogen (women)-
Effect on bile acid synthesis and composition
Decreasing synthesis of IGF-I
estrogen + progestins= 44% lower risk
cannot be taken routinely due to cardiovascular and breast cancer risks.

statins (but no RCT)
cannot be taken routinely

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44
Q

Systemic Manifestations of Iron Deficiency (late chronic) ?

A 
Behavioral and neuropsychiatric manifestations
Pica (pagophagia) 
Angular stomatitis cheilosis
glossitis 
Esophageal webs and strictures
Koilonychia
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45
Q

iron deficiency by serum Ferritin and transsferin saturation in adult?

A

Healthy or IBD-
F<30 T%<16

active IBD-
F<100 T%<16

adequate-
F>100 T%16-50

Potential iron overload
F>800 T%>50

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46
Q

GI-related etiology of IDA?

A

sever esophagitis
diaphragmatic hernia
cameroon ulcer

athrophic gastritis
H.pyloric

Dudenal ulcer

celiac

CRC
colitis
large polyp

arterio vascular malformations

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47
Q

בירור אנמיה מחוסר ברזל?

A

לברר כל אנמיה מחוסר ברזל

בירור “דחוף”:
גברים המוגלובין מתחת ל12
נשים בגיל פירון מתחת ל10

כל השאר ירד בגיידליננס החדשים

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48
Q

IDA inquiry management [AGA]?

A

1st- non-invasive test for all
stool/expiration test for H.pyloric
serology for celiac (anti TTG IgA)

2nd. Men and post menopausal women-
non invasive findings point to specific test
gastroscopy+ colonoscopy at same occasion for all
(cancer findings up to 10 times more in lower GI, 8.9% )

2nd. fertile women- the same buy
cancer findings up to 10 times more in lower GI, 2.0%
thus sole iron treatment can be offered

3rd. 
iron therapy in all
pillcam:
small intestine disease/ risk 
SI disease could obscure medications (e.g. anti coagulants)
acute anemia needing IV
iron treatment failure

4th.
Pill cam positive-
push endoscopy, angiography, intraoperative enteroscopy)

pill cam negative-
MRE/CTE

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49
Q

H. pylori infection Mechanism of iron deficiency?

A 
Occult GI bleeding
Competition for dietary iron 
achlorhydria
Low gastric juice ascorbic acid (ferric to ferrous)
Rugae are almost completely lacking
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50
Q

iron therapy manegement?

A

150-200Mg PO per day (debatably less)

response in more than a month?
exclude non compliance, low absorption or bleeding

3 month till normalized Hg
blood tests once a month till normalized Hg, THAN EVERY 3 MONTH FOR A YEAR, THAN AFTER A YEAR

parenteral in absorption defect (IBD, CKD {+epo}, Bariatric surgery)

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51
Q

Presentations of GI bleeding-

A

Hematemesis – vomiting blood (or coffee ground material) (bleeding proximal to the Treitz)

Melena – passage of black tarry stools > 50ml (proximal bleeding, nostly UGI but up to Rt colon)

Hematochezia- rectal bleeding
(mostly colon, massive UGI [no time for degradation, ‘cherry color’])

Occult bleeding – bleeding that is not apparent

Obscure bleeding – (can be occult) source not identified

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52
Q

Initial acute bleeding patient assessment?

A
  1. Assess severity of bleeding: Vital signs
  2. Resuscitation / history
  3. physical examination
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53
Q

initial acute bleeding patient assessment: Resuscitation?

A

2 large-bore IV lines
catheter (urine)
Oxygen (low Hg)
Careful hemodynamic & electrolyte monitoring (preferably in ICU)
Transfuse blood when indicated (Ischemia, Cardiac or Cerebral)
IV- PPI (before diagnosis)

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54
Q

initial acute bleeding patient assessment: history?

A

Age:
elderly bleed from lesions less common (i.e. diverticula, ischemic colitis, cancer)
Young pts - Meckel’s diverticula (congenital)

Previous bleeding:
ulcer
hereditary telangiectasia (Osler-Weber-Rendu)
diverticula

Previous surgery:
Aortic graft
Tumor

Known liver disease (or coagulopathy)
NSAID’s or Aspirin
Associated abdominal pain (ulcer, malignancy, mesenteric or colonic ischemia)
known Retching (Mallory-Weiss)
Change in bowel habits, anorexia, weight loss (suspect malignancy)

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55
Q

initial acute bleeding patient assessment: physical examination?

