גסטרו Flashcards
(150 cards)
1
Q
colonoscopy contraindications?
A
risk/ benefit no consent for non-urgent procedure acute diverticulitis fulminant colitis perforation (unless trying to close)
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
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%.
4
Q
Upper endoscopy Contraindications?
A
risk/ benefit
no consent for non-urgent procedure
5
Q
Upper endoscopy Preparation?
A
fast
6
Q
Upper endoscopy Risks?
A
Perforation of esophagus 0.03%
Sedation risks
Bleeding (therapeutic maneuvers)
7
Q
EUS Indications?
A
Staging cancer
gastrointestinal wall abnormalities
suspected choledocholithiasis
pancreatic abnormalities
8
Q
ERCP indications?
A
בעיקר צהבת חסימתית (טיפול)
CHOLANGITIS
ביופסיה
9
Q
ERCP risks?
A
pancreatitis:
Hartmann fluids
Prophylactic pancreatic stenting
NSAIDs - נר
bleeding 0.1% - 2% (sphincterotomy)
Perforation <1%
infection
sedation risks
10
Q
Dysphagia evaluations?
A
- fucking endoscopy!! (performed without stopping PPIs if needed)
- High resolution esophageal manometry
- essential for diagnosis of achalasia
- IRP(integrated relaxation pressure) - Barium swallow
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!!!
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
13
Q
EoE diagnosis?
A
biopsy only
also followup
14
Q
EoE endoscopy?
A
"טרכיאליזציה של הוושט" edema rings exudates furrows
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
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%)
17
Q
topical steroids for EoE?
A
Budesonide 8-12 weeks (Orodispersable tablets)
20% deep clinical, histologic and endoscopic remission
15% esophageal candidiasis, mild
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
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)
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»_space; feces, bile, blood, urine )
Accentuated by pressure or changes in tension “quite patient”
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?
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
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
24
Q
abdominal Vascular disturbances?
A
intestinal ischemia:
Acute mesenteric ischemia
Non-occlusive mesenteric ischemia (NOMI):
Abdominal angina
Vascular rapture (AAA)
Ovarian/testicular torsion
25
Acute mesenteric ischemia pain characteristics?
Acute obstruction (AF emboli?)
After few hours of ischemia -mucosal infarction and necrosis - peritoneal findings.
Pain typically poorly localized and visceral, without tenderness
26
Non-occlusive mesenteric ischemia (NOMI) pain characteristics?
Chronic partial obstruction
low-flow states pain (e.g. shock, hemodyalysis)
27
Abdominal angina pain characteristics?
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
28
Abdominal Wall pain characteristics?
constant and aching
29
abdominal neurological pain?
related to defecation
change of stool frequency
change in stool form
at least once a week for 3 months
30
important DD for abdominal pain?
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
31
Approach to PAIN – lab tests?
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?)
32
Approach to PAIN – radiology tests?
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
3. CT- very useful but radiation
33
polyp definition?
a grossly visible protrusion from the mucosal surface
34
Pathological classification of polyps?
Nonneoplastic hamartoma- congenital
cancerous potential (<1% become malignant):
Serrated (hyperplastic) polyp- BRAF, right colon
Adenomatous polyp- clearly premalignant, contain dysplastic tissue
35
Clinical factors to determine the probability of an adenoma becoming a cancer?
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
36
advanced adenoma criteria?
Adenoma >= 1 cm
Adenoma with high grade dysplasia
Adenoma with villous/tubulovillous histology
37
CRC screening Available tests?
Stool tests:
Fecal Occult Blood
exfoliated DNA- very limited today
Structural exams
Flexible sigmoidoscopy (FSIG)- canada only
Colonoscopy
Computed tomographic colonography (CTC)
38
Fecal Occult Blood test (FOBT) types?
```
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
39
exfoliated DNA test?
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)
40
stool tests Limitations?
