"Coffee grounds"

emesis
1a
suggests upper GI bleeding
as well as lower rate of
bleeding (enough time for
vomitus to tranform into
"coffee ground"
1b
"pencil stools" are
highly indicative of?
2a
Left sides tumors in
regards to CRC
2b
#1 cause of
PANCREATIC CA?
3a
SMOKING!
3b
% of patients with
HCC in patients with
diagnosed
CIRRHOSIS
4a
10-25%
4b
+ROVSINGS SIGN, +
PSOAS SIGN, +
OBTURATOR SIGN
5a
acute appendicitis
5b
47YO DM female presents with onset of tremors.
Undergone both pancreatic and renal transplantation
2/2 ESRD and DM. Takes medications including that
of immunosuppressants. BP 152/90 and pulse and
RR WNL. Examination shows gum hypertrophy and
labs show an increased BUN and inc CREATININE.
Which immunosuppressant is likely to be responsible
for the presentation of patient?
(Tacrolimbus, cyclosporine, AZA, Mycophenolate)
6a
CYCLOSPORINE!
most commonly used and acts by inhibiting the trancription of IL-2
and severeal other cytokines (mainly the THELPER LYMPHOCYTES
-nephrotoxic
-hypertension
-neurotoxic
-glucose inteleratnce
-infectoin
-malignancy of SQCC of skin and lymphoproliferative D/O
-gingival hyperplasia and hirsuitism
6b
80% of episodes of upper
GI bleeding stop
spontaneously and only
need supportive therapy - T
OR F?
7a
TRUE
7b
A lower GI bleed or positive
occult blood test in stool in
patients > 40YO is ___
___ until proven otherwise
8a
colon cancer
8b
A non-alcoholic patient has an
asymptomatic elevation of serum
transaminases (ALT/AST) and
increased serum iron and feritin
levels, and a family history of non-
alcoholic liver cirrhosis. This
diagnosis is strongly suggestive of?
9a
HEMOCHROMATOSIS
9b
Absolute criteria for
achalasia:
10a
Aperistalsis of
esophagus
Incomplete relaxation
of the LES
10b
Acalculous
cholecystitis
11a
Acute cholecystitis without stones that obstruct the
cystic duct (up to 10% of patients with acute
cholecystitis)
-idiopathic in patienst with underlying illness
associated to dehydration ischemia burns trauma
and a postoperative state
-signs and symptoms are the same as for acute
cholecystits
11b
ACHALASIA
12a
aquired motor d/o of the esophageal
smooth muscle in which the lower
esophageal sphinctor fails to
completely relax with swallowing and
abnormal peristalsis of esophgeal
body replaces normal peristalsis of
the esophageal body
12b
ACHALASIA HAS
NORMAL ____
PRESSURE UNLIKE
THAT OF DES
13a
normal LES pressure
13b
Acid suppression
therapy for pts with
PUD includes:
14a
H2 blockers; ranitidine;
famotidine; cimetidine;
PPI; esmoprezole;
omeprazole; lansoprazole;
pantoprazole, rabeprazole
14b
Acites is defined as the accumulation of
fluid into the peritoneal cavity 2/2 portal
HTN (increased hydrostatic pressure) and
________ (reduced oncotic pressure)
Diagnosis:
Treatment
15a
Ascited = portal HTN (increased hydrostatic pressure) and hypoalbuminemia
(reduced oncotic pressure). Thus will also have abdominal distenstion, shifting
dullness and fluid wave.
Abdominal ultrasound can detect >30mL fluid
Diagnostic = paracentesis to determine whether ascites 2/2 portal HTN or another
cause. Looks at cell count, ascites albumin, gram stain, culture to r/o SBP
(spontaneous bacterial pneumonitis)
-meausre the serum ascites albumen gradient. If >1.1g/DL, portal HTN likely. If <1.1
then portal HTN is unlikely and other cause.
TREATMENT:
1. Bed rest; low sodium diet; diuretics (furosemide and spironolactone)
2. Perform paracentesis if tense ascites, SOB or earlysatiety.
3. Peritoneovencous shunt or TIPS to reduce HTN
15b
Acute appendicitis with obstruction leads
to _____ of fluid and mucus, which
promotoes ________ growth leading to
inflammation. Distention of the appendix
can compromise ______ supply resulting
in ischemia and necrosis if untreated.
Necrosis results in perforation and
peritonitis.
16a
stasis
bacterial
blood
16b
Acute bacterial
sinusitis
17a
most common health problem in the US
-develops subsequent to viral
rhinosinusitis in 0.5-2% of all cases
-should be suspected in pts with symptoms
of virl rhinosinusitis that persis for more
than 10d or worsen after 5-7
17b
Acute gastritis is best
assessed by which
method?
18a
UPPER GI Endoscopy is the best
test for evaluating a pt with
epigastric pain. It can diagnose
PUD, gastritis, esophagitis and can
r/o CA of esophagus and stomach
and H. pylori with BIOPSY
18b
Acute infectious
diarrhea - top cases
are what organisms?
19a
1. Salmonella (14.6 cases)
2. Campylobacter (12.7 cases)
3. Shigella (4.7 cases)
4. E. Coli O157H7 (1.1)
5. Crptosporidia (3.0 cases)
19b
Acute infectious
diarrhea (stool
cultures: indications)
20a
-acutely ill patients with fever and
fecal WBCs
-diasease in very young and very old
-common source outbreaks
-food handlers
-persistent diarrhea after foreign
travel
20b
Acute Infectious
Diarrhea is defined as:
21a
increased frquency of defecation
(>/= stools/day) lasting
<14days
-accounts for 900k
hospitalizations and 6k deaths
annually
21b
Acute infectious
diarrhea options for
empirical therapy
22a
Ciprofloxacin 500 mg bid x 1-5d
Levofloxacin 500 mg daily x 1-5d
Erythromycin or azithromycin should
be added in the
immunocompromised host with
increased risk for possible FQ
resistant campylobactor infection
22b
Acute uncomplicated
UTI prevention of
precurrences
23a
Some supportive evdience
-cranberry juice (200-750 mL/d) or cranverryo
concentrate tablets (12-20% reduction)
-topical estrogen creams
-avoid exposure to vaginal spermicides
No supportive evidence
-postcoital voiding
-"enhanced" urinary hygiene
-oral estrogen replacement
23b
Acute UTI
uncomplicated
diagnosis:
24a
Consistent symptoms
+ positive dipstick
(U/A) = UTI (culture
NOT NEEDED)
24b
Acute versus Chronic
Mesenteric Ischemia
25a
ACUTE:
1. Results from a compromised blood supply, usually to the superior mesenteric vessels
2. Four types of acute mesenteric ischemia:
a. Arterial emboli (50% of cases) - cardiac origin (afibb, MI, valvular)
b. Arterial thrombi (25% of cases) - CAD, PVD, STROKE (atherosclerotic)
c. Nonocclusive mesenteric ischemic - splanchnic vasocontriction 2/2 CO dec
d. Venous thrombus - many predisposing factors - eg infection, hypercoag states, OCP, portal HTN, malig,
pacreatitis
3. Mortality rate for all types is about 60-70% - if bowel infarct occurred, rate >90%
Chronic
1. Caused by atherosclerotic occlusive disease of main mesenteric vessels (celiac artery, superior and inferior
mesenteric articles)
-abdominal angina, dull pain, typically postprandial (when there is increased demand for spanchnic blood flow);
analogous to anginal pain of CAD
-weight loss 2/2 abdominal angina
-mesenteric arteriography confirms the diagnosis
-surgical revascularization is definitive treatment and leads to pain relief in 90% of cases
25b
Adenocarcinoma of the
esophagus is one of two types of
esophageal CA that affects what
population?
Risk factors?
26a
Most common in white males
most common in distal 1/3 of esophagus @
GE junction
RF: GERD and Barretts esophagus are
main risk facors; alcohol and tobacco may
not be as important as in SCC
26b
Adenomatough polyps
differ from inherited
polyposis syndromes
in what way?
27a
Benign lesions that have
significant malignant
potential that are
precursors of
adenocarcinoma
27b
Adults respiratory distress
syndrome is a secondary
complication to acute
pancreatitis in what way?
28a
LIFE THREATENING
with high mortality
rate
28b
Albumin as a liver
function test:
29a
Albumin is decreased in chronic
liver disease, nephrotic
syndrome, malnutrition and
inflammatory states
*burns/sepsis/trauma
29b
Alkaline phosphatase
(ALK-P) is elevated in
which clinical
scenarios?
30a
1. ALK-P is elevated when obstruction to bile
flow(cholestasis); in any part or biliary tree. If normal,
unlikely biliary obstruction
2. IF EXCESSIVELY high (10 fold) think of extrahepatic
hiliary tree obstruction or intrhepatic cholestass (PBC or DI-
cirrhosis)
3. If level are elevated, measure the GGT (gamma-glutamyl
transferase) level to make sure the elevation is HEPATIC
origin (rather than bone or intestinal). If GGT is also
elevated, then strongly suggests hepatic origin. If GGT level
is normal but ALP elevated - think bone or pregnancy issue
30b
ALT and AST usually have
a similar increase, however
in alcoholics, we expect an
elevation in which enzyme?
31a
elevation is
AST>>>>ALT
31b
ALT is primarily found
in the ____
AST is primarily found
in the ____
32a
ALT - LIVER
AST - more nonspecific:
kidney, heart, brain,
skeletal muscle
32b
An autosomal RECESSIVE disease that is
2/2 copper metabolism. This normal
excess usually excreted by the liver
however whene the patients liver has a
deficiency in ++++++++, copper will
accumulated in the liver cells
(hepatocytes). What happens to the
hepatocytes?
33a
Wilsons disease
-cerruloplasmin
-as the hepatocytes die 2/2 to Cu2+
accumulation; the copper leaks into plasma and
accumulates in various organs (kidneys, cornea,
brain0
-most occurs during childhood/adolescence
(5YO)
-diagnosis within 5-35YO
33b
An underlying motility d/o is the cause of
both proximal (ZENKERS) and distal
(EPIPHRENIC) diverticula. Surgical
treatment is aimed at correcting the
motility d/o via ______.
A ______ is of 2ndary inportance in both
cases
34a
Myotomy
Divertoculectomy
34b
Angiodysplasia of the colon
(arteriovenous
malformations, vascular
ectasia)
refers to?
35a
-tortous, dilated veins in submuscosa of the colon (usually
proximal) wall
-a common cause of lower GI bleeding in patients over age
60YO
-bleeding usually low grade but 15% of patients may have
massive hemorrhage if veins rupture
-diagnosed by colonoscopy (preferred over angiography)
-in 90% of patients, bleeding stops spontaneously
-treated by colonoscopic coagulation of the lesion.
-if bleeding persists, a right hemicolectomy should be
considered
35b
Antibiotics for acute bacterial
sinusitis that is uncomplicated?
If complicated (severe sinusitis)
36a
Trial of symptomatic rx for 7days, if no
better than treat with amox, doxy or TSX
for 10days
consider CT scanning at baseline
treatment with azithro, FQs, or amox/clav
for 10-14d - if no better after 3 days then
change treatment
36b
AR disorder with increased
skin pigmentation, DM,
cirrosis and arthralgia in
late stages
37a
hemochromatosis
37b
Arteriography is used
for which reason in GI
BLEEDING?
38a
DEFINITIVELY LOCATES THE POINT
OF BLEEDING
-mostly used in pts with lower GI bleeding
-should be performed during active
bleeding
-potentially therapeutic (embolization or
intra-arterial vasopressin infusion)
38b
As many as 25% of patients with
bleeding AV malformations
have aortic stenosis however, no
____ and _____ relationship
has been noted.
39a
cause and effect (AVM
and AVS)
39b
Autosomal recessive -
Polyps plus cerebellar
medulloblastoma or
glioblastoma multiforme?
40a
TURCOTS
SYNDROME
40b
Barium enema are
good for?
41a
Evaluates the entire colon,
completmentary to fleximble
signmoidocopy - disadvantage is
that any abnormal finding
needs to be evaluated by
colonoscopy
41b
BARRETTS esophagus
42a
is a complication of longstanding
acid reflux disease in which thre is
columnar metaplasia of the
squamous epithelium. Patients with
Barretts esophagus are at increased
risk of developing adenocarcinoma of
the esophagus.
42b
Best diagnostic test for
esophageal
diverticulum
43a
Barium swallow
43b
BLACK GB STONES v.
BROWN GB STONES
44a
black 2/2 hemolysis
brown 2/2 biliary tract
infection
44b
Bleeding from small
bowel::
Bleeding from the
colon::
45a
-hematochezia,
melena
-occult blood,
hematochezia
45b
BLEEDING FROM THE
SMALL BOWL CAN
PRESENT AS EITHER
_____ OR ______
46a
Melena or
hematochezia
46b
Boas sign v. Murphys
sign v. Chargot's triad
47a
Boas sign - cholelithisis - gallstone - right
should/scapular pain
Murphy's sign - RUQ pain/tenderness on
inspiration and palpation
Chargots triad - RUQ pain, jaundice, fever
(seen in 70% of patients with this disease)
47b
Bowel duct stricture is 2/2 an _______ injury
(like that of biliary surgery or cholecystectomy,
liver transplantation); other causes include
recurring choldocholithiasis, chornic
pancreatitis, and PSC.
Clinical features: OBSTRUCTIVE JAUNDICE
48a
IATROGENIC
48b
CA-MRSA
1. Prevalence
2. Setting
3. Transmission
4. Strain
49a
1. emergence is nationwide
2. both children and adults in variety of settings
affected --> contact sports (wrestling, football
and fencing), correctional facilities, native
american communities, MSM
3. Transmission is person to person or by fomites
4. Strains causing MRSA (community) appear
distinct --> unique resistance cassette (SCC mec
IV) & broader susceptibility
49b
CA-P duration of
therapy
50a
1. ID society:
- s pneumona treat until
afebrile for >72 hr
- s aureus< GNRS, anaerobes,
atpicals, > 2 weeks
50b
CA-penumonia
diagnosis:
51a
Typical symptoms: cough,
SOB, sputum, pleuritic
chest pain
Infiltrate on CXR is gold
standard for dx
51b
Carcinoid tumor v.
Carcinoid syndrome
52a
Carcinoid tumors originate from neuroendocrine cells and secrete serotonin
-the most common site for these tumors is the appendix, but they can be found
in a variety of locations (small bowel, rectum, bronchus, kidney, pancreas)
syndrome results in 10% or patients with c. tumors.
-excess serotonin secretion can lead to carcinoid syndrome which is manifested
by cutaneous flushing, diarrhea, sweating, wheezing, abdominal pain, heart
valve dysfunctoin
-risk factors for mets increase with size of tumor - rare with appendiceal tumors
however ilieal tumors have greatest likelihood for malignancy - surgival
resection is tretament of choice.
52b
Carcinoma of the CB
53a
Most are adenocarcinomas and occur in the elderly
-associated with gallstones in most cases but include
cholescystemeric fisutla and porceliain gallbladder
-clinical features are nonspecific and suggest extrahepatic bile
duct obstruction: jaundice: biliary colic: weight loss: anorexia:
and RUQ mass
-difficult to remove with surgery: cholecystecotmy versus
radical cholecystectomy with wedge resection of the liver and
lymph node dissection - depending on depth of underlying
condition
-pronosis is POOR bc disease underdetected until it is
advanced.
53b
CAuses of acute
uncomplicated UTI in
women/males
54a
75-90% of cases E. coli
5-15% is S. saprophyticus
Probability of cystitis >90% in
woman with dysuria and
frequency w/o vaginal d/c
54b
Causes of BUDD-
CHIARI syndrome
55a
Hypercoaguable state
myeloproliferative d/o (polycythemia
vera)
pregnancy
chronic inflammatory diseases, infection
malignancies
trauma
-CONDITON is idiopathy in 40% of cases
55b
Causes of cirrhosis?
56a
1. Alcoholic liver disease (most common cause)
-range of conditions from fatty liver (reversible due to acute ingestions) to cirrhosis (irreversible).
-15-20% of heavy drinkings develop alcoholic cirrhosis
2. Chronic hepatitis B and C infections
3. Drug toxicity: acetaminophen toxicity, MTX
4. AI hepatitis
5. Primary biliary cirrhosis (PBC); secondary biliary cirrhosis
6. Hereditary metabolic diseases (Hemachromatosis, Wilson's disease (deposition of iron or copper)
7. Hepatic congestion 2/2 RHF or constrictive pericarditis
8. NASH
9. Hepato veno-occlusive disease can occur after bone marrow transplantation
56b
Causes of hepatic
encephalopathy:
57a
1. Toxic metabolites
2. occurs in 50% of all cirrhosis cases
3. Hypokalemia and alkalosis (2/2
diuretics), dedating drugs (narcotics,
sleeping meds), GI bleeding, systemic
infection, and hypovolemia
4. Clinical features: confusion, asterixis,
rigidity and fetor hepaticus
57b
Causes of SBO?