A

Skin:
Spider angiomata- upper back, CHepatic.d
Telangiectasia- oral mucosa
Hyperpigmentation of oral mucosa (Peutz-Jegher)

Abdomen:
Hepato-splenomegaly
Ascites
Caput medusae
Tenderness
Mass

Lymphadenopathy (left upper clavicular, convergence point)

hemodynamics, capillary filling, peripheral pulses cirrhosis, rectal exam

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56
Q

Lab interpretation in acute GI bleed?

A

CBC
coagulation
LFT
lactate

Hemoglobin:
does not reflect actual amount of blood loss

Chronic overt or occult bleeding:
hypochromic microcytic anemia reflecting iron deficiency

Urea:
may be elevated in upper GI bleeding out of proportion to elevation of creatinine (breakdown of blood proteins by bacteria)

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57
Q

acute Upper GI bleeding further assessment?

A

Following resuscitation the diagnostic tool of choice is gastroscopy (within 24h) (no good evidence for immediate endoscopy, unless unstable hemodynamic +- hematemesis== within 12h)

Timing

Visibility (erythromycin- adverse gastric emptying)

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58
Q

Acute upper GI etiology?

A

in approximate descending order of frequency

duodenal & gastric ulcer (most fucking common)
erosive/ severe gastritis (2nd)
erosive/ severe Esophagitis (3rd)
portal hypertension
vascular lesions
Mallory-Weiss Tear
malignancy
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59
Q

Acute upper GI: Esophagitis?

A

Tx – aimed at the cause – mainly PPI

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60
Q

Acute upper GI: Mallory-Weiss Tear?

A

mostly on 1st vomit (75%)
90% stop bleeding spontanuously
Endoscopic Tx if needed

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61
Q

Acute upper GI: portal hypertension (varices)?

A

Esophageal varices
Band ligation
iv PPI

Gastric (fundic) varices
iv PPI

Portal hypertensive gastropathy:
Somatostatin / Glipressin/ terlipressin (lower PHT by splenic vasoconstriction) (adverse scrotal necrosis)

Antibiotic prophylaxis (prevent bacteremia and death)

  • Fluoroquinolones
  • 3rd generation cephalosporin

endoscopic failure?

Balloon tamponade (Sengstaken-Blakemore tube)

  • no more than 24h
  • constant observation

Transjugular Intrahepatic Portosystemic Shunt (TIPS)
within 24-72hrs, high risk patients
higher risk of encephalopathy

62
Q

Acute upper GI: duodenal & gastric ulcer?

A

Most common etiology of UGI bleeding

Duodenum > stomach (IF STOMACH ALWAYS BIOPSY)

factors for bleeding –

  1. Gastric acid- initiator of ulcer [give PPi]
  2. H. Pylori- ALMOST ALL duodenal ucer, complete eradiction for prevention
  3. NSAIDs
    Gastric>duodenal
    Dose dependant risk
    Older age – higher risk for bleeding [+PPI / H2b for prevantion]

IHD, cerebrovascular disease (STRESS, more stomach)
Ethanol, anticoagulant Tx
Hospitalization- STRESS

63
Q

Management of ulcer bleeding?

A

Medical Tx – IV PPI, PO after

Endoscopic Tx:

  1. saline injection- pressurized closure
  2. Endoscopic coagulation
    - Bicap (spray)
    - ArgonPC
  3. clip (usualy both)

if needed:
3. Angiography + embolization

  1. Surgery
64
Q

gastric erosions etiology?

A

most common- NSAID’s
Stress
Alcohol abuse

65
Q

Acute upper GI: malignancy?

A

Malignant:
Esophageal cancer (rare to cause acute bleeding)
Gastric cancer > lymphoma
Small intestinal lymphoma > cancer

Benign:
Leiomyoma
Gastro-Intestinal-Stromal-Tumor (GIST) (rarely malignant)

66
Q

Acute upper GI: vascular lesions?

A

Dieulafoy- (mostly proximal stomach, can anywhere)
enlarged submucosal blood vessel that bleeds in the absence of any abnormality. Fluctuative bleeding thus recurrent gastroscopies required.

Angiodysplasia-
defect arteriovenous connection

Osler-Weber-Rendu syndrome [AD]

Gastric Antral Vascular Ectasia GAVE (Watermelon Stomach-
parallel erythematous folds traversing the gastric antrum
occult or overt bleeding
associated with hepatic, renal, and cardiac diseases

67
Q

Acute lower GI bleeding Initial management?