Limited sensitivity for adenomas
Lower sensitivity for Rt. colon cancer
Old versions of FOBT are not sensitive enough
41
CRC screening guidelines?
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
42
Colonoscopic surveillance (if was) guidelines?
```
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
43
Prevention of CRC?
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
44
Systemic Manifestations of Iron Deficiency (late chronic) ?
```
Behavioral and neuropsychiatric manifestations
Pica (pagophagia)
Angular stomatitis cheilosis
glossitis
Esophageal webs and strictures
Koilonychia
```
45
iron deficiency by serum Ferritin and transsferin saturation in adult?
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
46
GI-related etiology of IDA?
sever esophagitis
diaphragmatic hernia
cameroon ulcer
athrophic gastritis
H.pyloric
Dudenal ulcer
celiac
CRC
colitis
large polyp
arterio vascular malformations
47
בירור אנמיה מחוסר ברזל?
לברר כל אנמיה מחוסר ברזל
בירור "דחוף":
גברים המוגלובין מתחת ל12
נשים בגיל פירון מתחת ל10
כל השאר ירד בגיידליננס החדשים
48
IDA inquiry management [AGA]?
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
49
H. pylori infection Mechanism of iron deficiency?
```
Occult GI bleeding
Competition for dietary iron
achlorhydria
Low gastric juice ascorbic acid (ferric to ferrous)
Rugae are almost completely lacking
```
50
iron therapy manegement?
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)
51
Presentations of GI bleeding-
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
52
Initial acute bleeding patient assessment?
1. Assess severity of bleeding: Vital signs
2. Resuscitation / history
3. physical examination
53
initial acute bleeding patient assessment: Resuscitation?
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)
54
initial acute bleeding patient assessment: history?
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)
55
initial acute bleeding patient assessment: physical examination?
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
56
Lab interpretation in acute GI bleed?
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)
57
acute Upper GI bleeding further assessment?
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)
58
Acute upper GI etiology?
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
```
59
Acute upper GI: Esophagitis?
Tx – aimed at the cause – mainly PPI
60
Acute upper GI: Mallory-Weiss Tear?
mostly on 1st vomit (75%)
90% stop bleeding spontanuously
Endoscopic Tx if needed
61
Acute upper GI: portal hypertension (varices)?
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
Acute upper GI: duodenal & gastric ulcer?
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
Management of ulcer bleeding?
Medical Tx – IV PPI, PO after
Endoscopic Tx:
1. saline injection- pressurized closure
2. Endoscopic coagulation
- Bicap (spray)
- ArgonPC
2. clip (usualy both)
if needed:
3. Angiography + embolization
4. Surgery
64
gastric erosions etiology?
most common- NSAID’s
Stress
Alcohol abuse
65
Acute upper GI: malignancy?
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
Acute upper GI: vascular lesions?
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
Acute lower GI bleeding Initial management?
similar to acute upper GI bleeding
68
Acute lower GI bleeding presentation?
Mostly self-limiting (80%)
25 % will re–bleed
Usually painless
If painful, r/o mesenteric ischemia
69
Acute lower GI bleeding Diagnostic procedures?
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
Acute lower GI bleeding etiology?
diverticular disease of colon- most common generally
| hemorrhoids - most common in 50
71
Acute lower GI bleeding: diverticular disease of colon?
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
Acute lower GI bleeding: angiodysplasia?
70y
73
Acute lower GI bleeding: Hemorrhoids?
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
Acute lower GI bleeding: other causes?
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
Occult bleeding DIAGNOSIS?
if IDA or FOBT:
Colonoscopy
CTC
gastroscopy/VCE- controversial
76
Nutrition Screening Tools?
MUST
- BMI
- weight loss
- acute disease effect
NRS - nutrition risk score
77
Assessing Nutritional Status :Physical Examination
weight status
mobility
signs of nutrient deficiencies/malnutrition
hair, skin, GI tract including mouth and tongue
Fluid Balance (dehydration/fluid retention)
78
Anthropometric Data ?