58a
1. Adhesions from prior abdominal
surgery
2. Incaercerated hernias
3. Malignancy, intussusception, Crohns
disease, carcinomatosis and superior
mesenteric artery syndrome
(compression of third part of duodenum)
58b
Cavernosis
hemangiomas
59a
Vascular tumor that are small, asymptomatic and most
commony type of BENIGN liver tumor.
size increases 2/2 pregnancy or OCP use
complications: rupture with hemorrhage, obstructive
jaundice, coagulopathy, CHF seondary to a large AV shunt
and gastric outlet obstruction
Dx with US or CT with IV contrast - no biopsy indicated
59b
Celiac sprue
60a
Hypersensitivity to gluten
-weight loss, abdominal distention,
bloating diarrhea
-biopsy in prximal small bowel
reveals flattenng of villi which causes
malabsorption
-strict adherence to gluten free diet
60b
Characteristics of
jaundice:
61a
1. Yellow coloration of skin, sclera, mucous membranes, sclerae due
to over production or dec clearence of bilirubin
2. Clinical jaundice usually becomes evident when total bilirubin is >
2mg/dL
3. Conjugated v. unconjugated bilirubin
a. Conjugated (direct) -
loosely bound to albumin and therefore water soluble
when in excess, excreted in urine and is dark (only dark if conj br)
b. Unconjugated (indirect) -
tightly bound to albumin and therefore not water soluble
cannot be excreted in the urine even if blood levels are high
toxic, unbound form can cross BBB and cause neurologic deficits
4.
61b
Childs classification
system to assess
severity of LIVER
DISEASE
62a
CLASS A:
1. Ascites: NONE
2. Bilirubin: <2.0
3. Nutrtional status: excellent
4. albumin: > 3.5
Class B:
1. Ascites: controlled
2. Bilirubin: 2-2.5
3. Nutritional status: good
4. Encephalopathy: minimal
5. Albumin: 3-3.5
CLASS C:
1. Ascites: uncontrolled
2. Bilirubin: >3
3. Nutritional status: poor
4. Encephalopathy: severe
5. Albumin: <3
62b
Choledocholithiasis
clinical presentation:
63a
ASymptomatic for
years
-RUQ pain/epigastric
pain and jaundice
63b
Cholelithiasis v. Choledocholithiasis
Abnormality
Clinical features
Complications
Diagnosis
Treatment
64a
Cholelithiasis (A) and Choledocholithiasis (B)
I. Abnormality (A) - gallstone in gallbladder
(B) - stone in the COMMON BILE DUCT
II. Features (A) - asymptomatic + biliary colic if obstructed
stone 2/2 contracting GB
(B) - asymptomatic + RUQ pain/jaundice/eipgastric pain
III. Diagnostic (A) - US or CT
(B) - ERCP is the test of choice for RUQ US not sensitive
IV. Treatment (A) - resection if symptomatic (GB)
(B) - removal of stone via ERCP and spincterotomy
64b
Cholestasis referes to
obstruction of ____ _ from
ANY cause. If LFTs reveal
cholestasis (markedly elevated
ALKPHOS), then obtain?
65a
bile flow
abdominal or RUQ
ultrasound
65b
Cholesterol stones are one of
three major types of GB
stones that are _____ -
_____ in coloration and are
associated with the following:
66a
yelllow-green
1. obestity
2. DM
3. HLD
4. multiple pregnancies
5. Crohns dz
6. Native american ancestry
7. Cirrhosis
8. Cystic fibrosis
66b
Chronic gastritis
67a
MOST COMMON CAUSE = H PYLORI (>80%) cases
-autoimmune gastritis lads to chornic atrophic gastritis with
serum antipareital and anti-intrinsic factor antiboide
(possible dvelopment of pernicious anemia)
-most pts are asymptomatic and never develop
complications - manifests as epigastric pain similar to PUD
complications: gastritis, carcinoma, mucosa-associated
lymphoid tissue lymphoma (MALT)
-UPPER GI ENDOSCOPY WITH BIOPSY IS THE TEST OF
CHOICE FOR Dx OF CHRONIC GASTRITIS
67b
Cirrhosis of the liver v.
Hepatitis of the liver
68a
Cirrhoses - chronic liver dz characterised
by fibrosis, disruption of the liver
architecture and widespread nodules in
the liver (the fibrous tissue replaces
damaged or dead hepatocytes)
Hepatitis - inflammation of the liver
hepatocytes.
68b
Clinical features
associated with
esophageal
perforation?
69a
-PAIN (severe/retrosternal/chest/shoulder pain),
-tachycardia,
-hypotension,
-tachypnea,
-dyspnea,
-fever,
-hamman's sign ("mediastinal crunch") produced
by the heart beating against airfilled tissues,
pneumothorax or pleural effusion
69b
Clinical features of acute
mesenteric ischemia
versus chronic
mesenteric ischemia
70a
Acute: severe abdominal pain disproportionate to the physical
findings. Pain is due to ischemia or possibly infarction of
intestines analogous to MI in CAD. Abdomen may appear
benign even when there is severe schemia. This can lead t a
delay in dx. Acutesness and the severity of pain vary depending
on the type of acute mesenteris ischemia
-anorexia, vomiting
-GI bleeding (mild)
-peritonitis, sepsis, shock may be present in adv disease
Chronic: results in weight loss, abdominal angina
postprandially.
70b
Clinical features of
cholangiocarcinoma
71a
Obstructive jauntice and
associated symptoms - dark
urine, clay colored stool,
pruritis
weightloss
71b
Clinical features of
cholelithiasis?
72a
1. MAJORITY ARE ASYMPTOMATIC - if found
incidentally - dont touch it no need to remove
2. Biliary colic is due to temporary obstruction of
the cystic duct by a gallstone.
3. Pain is 2/2 the gallbladder contractng
AGAINST the obstruction
4. RUQ or epigastrium and mild-severe pain
5. BOAS SIGN - riht subscapular pain of biliary
colic
72b
Clinical features of
cirrhosis?
73a
-asymptomatic in early dz
-portal HTN, varices, ASCITES,
hepatic encephalopathy,
hepatorenal syndrome,
spontaneous bacterial
peritonitis, hyperestrinism
73b
Clinical features of
esophageal cancer:
74a
-dysphagia (MOST COMMON - to solids only then to liquids!)
-weight loss (second most common symptom)
-anorexia
-odynophasia (pain with swallowing)-late finding that suggests
extraesophageal involvement (mediastinal invasion)
-hematemesis, hoarseness of voice, recurrent laryngeal nerve
involvement
-aspiration pneumonia, respiratory symptoms due to
involvement of traceobronchial tree
-chest pain
74b
Clinical features of
PANCREATIC CA
75a
Very nonspecific - thus by the time dx is made, often too late
and incurable.
1. Abdominal pain
2. Painless jaundice bc @ head of pancreas
3. Weight loss
4. Onset of glucose intolerance but the GM is mild
5. Depression/weakness/fatigue
6. Migratory thrombophelbitis - develops in 10% of cases
7. Courvoisier's sign (palpable GB) present in 30% of
patients involved head of pancreas - presents without pain
75b
Clinical features of
PSC:
76a
1. Begin insidiously
2. Chronic cholestasis include
jaundive, pruritis; all patients
eventually present with chronic
obstructive jaundice.
3. Other symptoms include: fatigue,
malaise, weight loss
76b
Clinical features of
SBO?
77a
Cramping abdominal pain (if
continuous and severe then expect
strangulanous activity.
-n/v may be feculent
-obstipation (LACK OF STOOL and
FLATUS)
-abdominal distention
77b
Clinical features of UC
78a
1. Hematochezia
2. Abdominal pain
3. Bowel movement
78b
Clinical geatures of
HCC
79a
-abdominal pain
-hepatomegaly
-weiht loss, anorexia, fatigue
-signs and symptoms of CLD; portal HTN, ascites, jaundice,
splenomegaly
-paraneoplastic syndromes:
a. ERYTHROCYTOSIS
b. THROMBOCYTOSIS
c. HYPERCALCEMIA
D. CARCINOID SYNDROME
E. HYPERTROPHIC PULMONARY OSTEODYSTROPHY
F. hypoglycemia
g. HYPERCHOLESTEROLEMIA
79b
Clinical indicators of
Acute bacterial
sinusitis
80a
"double sickening"
unilateral pain
pain above or below the eyes on leaning forward
maxillary toothache
purulent rhinorrhea by hx
poor response to decongestants
0-1 = no treatment
2-3 = XR
4+ = ATB treatment
80b
CLinical signs of
appendicitis:
81a
1. Mcburneys point (tenderness)
2. Rebound tenderness, guarding, diminished bowel
sounds
3. Low-grade fever
4. Rovsings sign: deep palpation is LLQ causes
referred pain in RLQ
5. Psoas sign: RLQ pain when right thigh is extended
as patient lies on the L side
6. Obturator sign: pain in RLQ when flexed right
thigh is internally rotated when pt is supine.
81b
Clinical symptoms of
appendicitis:
82a
1. abdominal pain - starts in epigastrium,
moves toward umbilicus, then to RLQ with
distention of the appendix - the parietal
peritoneam may become irritated leading
to sharp pain
2. anorexia always present
3. nausea, vomiting (typically following
pain)
82b
Closed loop versus
open loop obstruction
in SBO
83a
Closed loop, the lumen is
occlused at two poitns by an
adheive band or hernia ring.
This can compromise blood
supple requiring emergent
surgery
83b
Clostridium difficile
presents with which
hypervirulent
features?
84a
Severe ileus
Fever
hypotension
marked leukocytosis (15k-50k)
ARF
Hypoalbuminemia
severe metaboli acidosis with elevated LACTATE
levels
Increased need for colectomy
84b
Coagulopathy occurs
2/2 synthesis of
clotting factors being
decreased:
85a
1. Prolonged PT; PTT may be
prolonged with severe disease
2. Vitamin K is ineffective
because it cannot be used by
diseased liver
3. Treatment of coag is FFP
85b
Colonoscopy identifies the
site of LOWER GI BLEED
IN ___% of cases and can
also be therapeutic
86a
70
86b
COmplication of
cholecystitis:
(inflammation of the
GB)
87a
1. Gangrenous cholecystitis
2. Perforation of GB
3. Emphysematous cholecystitis
4. CHolecystenteric fistula with
gallstone ileus
5. Empyema of the GB
87b
Complication of
diverticulitis:
88a
1. Abscess formation: drined either
percutaneously under CT guidance or sugically
2. Colovesicular fistula (50% of fistulsa
secondary to diverticulitis)
3. 50% close spontaneously
4. Obstruction-due to chronic inflammation and
thickening of bowel wall
5. Free COLONIC PERFORATION - uncommon
but catacstrophic and leads to peritonitis
88b
Complication of
diverticulosis versus
diverticulitis
89a
Diverticulosis: painless rectal
bleeding and diverticulitis
Diverticulitis: includes bowel
obstruction, abscess and fistulas
89b
Complication of liver
failure (AC, 9H)
90a
ASCITES
COAGULOPATHY
HYPOALBUMINEMIA
PORTAL HYPERTENSION
HYPERAMMONEMIA
HEPATIC ENCEPHALOPATHY
HEPATORENAL SYNDROME
HYPOGLYCEMIA
HYPERALBILIRUBINEMIA/JAUNDICE
HYPERESTRINISM
HEPATOCELLULAR CARCINOMA
AC,9H
90b
Complication to ACUTE
PANCREATITIS:
Ascending cholangitis and be 2/2
______ obstruction in the ampulla
of Vater, leading to infection of the
biliary tract.
91a
gallstone
91b
Complications
associated with
diverticulosis?
92a
1. Painless rectal bleeding (up to 40% of patients)
-bleeding is usually clinically insignificant and
stops spontaneously. No further treatment is
necessary in these patients.
-if bleeding beomes severe (5%) a colonoscopy
may be performed to locate the site of bleeding. If
doesnt stop, segmental colectomy may be
required
92b
COMPLICATIONS OF
CBD stones
93a
Cholangitis
Obstructive jaundice
Acute pancreatitis
Biliary colic
biliary cirrhosis
93b
Complications of
cholelithiasis?
94a
1. Cholecystitis
2. Choledocholithiasis with
assoicated symptoms
3. Gallstone ileus
4. Malignancy
94b
Complications of
hemachromatosis:
95a
#CIRRHOSIS INCREASES RISK OF HCC BY 200; PRESENSE OF LIVER
DISEASE IS ESSNTIAL FOR PROGNOSIS OF DZ
#Cardiomyopathy - CHF, arrhythmias
#DM - due to iron deposition in the pancreas
#Arthritis-most common sites are the 2nd and 3rd metacarpelphysial joints
HIPs and KNEES
#Hypogonadism - loss of labido, mensus, impotence
#hypothyoid
#hyperpigmentation of skin
95b
Complications of UC
96a
1. IDA
2. Hemorrhage
3. Lytes and h20
4. Structures, benign, malignant usally malignant
5. Colon ca- increas risk
6. Cholangiocarcinoa (half of all biles duct CA are
associated with UC)
7. Sclerosing cholngitis
8. Toxic mega
9. MR
96b
Complications with
CHRONIC
pancreatitis:
97a
1. Narcotic addiction - most common complication
2. DM/impaired glucose tolerance
3. Malapsorption/steatorrhea
4. Pseudocyst formation
5. Pancreatic ductal dilitation
6. CBD obstruction (2/2 to fibrosed portion in head
of gland)
7. VItamin B12 malabsorption
8. Effusions (pleural, pericardial, peritoneal)
9. Pancreatic carcinoma (increased risk)
97b
COMPLICATIONS
WITH CROHNS!
98a
1. fistula between colon and other
segments of intestine (enteroenteral),
bladder, and vagina and skin.
-anorectal dz in 30% pateints - fissues,
abscesses, perianal fistulas
-SBO 20-30%
-malignancy
-
98b
Considerations with acute
bacterial sinusitis that
recurs?
99a
1. Inadequate course of therapy
2. Concurrrent allergic rhinitis
3. Anatomic abnormalities that block ostia
4. undiagnosed immundeficiency states
-cystic fibrosis
-common variable immunodeficiency
-immotile cilia syndrome (karteganer's)
99b
Crohns disease
100a
1. chornic TRANSMURAL inflammatory dz that
affects any parrt of GI mouth to ANUS ubt most
commonly involves small bowel at terminal ileum
2. three major patterns: 1-40% have disease
at ileum and cecum. 2-30% of patients have
disease confined to small intestine. *3 25%
patients have disease at colon ONLY
100b
Crohns disease has a chroni, indolent
course characterized by unpredictable
flares and remissions. The
effectiveness of medical treatment
will ____ with advaning disease and
complications eventually develop
requiring surgery.
101a
decrease
101b
CROHNS v. UC
102a
CHRONS: involves transmural wall from mucosa to
serosa; discontinous with skips
UC: mucosa and submucosa
CD: termianl ileum most commmon but can involved
any part of GI
UC: colon and rectum - starts at rectum nd goes up
CD: fistula and abscesses
UC: SC and colorectal CA
102b
Dark urine and pale
stools signal a
diagnosis of?
103a
CONJUGATED
HYPERBILIRUBINEMIA
103b
Decreased liver syntheic function will
cause a decrease in serum albumin
concentration and an increase in INR
(why?) Hypoalbuminemia can contribute
to edemain end stage liver disease.
104a
because the liver produces albumin
and clotting factors. If clotting
factors are low, then PT and PTT
times will take longer and the INR
will be hypercoaguable because
there are minimal being produced
104b
Diagnos gastric CA
Stage gastric CA
105a
Endoscopy with
multiple biopsies
Abdominal CT
105b
Diagnosis for UC
106a
1. Stool culture for cdiff ova
parasits
2. fecal leukocytosis
-WBCs can appear in UC
ischemic colitis or infectious
disease
106b
Diagnosis of
ACHALASIA
107a
Dx: barium swallow ("birds beak") beak-like
narrowing of distal esophagus and a alrge, dilated
esophgus proximal to the narrowing
dx: UPPER GI endoscopy to r/o secondary causes of
achalasia (gastric carcinoma) and retention
esophagitis or esophageal CANCER
dx: manometry to confirm the dz; reveals failure of
LES relaxation and aperistalsis of esophageal body
107b
Diagnosis of acute
cholangitis versus
other biliary tract
issues?
108a
1. RUQ US is the initial study
2. Lab: hyperbilirubinemia, leukocytosis, mild
elevation in ALT/AST
3. Cholangiography (PTC or ERCP) - definitive test
but not perfrmed during the acute phase of illness.
Once resolved, then proceed with PTC or ERCP.
PTC before ERCP when the duct system is dilated
(per US) and use ERCP when the duct system is
normal
108b
Diagnosis of
appendicitis:
109a
acute appendicitis is a clinical diagnosis
-lab: leukocytosis
-imaging: CT scan (lowers false postivie rate
significantly)
Ultrasound
109b
diagnosis of
cholangiocarcinoma
110a
1. PTC/ERCP for diagnosis and
assesssment of resectability
2. IF patient has an unresectable tumor
(more likely the case with proximal than
distal bile duct tumors) - stent placement
is an option during PTC or ERCP to relieve
the obstruction
110b
Diagnosis of
choledocholithiasis:
111a
Order CMP with LFTS:
1. Labs: total and direct bilirubin
levels are elevated and ALK-P
2. RUQ ultrasound usually intial
study but will perform ERCP as the
gold standard
3. PTC is an alternative to ERCP
111b
Diagnosis of chronic
pancreatitis:
112a
CT scan is the initial study of choice - shows calcifications not seen
on plain film. Mild to moderate cases may not be detectable, so a
normal CT scan doesnt rule out chronic pancreatitis.