A

similar to acute upper GI bleeding

68
Q

Acute lower GI bleeding presentation?

A

Mostly self-limiting (80%)

25 % will re–bleed

Usually painless

If painful, r/o mesenteric ischemia

69
Q

Acute lower GI bleeding Diagnostic procedures?

A

X-ray or CT not helpful

Colonoscopy (80 accuracy, only after purgatives)

Tagged RBC- scintigraphy – low predicrive value

Angiography + embolization if heaby bleeding (low visibility, less in colon)

Surgery (rare)

70
Q

Acute lower GI bleeding etiology?

A

diverticular disease of colon- most common generally

hemorrhoids - most common in 50

71
Q

Acute lower GI bleeding: diverticular disease of colon?

A

15% to 55% of cases
painless, bright red, maroon or melena (depending on site)
Start – stop pattern; “water faucet”
May compromise hemodynamics (elderly)

Diagnosis: per exclusion

Significant recurrence (30%)

Tx: most subside spontaneously (95%), some need angiographic embolization or surgery

72
Q

Acute lower GI bleeding: angiodysplasia?

A

70y

73
Q

Acute lower GI bleeding: Hemorrhoids?

A

recurrent low-volume bright red blood on the paper or on stool

Straining aggravates bleeding

NEVER!!! relate bleeding to hemorrhoids before exclusion of other lesions!!!

ALWAYS!!! colonoscope after age 50.
Otherwise at least sigmidoscope.

74
Q

Acute lower GI bleeding: other causes?

A

Meckel’s diverticulum (young children)

Infectious colitis:
Shigella; Salmonella > campylobacter
Pseudo-membranous colitis (rarely bloody; C.diff > Klebsiella sp.)

Radiation proctitis

Ischemic colitis- mostly splenic flexure and sigmoid, watershed areas

IBD – colitis

75
Q

Occult bleeding DIAGNOSIS?

A

if IDA or FOBT:
Colonoscopy
CTC
gastroscopy/VCE- controversial

76
Q

Nutrition Screening Tools?

A

MUST

  • BMI
  • weight loss
  • acute disease effect

NRS - nutrition risk score

77
Q

Assessing Nutritional Status :Physical Examination

A

weight status

mobility

signs of nutrient deficiencies/malnutrition
hair, skin, GI tract including mouth and tongue

Fluid Balance (dehydration/fluid retention)

78
Q

Anthropometric Data ?

A

BMI

Body Fat Measurements

79
Q

cachexia definition?

A

multifactorial wasting syndrome characterized by involuntary weight loss of skeletal muscle mass with or without loss of fat mass

80
Q

sarcopenia definition?

A

condition characterized by loss of muscle mass and muscle strength
high fat to muscle ratio
need a CT for calculation
prevalent in cancer ptx

81
Q

Approach a Pancreatic Lesion?

A

Age

Comorbidities

Lifestyle habits- alcohol and smoking

Systemic signs

  • Weight loss
  • Loss of appetite
  • Painless jaundice- problematic

Recent onset diabetes mellitus

Imaging

82
Q

“Double duct sign” in pancreatic imaging?

A

usually indicates a mass at the head of pancreas

83
Q

Contrast enhanced EUS in pancrease?

A

lesion-
hypoechoic but after contrast hyperechoic?
Most probably a neuroendocrine tumor-
highly vascular
Mostly benign
if small and non-functional, we may surveille only

hypoechoic after contrast?
most probably adenocarcinoma

84
Q

Cystic pancreatic lesions characteristics?

A

serous cystic neoplasm- benign, 75% grandma
mucinous cystic neoplasm- potentially malignant, 99% mother
main duct IPMN 70% > side duct IPMN 0.8%malignancy, m=f 60-80y
if IPMN- surgery

85
Q

pancreatic cyst biopsy lab findings?

A

AMYLASE (ductal involvement)-
IPMN and Pseudocysts

CEA (Mucinotic)-
musinous cystic neoplasm or IPMN

86
Q

Bilirubin Metabolism?

A

hemoglobin degradation (80%)
biliverdin
macrophages (BM and spleen) - unconjugated bilirubin
unc-bilirubin connects to Albumin and enters hepatocyte
conjugation with glucuronic-acid by B-UGT
secreted by cuniculi Bile
or secreted to blood (5% of all bilirubin in blood)

87
Q

Bilirubin Measurements?

