Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clin Med 3 > Biliary Diseases > Flashcards

Biliary Diseases Flashcards

1
Q

what are the liver function tests?

A

ALT, AST, Alkaline Phosphatase, GGT, LDH, Bilirubin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is ALT? found where? released when? normal range?

A

type of LFT

found primarily in hepatocytes

released when cells are hurt or destroyed

normal is b/w 7-55 U/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

when does ALT increase?

A

whenever the hepatocytes are injured

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

do the LFTs test the function of the liver?

A

NO!!! they are just enzymes that are created in the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is AST? found where?

A

type of LFT

Found in liver, heart, muscle, intestine, pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

is the AST specific for liver disease?

A

no!!! when it goes up, doesn’t always mean the liver or hepatocytes are damaged - could be something else

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what does the AST follow?

A

the ALT - when ALT increases, so does AST

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

when is AST elevated 2 or 3x (vs ALT) giving an AST/ALT ratio >3?

A

Elevated 2 or 3x (vs ALT) in alcoholics

AST/ALT ratio >3 = alcohol underlying cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

AST normal range

A

8-48 U/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is alkaline phosphatase? found where?

A

type of LFT

found in liver (esp biliary tract), bones, intestines, & placenta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

when does the liver alkaline phosphatase rise? GGT?

A

with obstruction or infiltrative diseases (i.e. gallstone or tumors)

GGT is considered more specific to liver than AP (helps you determine if AP is elevated d/t biliary disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the normal range of alkaline phosphatase?

A

45-114 U/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is GGT?

A

enzyme found in many organs - highest concentration in the liver

a type of lLFT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

when is GGT elevated?

A

elevated in blood in most diseases that cause damage to liver or bile ducts

the first enzyme to be elevated in damage to the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

if alk phos is elevated and unsure if d/t bone or liver, what do you check?

A

the GGT

if normal GGT then likely d/t bone disease

if GGT elevated in setting of Alk phos, d/t liver disease

(elevated in 75% of ETOH abuse)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is LDH? elevated in? found where?

A

type of LFT

enzyme found in blood and liver

elevated in tissue damage, so if liver damaged, may be elevated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is bilirubin?

A

yellow pigment formed in the liver by the breakdown of Hgb and excreted in bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

when is bilirubin elevated?

A
  • jaundice
  • liver disease and blockage of the bile ducts
  • any process which increases the breakdown of RBCs (hemolytic anemia)
  • anything that affect the production or elimination of bilirubin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the 2 forms of bilirubin?

A

unconjugated bilirubin “indirect”

conjugated bilirubin “direct”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is unconjugated bilirubin “indirect”?

A

heme that is released from Hgb is converted to unconjugated bilirubin

it is carried by proteins to the liver

small amounts may be present in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is conjugated bilirubin “direct”?

A

when unconjugated bilirubin gets sugars added to it in the liver

it enters the bile and passes from the liver to the small intestines and is eliminated in the stool

normally, no conjugated bilirubin is present in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

total bilirubin range?

A

0.3 - 1.9 mg/dL

conjugated + unconjugated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

normal range of bilirubin?

A

0-0.3mg/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

hepatocellular pattern of liver enzymes

A

increased AST and ALT compared to Alk phos, bili +/- elevated

Ex: intrahepatic injuries

Hepatocytes damaged -> ALT and AST released from cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

cholestatis pattern of liver enzymes

A

increase in alk phos compared to AST, ALT, bili +/- elevated

elevated in biliary obstruction or duct injury d/t retention of bile acids in the liver

Extrahepatic - ex. biliary obstruction

Intrahepatic - ex. primary biliary cholangitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

isolated hyperbilirubinemia pattern of liver enzymes

A

increase in bilirubin but the AST/ALT and alk phos are normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what are the 3 sections of the gallbladder?

A

fundus, body, neck

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is the common bile duct?

A

cystic duct + hepatic duct join

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is the fxn of the gallbladder?

A
  • stores bile

- bile emulsifies fats - assisting in absorption of fats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is bile?

A

bile acids + phospholipids + cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is the function of bile?

A

used to help excrete cholesterol, aid in the digestion and absorption of fat, cholesterol and fat soluble vitamins in the intestines (A, D, E, K)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

where are bile acids stored?

A

in the gallbladder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

where are bile acids reabsorbed?

A

in the terminal ileum and then carried through the portal blood circulation to be reconjugated and secreted back into the bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what is cholestasis?

A

something is obstructing the secretion of bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

causes of cholestasis?

A
  • gallstones
  • gallstones in common bile duct
  • tumors
  • cysts
  • pancreatic problems
  • liver disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

cholestasis s/sx’s

A

RUQ pain, colicky, jaundiced, dark urine, weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what liver enzyme will be elevated in cholestasis?

A

alk phos will be elevated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

dx of choelstasis

A

US to look for stones, tumor or cause of blockage

CT or MRI (liver disease)
-MRI better for looking at liver, but can do CT if uncertain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what is cholelithiasis?

A

gallstones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

pathophysiology of cholelithiasis?

A

-form secondary to abnormal bile constituents

mechanism of gallstone formation:

  • increased biliary secretion of cholesterol
  • cholesterol crystals precipitate and form stone
  • gallbladder hypomotility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what are the 2 types of gallstones and which one is most common?