Abdominal radiographs: pacreatic calcification = 99% specific but
only found in 30% of cases
ERCP is the GOLD STANDARD but not done routinely because of its
invasiveness
Lab studies not helpful because serum amylase and lipase levels
arent elevated in CHRONIC pancreatitis
112b
Diagnosis of crohns
113a
-diarrhea (nonbloody)
-malabsorption and weight loss
-abdominal pain RLQ n/v
-fever malaise
-extraintestinal manifestiations in 15% - uveitis,
arthritis, anklosing SpA, erythema nodosum,
pyoderma gangrenosum, aphthough oral ulcers
cholelithiasis and neprholithiasis
113b
Diagnosis of crohns
114a
endoscopy (sigmoidoscopy or colonoscopy) with
BIOPSY - typical findings are apthous ulcers,
cobblestone appearance, pseudopolyps, patchy
skip lesions
barium enema
upper GI with SBfollow through
114b
DIAGNOSIS OF
ESOPHAGEAL
HIATAL HERNIA
115a
barium swallow
115b
Diagnosis of gastric
CA
116a
Endoscopy with multiple biopsies is the most
accurate!
-barium upper GI series less accurate but can
completment upper endoscopy biopsy findings
-abdominal CT scan to stage and detect mets
-FOBT
116b
Diagnosis of HCC
117a
Liver biopsy - required for definitive diagnosis
-lab tests (hepatitis B and C serology, LFTs,
coagulation tests
-imaging studies: US, CT scan (chest abdomen pelvis;
MRI/MRA if surgery is an options because they
provide more detail about anatomy.
-tumor marker elevation of AFP is useful as a
screening tool. AFP level may be elevated in 40-70%
of patients with HCC and is also helpful in
monitoring response to therapy.
117b
Diagnosis of
PANCREATIC CA:
118a
ERCP most sensitive test to distinguis CA of head
of pancreas from tumors of the ampulla and
lymphomas.
CT scan is the perferred test for diagnosis and
assessment of DISEASE SPREAD
tumor markers: CA19-9 (83 sensitivity nd 82
specificity) CEA (sensitivity of 56% and
specificity 75%)
118b
Diagnosis of
PBCirrhosis:
119a
1. Laboratory findings - cholestatic LFTs (elevated ALKphos)
-positive antimitochondrial antibodies (AMAs) found i n90% to
95% of patients
-this is hallmark of the disease (specificity) of 98%; if serum is
positive for AMAs, perform liver biopsy to confirm diagnosis
-elevated cholesterol, HDL
-elevated immunoglobulin M
2. Liver biopsy - percutaneous or laparacopic to confirm ddx
2. Abdominal US or CT scan to rule out biliary obstruction
119b
Diagnosis of
pseudomembranous
colitis
120a
C. diff toxins in stool is diagnostic but
results take at least 24 hours (95%)
sensitivity
-flexible sigmoidoscopy is most rapid test
and is diagnostic but not frequently done
-abdominal radiograph to r/o toxic
megacolon and perforation
-leukocytosis
120b
Diagnosis of SBO
1. Abdominal plain films (DILATED LOOPS OF
SMALL BOWEL WITH AIR DLUID LEVELS
PROIMAL TO POINT OF OBSTRUCTION ON
UPRIGHT FILM AND MINIMAL GAS IN
COLON *if complete SBO
What 2 other tests?
121a
1. Barium ENEMA - to rule out colonic
obstruction if plain film do not distinguish
small from large bowel obstruction;
barium enema identifies sites of
obstruction
2. Upper GI series with small bowel
follow-through if above are not diagnosed
121b
Diagnosis of UC
(perform these
studies)
122a
1. Stool cultures for
cdiff, oca, parasites to
rule out infection
122b
Diagnosis regarding
esophageal CA
123a
Barium swallow - useful for dysphagia
-UPPER endoscopy with biiopsy and brush
cytology is required for deinitive diagnosis. It
confirms the diagnosis in 95% if cases
-TEE US to determine the depth of penetratoin of
the tumor *most reliable to test staging of local
CA
-full metastatic workup (CT scan of
chest/abdomen, CXR, bone scan)
123b
Diagnostic test of choice for
diverticulosis (LLQ,
painless rectal bleeding,
constip/diarrhea) and
bloating)
124a
Barium enema is the test of
choice
-abdominal xrays are
usually normal and are not
diagnostic for diverticulosis
124b
Diseases of the
appendix:
Acute appendicitis:
125a
Lumen of the appendix is obstructed by:
1. Hyperplasia of lymphoid tissues (60%)
of cases
2. Fecalith (35% of cases)
3. Foreign body
4. PARASITE/CARCINOID TUMOR
(other rare causes)
125b
Diseases of the esophagus:
Two types of esophageal
cancer?
126a
SCC and
Adenocarcinoma
126b
Diverticulitis can occur in 15-25% of
all patients with diverticulosis
however this is not always a
precedent of diverticulitis.
Pathophysiology of diverticulitis?
Diagnostic examinations?
127a
1. Occurs when the feces become impacted in the diverticulum, leading to
erosion and microperforation
2. Clinical features; fever, LLQ pain, leukocytosis (elevated WBC); alteration in
bowel habits, vomiting, sometimes a painful mass on rectal exam if
inflammation is near the rectum.
Diagnostic tests for diverticulitis:
1. CT scan of abdomen and pelvis with ORAL and IV contrast is the test of
choice
-reveals a swollen, edematous bowel wall or an abscess.
2. Abdominal radiographs help in excluding other potential causes of LLQ pain
that can rule out obstruction or ileus.
3. Barium enema and colonoscopy are contraindicated in ACUTE
DIVERTICULITIS due to the risk of perforation
127b
Diverticulitis recurs in about --
% of pateints treated medically,
usually within the first 5 years.
Lower GI bleeding is RARE in
diverticulitis but common in
diverticulosis.
128a
30%
128b
Duodenal ulcer differs
from gastric ulcer in
what ways?
129a
1. Duodenal: by an increase in offensive factors (higher rates of basal and stimulated gastric acid secretion). H.
pylori in 70-90% of patients. LOW MALIGNANCY; majority are located within 1-2cm distal to pylorus usually on
posterior wall. Age is YOUNGER (<40). BLOOD TYPE O. Risk factors includes NSAID use. Other - eating usually
relieves pain and NOCTURNAL pain is more common than in gastric ulcers.
2. Gastric ulcers - caused by decrease in defensive factors (gastric acid level is normal) low unless ulcer is pyloric or
prepyloric. H. pylori infection in 60-70%. HIGH LEVEL MALIGNANCY - must undergo biopsy to rule out
malignancy). Location:
Type I: most common - 70% on lesser curvature
Type II: gastric and duodenal ulcer
Type III: Prepyloric (within 2 cm of pyloris)
Type IV: near esophagogastric juntion
Age distribution occurs in older patients (>40). BLOOD TYPE A. RIsk factors smoking. Eating does not usually
relieve pain. Complication rates are higher than those of duodenal ulcers. There is a higher recurrence rate with
medical therapy alone.
129b
EMPIRIC THERAPY
FOR SKIN AND SOFT
TISSUE INFECTION
(SSTI)
130a
Depending upon clinical setting/features
-risk of CA-MRSA: TSX, clinda or minocycline
-Cat bite: augmentin
-DM foot ulcer: cipro/clinda
-noncholera vibrio: doxy
-erysipelas: PCN or amoxicillin
If hospitalized (IV)
-MRSA: Vanc (or linezolid or dapto)
-Cat bite: Unasyn
-DM infectoin: ERTAPENAM
130b
Empiric treatment for
cat bite?
131a
Augmentin
131b
Empirical treatment
for CA-MRSA:
132a
TSX, clinda, mino
132b
EPIGASTRIC abdominal pain that
radiates to the back in 50% of
patients that is often steady, dull, and
severe that gets WORSE WHEN
SUPINE and POSTPRANDIALLY.
Diagnosis?
133a
Acute pancreatitis
133b
EPIGASTRIC PAIN that is
aching/gnawing in nature with
NOCTURNAL SYMPTOMS and the
EFFECT OF FOOD ON SYMPTOMS
is present.
+/- Upper GI bleeding
134a
PUD
134b
Esophageal
Diverticula
135a
Most esophagel diverticula are
caused by an underling motility
disorder of the esophagus:
1. Zenkers diverticulum
2. Traction diverticulum
3. EPiphrenic diverticula
135b
Esophageal hiatal
hernia has two main
types:
136a
Two main types:
1. Sliding
2. Paraesophageal
hiatus
136b
Esophageal
manometry is
diagnostic -
137a
simultaneous, multiphasic,
repetitive contraction that
occur after a swallow;
spinhicter response is
normal
137b
Esophageal/gastric varices are a
complication of cirrhosis. What
are the clinical findings? How is
it diagnosed and how is it
treated?
138a
1. Massive hematemesis, melena, exacerbation of
hepatic encephalopathy; esophageal >90% and
gastric >10%.
2. Diagnosis emergeent upper GI endoscopy once
patient is stabilitys if patient presents with
hematemesis.
3. Initial treatment: FLUIDS to maintain BP and get
hemodynamically stable
4. 2/2: administer BB as LT therapy to prevent
rebleeding.
138b
Etiology of biliary cirrhosis -
this disease occurs in response
to chornic biliary obstruction
from the following:
139a
1. Long-standing
mechanical obstruction
2. Sclerosing cholangitis
3. Cystic fibrosis
4. Biliary atresia
139b
Factors increasing
mortality of GI
bleeding
140a
>65YO, severity of initial bleed
extensive comorbid illnesses
onset or recurrency of bleeding while hospitalize
for another condition
need for emergency surgery
transfusion requiresments
diagnosis (esophageal varices have a 30%
mortality rate)
endoscopic stigmata of recent hemorrhage
140b
Familial juvenile
polyposis coli
141a
RARE = in childhood; only
small risk of CRC
-more than 10 and up to
hundred of juvenile colon
polyps.
141b
Focal nodular
hyperplasia
142a
benign liver tumor without malignant
potential that occurs in women of
childbearing years with NO
assciaation with oral contraceptives
-usually asymptomatic. Hepatomeg
present
142b
For diverticulosis - test
of choice?
For diverticulitis - test
of choice?
143a
1. Barium enema
2. CT scan (barium
enema is contraindicated
2/2 to acute bleeding)
143b
Forceful dilation and
what other surgical
methods can treat but
NOT CURE achalasia?
144a
Forceful dilatation - mechanical, pneumatic, or hydrostatis
a. pneumatic balloon dilatation is most effective
b. Lowers basal LES tone by distrupting the muscular ring
c. Can be effective but there is a 5% risk of performation
Surgical
a. "HELLER MYOTOMY" - circular muscle layer of LES is
incised
b. usually reserved for patients who do not respond to
dilation therapy
144b
Gastric lymphoma
145a
A type of NHL that
arises in the stomach
145b
Gastric lymphoma
146a
NHL in stomach with features similar to those of
adenocarcinoma of the stomach however
includes bleeding, obstruction and perforation.
-EGD is standard diagnosis - same as
adenocarcinoma of stomach.
-treatment depends upon the stage of the disease
and complications
146b
GGT is often used to confirm
that the elevated ALK-P is of
hepatic origin
T or F
147a
True
147b
GI bleeding
1. Upper GI bleeding
v. Lower GI bleeding
148a
UPPER GI bleeding: source of
bleeding above the ligament of
trietz
LOWER GI BLEED: source of
bleeding below the ligament of
trietz
148b
GI bleeding is a
complication
associated with PUD:
149a
bleeding may be slow (anemic symptoms) or rapid
and severe (leading to shock)
Dx studies: STOOL GUIAC, UPPER GI ENDOSCOPY
Resuscitation: daignose site of bleed via endoscopy
and test: performatm surgery for acute bleeds that
require transfusion of >6U
-most common cause of upper GI bleeding is 2/2
149b
Gilbert's syndrome
Characteristics:
Findings:
Treatment:
150a
Occurs in 7% of population-autosomal dominant condition in
which there is decreased activity of hepatic uridine diphosphate
flucuronyl transferase activity (UDP transferase);
DIAGNOSIS: MOST COMMON CAUSE OF ISOLATED
ELEVATION IN UNCONJUGATED BILIRUBIN. +/- jaundice
NO TREATMENT NECESSARY AND LIVER BIOPSY RESULTS
ARE OFTEN NORMAL.
150b
Gray turners sign,
cullens sign, foxs sign
=
151a
ACUTE
PANCREATITIS
151b
HCC is likely in a patient with
cirrhosis who has a palpable
liver mass and elevated AFP:
T or F
152a
T
152b
Hematemesis
153a
vomiting blood;
suggest uper GI
bleeding
153b
Hematochezia
154a
bright red blood per rectum
-represents lower GI source
(LEFT COLON OR RECTUM)
-consider diverticulosis,
arteriovenous malformations,
hemorrhoids, and colon CA
154b
Hemochromatosis v.
Hemosiderosis?
155a
Hemochromatosis: common AR disease in US homozygous for C282Y on chromosome
6. Causes increase intestinal iron absorptino with elevated accumulation of iron in the
liver, pancreas, heart adrenals tests pituitary kidneys joints and skin. Disease onset is
after age 50 with nonspecific symptoms in early stages. Later signs include
arthropathy, hepatomegatly, skin pigmentation and cardiac enlargement, DM and
impotention. Patients WILL DEVELOP HEPATIC AND PACNREATIC
INDUFFICIENCY with possibly CIRRHOSIS and HCC, CHF, and hypogonadism.
Lab findings will be elevated LFTs with elevated plasma iron and increase 50% sat of
TIBC and elevated ferritin.
Hemosiderosis is the deposition of excessive iron in the tissues. This is caused by a
variety of inherited metabolis disorders or by environmental exposures to iron
containing substances and is therefore NOT considered to be a distinct disease entitiy.
155b
Hemochromatosis:
156a
Autosomal recessive disease of iron absorption-
-escessive iron absorption in the intestine leads to
ncreased assumulation of inro (as ferritin and
HEMOSIDERIN) in varous organs. Over years,
fibrosis isn involved organs will occur seoncdary
to OH free radials generated by excess iron
156b
Hemorrhagic
pancreatitis is another
complication of acute
pancreatitis:
157a
Cullen's sign (periumbilical bleeding)
Grays sign (flank ecchymoses)
Fox's sign (inguinal ecchymoses)
CT scan with TV contrast is the study of
choice
157b
Hepatic abscess is the
most serious complication
of acute cholangitis with a
HIGH _____ _____
158a
mortality rate
158b
Hepatocellular
adenoma
159a
benign liver tumor seen in females 15-40YO 2/2
OCP use, anaboli steroid use with RUQ pain or
fullness.
diagnose with CT scan, US
Treatment: d/c OCP; surgically remove tumors
>5cm that do not regress s/p OCP d/c
159b
Hepatocellular CA accounts for >
80% of primary liver CA and
although rare in US, accounts for
most deaths 2/2 cancers world wide.
Highest in Africa and asia.
What are the two pathologic types?
160a
nonfibrolamellar
carcinoma
fibrolamellar carcinoma
160b
HIGH fat and LO
FIBER diets increase
the risk of?
161a
CRC
161b
HNPPCRC - without
adenomatous
polyposis
Lynch I v. Lynch II
162a
Lynch syndrome I: site specific CRC - early
onset CRC without multiple polyposis
Lynch syndrome II: cancer family
syndrome - all features of lunch 1 plus
increased number and early occurrence of
other cancers (female genital tract, skin,
stomach, pancrea, brain, breast, biliary
tract).
162b
How are CIRRHOTIC
patients managed
LONGTERM?
163a
1. Periodic lab values 3-4 months (CBC,
CMP, RFTs, LFTs, coagulation tests)
2. Perform an endoscopy to determine the
presense of varices
3. If hepatocellular carcinoma is suspected
then perform a CT guided biopsy for
diagnosis
163b
How do signs and
symptoms change in
relation to the effected
side of colon (right v. left)
164a
Right sided colon tumors:
-obstruction is unusual because of the larger luminal
diameter (the cecum has the largest luminal diameter
of any part of the colon that often allows for tumor
growth to go undetected.
-common finding is occult blood in stool , iron
deficiency anemia and MELENA (BLACK STOOL)
-change in bowel habits is uncommon
-triad of anemia, weakness, RLQ mass (occasionally)
is present
164b
How does
cholangiocarcinoma
differ from carcinoma
of the gallbladder?
165a
This is a tumor of the intrahepatic or
extrahepatic bile ducts: most adenocarcinomas
-7th decade diagnosis
-located in three regions: (1) proxmial 1/3 of
CBD, (2) distal extrahepatic, (3) intrahepatic)
-most likely to be resected is distal and least
likely is intrahepatic.
165b
HOW does CRC
spread?
166a
Direct extension - circumferencially and then through
the bowel wall to invade other abdominal organs.
hematogenous
-portal circulation to the liver, liver is the most
common site of distant spread
-lumbar/vertebral veins to lungs
-lymphatic (regionally)
-transperitoneal and intraluminal
166b
How does DES
(diffuse esophageal
spasm) differ from
achalasia?