A

Normal bilirubin level (adult)
Less than 1-1.5 mg/dL

Clinical Jaundice
Bilirubin >3 mg/dL

88
Q

high Bilirubin DD?

A

prehepatic- hemolysis
hepatic- hepatocytes
post hepatic- obstructive or surgical

89
Q

obstructive jaundice DD?

A

intraluminal:
choledocholithiasis
clonorchis sinensis
ascariasis @ schistosomiasis

mural (wall):
cholangiocarcinoma-Rare, Highly lethal
Sclerosing cholangitis

Extrinsic:
CA of head of pancrease
periampullary carcinoma
Mirrizi’s syndrome

90
Q

choledocholithiasis?

A

in common bile duct (cysto- gallbladder)

20-30% of >50 women
10-15% of >50 men

75% asymptomatic- no intervention

20% biliary colic-
intermittently obstruction of cystic duct
transient RUQ/ epigastric pain after meal (as fatty as painfull)

10% cholecystitis
stone impacted in cystic duct
can have fever, constant pain

5% cholangitis/pancreatitis/jaundice
common bile duct obstruction

91
Q

choledocholithiasis Diagnosis?

A

History (abdominal pain!, if not probably Pancreas head carcinoma)

physical's:
Murphy’s sign – acute cholecystitis
Fever
Abdominal Tenderness
Palpable abdominal mass

U.S-
>95% sensitivity &specificity for >2 mm gallbladder stones
50% sensitivity for bile duct stones

MR(I)CP-
>95% sensitivity for common bile duct stones
no contrast

EUS-
>95% sensitivity for common bile duct stones
Pancreatic head carcinoma
Cholangiocarcinoma
biopsies 
somewhat invasive

HIDA scan
Limited hepatic uptake of HIDA when bilirubin>7mg/dL

92
Q

choledocholithiasis Treatment?

A

not diagnostic!!!
will choose when jaundice and dilated bile ducts

adverse:
pancreatitis

PTC/PTBD-
Therapeutic procedure similar to ERCP

(mostly) Surgery- Laparoscopic cholecystectomy
Need to clear bile duct first
Intra-operative cholangiography if needed

93
Q

primary sclerosing cholangitis?

A

Chronic
Progressive
“Beads on string”
Bile duct strictures (intra and extra hepatic)

94
Q

normal mass of stool per day?

A

200gr

95
Q

איטיולוגיה של שלשול?

A

מיימי – אוסמוטי / סקרטורי
אינפלמטורי
שומני
הפרעות בתנועתיות המעי

96
Q

שלשול מיימי אוסמוטי או סקרטורי ?

A

בדרך כלל ישנו מרכיב משולב
אוסמוטי בד”כ פחות מ200 מ”ל

אוסמוטי- חומר אוסמוטי המושך מים לתוך הצואה ולכן צום יעזור.

סקרטורי- פגיעה במנגנון ההפרשה עקב תרופות, ממאירות, פגיעה במעי, לכן צום לא יעזור

נבדיל ע”י
290 mOSm/kg – 2 * (Na+k) = Osmotic Gap
אם ההפרש קטן, הצואה דומה בתכולתה להרכב הנוזלים בגוף, משמע אוסמוטית.

97
Q

שלשול אינפלמטורי ?

A

שלשול עם דם (בעיקר דלקת קולונית)
עליה בקלפרוטקטין (חלבון שנמצא בפולימורופנוקליאריים)
IBD, GVHD

98
Q

שלשול שומני?

A

סוג של אוסמוטי (השומן מושך מים)
גושי, ריח רע, חיוור, צף
נובע מתת ספיגה אינטרא-לומינאלית או מוקוזלי

99
Q

דגלים אדומים בשלשול?

A 
הסתמנות בגיל מעל 50
דימום רקטלי / מלנה
כאב/שלשול ליליים
כאב בטני מתקדם
ירידה במשקל / סימנים סיסטמיים
שינויים מעבדתיים (לדוג' אנמיה, עליה במדדי דלקת)
family history of IBD or GI malignancies
100
Q

chronic diarrhea duration?

A

over 4 weeks

101
Q

chronic diarrhea physical exam?