BMI
| Body Fat Measurements
79
cachexia definition?
multifactorial wasting syndrome characterized by involuntary weight loss of skeletal muscle mass with or without loss of fat mass
80
sarcopenia definition?
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
Approach a Pancreatic Lesion?
Age
Comorbidities
Lifestyle habits- alcohol and smoking
Systemic signs
- Weight loss
- Loss of appetite
- Painless jaundice- problematic
Recent onset diabetes mellitus
Imaging
82
“Double duct sign” in pancreatic imaging?
usually indicates a mass at the head of pancreas
83
Contrast enhanced EUS in pancrease?
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
Cystic pancreatic lesions characteristics?
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
pancreatic cyst biopsy lab findings?
AMYLASE (ductal involvement)-
IPMN and Pseudocysts
CEA (Mucinotic)-
musinous cystic neoplasm or IPMN
86
Bilirubin Metabolism?
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
Bilirubin Measurements?
Normal bilirubin level (adult)
Less than 1-1.5 mg/dL
Clinical Jaundice
Bilirubin >3 mg/dL
88
high Bilirubin DD?
prehepatic- hemolysis
hepatic- hepatocytes
post hepatic- obstructive or surgical
89
obstructive jaundice DD?
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
choledocholithiasis?
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
choledocholithiasis Diagnosis?
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
choledocholithiasis Treatment?
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
primary sclerosing cholangitis?
Chronic
Progressive
“Beads on string”
Bile duct strictures (intra and extra hepatic)
94
normal mass of stool per day?
200gr
95
איטיולוגיה של שלשול?
מיימי – אוסמוטי / סקרטורי
אינפלמטורי
שומני
הפרעות בתנועתיות המעי
96
שלשול מיימי אוסמוטי או סקרטורי ?
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
שלשול אינפלמטורי ?
שלשול עם דם (בעיקר דלקת קולונית)
עליה בקלפרוטקטין (חלבון שנמצא בפולימורופנוקליאריים)
IBD, GVHD
98
שלשול שומני?
סוג של אוסמוטי (השומן מושך מים)
גושי, ריח רע, חיוור, צף
נובע מתת ספיגה אינטרא-לומינאלית או מוקוזלי
99
דגלים אדומים בשלשול?
```
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
chronic diarrhea duration?
over 4 weeks
101
chronic diarrhea physical exam?
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
chronic diarrhea Assessment (lab, imaging)?
```
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
ROME criteria for IBS?
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
PPI for bleeding ulcer mechanism?
higher PH thus stopping ulcer propagation
higher PH induce/ propagates coagulation
thus reduction of Endoscopy usage
105
forest classification of bleeding peptic ulcer?
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
Esophagogastroduodenoscopy (EGD) comlications?
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
managing anti-platelet agents in UGIB?
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
Hepatocellular injury- Lab?
↑ALT/AST >>↑ALK PHOS
+/- Bilirubin
+/- synthetic function – albumin, INR
109
Cholestatic injury- Lab?
↑ALK PHOS >>↑ALT/AST
GGT
+/- bilirubin
+/- synthetic function – albumin, INR
110
LFTs normal values?
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
liver injury physical exam?
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
ALD LAB?
AST:ALT >>2
| ↑GGT
113
transaminases (ULN) lvl interpretation?
>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
acute liver failure definition?
severe acute liver injury (LFTs) + encephalopathy + impaired synthetic function (INR of ≥1.5)
without cirrhosis or preexisting liver disease.
<26W
115
acute liver failure classification and etiology?
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
liver failure symptoms?
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
encephalopathy presentation?`
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
acute liver failuer lab?
Hemolytic anemia- wilson
```
Elevated
creatinine, urea
amylase and lipase
ammonnia
LDH
```
```
Hypo
glucose
phosphate
Mg
k
```
Acidosis or alkalosis
119
acute liver injury pattern: Acetaminophen?
aminotransferase >3500
low bilirubin
high INR
120
cute liver injury pattern: Ischemic hepatic injury?
aminotransferase 25 to 250XULN,
LDH +
fast elevation followed by fast reduction
121
acute liver injury pattern: Hepatitis B virus?