167a
DES - nonperistaltic sponaneous contraction of the
esophageal body - several segments of the
esophagus contract simultaneously and prevent
appropriate advancement of food bolus
ACHALASIA - spincter function is normal (normal
LES pressure)
167b
How does hyperestrinism
result in patients with
CIRRHOSIS of the lIVER?
168a
1. SPinder angiomas-dilated
cutaneous arteriold with central red
spot and reddish extensions that
radiate ourward like a spiders web.
2. Palmer erythema
3. Gynecomastria
3. Testicular atrophy
168b
How does PRIMARY
BILIARY CIRRHOSIS
differ from PRIMARY
SCLEROSING
CHOLANGITIS?
169a
1. Chronic/progressive/ cholestatic LD/characterised by destruction of intrahepatic bile ducts
with PORTAL inflammation and scarring - INTRAHEPATIC DUCT SPECIFIC
2. SLOWLY progressive dz with variable course can progress to cirrhosis and End stage liver
dz
3. THIS IS AUTOIMMUNE WITH ANTI-MITOCHONDIAL AB, CARDIOLOPIN - and is often
associated with other autoimmune disorders.
4. It is most common in middle-aged women
biliary cirrhosis, often abbreviated PBC, is an autoimmune disease of the liver[1] marked by
the slow progressive destruction of the small bile ducts (bile canaliculi) within the liver. When
these ducts are damaged, bile builds up in the liver (cholestasis) and over time damages the
tissue. This can lead to scarring, fibrosis and cirrhosis. It was previously thought to be a rare
disease, but more recent studies have shown that it may affect up to 1 in 3-4,000 people; the
sex ratio is at least 9:1
169b
How is ACUTE
CHOLANGITIS
treated:
170a
1. IV AB and IV fluids
-close monitoring of hemodynamics, BP and urine OUTPUT
is important
-most patients respont rapidly. Once patient stabilized -
ERCP or PTC performed for evaluation of underlying
condition.
2. Decompress the CBD via PTC (catheder drain); ERCP
(spincterectomy or laparotomy) - (T tube insertion) once the
patient is stabilized, or emergently if the condition doesnt
respond to the antibiotics.
170b
How is acute
cholecystitis
diagnosed?
171a
RUQ ultrasound is the test of choice
a. HIGH sensitivity and specificity
b. Findings include thickened gallblasdder wall, pericholecystic fluid, distended
gallbladder and presnse of stone(s).
CT Scan is as accurate as ultrasound but is more sensitive in identifying
complicatons of acute cholecystitis (performation, abscess, pancreatitis)
RADIONUCLEOTIDE scan (HIDA-hepatoiminodiacetic acid)
-used when US is inconclusive-its sensitivity and specificity paralel that of
ultrasound. If HIDA scan is normalthen acute cholecystitis can be ruled out
-positive HIDA scan means the gallbladder is not visualized
-if GB not visualized 4 hours after injection, diagnosis of acute cholecystitis is
confirmed
171b
How is budd-chiari
diagnosed?
172a
hepatic venography,
serum ascites albumin
gradient > 1.1 g/dL
172b
How is hepatic
functional reserve
assessed?
173a
Child's classification
-estimates hepatic reserve in liver failure;
it is used to measure disease severity and
is a predictor of morbidity and mortality.
-childs class C is the most severe disease
and childs class A is the least severe
disease.
173b
How is spontaneous
bacterial peritonitis
diagnosed?
174a
Estalished by paracentesis and
examination of ascitic fluid for WBCs
*especially PMNs) gram stain with culture
and sensitivies.
=WBC >500
=PMN >250
=+ ascites culture - culture neg CBP is
common
174b
How is wilsons disease
dx? How is it treated?
175a
Dx: Hepatic dz w/ elevated ALT>AST with impaired syn of clotthing factors
-decreased serum ceruloplasmin levels although ranges within normal dont
exclude dx
-liver biopsy (elevated Cu2+)
-if dx, then warn first degree relatives
Rx: chelating agents - penicillamine that removes nad detoxifies the excess
Cu2+ deposits.
-ZINC - prevent uptake of Cu2+
=liver transplantation if unresponsive to chelation + zinc
-montior Cu2+ levels, urinary copper excretion, ceruloplasmin and liver
function: phsycial examination for isgns of liver or nerologic disease -
psychological health
175b
HOw long might it
take a pancreatic
abscess to form in
acute pancreatitis?
176a
Although RARE< will
occur 4-6 weeks post
acute pancreatitis
176b
How might colonic
volvulus be
diagnosed? What are
the two types?
177a
Colonic volvulus can most commonely be in the sigmoid colon 75%
or the cecum 25%.
-cecal volvulus most commonly occurs in younger population. Cecal
due to lack of right colonic fixation to retroperitoneam.
Diagnosis:
1. Plain abdominal film: sigmoid looks like an omega loop; cecal
looks like coffee bean.
2. Sigmoidoscopy preferred diagnosetic and therapeutic test for
sigmoid volvulus (NOT SECAL!); leads to successful treatment in
many cases.
177b
How might HIDA
diagnose that of acute
cholecystitis? When is
it superior to an US?
178a
HIDA - radionuclide scan - hepatoiminodiacetic
acid) is used to diagnose inflammation of the GB
when US is inconclusive. If the scan is normal,
then acute cholecystitis can be ruled out. If the
test is positive then the GB cannot be visualized 4
hours after injection, diagnosis of acute
cholecystitis is confirmed
178b
How might one
determine whether or
not a polyp is
malignant?
179a
1. Size (the larger the polyp, the
greater the malignant potential)
2. Histologic type
3. Atypia of cells
4. Shape (sessile-flat, more likely to
be malignant) versus pedunculated
(on a stalk)
179b
How might PUD be
diagnosed?
180a
Endoscopy is the most accurate. Essnetial in
diagnosis of gastric ulcers because a BIOPSY is
req to rule out melignancy of duodenal ulcers do
not require biopsy bc dec likelihood.
-preferred when severe or acute bleeding is
present (can perform electrocautery of bleeding
ulcers) - biopsy can also be taken for H. pylori
test if gastric also.
180b
How should
JAUNDICE be
evaluated?
181a
Initial step:
--> Hx, PE, LABS: ALT, AST, Bilirubin, ALKPHOS, ALBUMIN, PT
If normal LFTs (ALT, AST, ALKPHOS, albumin, PT)
-->conjugated hyperbilirubinemia
-DJ syndrome/rotors syndrome
-->unconjugated hyperbilirubinemia
-see test for differential; hemolysis and gilberts syndrome most common
If abnormal LFTS (intrahepatic issue)
-->suspected intrahepatic disease based on LFT
-viral seriology/AMA/ANA/SMA/cerruloplasmin/Fe-TIBC/AAT
-STOP drugs
-consider liver bx
-consider CT scan to r/o structureal dz
-medical management v. observation
-ducts will be normal
-->suspected extrahepatic obstruction
-noninvasive imaging (US/CT)
a. Normal ducts
b. Normal ducts but suspecte extrahepatic cholestasis
c. Dilated ducts
i. Direct duct visulaization - ERCP or PTC
--> if seen, then relieve obstruction
(surgically, endoscopicallly, percutaneously)
181b
Hundreds of adenomatous polyps in
the clon, the colon is always involved
and the duodenum is involved in
90% of cases . Polyps may also form
in the stomach, jejunum and ileum.
This is an autosomal dominant d/o
182a
FAP
182b
Hypo or
hypercalcemia results
from acute
pancreatitis?
183a
HYPOcalcification is due
to fat saponification: fat
necrosis binds to
calcium
183b
IDSA/SHEA Tretment
recommendations for
C. Diff Acute Diarrhea
(CDAD)
184a
Mild-moderate:
-(WBC<15k, crt WNL/unchanged)
-drugs: metronidazole 500 po 10-14d
Severe uncomplicated
-(WBC >/= 15K or inc serum creat; >50% baseline preCDAD
-drugs: Vancomycin 125mg po or via NGT qid 10-14day
Severe complicated
-(WBC>above criteria with dec BP or shock, megacolon, perforation or severe colitis on CT)
-if NO ILEUS: Vancomycin 500mg po qid + metronidazole 500-750mg IV Q8hr
-if ILEUD: Vancomycin 500 mg via NGT or po + Metronidazole 500-750 IV Q8 + Vanc
enema
First recurrance: same as initial episode
Second or further: PO vanc taper or pulse
184b
if a patient presents with peritoneal
fluid excess with exertional dyspnea.
What is likely the cause of the
patients distended abdomen and
edema if a paracentesis shows an
albumen level of 2.5 and a blood
study shows an albumin of 3.8?
185a
SAAG - serum albumen ascites gradient
serum albumin - ascites albumin = 1.3
therefore because it is greater than 1.1, we
can denote his cause to portal HTN
185b
If a patient with GERD also
has a diatal hernia, the
hernia often wrosens the
symptoms of GERD - T or F
186a
T
186b
IF a PEPTIC ULCER is
uncomplicated, then a _____
_____ or ______ is not needed
initially. Initiate empiric therapy. If
you suspect any complications of
PUD, order confirmatory testss
187a
barium swallow,
endoscopy
187b
If ALT and AST levels
are mildly elevated
(low hundreds), think
of what diagnosis?
188a
Chronic viral hepatitis
or acute alcoholic
hepatitis (AST < 500)
and (ALT < 300)
188b
IF ALT and AST levels
are moderately
elevated (Low
hundreds) think of?
189a
acute viral hepatitis
189b
IF AST and ALT are
severely elevated (>10,000)
extensive hepatic necrosis
has occured. This includes:
190a
1. Ischemia
2. Shock liver (prolonged
hypotension or circulatory
collapse)
3. Acetominophen toxicity
4. Severe viral hepatitis
190b
If prolonged PT -
191a
advanced liver disease
191b
If there is not hemolysis,
isolated hyperbilirubinemia
(unconjugated) may indicate
_______ syndome which is
assymptomatic and requires no
rx.
192a
Gilberts
192b
In acute pancreatitis:
1. Serum amylase:
2. Serum lipase:
3. LFTs:
4. Hyperglycemia/hypoxemia/leukocytosis:
5. Order the following for assessment of
prognosis:
"ransons criteria"
193a
1. Amylase = most common tests but many
conditions cause hyperamylasemia and its absense
doesnt rule out acute pancreatitis. If levels are >5x
NL then highly specific for acute pancreas.
2. Lipase = more specific for pancreatitis than
amylase
3. LFTs - to identify cause (gallstone pancreatitis)
4. Glucose, Ca@+. hct, BUN, ABG, LDH, WBC
count
193b
In cholelthiasis, biliary colic can
lead to acute ________.
In choledocholithiasis, onset of
symptoms leads to _____
and/or ______ which are life
threatening causes.
194a
Acute cholecystitis (obstruction of
the GB leading to inflammation -
not due to infection).
Acute pancreatitis or
CHOLANGITIS
194b
In patients with CIRRHOSIS (fibrosis
of liver tissue), the ALT/ASTs are
____ or ______ or meatstatic liver
disease because the number of ealthy
functioning hepatocytes are markedly
decreased.
195a
normal to low
195b
In patients with GI
bleeding, always ask if
taking >>>>, >>>>,
>>>> po, prn.
196a
NSAIDS, ASA,
anticoags
196b
Incidence of CRC at
20 years with UC is?
At 30 years?
197a
CRC + UC at 20 years
- 5-10%
CRC + UC at 30 years
-12-20%
197b
Increased capillary
permeability is the
mechanism by which
_____ ascites forms.
198a
exudative
198b
Increased glomerular filtration
pressure will increase
glomerular _____ rate and
decrease the serum ______
concentration. This will NOT
cause ascites
199a
filtration
creatinine
199b
Indication for sinus
aspiration 2/2
bacterial sinusitis
(acute)
200a
-associated with intracranial complications
(empyema, meningitis, brain abscess)
-sinusitis in the immuncompromised host
-sinusitis that fails to respond to a
"readonable course" of "appropriate" ATB
reaction
200b
Inflammatory bowel
disease (IBD)
201a
1. Regional enteriritis
(CROHNS DZ)
2. Ulcerative enteritis
201b
Inflammatory bowel
disease v. CRC
202a
Both UC and Crohns
increase risk, but
UC>>> than crohns
202b
Initial empirical
therapy for CA-P
203a
Outpatient: if healthy without recent ATB: treat with
macrolide or doxy; if recent ATB then use FQ or
macrolide+amox
Comoribitidies - no recent ATB : adv macrolide or FQ; recent
ATB treatment FQ or Adv macrolife + b-lactam
Inpatient: 3rd gen ceph + FQ or macrolide; at risk for
pseudomonas then used antipseudomonal B lactam
+AMG+FQ or macrolide or antipsydomonary b-lactam +
cipro
203b
It can be difficult to distinguish
the CHEST pain of DES from
cardiac chest pain - thus what
work up must be done?
204a
Cardiac catheterizaton to r/o ischemic
causes of chest pain, before an
esophageal cause is investigated
-then perform ESOPHAGEAL
MANOMETRY IS DIAGNOSTIC
-then perform upper GI barium swallow
204b
Laboratory testing
(NOT IMAGING OR
BIOPSY) for PUD?
205a
REQUIRED to diagnose H. pylori
1. Biopsy by endoscopy: histologic ecal of endoscopic
biopsy is gold standard.
2. UREASE detectoin via urea breathe test is the
most convenient test (Sensitivity and Specificity >
95%)
3. Serology - presense of AB to H. pyloris doesnt
indicate a CURRENT infection bc AB to H pylori can
remain levated for mo-yrs post eradication of
infection.
205b
Large bowel
obstruction:
206a
1. Causes: volvulus,
adhesions, hernias, COLON
CANCER (#1)
2. LBO v. SBO: LBO has
less fluid and lyte loss
206b
Left sided colonic
tumors and
symptoms:
207a
1. Smaller luminal diameter, signs of
obstruction are more common -
change in bowel habits more
common - alternating
constipation/diarrhea narrowing of
stools ("pencil stools")
2. Hematochezia more common
207b
LFT Pearls:
1. Cholestatis LFTS:
2. Hepatocellular
necrosis/inflammation
208a
1. markedly elevated ALK-P and
GGT; slightly elevated AST and
ALT
2. normal or slightly elevated
ALK-P and markedly elevated
ALT and AST
208b
Major differential
points of SSTI's (skin
and soft tissue
infections)
209a
Community v. Hospital acquired
-community: s aureus >>> group A
streptococci and GBS
-hospital: s aureus, GNRs, enterococci
Erythema only v. pus &/or open wound
-erythema only: strept
-pus/open wound: s aureus
209b
Mallory Weiss
syndrome
210a
MUCOSAL tear at the GE jundtion as a result of forceful
vomiting or restching. It usually occurs after repeated
episodes of vomiting but it may occur after one episode
-most commonly associated with binge drinking in
alcoholics but any isorder that causes vomiting can induce
the musocal tear
210b
Management of
uncomplicated UTI
(acute)
211a
1-2 recurrences per year
-intermittent self treatment (educable, typical sxs)
-TSX, TMP, FQ x 3 days
>2 recurrences/yr associated with coitus
-postoital prophylaxis
-TSX, NTF, or FQ after intercourse
>2 recurrentces without coitus
-continuous prophylaxis (95% reduction)
-TSX, TMP, NTF, F! qhs x 6 mo
211b
Manifestations of strangulated bowel
in SBO includdes fever, severe and
continuous pain, hematemesis,
schock, gas in bowel wall or PV,
adbominal free air, peritoneal signs
and _____. Will check _____
_____ to see if gut ischemia present
212a
acidosis, lactice acid
increased
212b
Melena
213a
-black tarry lquid foul smelling stool
-caused by depradation of hgb by bacteria in teh colon; presense of
melena indicates that blood has remained in the GI tract for several
horus
-the further the bleeding site fom retum, the more likely melena will
occur
-note that dark stools can also result from BISMUTH, IRON,
SPINACH, CHARCOAL, LICORICE
-melena sugests upper GI bleeding (esophagus, stomach,
duodenum) - occasionally the jejunum or ielum is source but usualy
if caused but colonic lesions - but if so then the ASCENDING
COLON is the most common colonic location
213b
Metabolic activity post
SBO?
214a
Hypovolemia,
tachycardia, hypotension,
teachypnea, AMS,
oliguira
214b
Metastasis of
GASTRIC carcinoma
215a
1. Krukenberg's tumor: metastasis to ovary
2. Blumer's shelf: metastasis to rectum
3. Sister Mary Josephs node: met to
periunbilival lymph node
4. Virchows node - metastasis to the
supraclavicular fossa nodes
5. Irish's node (metastasis to the left
axillary adenompathy
215b
METASTATIC
WORKUP REQUIRES
WHAT IMAGING
STUDIES:
216a
CT CHEST
CT ABDOMEN
CXR
BONE SCAN
216b
Most common cause of LOWER GI
BLEED IN PATIENTS < 60YO?
Most COMMON cause of LOWER
GI BLEED in PATIENTS > 60YO?
217a
Angiodysplasia if
>60YO
Diverticulosis if
<60YO
217b
Most common causes
of ACUTE
pancreatitis:
218a
1. ALCOHOL
2. GALLSTONES
218b
Most common type of
tumor within the
intra/extra hepatic
bile ducts
219a
KLATSKIN's TUMOR
-tumors in proximal third of the CBD
- involve the junction of the right and
left hepatic ducts with very POOR
prognosisbecausethey are
unresectable.