A

anemia, dermatitis herpetiformis (celiac) , edema, clubbing (IBD or malabsorption)
erythema nodosum (UC)
flushing (carcinoid, serotonin / vasoactives)
oral ulcers (IBD, Celiac)
abdominal mass or tenderness
rectal mucosa, rectal defects, altered sphincter functions?

102
Q

chronic diarrhea Assessment (lab, imaging)?

A 
calprotectin
TSH
celiac serology 
CRP
CBC
Biochemistry - 5HTT, anti gliadin, anti tTg
CDT
stool culture
albumin, VIT D
fast gastrin 
vasoactive intestinal polypeptide

IF RED FLAGS- colonoscopy / gastroscopy

103
Q

ROME criteria for IBS?

A

Recurrent abdominal pain, at least 1 day per week in the last 3m
+
2/3:
1. Related to defecation
2. Associated with a change in stool frequency
3. Associated with a change in stool form (appearance)

104
Q

PPI for bleeding ulcer mechanism?

A

higher PH thus stopping ulcer propagation
higher PH induce/ propagates coagulation
thus reduction of Endoscopy usage

105
Q

forest classification of bleeding peptic ulcer?

A

grading goes with mortality:

1a. spurting hemorrhage
1b. oozing hemorrhaged
2a. non bleeding visible vessel
2b. adherent clot
2c. flat pigmented spot
3. clean bed (55%

106
Q

Esophagogastroduodenoscopy (EGD) comlications?

A

Aspiration
Desaturation or respiratory distress
conscious sedation risks

↑risk of complications with:
Inadequate resuscitation or hypotension
Comorbidities

Consider elective intubation prior to EGD if active bleeding, altered respiratory or mental status

107
Q

managing anti-platelet agents in UGIB?

A

continuation of low dose aspirin- if discontinuation than up to 7 fold death risk

but if given for 1st (before) CV prophylaxis-
can discontinue and resume after resolution

2nd (after) CV prophylaxis- don’t discontinue

Dual therapy? (ASA+ Plavix [clopidrogel])
temporarily Plavix discontinuation, resumed within 1-7 days

108
Q

Hepatocellular injury- Lab?

A

↑ALT/AST&raquo_space;↑ALK PHOS
+/- Bilirubin
+/- synthetic function – albumin, INR

109
Q

Cholestatic injury- Lab?

A

↑ALK PHOS&raquo_space;↑ALT/AST
GGT
+/- bilirubin
+/- synthetic function – albumin, INR

110
Q

LFTs normal values?

A

AST<30
ALT<30

ALK PHOS<120
is secreted by bones and liver thus adolescents, children- higher UNL
same with pregnant women (renal secretion)

GGT-38
LDH-480

111
Q

liver injury physical exam?

A

acute +-
chronic -
cirrhosis +++

spider nevi 
gynecomastia 
caput medusa
jaundice 
ascites
portal hyper tension- splenomegaly, pancytopenia
flapping
testicular atrophy 
loss of pubic hair
anemia (macrocytic, or iron deficency)
clubbing
palmar erythema 
leukonychia 
muehrcke lines
Dupuytren contracture (tendons hardening)
112
Q

ALD LAB?

A

AST:ALT&raquo_space;2

↑GGT

113
Q

transaminases (ULN) lvl interpretation?

A

> 50X Ischemic hepatitis

> 25X Acute hepatitis (viral/toxic)

10X HBV flare-up (C doesn’t cause flare-up)

2-10X Chronic HBV/HCV (fluctuating)

<4X NASH/NAFLD

114
Q

acute liver failure definition?

A

severe acute liver injury (LFTs) + encephalopathy + impaired synthetic function (INR of ≥1.5)

without cirrhosis or preexisting liver disease.

<26W

115
Q

acute liver failure classification and etiology?

A

hyperacute (<7 days), acute (7 to 21 days)

  1. drug (acetaminophen) toxicity
  2. viral (hepatitis B, C, A, D, E(endemic))

subacute (>21 days and <26 weeks)-
Acute kidney injury 30-70% , portal hyper tension, Wilson disease

116
Q

liver failure symptoms?

A

Fatigue/malaise, Lethargy- may become confused or eventually comatose (encephalopathy, have grades)

herpes simplex virus- 30 to 50% Vesicular skin lesions
Anorexia
Nausea and/or vomiting
Right upper quadrant pain
Pruritus
Jaundice
Abdominal distension from ascites (can be acute too)

117
Q

encephalopathy presentation?`

A

cerebral edema-
grade 1-2 uncommon
grade 3 25%
grade 75%

pupils-
normal response- grade I 
hyperresponsive- grade II to III
slowly responsive- grade III to IV
fixed miosis- brainstem herniation

Cushing’s triad-
systemic hypertension
bradycardia
respiratory depression

Seizure- 32% subclinical seizure activity detected by electroencephalogram

118
Q

acute liver failuer lab?