Aminotransferase 1000 - 2000 common
| ALT+++ > AST++
122
acute liver injury pattern: Wilson disease?
```
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
acute liver injury pattern: Acute fatty liver of pregnancy/HELLP syndrome
Aminotransferase <1000
elevated bilirubin
low platelet count
124
acute liver injury Imaging?
CT- liver less dense than skeletal muscle (darker)
Cirrhosis- nodular
CRF?
do U.S
125
acute liver failure Treatment?
acetaminophen, alcohol-
give N-acetylcysteine (NAC), can cause anaphylaxis (rare)
liver transplant- 90% success
126
liver biopsy?
A transjugular approach is preferred -concerns over bleeding (coagulopathy)
127
Central Event in Liver Fibrosis?
Hepatic Stellate cell Activation (perisinusoidal, Ito)
| In space of Disse
128
liver fibrosis magnitude evaluation?
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
West Haven Scale (encephalopathy)?
```
0,1- personality change
2- disorientation, impaired motor skills
3- stupur
4-coma
death
```
130
Ascites & Caput Meduza in portal hypertension characteristics?
↓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
Child-Turcotte-Pugh (CTP) of cirrhosis severity?
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
Model for End stage Liver Disease (MELD)?
```
creatinine, bilirubin, INR, Sodium
3 month observed mortality
≥40 71%
30–39 53%
20–29 20%
10–19 6.0%
<9 2%
```
133
Hepatic Venous Pressure Gradient (HVPG)?
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
hepatocellular carcinoma (HCC)?
↑ 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
Milan Criteria?
Liver Transplantation for HCC
1 lesion ≤ 5 cm
2 to 3, none < 3 cm
136
Modified BCLC staging system and treatment strategy ?
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
charcot triad?
jaundice;
fever, usually with rigors;
RUQ pain
138
reynold pentad?
charcot triad
hypotension
confusion
139
Enzymes raised in cholestasis (hepatobiliary)?
ALP
GGT
ALP isoenzymes are also present in bone & placenta
lone elevation in GGT levels – Fatty liver, alcoholic liver disease
140
Clinical PBC?
Pruritus (related to retention of bile acids, CAN BE VERY SEVERE, INDICATION FOR TRANSPLANT)
Fatigue.
Xanthomas/xanthalasmas
Osteoporosis.
Portal hypertension.
Jaundice
141
Primary Biliary Cholangitis characteristics?
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
Laboratory Findings for PBC?
Serum ALP- elevated1:40) strongly suggestive (95%)
ASMA- may be positive
ANA- may be positive
IgM- high
IgG/A- normal
143
Liver biopsy requirement for diagnosis of PBC?
1. PBC-specific antibodies are absent
2. Co-existent AIH or NASH is suspected
3. With other systemic/extrahepatic co-morbidities
144
Histologic stages of PBC?
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
PBC treatment?
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
Primary sclerosing cholangitis (PSC) characteristics?
autoimmune
Relative preservation of hepatocytes
middle-aged men
strongly associated with IBD mainly UC
often complicated cholangiocarcinoma
higher risk of colorectal cancer
147
PSC clinical findings?
Jaundice
Biliary infection(cholangitis)- acute/ stagnant
Cirrhosis
148
PSC typical LAB?
Alk Phos- 875
Bilirubin- 2.0-5.0
AST/ALT- 75-150
Albumin- 3.5 (early normal, will reduce)
PT-11s and progresses
149
PSC diagnosis?
MRCP
| very very rarely biopsy- onion-skinning fibrosis
150
PSC treatment?
(UDCA) improves the liver function profile in some patients
Liver transplantation
85% 5 years
70% 10 years
development of IBD persists even after transplantation