219b
Most patients with acute pancreatitis
have mild to moderate disease, but to
up 25% have severe disease
What are the causes of acute
pancreatitis:
220a
1. Alcohol abuse (40%)
2. gallstones (40%) - galllstone passes into the bile duct and blocks the ampulla
of vater
3. post ERCP - pancreatitis occurs in up to 10% of patients undergoing ERCP
4. VIral infections (mumps or COXSACKIEBVIRUS)
5. Drugs (sulfonamides), HCTZ, ferusemide, estrogens, HIV medications, and
many other drugs have been implicated
6. Post operative complications (HIGH MORTALITY RATE)
7. Scoprion bites
8. Pncreas divisum
9. Pacnreatic CA
10. HyperTG hyperCa
11. uremia
12. blunt abdominal trauma (most common cause of pancreatitis in children)
220b
Most sensitive and
specific test for CRC
221a
Colonoscopy
221b
Multiple hamartomas that may be
scattered through the GI tract that
cause pigmented spots around the
lips, oral mucosa, face, genitalia and
palmar surfaces. These are very low
malignant potential. Intussesception
or GI bleeding may occur.
222a
Peutz Jeghers
222b
Murphys sign v. BOAS
sign
223a
Murphy's sign: RUQ pain, inspiratory
arrest during deep palpation of RUQ,
not present in many causes) - fever
and leukocytosis - cholecystitis
BOAS sign - right should pain 2/2
that of gall stone - cholelithiasis
223b
NASH histologically is
identical to patients with
____ liver disease, but these
patients do not usually have a
history of substance abuse.
224a
alcohol
224b
Nasogastric tube and
diagnosis of GI
bleeding>
225a
Initial procedure for determining whether GI bleeding is an upper or
lower GI source
-use the NG tube to empty the stomach to prevent aspiration
-false negative findings are possible if upper GI bleeding is
intermittent or from lesion in the duodenum
-evaluation of aspirate
-bile but no blood --> UPPER GI BLEED UNLIKELY; source
probable distal to lig of trietz
-BRIGHT red blood or "coffee" grounds appearance - upper GI
bleeding
-nonbloody aspirate (clear gastric fluid) - upper GI bleeding unlikely
but cannot be ruled out definitively (source may possibly be in the
duodenum)
225b
nonfibrolamella
carcinoma of the liver:
226a
(most common HCC) - usually associated with
hepatitis B or C and cirrhosis. Unresectable with
very short survival time (months)
Fibrolamellar - usually not associated with hepa
B and C; is resectable; relatively llonger survival
timel seen most commonly in adolescenets and
young adults.
226b
Occult blood in the
stool
227a
source of bleeding can
be anywhere along the
GI
227b
ORGANS effected by
Wilsons dz v.
Hemochromatosis
228a
Kidney, liver, cornea = wilsons
liver (primary), pancreas,
heart, joints, skin, thyroid,
gonads, hypothalamus = hemo
228b
Pacnreatic ascites/pleural
effusion is the MOST COMMON
CAUSE OF INFLAMMATION of
the PERITONEAL SURFACE.
TRUE/FALSE?
229a
TRUE!
229b
Pain in acute cholecystitis is 2/2
gallbladder wall inflammation
whereas pain in biliary colic is 2/2?
230a
contraction of the gallbladder
against the obstructed cystic
duct. ALso the pain of acute
cholecytitis persists for several
days whereas the pain of biliary
colic lasts only a few hours.
230b
PAINLESS
JAUNDICE IS NOT A
COMMON FINDING
IN _________ CA
231a
PANCREATIC
231b
Pancreatic cancer -
what are the general
characteristics?
232a
Elderly (75% > 60YO); rare before
40YO; common to AA
Location: Pancreatic head (75%);
pancreatic body (20%); pancreatic
tail (5-10%)
232b
Pancreatic necrosis is a complication
of ACUTE pancreatitis. What are the
two main types of necrosis:
1.
2.
233a
1. Sterile pancreatic necrosis and
infected pancreatic necrosis differ
by a CT GUIDED
PERCUTANEOUS ASPIRATION
WITH A GRAM STAIN/CULTURE
OF ASPIRATE
233b
Paraesophageal hernias tend to
enlarge with time, and the entire
stomach may ultimately move into
the _____. Type 3 hernias
(combination of type 1 and 3) are
treated as type _____ surgically.
234a
thorax
type 2
234b
Paraesophageal hiatal
hernia accounts for
<5% of cases. Describe
dx
235a
The stomach herniates into thorax through
the esophgeal hiatus but the GE junction
doesnt, it remains below the diaphragm.
THis uncommon hearnia can become
strangled and should be repaired
surgically
235b
Paralytic ILEUS
236a
peristalsis is decresd or absent without mechanical obstruction
-resolves with time or when the cause is adddresed medically -
surgery is not usually needed.
CAuses: medications (narcotics, anticholinerguc effects) post
operative state, spnal cord injury, shock, metabolic disorders
(espcially hypokalemia) and eritonitis
-abdominal plain filmss show a unifrom distribution of gas in small
bowel, colon and rectum
-failure to pass contrast medium byuond fized point is diagnostic.
RX: FLUIDS - NPO, correcton of electrolytes; NG suction if
necessary and placeebt if long tube if ileus persists postoperatively
236b
Partial v. complete
obstruction
237a
Partial: with partial obstruction, patients are
able to pass gas or have bowel mvmts as opposed
to complete obstruction however patients with
complete obstruction may occasionally be able to
pass gas or stool because they may have residual
stool or gas in the colon
237b
Pateint with a history of AORTIC GRAFT SURGERY
who has a small bleed of GI involving the duodenum
before massive, fatal hemorrhage hours to weeks
later.
Performing an endoscopy or surgery during this small
window of opportunity to prevent death is
quinticential to survivial.
DX:
238a
AORTOENTERIC
FISTULA
238b
Pathology of Crohns
239a
terminal ileum is hallmark location but other sites of
GT tract may also be seen
-skip lesions
-fistula
-luminal strictures
-noncaseating granulomas
-transmural thicknening and infalmation *full
thickness wasll involvement)
Mesenteric: fat creeping" onto antimesenteric border
of small bowel
239b
Pathology of UC
240a
1. Uinterupted involvement of
the rectum and the colon
without skip lesions
-inflammation is not transmural
like CROHNS - here it is only
mucosal and submucosa
240b
Pathophysiology of
SBO
241a
Dehydration is a key event in SBO
-intesntinal distention causes reflex
vomiting, increased intesinal secretion
proimal to point of obstruction and
decreased absorption. This leads to
hypochloremia, hypokalemia and
metabolic alkalosis
241b
PATIENTS with colonic
distention that exceeds that of
10cm increases the risk of bowel
ruptures leading to either
peritonitis and even death -
treatment?
242a
Decompress
immediately.
242b
Patients with UC may have
______ ____ at first with
eventual progression to
bloody diarrhea
243a
nonbloody diarrhea
243b
PBC can occur
secondary to PSC
T or F
244a
TRUE
244b
Percent of women per
year diagnosed with
acute uncomplicated
UTI (cysitis)?
245a
11%
245b
Performance of surveillance
_______ in patients with
known achalasia has been
shown to detect the tumor at
an early stage.
246a
esophagoscopy
246b
Peritoneal fluid (third space) can develop
due to many causes - one of which being
portal HTN, trauma, pancreatitis and
malignancy.
How might one distinguish a diagnosis
amongst the above as the causitive agent of
the abdominal distention?
247a
1. distinguish exudative from transudative fluid
accumulation
-use SAAG which (serum ascites albumin
gradient) is calculated bysubtracting the ascites
albumin concentration from the serum albumin
concentration.
-A difference of 1.1 g/dL or greater is 95%
accurate in diagnosing a transudative process
consistent with portal hypertension.
247b
PERSISTANT OR CONTINUING
INFFLAMMATION OF THE PANCREAS WITH
FIBROTIC TISSUE REPLACEMENT OF
PANCREATIC PARENCHYMA AND
ALTERATION OF PANCREATIC DUCTS
(AREAS OF STRICTURE/DILATION);
EVENTUALLY RESULTS IN IRREVERSIBLE
DESTRUCTION OF THE PANCREAS
248a
CHRONIC PANCREATITIS
- BOTH ENDOCRINE
(INSULIN) AND
EXOCRINE (ENZYMES)
ARE AFFECTED
248b
Pigmented stones are
the second type of GB
stones that occur 2/2?
249a
Black stones found in the GB associated with
HEMOLYSIS, SCA, THALASSEMIA, HEREDITARY
SPHEROCYTOSIS, ARTIFICIAL VALVES,
ALCOHOLIC CIRRHOSIS
BROWN stones are usually found in BILE ducts
and are associated with a BILIARY tract infection
249b
Polyposis PLUS osteomas, dental
abnormalities, benighn soft tissue
tumors, desomis tumors, sebaceous
cysts. The risk of CRC is ____% by
approximately age 40.
Syndrome?
250a
100%
Gardners syndrome
250b
Porcelain gallbladder
is defined as:
251a
intramural calcification of the
gallbladder wall
-prophylactic cholecystectomy
is recommended bc 50%
becomes malignant
251b
Portal HTN as a
complication of
cirrhosis (severe liver
disease)
252a
-bleeding/hematemesis, melen, hematochezia)
2/2 esophagogastric varices is the most life-
threaning complication of portal HTN.
-diagnose based upon clincial presense of about.
paracentesis can help dx
-use transjugular intrahepatic portal-systemic
shunt (TIPS) to lower portal pressure
252b
Presentation of a young, non-obese and on-blacnk patient
with HTN should rasie suspician for ______ _______.
FUrther, lab values with severe HTN, and elevated HR with
serum chemistry levels revealing normal glucose, and
normal serum creatinine, elevated sodium and low
potassium, and a CT scan with a 2cm mass on left adrenal
gland should be indicative of?
What would plasma renin be? what would serum
aldosterone be? What would serum bicarbonate be?
253a
-secondary HTN
-primary hyperaldosteronism causes HTN, hypernatremia, hypokalemia, and
metabolic alkalosis
-excess aldosterone promotes distal tubular reabsorptin of sodum which results
in volume expansion and secretion of poassium and ydroge ions. he mass on pt
CT likelt to be adrenal adenoma. Likewise, Conn's syndrome should have
aldosterone levels and renin levels checked. Aldosterone release is regulated by
renin and therefore while aldosterone levels are increased, renin levels will be
decreased 2/2 feedback inhibition. Muscle weakness and exercise intolerance
are the result of hypokalemia
-the HIGH levels of serum bicarb are what will be present 2/2 the effect of
aldosterone on intercalated B cells. decreased K+ causes deposition of intersitial
cells and uptake of H+ ions which further increases the serum pH
253b
Primary
hemochromatosis
verus secondary
hemachromatosis?
254a
Primary - early diasnogsis and treatment
before development of complications
(primary cirrhosis ut also heart dz and
diabetes) imrpoves survival.
Secondary - iron overload 2/2 multiple
blood transfusions or in CHRONIC
HEMOLYTIC ANEMIA!
254b
Primary sclerosing
cholangitis (PSC)
-general characteristics
include:
255a
1. Chronic/idiopathhic/progressive intrehepatic or
extrahepatic duct disease
2. Thickened bile duct walls ad narrowing of their
lumens; leads to cirrhosis, portal hypertension and
liver failure.
Strong associates with UC (less with that of Crohns) -
UC is present in 50-70% of patients with PSC; often
the UC dominates the clinical picture. The course of
PSC is unaffected by a colectomy done for UC
255b
Prognosis of
carcinoma of the GB
256a
90% die of advanced
disease within 1 year
of dx 2/2
underdetection
256b
Prognosis of
PANCREATIC CA?
257a
Dismal - diet within
months of diagnosis
257b
Prothrombin time as a
LFT describes?
258a
THe liver synthesizes clotting factors I, II, V, VII, IX,
X, XII, XIII, the function of which is reflected by PT
PT is not prolonged until most of the liver's synthetic
capacity is lost which corresponds to advanced liver
disease.
258b
Proximal v. distal SBO
259a
Distal obstruction causes
distention of proximal
bowel segments, making
the diagnosis easier on
plain radiograph
259b
PSEUDOCYSTS may be
present at sites distant to
the ______ but are still
2/2 acute pancreatitis.
260a
pancreas
260b
Pseudomembranous
colitis
261a
-Antibiotic associated colitis because many patients do not have
grossly visible pseudomembranes
a. AB rx kills organisms that normally inhibit the growth of Cdiff.
b. Overgrowth of C. diff and toxin production
c. almost all antibiotics have been associated but the most common
include;
i. Clindamycin
ii. Ampicillin
iii. Cephalosporins
Symptoms usually begin during first week of antibiotic therapy but
can continue 6 weeks after stopping AB.
261b
Radiation therapy is indicated in
patients with ____ cancer but
NOT indicated in patients with
>>>>
262a
Can use for patients with
rectal cancer
Cannot use for patients
with colon CA
262b
Rectal CA v. Colon CA
263a
Rectal CA has a higher
recurrence rate and a
lower 5 year survival
rate than colon CA
263b
Rectal cancer versus
CRC
264a
20-30% of all CRC are rectal
1. Hematochezia is the most
common symptom
2. Tenemus
3. Rectal mass, feelin of incomplete
evacuation of stool due to mass
264b
Reynolds pentad is associated
with ____ _ and is a highly
toxic state that requires
emergency treatment and can
be rapidly fatal
265a
acute cholangitis
265b
RISK FACTOR FOR
CHOLANGIOCARCINOMA:
266a
1. PSC major RF
2. UC
3. CHoleochal cysts
4. Clonorchis sinensis
infestation (Hong kong)
266b
Risk factors associated
with HCC
267a
Cirrhosis-especially in associated alcohol or
hepB/C; forms in 10% or cirrhostic pts
Carcinogens (aflatoxin, vinyl chloride, thorotrast)
AAT deficiency
Hemocrhomatosis, Wilsons dz
schistosomiasis
hepatic adenoma (10% risk of malignant
transformation
cigarette smoking
267b
RIsk factors for CRC
268a
1. Over 50yo
2. Adenomatous polyps (premalignant lesions but most do not
become CA)
-villous adenomas have higher malignant potential than tubular
ademona
-the larger the size the greater the number of polyps the higher the
risk of malignancy
3. Personal history or prior CRC
4. IBD
5. Family Hx
6. Dietary factors
7. Major polyposis syndromes
268b
RISK FACTORS of
gastric CA:
269a
1. atrophic gastritis
2. adenomatoush gastric polps
3. H pylori infecction -3-6x inc
4. Postantrectomy - many causes post billroth II
anastomosis (15-20yrs post surgery)
5. PERNICIOUS ANEMIA
6. Menetriers disease
7. High intake preseved foods
8. Blood type A
269b
Risk factors regarding
pancreatic cancer:
270a
1. CIGARETTE SMOKING
2. Chronic pancreatitis increases risk
3. DM
4. Heavy alcohol use
5. Exposure to chemicals-benzidine
and b-naphthlyamine
270b
RUQ ultrasound has high
sensitivity AND specificity
when accounting or
stones that are > ___mm.
271a
2
271b
SBO (small bowel
obstruction): Three
points to differentiate
between:
272a
1. Partial v. complete
obstruction
2. Closed loop v. open loop
obstruction
3. Proximal v/ distal loop
obstruction
272b
SBP: SPONTANEOUS
BACTERIAL
PERITONITIS is
indicative of?
273a
Infection ascites fluid that occurs in up to 20% of
patients hospitalized for ascites
1. occurs in patients with ascites caused by chronic
liver disease with HIGH mortality rate 20-30%
2. high recurrence rate (70%)
3. E. Coli, Klebsiella, Streptococus penumoniae
4. CLinical features: abdominal pain, fever, vomiting,
rebound tenderness. SBP can lead to SEPSIS
****REBOUND TENDERNESS! = SBP!
273b
SCC is most commonly
seen in which patients
regarding esophageal
CA?
274a
black males
most commonly located in upper thoacic
and mid thoacic esophagus
1/3 in distal 10 cm of esophagus
RF: alcohol and tobacco use, nitrosamines
(diet), achlasia, PV syndrome, caustic
ingestion, nasopharyngeal carcinoma
274b
SCHATZKIS RING
(Distal esophageal
web)
275a
circumferential ring in the lower
esophagus that is always
accompanied by a sliding hiatial
hernia.
275b
Screening for CRC
276a
Fecal occult blood testing annually
(poor sensitivity/specificity)
Colonoscopy every 10 years
(over the age of 50 OR 10 years prior
to the diagnosisof CRC in family
member)
276b
SIGNS OF ACUTE
CHOLECYSTITIS
277a
RUQ tenderness, rebound tenderness in
RUQ
-murphys sign is pathogmonic (inspiratory
arrest during deep palpation of the RUQ;
not present in many cases)
-hypoactive bowel sounds
-lowgrade fever with leukocytosis
277b
Signs of acute liver
failure:
278a
1. Jaundice
2. Elevated LFTs
3. Coagulopathy
4. Hypoglycemia(liver stones glycogen)
5. Hepatice encephalopathy 2/2 ammonia
intoxication
-Infection
278b
Signs of biliary tract
obstruction
279a
INC alk-phos and inc GGT
elevated conjugated BR
elevated jaundice
pruritis
dark urine
pale stool
279b
Signs of intestinal
infarction:
280a
hypotension, tachypnea, lactic
acidosis, fever and AMS
-CHECK THE LACTATE
LEVEL IF ACUTE
MESENTERIC ISCHEMIA IS
SUSPECTED
280b
Skin and soft tissue infections
(SSTI's) are the most common
of all infections
What are the categories?