A

Hemolytic anemia- wilson

Elevated 
creatinine, urea
amylase and lipase
ammonnia
LDH
Hypo
glucose
phosphate 
Mg
k

Acidosis or alkalosis

119
Q

acute liver injury pattern: Acetaminophen?

A

aminotransferase >3500
low bilirubin
high INR

120
Q

cute liver injury pattern: Ischemic hepatic injury?

A

aminotransferase 25 to 250XULN,
LDH +
fast elevation followed by fast reduction

121
Q

acute liver injury pattern: Hepatitis B virus?

A

Aminotransferase 1000 - 2000 common

ALT+++ > AST++

122
Q

acute liver injury pattern: Wilson disease?

A 
Coombs-negative hemolytic anemia, 
aminotransferase <2000
AST to ALT >2, 
alkaline phosphatase ==<40
alkaline phosphatase to total bilirubin (mg/dL) ratio <4, rapidly progressive renal failure
low uric acid
123
Q

acute liver injury pattern: Acute fatty liver of pregnancy/HELLP syndrome

A

Aminotransferase <1000
elevated bilirubin
low platelet count

124
Q

acute liver injury Imaging?

A

CT- liver less dense than skeletal muscle (darker)

Cirrhosis- nodular

CRF?
do U.S

125
Q

acute liver failure Treatment?

A

acetaminophen, alcohol-
give N-acetylcysteine (NAC), can cause anaphylaxis (rare)

liver transplant- 90% success

126
Q

liver biopsy?

A

A transjugular approach is preferred -concerns over bleeding (coagulopathy)

127
Q

Central Event in Liver Fibrosis?

A

Hepatic Stellate cell Activation (perisinusoidal, Ito)

In space of Disse

128
Q

liver fibrosis magnitude evaluation?

A

NAFLD Fibrosis Score (NFS)
Age, BMI, IFG/DM, AST/ALT, Platelets, Albumin
0.676 85% PPV

FIB-4
Age, AST, ALT, Platelets
<1.3 90% NPV
1.3-2.67 intermediate 
>2.67 80% PPV

Fibroscan- U.S basically
fibrosis + fattiness

129
Q

West Haven Scale (encephalopathy)?

A 
0,1- personality change 
2- disorientation, impaired motor skills
3- stupur
4-coma
death
130
Q

Ascites & Caput Meduza in portal hypertension characteristics?

A

↓Hypoalbuminemia
↑Na retension

Serum Ascites Albumin Gradient (SAAG) >1.1
albumin does not move in or out thus higher hydrostatic pressure induce water movement out of vessels , thus concentrating intra-vessels albumin and diluting ascetic albumin

± Chylus Ascites- high triglycerides due to lymphatic involvement

± SBP- spontaneous bacterial peritonitis
Positive Gram Stain
PMN > 250 cells/μL
give: Cefotaxim (3rd generation) , Ab Prophylaxis

131
Q

Child-Turcotte-Pugh (CTP) of cirrhosis severity?

A
  1. total billirubin
    <34, 34-50, >50
  2. serum albumin
    >3.5, 3.5-2.8, <2.8
  3. INR
    <1.7, 1.7-2.3, >2.3
  4. ascites
    none, mild, moderate to severe
  5. hepatic encephalopathy
    none, grade 2-3, grade 3-4

grade A- 5-6 points, 100% 1y.sur
grade B- 7-9 points, 80% 1y.sur
grade C- 10-15 points, 45% 1y.sur

132
Q

Model for End stage Liver Disease (MELD)?

A 
creatinine, bilirubin, INR, Sodium 
3 month observed mortality
≥40 		71% 
30–39 	53% 
20–29 	20% 
10–19 	6.0% 
<9 		2%
133
Q

Hepatic Venous Pressure Gradient (HVPG)?

A

HVPG = Free Hepatic Venous Pressure – Wedged Hepatic Venous Pressure

can determine cause of HHP:

post sinusoidal- both elevated
sinusoidal- both elevated
pre-sinusoidal- both normal

134
Q

hepatocellular carcinoma (HCC)?