281a
Superficial uncomplicated infections
Necrotizing infections
Infections associated with bites and
animal contact
surgical site infections
infections of the
immunocompromised host
281b
Special associations
during skin and soft
tissue infections
282a
1. Recurrent boils
2. DM
3. Neutropenia
4. Bite wounds (human, cat, dog, eikenella, pasturella
multiocida, capnocytophaga)
5. Water exposure
6. MRSA/MSSA
7. S aureus, GBS, others
8. P aeruginosa, GNRs
9. Vibrios, Aeromonas, M,marinum
282b
SQAA of the
esophagus
283a
20% survivial rate at 1
year
5% survival rate at 5
years
283b
Staging esophageal cancer that
have invaded the muscularis
propria and has positive regional
nodes:
284a
STAGE IIB
Stage 1: tumor invades lamina propria or submucosa; nodes
negative
Stage 2a: tumor invades muscularis proprai or adventitia;
nodes negative
Stage 2B: tumor invases up to muc propria with positive
regional nodes
Stage 3: tumor invades adventitia (positive reional nodes) or
tumor invades adjacent structures (positive or negative nodes)
Satge 4: distant mets
284b
Staging for CRC using
Dukes' staging
285a
Performed cia CT scan of abdomen and CXR
Stage A - stage I limited to muscularis mucosa
Stage B - stage II that goes past mm without node
involvement
B1 - into submucosa/muscularis propria
B2 - through entire bowel wall
B3 - through bowel wall into adjacent structures
Stage C - positive regional lymph nodes
Stage D - stage IV goes to distant metastasis
285b
Sulfasalazine is
metabolized by bacteria to
5-ASA and sulfapyridine.
5ASA is the _____
_______ of the drug
286a
effective moality
286b
Surgical intervention
in CROHNS
287a
1. reseve for complication of crohns dz.
Sedmental resection of involved bowel.
Recurence rate after surgery byyt up to
50%
2. Indications: SBO, fistula, diabling
disase, performation of abscess...
287b
Symptoms of acute
cholecystitis:
288a
-Pain is always present and is
located in RUQ or epigastrium;
it may radiate to the right
schould or scapula (BOAS
SIGN)
-n/v/anorexia
288b
Symptoms of
SCHATZKIs RING v.
PV SYNDROME
289a
SR: moderate dysphagia may be present; 2/2 alkali, acids,
bleach, detergents (suicide attempts). Stricture formation
indicates inc risk for esophageal cancer
Treatment: esophagectomy i full thickness necrosis has
occurred. Pt should avoid vomiting, gastric lavage and all
orgal intake which cnan compound the original injury. Give
the pt steroids and AB its well
PVS: Anemia, oral mucosa, upper GI esophageal webbing
causing dysphagia
289b
Term used to describe esophageal
perforation:
2/2: BLUNT TRAUMA, MEDICAL TUBES,
INSTRUMENTS, FORCEFUL VOMITING
ASSOCIATED WITH THAT OF
ALCOHOLISM OR BULIMIA
290a
Boerhaave's syndrome
290b
Tests to order in
patients with GI
bleeding and
hematochezia:
291a
first rule out anorectal cause
(hemorrhoids). Colonoscopy is
the intial test bc colon cancer is
the main concern in patients >
50YO
291b
Tests to order in
patients with GI
bleeding and
MELENA
292a
UPPER ENDOSCOPY intitial test bc
the most likely bleeding site is in the
upper GI tract.
ORDER COLONOSCOPY if no
bleeding site is identified from the
endoscopy
292b
Tests to order in
patients with GI
bleeding and OCCULT
BLOOD
293a
colonoscopy is the initial test in
most cases (colon CA is the
main concern) Order and upper
endoscop if no bleeding site
identified from the colonoscopy
293b
Tests to order in
patients with GI
bleeding with
HEMATEMESIS:
294a
UPPER GI
ENDOSCOPY = #1
TEST
294b
The development of a palpable
mass in the epigastrium four
weeks after the onset of acute
pancreatitis is HIGHLY
suggestive of a ______
_______ formation
295a
Pancreatic pseudocyst
formation
295b
The diagnosis of acute
pancreatitis is
normally made by:
296a
1. Clinical presentation.
2. Lab studeies are
supportive (amylase/lipase)
3. and CT scan is
confirmatory
296b
The distortion of the liver
anatomy in CIRRHOSIS causes
which two major events:
1.
2.
297a
1. Decreased blood flow through the liver and thus causing
PORTAL HTN (therefore associated ascites, esophageal
varices, splenomegaly, peripheral edema, variscosity of veins
"back stream" in circulation, hemorrhoids)
2. Hepatocellular failure that leads to impairment of
biochemical functions such as decreased albumin synthesis
and decreased clotting factor synthesis (thus can no longer
carry Ca2+ or protein and will have increased bleeding 2/2
decreased coag.
297b
The higher the AST-ALT ratio
the greater the likelihood that -
----- is contributing to the
abnormal LFTs
298a
alcohol
298b
The level of either _____
or _______ in acute
pancreatitis does not
reliably predict the severity
of disease.
299a
amylase
lipase
299b
Third most common
cancer in the United
States (in men and
women)
300a
CRC
300b
Three types of
adenomatous polyps:
301a
1. Tubular
2. Tubulovillous
3. Villous
*tubular is the most common type in up to 60-80% of
cases
*tubulovillous has an intermediate risk of malignancy
*villous is the GREATEST risk of becoming malignant
301b
Toxic megacolon, growth
retardation, narcotic abuse
all can result from Crohns.
T or F
302a
T
302b
Transmural tear
throught the
esophagus via the GEJ
v. Muscosal
303a
Boerhaave's syndrome
MW syndrome
303b
Treatment for acute
pancreatitis?
304a
Bowel rest (go NPO) - goal to REST THE
PANCREAS
-IV FLUIDS - may have severe intravascular
volume depletion
-Pain control - be cautious with narcotic
-Nasogastric tube if severe nausea/vomiting or
ileus present; routine use is controversal
304b
Treatment for acute
primary biliary
cholangitis: (PSC)
305a
1. No curative treatment other than liver
transplantation
2. When dominant stricture causes
cholestasis, ERCP with stent placement for
biliary drainage and bile duct dilatation
may relieve symptoms
3. use cholestyramine for symptomatic
relive to decrease pruritis
305b
Treatment for BUDD-
CHIARI syndrome
306a
1. Medical therapy is uaually
unsatisfoatory (anticoag, thrombolytics,
diuretics)
2. Surgery is eventually necessary in most
cases (balloon angioplasty with stent
placement in IVC, portocaval shunts)
3. LIVERTRANSPLANT if cirrhosis is
present!
306b
Treatment for C diff
colitis:
307a
d/c offending agent
-metronidazole is the drug of choice (cannot be
used if infant/preg)
-oral vanc used if patient resistance to met or
cannot tolerate it
-redarless of choice of AB, recurrence may occur
within 2-8 weeks after stopping the AB
-CHOLESTYRAINE MAY BE USED AS
ADJUVANT TO IMPROVE DIARRHEA.
307b
Treatment for
cholangiocarcinoma:
308a
1. most patients do not have
resectable tumors at diagnosis
2. survival rate low despite
aggressive therapy and
stenting or biliary drainage
308b
Treatment for DES?
309a
-nitrates and CCB which
decreases contractions but
not curative
-TCAs
-esophagomyomotomy
309b
Treatment for
ESOPHAGEAL CA
310a
Palliation is the goal in most patients becase the
disease is usually advanced at presentation
HOWEVER PERFORMATION OF AN
ESOPHAGECTOMY MAY BE CURATIVE IF
STAGE 0,1,2A.
-CHEMO + RADIATION B4 SURGERY
PROLONGS SURVIVAL
310b
Treatment for gastric
CA
311a
Surgical resection with wide (>5cm)
margins (total or subtotal
gastructomy) with extended lymph
node dissection
-chemotherpay may be appropriate in
some causes
311b
Treatment for patients
with achalasia
312a
1. Adaptive measures: chew food to consistency of pea soup
b4 swallowing; sleep with trunk elevated, avoid eating
before sleeping
2. Medical therapy
a. antimuscarinics (DICYCLOMINE) usually unsatisfactory
b. sublingual nitroglycerine - long acting nitrates, CCB
3. injection of outlimun toxin into the LES during endoscopy
-blocks cholinergic activity in the LES
-can be effective in up to 65% of cases; however, repeat
procedure needs to be performed every 2 hrs
312b
Treatment for PUD:
Medical
313a
SUPPORTIVE!
1. d/c nsaids/asa
2. rstrict -OH use but not foods
3. Stop smoking/dec emotional stress
4. Avoid eating before bedtime and dec coffee intake
ACID RESTRICTION!
1. H2 blockers, PPIs, antacids
ERATICATE H. PYLORI with tripple therapy regimen
CYTOPROTECTION - sucralfate and MISOPROSTOL
Surgical: Rarely needed - required for ocmplication of PUD(bleeding
performation gastric outlet obstruction
313b
Treatment for SBO
314a
1. If incomplete - nonoperative management
2. IV fluids establish urine output; add K+ to correct
hypokalemia
3. NG tube to empty stomach (gastric decompresion)
4. AB
5. Surgery is indicated for complete obstruction, for
patial obstruction that s persistent and or associated
with constant pain or if strnagulation is suspected.
Perform an exploratory laparomty with lysis of
adhesions and resection of necrotic bowel.
314b
Treatment of
acalculous
cholecystitis
315a
Emergent cholecystectomy is the
treatment of choice - patients who
are too ill for surgery, perform
percutaneous drainage of he GB
with cholecystostomy
315b
Treatment of acute
cholecystitis?
316a
Conservative meausres: (1) hydration with IV fluids
(2) NPO (3) IV antibiotics (4) analgesics
Surgery: cholecystectomy is indicated in most
patients with symptomatic gallstones. Early
cholecystectomy is preferred (first 24-48 hours)
316b
Treatment of
appendicitis:
317a
APPENDECTOMY - usually laparoscopic. Up to 20%
of patients who are dx with acute appendicitis are
found to have a normal appendix during surgary.
Because illness is potentially life threatening,
acceptable risk even during pregnancy.
317b
Treatment of bleeding
esophageal VARICES:
318a
1. VARICEAL LIGATION/BANDING
-initial endoscopic treatment of choice; effective control of ACTIVE BLEEDING
-lower rate of rebleeding than scleotherapy
2. ENDOSCOPIC SCLEROTHERAPY:
-sclerosing substance is injected into varices during endoscopy
-this controls acute bleeding in 80-90% of cases with 50% haveing rebleeds
3. IV vasopressin
-alternative to octraotide but LESS POPULAR due to risk of complication.
-vasoconstriction of mesenteric vessels reduces portal pressure
-NG is admin to prevent side effects of vasopressin (coronary vasoconstrict/MI, decreased CO/HTN)
3. IV octreotide
-now replacing vasopressin as firstline therapy; causes splanchnic vasoconstriction and reduces portal pressure
-fewer side effects
318b
Treatment of
choledocholithiasis
319a
ERCP with sphincteromtomy and
stone extracton with stent
placement (successful in 90%) of
patients with it.
-laparoscoptic choledocholithiotomy
in select cases
319b
Treatment of cirrhosis
of the liver:
320a
1. Treatment of underlying cause (alcohol, interferons
for hepC/B)
2. Once cirrhosis develops aim to treat via
managment the complicatoin. Most serious
complication is the esophageal varices that are
actively bleeding and hepatic encephalopathy
3. Liver transplant is the only hope for a cure.
Abstinence from alcohol for more than 6 months is
requiredbefore a patient is eligile for transplantation
320b
Treatment of colonic
volvulus
321a
Sigmoid volvulus: nonoperative reduction
(decompression) is successful in 70% of
cases. The recurrent rate is HIGH so
elective sigmoid colon resection is
recommended
Cecal volvulus: emergent surgery
321b
Treatment of CRC
322a
1. Surgical resection of tumor containing bowel as well as redection of regional
lymphatics
2. CEA level should be obtained before surgery
3. Adjuvant therapy:
-Dukes C colon ca: postoperative chemo (5FU and leucovorin) but no radiation
-Dukes B2/C rectal: both chemo (5FU) and radiation therapy postoperatively
4. F/u is important and caries among physicians
-stool guiac test
-annual CT scan of abdomen/pelvis/CXR for up to 5 years
-colonoscopy 1 year then every 3 years
-CEA levels are checked periodically (3-6 mo)
i. Postop CEA <2-3 good prognosis
ii. Subsquent increase in CEA is marker for recurrance
iii. often, second look operations are based on HIGH CEA levels post resection
iv. VERY HIGH ELEVATIONS OF CEA suggest liver involvment
322b
TREATMENT OF
CROHNS
323a
1. Medical
a. Sulfasalazine (useful if colon involved bc is a 5-ASA *mesalamine) as tha
active compound released in colon that is more useful in uS than in Crohns, 5-
ASA compounds bock PGE release and serve to decrease inflammation
-there are preparations of 5ASA that are more useful in distal small bowel
disease.
b. Metronidazole
c. corticosteroids *prenisone for exacerbations and if no repsonse to
metronidazome)
d. immunosuppressants AZA 6MP) with steroid if patients doesnt responseto
above agents
e. BA sequetrants (cholestyramine or colestipol) pts with severe ileal disease
who cannot absorb bile acids
323b
Treatment of
diverticulitis:
324a
1. If initial episode of diverticulitis (fever, LLQ pain,
leukocytosis)
a. Use of IV antibiotics, bowel rest (NPO), IV fluids.
b. Mild episodes can be treated outpatient basis if patient is
reliable and has few or no comorbiditie.
c. IF persists > 3-4 days then require surgery
2. If second or subsequent episodes of diverticulitis:
a. surgery is recommended (resectionof involved segment) once
acute inflammation resolves
3. Low-residue diet (eg: no nuts, seeds)
324b
Treatment of
epiphrenic
diverticulum (distal
1/3)
325a
esophagomyotomy
325b
Treatment of
esophageal hiatal
herniation
326a
1. Sliding: medically with antacids, small meals, and elevation of
head post meals; 15% requires a nissens fundoplication
2. Paraesophageal: treatd with elevtice surgery due to risk of above
complications
326b
Treatment of GALLSTONES
symptomatic v. asymptomatic
327a
SYmptomatic-elective
cholecustectomy for patients
with recurrent bouts of biliary
colic
asymptomatic - no treatment
327b
Treatment of HCC
328a
1. Liver resectoin (in the
10% of patients who have
resectable tumors)
2. Liver transplantation if
diagnosis is made early
328b
Treatment of
hemochromatosis?
Diagnosis?
329a
1. Marked elevation in serum iron and serum ferritin
2. Elevation of iron saturation (transferritin sat)
3. Decreased TIBC
4. Liver biopsy (determines hepatic iron concentration)
5. Genetic testing for chromosomal abnormality
TREATMENT: perform phlebotomies to removes excessive
serum iron
-treat any complications (CHF. DM. hypothyroidism,
arthritis) and consider liver transplantation if late stage
hemacrhomatosos
329b
Treatment of hepatic
encephalopathy?
330a
Lactulose prevents absorption of amonia. Metabolism
of lactulose by bacteria in colon favors the formation
of NH4+ which is poorly absorbed from GI tract,
thereby promoting excretion of ammonia.
-NEOMYCIN (AB) kills the bowel flora, so decreases
the ammonia production by intestinal bacteria
-DIET: limit protein to 30-40 mg/day
330b
Treatment of MW
syndrome/tear
331a
upper endoscopy is diagnostic, most
causes stop bleeding without any
treatment but if treatment is required it is
surgical (overing the tear) or angiographic
embolization if bleeding continues, but
this is raraely necessary. Acid suppression
is used to promote healing.
331b
Treatment of
pancreatic CA
332a
1. Whipples procedure is the only hope for cure; only
a minority of tumors resectable. Pronosis post
resection with 5 year survival rate of 10% - grim.
2. If the tumor is unresectable and biliary obstruction
is present , perform PTC or ERCP with stent
placement across the obstruction for palliation.
332b
TREATMENT OF
PLUMMER VINSON
SYNDROME
333a
ESOPHAGEAL
DILITATION
333b
Treatment of SBP:
334a
spontaneous bacterial peritonitis
1. Broad spec therapy then give specific once
identify bacteria.
-clinical improvement should be seen within 24-48
hours. Repreat paraventesis in 2-3 days to
document a decrease in ascitis fluid PMN < 250
334b
Treatment of two
possible causes of liver
cysts:
335a
1. Polycystic kidney disease:
no treatment necessary
2. Hyadatid cysts: surgical
resection without spilling +
mebendazole
335b
Treatment of UC:
336a
medical: corticosteroids for acute
exacerbaton
-SULFASALAZINE is he mainstay of
treatment - it is effective
-immunosuppressives
surgical - curative (UNLIKE CROHNS
disease) involves total colestomy
336b
Treatment of zenkers
diverticulum
337a
surgical:
cricopharyngeal
myotomy
337b
Treatment options for
acute uncomplicated
UTI
338a
1. TMP-SMX 1 DS po bid x3day
-success rate 94%
-first line unless local resistance >15-20%
2. FQ (NOT moxi) x 3d
-success >94%
use when rx with TSX is contrandicated
3. Nitrofurantoin (***can instigate G6PD/exacerbate it!)
100mg po bid x 7d
4. Fosfomycin 3 gm po x 1 dose
338b
Two main types of
LIVER CYSTS:
339a
1. Polycystic liver cysts
2. Hyatid liver cysts
339b
Two types of liver
cysts and causes:
340a
1. Polycystic liver cysts: AD usualy associated with ADPKD. Results in renal
failure and is the main determinant of the prognosis whereas the liver cysts
RARELY lead to hepatic fibrosis and liver failure.
-usually asymptomatic; some patients have absominal pain and upper
abdominal masses
-treatment: unneccessary
2. Hyadatid liver cysts: caused by infection from the tapeworm
ECHINOCOCCUS GRANULOSUS or ECHINOCOCCUS MULTIOCULARIS.
Cysts most commonly occur in the RL of the liver.
-small cysts are asymptomatic; larger cysts may cause RUQ pain and
RUPTURE into the peritoneal cavity, causing fatal anaphylactic shock.
-treatment: SURGICAL resection (caustion to avoid spilling contents of the
cysts into the peritoneal cavity). Mebendazole is given after surgery
340b
Types of varices 2/2 liver
disease:
341a
1. Esophageal
2. Gastric
3. Hemorrhoids
4. Caput medusae (distention
of abdominal wall veins)
341b
Ulcerative colitis:
342a
CHRONIC INFLAMMATORY DISEASE of colon or rectal
mucosa that occurs at any age but usually young adulthood.
-distribution os UC involves to rectum in all caes and can
involve the colon paritally or entirely
a. rectum along (10%)
b. rectum and left colon (40%)
c. rectum, left colon, right colon *30%)
d. pancolitis
unpredictable course and variable
342b
What accounts for
60% of all cases of
ascending cholangitis?
343a
Choledocholithiasis
343b
What are
CHOLEDOCHAL
CYSTS
344a
Cystic dilitations of biliary tree involving either the extrahepatice or
intrhepatic duct or both; more common in women (4:1)
-EPIGASTRIC PAIN, jaundice, fever, and RUQ mass
-complications: CHOLANGIOCARCINOMA (MOST FEARED);
HEPATIC ABSCESS< RECURRENT cholangitis/pacreatitis,
rupture, biliary obstruction, cirrhosis, and portal HTN
-US is the best noninvasive tests, and ERCP is definitieve diagnosis
Treatment is surgery: complete resection of the CYST with a biliary-
enteris anastomosis to restore continuity of biliary system with
bowels
344b
What are the causes of
CONJUGATED
hyperbilirubinemia?
345a
-Urine positive for bilirubin
1. Decreased intrahepatic excretion of bilirubin
-hepatocellulr disease (viral, or alcoholic hepatitis, cirrhosis)
-inherited disorders (DUBIN-JOHNSON syndrome, Rotor's syndrome)
-drug-induced (OCP)
-PBC, PSC
2. Extrahepatic biliary obstruction
-gallstones
-carcinoma of head of pacreas
-cholangiocarcinoma
-periampullary tumor
-extrahepatic biliary atresis
345b
What are the causes of
unconjugated
hyperbilirubinemia?
346a
(Urine negative for bilirubin)
1. Excess production of BR - hemolytic anemias
2. reduced heaptic uptake of BR or impaired conjugation
-GILBERTS syndrome
-drugs (sulfas, penicillin, rifampin, radiocontrast agents
-criggler najjar syndrome types I/II
-physiologic jaundice of newborn (immature conjugating
system)
-diffuse liver dz (cirrhosis/hepatits)
346b
What are the clinical
feature of budd-chiari
syndrome:
347a
Hepatomegaly,
ascites, abdominal
pain RUQ; jaundice,
variceal bleeding
347b
What are the clinical
features of achalasia:
348a
1. Dysphagia (odynophgia less common) -
both solids and liquids
2. Regurgitation
3. Chest pain
4. Recurrent pulmonary complications
secondary to aspiration, which may cause
lung abscess, bronchiectasis, hemoptysis
348b
What are the clinical
features of CHRONIC
pancreatitis?
349a
1. Epigastric pain
2. Recurrent abdominal pain
3. May be aggravated bya a drinking episode or by
eating
4. Radiates to the back (in 50% of cases)
5. WEIGHT lOSS 2/2 malabsorption, alcohol abuse,
DM; steatorrhea 2/2 to malabsorption
349b
What are the clinical
features of CRC?
350a
Abdominal pain is that most common feature - where
CRC is the most common cause of large bowel
obstruction in adults
-weight loss
-blood in stool
-colonic perforation is the most life threatening
-anemia
350b
What are the clinical
features of
diverticulosis?
351a
-Asymptomatic and dsicovered
incidentally on barium enema or
colonoscopy done for another reason.
-Vague LLQ discomfort, bloating,
constipation/diarrhea may be present
-only 10-20% become symptomatic
(develop complications)
351b
What are the clinical
features of Esophageal
Hiatal Hernias?
352a
asymptomatic,
incidentally found
-heartburn, chest pain,
dysphagia
352b
What are the clinical
features of gastric
cancer
353a
abdominal pai and unexplained weight
loss are most common symptoms; reduced
appetitie, anorexia, dyspepsia, early
satiety, nausea and vomiting, anemia,
melena, guiac positive stool
353b
What are the clinical
features of
pseudomembranous
colitis?
354a
1. Profuse watery diarrhea
2. Crampy abdominal pain
3. Toxic megacolon with
risk of perforation
354b
WHAT ARE THE
CLINICAL
FEATURES OF
WILSONS DISEASE
355a
1. Liver disease with acute hepatitis, cirrhosis or fulminant hepatic
failure
2. KAYSER-FLEISCHER RINGS (yellow rings in the cornea
representative of cu2+ accumulation and deposition in cornea...do
not interfere with vision.
3. CNS findings:
-extrapyramidal signs= parkinsonian symptoms with resting tremor,
rigitity, radykinesia, chorea, drooling, incoordination due to copper
depostition in BG
-psychiatric distrubances - depression, neuroses, peraonlity changes,
psychosis
4. Renal involvment
-aminoaciduria, neprhocalcinosis
355b
What are the clinical
findings in patients with
hepatic encephalopathy?
356a
Decreased mental function, confusion, poor
concentration, stupor, coma
Asterixis (hand flapping tremor)
Rigidity and hyperreflexia
Fetor hepaticus (MUSTY ODOR OF BREATH)
356b
What are the clinical
symptoms of primary
biliary cirrhosis of the
intrahepatic bile ducts?
357a
Fatigue
Pruritis
Jaundice
RUQ discomfort
Xanthomata and xanthelasmata
Osteoporosis
Portal HTN with resultant sequelae
357b
What are the common
comorbitidies
associated with
NASH?
358a
1. Obesity
2. Hyperlipidemia
3. DM (some patients have none of these)
4. Usually asymptomatic and a benign course
(but cirrhosis develops in 10% to 15%)
5. Typically discovered on routine laboratory
tests (mild elevation in ALT and AST)
6. Treatment is not clearly established
358b
What are the
complications of acute
pancreatitis?
359a
Complications of pancreatitis (ACUTE):
1. Pancreatic necrosis - can be sterile or infected
a. sterile heals on own
b. infected has high mortlatlity rate 2/2 multiple organ failure in 50% of causes;
surgical debridement and antibodics indicated
2. Pancreatic pseudocyst
a. encapsulated fluid collection that appears 2-3 weeks after an acute attack -
unlieke a true cyst, it lacks an epitheliel lining.
b. complications of untreated pseudocysts include rupture, infection, gastric
outlet obstruction, fistula, hemorrhage into cyst, and pancreatic ascites. It may
impinge on adjacent abdominal organs (duodenum, stomach, transverse colon)
if large enough; or if located at the head of the pancreas, can cause
comepression of the CBD
c. diagnosis by CT
d. IF cysts < 5cm then observe, if > 5cm then drain
359b
What are the
complications of severe
pseudomembranous
colitis?
360a
Toxic megacolon
Colonic perforation
Anasarca, electrolyte
disturbances
360b
What are the key
features of the
plummer vinson
syndrome?
361a
UPPER ESOPHAGEAL WEB + IRONDEF
ANEMIA + ATROPHIC ORAL MUCOSA
-also KIOLONYCHIA (spoon shaped fingernails)
-10% develop SCC of the oral cavity,
hypopharynx or esophagus
-treatment: ESOPHAGEAL DILITATION -
CORRECT NUTRITIONAL DEFICIENCY
361b
What are the majority
of cases regarding
PUD related to?
362a
1. Helicobactor pylori infection
2. NSAIDS-inhibit prostaglandin
production which leads to impaired
mucosal defenses.
3. Acid hypersecretory states like ZE
syndrome (excessive production of
gastrin)
362b
What are the risk
factors for acquisition
of clostridium
difficile?
363a
Hospitalization or residence in a
chronic care facility
-AB exposure - nearly all AB
implicated however the big three
(CLINDA, CEPHS, FQ)
-Advanced age (esp >65)
363b
What are the signs
associated with acute
pancreatitis?
364a
1. Low grade fever, tachycardia, hypotension,
leukocytosis
2. Epigastric tenderness, abdomial distention
3. Decreased or absent bowel sounds indicate patial
ileus
4. The following signs are seen with hemorrhagic
pancreatitis as blood tracks along fascial planes:
-Grey turners sign (flank ecchymoses)
-Cullen's sign (periumbilical ecchymoses)
-Fox's sign (ecchymosis of inguinal ligament
364b
What are the signs of
appendiceal rupture
2/2 untreated acute
appendicitis?
365a
Complications -20% of cases
RF: delay in treatment (>24 hours) and
extremes of age
-signs of appendiceal rupture (high fever,
tachycardia, marked leukocytosis,
peritoneal signs, toxic appearance)
365b
What are the three
major causes of
JAUNDICE:
366a
1. Hemolysis of RBC
2. Liver DZ
3. Biliary obstruction
366b
What are the two
etiologies of a LIVER
ABSCESS?
367a
1. Pyogenic liver abscess: most common cause is biliary tract obstruction - obstruction of bile flow allows baterial
proliferation. Other causes include GI infection (diverticulitis, appendicitis) with spread by the portal veonous
system and penetating liver trauma (GUNSHOT WOUND, SURGERY)
-causative organisms: E. coli, klebsiella, proteus, eneterococcus, anaerobes
-features: fever, malaise, anorexia, weight loss, nausea, comiting, RUQ pain, jaundice.
diagnosis by US or CT scan: elevated LFTs
-treatment: FATAL if untreated *treatment with IVAB and percutaneous drainage of the abscess. which reduces the
mortality to about 5-20%. Surgical drainage is sometimes considered
2. Amebic liver abscess: most common in men (9:1); homosexual. Fecal oral contact transmission. Caused by
intestinal amebiasis (e. histolytica) - the amebae reach the liver via the hepatic portal vein.
-clinical features: fever, RUQ pain, n/v, hepatosplenomegay, diarrhea
-seriological testing (immunoglobulin G enzyme immunoassay) will estbolish diagnosis. Elevated LFTs; E.
histolytica stool antigen test *detects protozoe in the stool). Imagine studies (US/CT) identifies the abscess but it is
difficult to distinguish from a pyogenic abscess.
-IV metronidazole is effective treatment in most cases. Therapeutic aspiration of the abscesss (IMAGE_GUIDED
percutaneous aspiratoin causses. Therapeutic aspiration of the abscess may be necessary if the abscess is larger
(HIGH RISK OF RUPTURE) or if there is no response to medical therapy
367b
What causes the elevation
in ALT or AST levels in
asymptomatic patients
(ABCDEFGHI)
368a
Autoimmune hepatitis
Hepatitis B
Hepatitis C
Drugs or toxins
Ethanol
Fatty liver (TG)
Growths (tumors)
Hemodynamic disorders (CHF)
Iron (hemachromatosis), copper (wilsons), AAT
deficiency
368b
What diagnosis does an upper
GI barium swallow show
("corkscrew esophagus") - in
50% which represents multiple
simultaneous contractions?
369a
DES
369b
What exacerbates
GILBERTS syndrome?
370a
fasting (crash diets); fever,
alcohol, and infection.
Asymptomatic in most cases,
but occasionally jaundice is
seen.
370b
What imaging can be
done for upper GI
bleeds:
371a
Upper endoscopy
NG tube
Anoscopy or proctosignmoidoscopy
COlonoscopy
Bleeding scan
Arteriography
Exploratory laparatomy - last resory
371b
What imaging studies can
be performed in patients
with acute pancreatitis that
will lead to its diagnosis?
372a
1. Abdominal radiograph - has a limited role in dx of acute pancreatitis; instead rules out that of other diagnosis
such as intestinal perforation (free air)l presense of calcification suggests CHRONIC, not acute PANCREATITIS.
2. Abdominal ultrasound - helps identify the cause of pancreatitis (gallstone) and useful for pancreatic abscesses or
pseudocysts
3. CT scan of the abdomen - most accurate test for dx of acute pancreatitis and for identifying complications of the
disease
4. ERCP - severe gallstone pancreatitis with biliary obstruction; identidy uncommon causes of acute pancreatitis if
the disease is recurrent
372b
What indicates a non-
neoplastic polyp?
373a
A benign lesions with no malignant potential
-hyperplastic (metaplastic polyp) most common
(90%); generally remain small and asymptomatic
-no specific therapy required but difficult to
distinguish from neoplastic polyps
-juvenile polyps are highly vascular and common
(if younger than 10) so remove
-inflammatory polyps (pseudopolyps) are
associated with UC
373b
WHAT IS "BOAS"
SIGN?
374a
RIght scapular pain
2/2 biliary colic
374b
What is a bleeding
scan?
375a
radionucleotide scanning that reveals
bleeding even with a low rate of
blood loss. It does not localize the
lesion; it only identifies continued
bleeding. Role is controversial but it
may help determine where
arteriography is needed
375b
What is a flexible
sigmoidoscopy?
376a
Can be used to reach the area
where approximately 50-70% of
polyps and CA occur
Can be diagnostic in about 2/3
of all CRCs
376b
What is ACUTE
CHOLECYSTITIS
377a
Obstruction of the cystic duct (not infection)
induceing acute inflammation of the
gallbldder wall
-chronic forms when recurent bouts of acute
cholecystitis
-10 percent of patients with gallstones
develop acute cholecystitis
377b
What is ACUTE
GASTRITIS?
378a
inflammation of the gastric mucosa 2/2
NSAIDS/ASA, H. pylori, alcohol, heavy cigarette use,
smoking, caffeinel extreme physiologic stress (eg
shock, sepsis, burns). It can either be asymptomatic
or cause epigastric pain. The relationship between
eating and pain is NOT consistent.
IF LOW PAIN or MODERATE and not worrisome,
empiric therapy + acid suppress is good treatment
with the stopping of NSAIDs
378b
What is acute
pancreatitis:
379a
inflammation fo the pancreas
resulting from prematurely
activated pancreatic digestive
enzymes that invoke pacreatic
tissue autodigestion
379b
What is alreay present
(symptomatically) in a
MW syndrome
380a
Hematemesis is always
present - it varies from
steaks of blood in vomitus
to massive bright red
blood.
380b
What is Budd-chiari
syndrome?
381a
Liver disease caused by the occlusion of the hepatic
venous OUTLFLOW which leads to hepatic
congestions and microvascular ischemia.
-variable vourse - indoent, gradual development of
portal HT and progressive deterioration of Liver
FUNC
-can lead to acute liver failure, which can be fatal
without immediate therapy
381b
What is CEA?
382a
Tumor marker for pancreatic
cancer, not useful for screenin;
useful for baseline and
recurrence surveillence
382b
What is
CHOLANGITIS?
383a
INFECTIOn of the biliary
tract 2/2 to obstruction
which leads to biliary stasis
and bacterial overgrowth.
383b
WHat is
choledocholithiasis?
384a
Gallstones that are found in the CBD
-primary v. secondary causes;
primary-originate in the CBD (usually
will be pigmented)
secondary - originate in the GB and
then pass into the CBD (usually
cholesterol/mixed) - 95% of all cases
384b
What is cholelithiasis?
What are the three
types of GB stones?
385a
stones in the gallbladder
1. Cholesterol stones
2. Pigmented stones
3. Mixed stones (cholesterol and
pigment) - most common
385b
What is cholestasis?
386a
Blocking of bile either intrahepatically or
extrahepatically with increased conjugated bilirubin
levels.
symptoms: jaundice, gray stools, darkened urine, bile
salt deposition in skin causing pruritis, elevated
serum alkphos, elevated serum cholesterol (impaired
excretion), skin xanthomas (local accumulation of
cholesterol), malbsorption of fats and fat soluble
vitamins.