A

↑ Viral Hepatitis- Eastern Asia , Sub- Saharan Africa
chronic alcohol use
NAFLD

Up to 90% of HCC with background of cirrhosis

U.S-method of choice for screening
hypoechoic nodules or masses

135
Q

Milan Criteria?

A

Liver Transplantation for HCC
1 lesion ≤ 5 cm
2 to 3, none < 3 cm

136
Q

Modified BCLC staging system and treatment strategy ?

A

Very early stage (0)- ablation, resection
Single <2 cm
Child-Turcotte-Pugh A, no ascites

Early stage (A)-resection, transplant, ablation
Solitary or 2–3 nodules <3 cm
Child-Turcotte-Pugh A, no ascites

Intermediate stage (B)- chemoembolization
Multinodular
unresectable
Child-Turcotte-Pugh A, no ascites

Advanced stage (C)- systemic therapy
Portal invasion/extrahepatic spread
Child-Turcotte-Pugh A, no ascites

systemic therapy:
Atezolizumab with Bevacizumab (becoming 1st line)
sorafenib, lenvatinib (current 1st line)

Terminal stage (D)- best supportive care
Not transferable HCC
End-stage liver function
137
Q

charcot triad?

A

jaundice;
fever, usually with rigors;
RUQ pain

138
Q

reynold pentad?

A

charcot triad
hypotension
confusion

139
Q

Enzymes raised in cholestasis (hepatobiliary)?

A

ALP
GGT

ALP isoenzymes are also present in bone & placenta

lone elevation in GGT levels – Fatty liver, alcoholic liver disease

140
Q

Clinical PBC?

A

Pruritus (related to retention of bile acids, CAN BE VERY SEVERE, INDICATION FOR TRANSPLANT)

Fatigue.

Xanthomas/xanthalasmas

Osteoporosis.

Portal hypertension.

Jaundice

141
Q

Primary Biliary Cholangitis characteristics?

A

Chronic, slowly evolving cholestatic disorder.
T cell mediated destruction of intrahepatic bile ducts

Relative sparing of hepatocytes with relative preservation of liver function

middle-aged women

142
Q

Laboratory Findings for PBC?

A

Serum ALP- elevated1:40) strongly suggestive (95%)
ASMA- may be positive
ANA- may be positive

IgM- high
IgG/A- normal

143
Q

Liver biopsy requirement for diagnosis of PBC?

A
  1. PBC-specific antibodies are absent
  2. Co-existent AIH or NASH is suspected
  3. With other systemic/extrahepatic co-morbidities
144
Q

Histologic stages of PBC?

A

stage 1-
intense lymphocytic inflammation surrounding the bile ducts

Stage 2-
bile ductular proliferation
+-hepatocyte injury and/or piecemeal necrosis.

Stage 3
development of bridging fibrosis.

Stage 4
presence of cirrhosis.

145
Q

PBC treatment?

A

UDCA- Ursodeoxycholic acid
Stabilizes biliary epithelial cell membranes
Replacement of hepatotoxic (endogenous) bile acids
Alters HLA I-II expression on biliary epithelial cell
Inhibits biliary cell apoptosis
Promotes endogenous bile acid secretion

no good?

OCALIVA- farnesoid X receptor (FXR) agonist
anticholestatic effects
preventing the toxic buildup of bile acid

liver transplant-
only curative treatment
MELD scoring system is used to prioritize patients (3M)
PBC recur but does not generally reduce patient or graft survival substantially.

146
Q

Primary sclerosing cholangitis (PSC) characteristics?

A

autoimmune

Relative preservation of hepatocytes

middle-aged men

strongly associated with IBD mainly UC

often complicated cholangiocarcinoma

higher risk of colorectal cancer

147
Q

PSC clinical findings?

A

Jaundice
Biliary infection(cholangitis)- acute/ stagnant
Cirrhosis

148
Q

PSC typical LAB?

A

Alk Phos- 875
Bilirubin- 2.0-5.0
AST/ALT- 75-150
Albumin- 3.5 (early normal, will reduce)

PT-11s and progresses

149
Q

PSC diagnosis?

A

MRCP

very very rarely biopsy- onion-skinning fibrosis

150
Q

PSC treatment?

A

(UDCA) improves the liver function profile in some patients

Liver transplantation
85% 5 years
70% 10 years
development of IBD persists even after transplantation

מבואות (8 decks)

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