386b
What is diagnostic for
CHRONIC
PANCREATITIS?
387a
1. COMBINATION OF: CHRONIC EPIGASTRIC PAIN
2. CALCIFICATION OF PANCREAS ON PLAIN
ABDOMINAL FILMS
Triad of symptoms:
1. Steatorrhea
2. DM
3. Pancreatic calcification of plain films or CT
= DIAGNOSTIC
387b
What is diverticulosis?
388a
pouches in the colon wall that
should be distinguished from
diverticulitis, which refers to
inflammations or infections of
the diverticula and is a
complication of diverticulosis.
388b
What is GALLSTONE
ILEUS?
389a
Gallstone enters the bowel lumen via
cholecystenteric fistula and gets stuck in
the terminal ileum and causes obstruction
at the ileocecal valve - causes obstruction
and accounts for 1-2 % of bowel
obstructions
389b
What is hemobilia?
390a
When blood fraining into the duodenum via the common bild duct.
Soundce of bleeding can be anywhere along the biliary tract, the
liver, or the ampullary region.
Causes: TRAUMA (MOST COMMON); PAPILLARY THYROID
CARCINOMA; SURGERY 2/2 CHOLESCYSTECOMY
Diagnostic: Arteriogram is diagnostic - upper GI endoscopy shows
blood coming our of the ampulla of vater
Treatment: resuscitation (+/- transfusoin) If bleeding is severe,
surgery is necessary (options include ligation of hepatic arteries or
arteriogram with emnolization of vessel).
390b
What is hepatorenal
syndrome?
391a
progressive renal failur in advanced liver disease, 2/2 enal
hypoperfusion resulting from vasoconstriction of the renal vessels
that is precipitates by infection or diuretics.
-functional renal failure where the kidneys are normal in terms of
morphology and no specific causes of renal dysfunction are
eventend. The condition doesnt responde to volume expansion and
thus asotemia, oliguria, hypoantrmia, hypotension and lo urine
sodium results.
Treatment is by liver transplantation ONLY
391b
What is NASH?
392a
Non-alcoholic
steatohepatitis
(NASH)
392b
What is OGILVIE'S
SYNDROME
393a
Signs, symptoms, radiographic evidence of large bowel obstruction are present
but no mechanical obstruction.
-causes: surgery, trauma, serious medical illness (sepsis, malignancy) and
medications (narcotics, psychotrpoic drugs, anticholinergics)
-diagnosis: not confirmed until mechanical obstruction of colon is exluded
-treatment: stop offending agent (narcotic) or supportive measures (IV
fluids/electrolyte repletion)
-decompression with gentle enemas or NG suctions may be helpful
-colonoscopic decompression is usually successful
-surgical decompression with cecostomy or colostomy is LAST result
393b
What is REYNOLDS
PENTAD?
394a
Charcots triad (fever,
jaundice, RUQ pain) +
septic shock + AMS (CNS
depression - coma-
disorientation)
394b
What is the "best" rx
for C. diff acute
diarrhea in 2011?
395a
Traditional treatment
-d/c the offending ATB (if possible)
-avoid narcotics and anti-motility agents
-oral metronidazole >>> oral vanc
New recommendations
-treatment based on dz classification: mild,
moderate, severe, severe complicated
-increase role for po vanc
395b
What is the biliary dyskinesia?
Diagnosis:
Treatment:
396a
Motor dysfunction of the sphincter of Oddi which leads to
recurrent episodes of biliary colic without any evidence of
gallstones on diagnostic studies such as ultrasound, CT
scan, ERCP
Dx: made by HIDA scan - once the gallbladder is filled with
labeled radionuclide; give CCK IV then determine the
ejection fraction of the GB. If low then dyskinesia likely
Treatment: laparoscopic cholecystectomy and endoscopic
spincterotomy
396b
What is the DEFINITIVE
DIAGNOSTIC STUDY to
diagnose esophageal
perforation?
397a
CONTRAST ESOPHAGRAM = soluble gastrografin swallow
preferred
-then a CXR shows air in the mediastinum
-if stable and perforation is small, medical management is
appropriate (IV FLUIDS< NPO, AB, H2 blockers)
-if patient is ILL and perforation is large (or communication
into the cavity, surgery should be performed within 24 hours
of presentation = success rate is higher)
397b
What is the diagnosis
of jaundice?
398a
Serum levels of unconjugated v. conjugated BR.
-if unconjugated, then there must have been an issue prior to
hepatic uptake and thus check CBC, reticulocyte count, haptoglobin,
and LDH (with peripheral smear) to r/o hemolytic anemia
-if conjugated hyperbilirubinemia, then there must have been an
issue after the bilirubin-albumin complex formed and after hepatic
uptake either within or after the hepatic ducts. LFTS may points to
cause
-get US/CT to assess biliary tract for obstruction or anatomic
changes
-additional tests ERCP if conj with obstruction 2/2 US/CT
-liver biopsy is the last resort and indicated in some cases to
determine cause of HCC injury
398b
What is the general
characteristic of
diverticulosis?
399a
1. Increased intraluminal pressure-inner layer of
colon bulges through focal area of weakness in colon
wall (usually an area of blood vessel penetration)
2. LOW FIBER diets: contipation cause sintraluminal
pressures to increase with a positive family history
increases the risk
3. Most common location is the sigmoid colon
however diverticula may occur anywhere in the colon.
399b
What is the hormone
that relaxes the sphictor
of Oddi and contracts
the gallbladder:
400a
CCK
400b
What is the LAB TEST that
diagnosis for GI bleeding?
401a
-stool guiac for occult blood
-Hgb/hct level (may not be decreased in acute bleeds)
-A hgb level >7-8 acceptable in young health patients without active
bleeds
-A hgb level in most elderly patients should have hgb level ?10 g/dL
-low MCV is suggestive of iron deficiency anemia and chronic blood
loss
-coag profile (plt ct, PT, PTT, INR)
-LFTs, renal function
-the BUN-creatinine ratio is elevated with upper GI bleeding. This is
suggestive of upper GI bleeding if patient has no renal insufficiency
401b
What is the metabolism of
BILIRUBIN
402a
-80% of BR is derived from hemoglobin (RBC breakdown). The rest
comes from myoglobin breakdown and liver enzymes
-hemoglobin is coverted to BR in the spleen. This unconjugated BR
circulates in plasma, bound to albumin. This BI-albumin complex is
not water soluble; therefore it is not excreted in the urine.
-in the liver, it dissciates from albumin and the BR is conjugated and
excreted into the intestine, where bacteria act on it to produce
urobilinogen and urobilin
-therefore, unconjugated hyperbilirubinemia results when there is a
defect BEFORE hepatic uptake. Conjugated hyperbilirubinemia
results when there is a defect AFTER hepatic uptake
402b
WHAT IS THE MOST
COMMON CAUSE OF
CHRONIC PANCREATITIS?
403a
ALCOHOLISM
403b
What is the most common
causes of cirrhosis?
What is the primary
method of diagnosis?
404a
1. Alcoholic liver disease
2. Hepatitis C
Dx by liver biopsy (gold
standard)
404b
What is the most
common location for
liver abscesses (both
pyogenic and amebic)?
405a
Right lobe of the liver
405b
What is the peak
incidence of
appendicitis?
406a
Peaks in the teens and mid-
20s - prognosis worse in
infants and elderly 2/2
higher rates of perforation
406b
What is the prognosis
of acute pancreatitis?
WHAT IS RANSON'S
CRITERIA?
407a
RANSON'S CRITERIA is used to determine the prognosis and mortality rates:
*pts with more than 3 or 4 Ranson's criteria should be monitored in ICU
1. (GALAW) Admission criteria:
Glucose >200;
Age>55YO;
LDH >350;
AST>250;
WBC>16,000
2. Initial 48 hours criteria (C HOBBS)
Ca2+ < 8 mg/dL
Decrease in Hematocrit (>10%)
PaO2 < 60 mm Hg
BUN increase >8mg/dL
Base deficit > 4 mg/dL
Fluid sequestration > 6L
3. Mortality
<3 criteria - 1%
3-4 criteria - 15%
5-6 criteria - 40%
>7 criteria - 100%
407b
What is the prognosis
of HCC?
408a
If it is unresectable then the
prognosis is less than 1 year
-if it is RESECTABLE then 25%
of patients can live > 5 years
408b
What is the recurrence
rate post surgical
resection of CRC
within 3 years?
409a
90%
409b
What is the risk of
CRC in patients with
FAP?
410a
100% by age 30 or 40 thus
requires prophylactice
colectomy for treatment
410b
What is the treatment for acute
mesenteric ischemia?
411a
Supportive: IV fluids, broad-spec antibiotics
-direct intr-arterial infusion of papaverine (vasodilator) into the
superior mesenteric system during arteriography is the therapy of
choice for all arterial causes of acute mesenteric ischemia
-direct intra-arterial infusions of thrombolytics or embolectomy
inficated in pations with embolic acute mesenteric ischemia
-heparin anticoagulation is the treatment of choice for venous
thrombosis
-surgery (resection if nonviable bowel) may be needed in all types of
acute mesenteric ischemia if signs of peritonitiis develops
411b
WHAT IS THE
TREATMENT FOR
BILE DUCT
STRICTURE
412a
ENDOSCOPING STENTING IS
PREFERRED OR SURGICAL
BYPASS IF OBSTRUCTION IS
COMPLETE OR IF
ENDOSCOPIC
SPINCTEROTOMY
412b
What is the treatment
for chronic
pancreatitis?
413a
Nonoperative management: narcotic analgesics for pain; bowel rest
(NPO); pancreatic enzymes inhibit CCK release and thus decrease
pancreatic secretions after meals; H2 blockers inhibit gastric acid
secretion, preventing degradation of the pacnreatic enzyme
supplements by gastric acid; INSULIN may be necessary if SEVERE
pancreatitis; alcohol abstinence; small volume low fat meals - may
improve abdominal pain.
Surgical managment on chronic pancreatitis: main goal is relief of
incapacitating abdominal pain.
1. pancreaticojejunostomy (Pancreatic duct drainage procedure to
decompress the dilated pancreatic duct - most common)
2. Pancreatic resection (distal pancreatectomy, Whipples procedure)
413b
What is the treatment
for diverticulosis?
414a
1. High fiber foods (bran)
increase the stool bulk
2. Psyllium *if the patient
cannot tolerate bran)
414b
What is the treatment
for GI bleeding:
415a
1. If the patient is hemodynamically unstable, resuscitation is always TOP priority
-remember CABs - once the patient is stabilized , obtain a diagnosis
A. supplemental O2
B. place two large bore IV lines. Give IV fluids or blood if pateint is volume dep
C. draw blood for hgb, hct, PT, pTT, plt, INR; monitor hgb Q4Q8
D. Continue to monitor until 24 hours of stable hgb
E. type and crossmatch adequate blood (PRBCs). Transfuse as the clinical condition demands *shock, patients with
cardiopulmonary DZ
2. Treatment depends on the CAUSE/SOURCE
A. UPPER GI BLEED
i. EGD with coag of bleeding vessel. If bleeding cont, repeast endoscopic therapy or proceed with ligation therapy
B. LOWER GI BLEED -
i. colonoscopy - polyp excision, injection, laser, cautery
ii. arteriogrphic vasoconstrictor infusion
iii. surgical resection of involved area - last resort
3. Indications for surgery
-hemodynamically unstable patients who have not responded to IV fluid, transfusion, endoscopic intervention or correction of
coags
-severe initial bleed or recurrence of bleed post treatment
-continued bleeding for more than 24 hours
-visible vessel at base of ulcer (30-50%) chance of rebleed
-ongoing transfusion requirement (5U within first 4-6 hours)
415b
What is the treatment of
patients with suspected
ascending cholangitis?
416a
1. Blood cultures
2. IV fluids
3. Empiric antibiotics with good
anaerobe and gram - coverage -
4. Decompress the CBD when patient
becomes hemodynaicmally stable.
416b
What is the
TREATMENT of PBC?
417a
Rx:
1. Cholestyramine for the pruritis
2. Vitamin D, Calcium, Bisphosphonates for
osteoporosis
3. Ursodeoxycholic acid (hydrophilic bile acid) has
been shown to slow progression
4. Liver transplantation is only curative therapy.
AUTOIMMUNE AB: (+) antimitochondrial
antibodies
417b
What is the treatment
regimen for H
PYLORI
418a
Triple therapy: PPI + 2 AB --> take 2x daily --> more exp than bismuth-based
Quadruple therapy: PPI + BISMUTH + 2 AB --> dalf the time as triple therapy
(1-week program opposed t 2 weeks for triple) --> expensive of PPI
-If H. pylori test positive then begin eradication therapy with triple or quad
therapy. BEGIN ACID SUPPRESSION WITH ANTACIDES OR A PPI
-if ACTIVE NSAID induecd ulcer - stop NSAID USE. Also begin with either PPI
or misoprostol. Continue 4-8 weeks depending on severity - treat the H. Pylori
infection
418b
What is the treatmet
for colonic polyps?
419a
Complete removal of the
polyp
419b
What medication should
be avoided in patients
with mesenteric ischemia?
420a
Vasopressors because
it worsens the
ischemia.
420b
What patients should
not be treated if acute
infections diarrhea is
clinically present?
421a
Pts with mild disease without systemic
toxicity or dehydration
pts with spontaneously remitting sxs
pts with suspected shiga toxin-producing
e. coli infection (O157H7) --> bloody
diarrhea in an afebrile pt with a h/o eating
raw hamburger or seed sprouts or visiting
a petting zoo
421b
What percent of patients
with biliary coloic
develop acute
cholecystitis in 2 years?
422a
33%
422b
What risks can
exacerbate PUD?
423a
1. Smoking
2. Alcohol and coffee
3. Emotional stress
and type A personality
423b
What type of hernia (esophageal) accounts for
90% of cases. Both the gastroesophageal juntion
and portion of the stomach herniates into the
thorax through the esophageal hiatus (so that the
GE junction is above the diaphragm)
This is also the most common and benign finding
that is assocated with GERD
424a
SLIDING HERNIA
424b
When is discharge
appropriate for CA-P?
425a
When VS are stable for 24hr (temp <100;
RR<24; HR<100, SBP >90, sat 90%)
-able to take ATB po
-able to maintain hydration and nutrition
-MS is normal or at baseline
-no other active clinical or psychosocial
issues requireing ongoing hositalization
425b
When might an upper GI bleed
result in hematochezia?
426a
If the bleeding is very briskand doesnt
remain in colon to turn into melena
-this indicated heavy bleeding and patient
often has some degree of hemodynamic
instability
-an upper GI leed source is present in 5%
of patients with hematochezia
426b
When should a
CULTURE be drawn
on a skin and soft
tissue infection:
427a
Systemic symptoms/signs
sepsis syndrome
abscess or draining pus
necrotizing infection
immunocompromised host
DO NOT ATTEMPT TO CULTURE
CELLULITIS IN PTS WITH INTACT SKIN
427b
When should a patient be
hospitalized for CA-pnemonia?
428a
CAP The CURB-65 score
1. Confusion (1 point)
2. BUN >19 (1 point)
3. RR >/= 30 (1 point)
4. SBP <90 or DBP </= 60 (1 point)
5. Age >/= 65 (1 point)
CURB score: 0-1 low risk, outpt rx; 2 short inpatient stay or
closely monitored supervised outpt treatment; 3-5 severe
pneumonia, inpt managment
428b
When should therapy
be considered in acute
infectious diarrhea?
429a
Treatment for febrile, CA-diarrhea should be
considered for the pt with:
1. sig systemic tox and dehydration esp in ver
young and very old (>70)
2. bloody diarrhea or dysentery
3. fecal WBCs or lactoferrin
4. immunocompromising conidtions
5. suspected complicating bacteremia
429b
Where are most
polyps found?
430a
rectosigmoid region and
most patients are
assymptomatic
-#1 symptoms is rectal
bleeding
430b
Which
aminotransferase is
more specific for liver
damage?
431a
ALT>AST
431b
Which esophageal cancer is the
most common in the USA?
432a
Used to be SCC > 90%
cases but not the incidence
of adenocarcinoma has
increased dramatically in
the US
432b
Why might a serum
gastrin level be used in
the dx of PUD?
433a
If potential for ZE
syndrome as a diagosis
433b
Zenker's Diverticula v.
Traction Diverticula v.
Epiphrenic diverticula
434a
Zenkers - most common type; found in upper 1/3 of the esophagus: failure of the
cricopharyngeal muscle to relax during swallowing leads to increased intraluminal pressure.
This causes outpouching of mucosa through an area of weakness in the pharyngral
constrictors.
CLINICALLY: dysphagia, regurgitation, halitosis (BAD BREATH), weight loss, chronic cough
Traction diverticula: located in the midpoint of the esophagus near tracheal bifurcation. Due
to traction from continguous medistinal inflammation and adenopathy (pulmonary
tuberculosis). Tb causes hilar node scaring which causes retraction of the esophagus...it is
usually asym and causes no treatment
Epiphrenic diverticula: found in the lower third of the esophagus. It is usually associated with
spastic esophageal dysmotility or achalasia. Symptoms of dysphasia are more often realted
to the udnerlying motility disorder unless the diverticulum is very large.
434b