A

cholesterol stones (MOST COMMON)

pigment (calcium) stones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

cholelithiasis epidemiology

A

women > men

increases with age

native Americans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

cholelithiasis risk factors

A
  • **4 Fs
  • Fat, Fertile, Forty, Fair
  • obesity, pregnancy/OCP, age, fair skin

-forty is the magic number - incidence 4x higher b/w ages 40-69

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

cholelithiasis clinical presentation

A

-MANY ARE ASYMPTOMATIC (until stone gets stuck)

  • intermittent severe RUQ pain radiation to the scapular region (d/t diaphragm innervation)
  • pain can be epigastric w/radiation to the RUQ

-onset is sudden and can last from 30min - 5 hrs

  • N/V w/pain
  • pain can occur after eating high-fat meal
  • night>day
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

cholelithiasis dx

A

US - very sensitive even for small stones
-can use the US to assess the emptying and filling of the gallbladder

Plain film - won’t see many cholesterol stones (see pigment stones)

HIDA - looks at the functioning and emptying of the gallbladder
-determines if a cystic duct obstruction is present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what does the HIDA scan do?

A

looks at the functioning and emptying of the gallbladder
-determines if a cystic duct obstruction is present

used in cholelithiasis dx

US may not show obstruction so use HIDA scan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

when do you treat cholelithiasis?

A

only if pt is symptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

tx of cholelithiasis

A

laparoscopic cholecystectomy for symptomatic patient
-outpatient, w/ quick recovery, not for urgent/emergent

chenodeoxycholic and ursodeoxycholic acid if pt is symptomatic

  • requires lifelong administration
  • bile salt given PO to dissolve stones over 2 years time
  • for pts who refuse surgery and have a functioning gallbladder
  • gallstones do recur
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

who is chenodeoxycholic and ursodeoxycholic for?

A

its for tx of cholelithiasis if pt is symptomatic

-for pts who refuse surgery and have a functioning gallbladder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

acute cholecystitis caused by?

A 
gallstone obstruction (most of the time)
-gallstones obstruct the cystic duct
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

acute cholecystitis sx’s? PE signs?

A

RUQ/epigastric pain that is continuous and gradually worsens

fever, leukocytosis, N/V, anorexia

PE signs:
+ Murphy’s sign (pain on inspiration while press on RUQ)

-Courvoiser’s sign: a palpable gallbladder on PE b/c gallbladder dilates d/t obstruction of common bile duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what is acalculus cholecystitis?

A

an acute inflammatory condition in pts w/out gallstones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

acute cholecystitis labs

A

***elevated WBC (b/c of infection) - (leukocytosis with left shift)

-increased bili, increased AST/ALT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

acute cholecystitis imaging

A

RUQ US - shows stone and inflammation but not obstruction

Sonographic Murphy’s sign (+ Murphy’s sign when press US into RUQ)

HIDA scan - shows cystic duct obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

acute cholecystitis tx

A

NPO, IVF, Pain control (caution with Morphine)

IV abx (3rd gen cephs + Flagyl; severe cases need Fluoroquinolone + Flagyl)

LAP CHOLECYSTECTOMY - MAINSTAY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

why must you be cautious with Morphine when treating the pain of acute cholecystitis?

A

b/c Morphine can cause spasm of the sphincter of Oddi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

what is the mainstay of tx for acute cholecystitis?

A

lap cholecystectomy

often done w/in first 24-48 hrs after presentation or, less often, 4-8 wks after an acute episode

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

tx for acute cholecystitis pts that aren’t surgical candidates

A

percutaneous drainage

-relieves pressure in gallbladder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what is choledocolithiasis?

A

stone that gets into the common bile duct
-can form spontaneously in the duct even after cholecystectomy

COMPLICATION OF CHOLELITHIASIS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

choledocolithiasis labs

A

very elevated ALT/AST from obstruction, often >1000

elevated bilirubin

alk phos will rise slowly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

choledocolithiasis imaging

A

RUQ US and CT will show dilated ducts from stuck stone causing inflammation

MRCP (special type of MRI)

ERCP - reserved for therapeutic interventions - do sphincterotomy w/stent placement (take out stone and put in stent)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

what is cholangitis?

A

inflammation of the bile duct, complication of choledocolithiasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

cholangitis s/sx’s

A

CHARCOT’S TRIAD - fever, jaundice, severe RUQ pain

pruritis (b/c elevated bilirubin), dark urine, alcoholic stools

REYNOLDS PENTAD = Charcot’s triad + Hypotension and AMS

***THESE PTS ARE SICK, ENDOSCOPIC EMERGENCY

64
Q

what is Charcot’s triad?

A

fever, jaundice, severe RUQ pain

indicative of cholangitis

65
Q

what is Reynolds pentad?

A

Charcot’s triad (severe RUQ pain, fever, jaundice) + hypotension and AMS

66
Q

is cholangitis an emergency?

A

YES!!! ***THESE PTS ARE SICK, ENDOSCOPIC EMERGENCY

67
Q

cholangitis tx

A

Hang IV abx and go to ERCP stat (endoscopic sphincterotomy and stone extraction is key!!!)
-Ampicillin + Gentamycin or Cipro + Flagyl

After pt stable and stone is out, then do lap cholecystectomy

68
Q

what is key for cholangitis tx?

A

Endoscopic sphincterotomy and stone extraction

69
Q

once cholangitis pt is stable, how are they treated?

A

lap cholecystectomy

70
Q

what is primary sclerosis cholangitis?

A

chronic diffuse inflammation of the biliary system

leads to fibrosis and stricture of the biliary ducts

very rare

71
Q

primary sclerosis cholangitis risk factors

A
  • ***UC

- Crohn’s, 1st degree family member, HLA-88, DR-3, DR-4

72
Q

primary sclerosis cholangitis epidemiology

A

Men > women

age 20-50

73
Q

primary sclerosis cholangitis clinical presentation

A
  • progressive obstructive jaundice
  • fatigue
  • pruritis
  • anorexia
  • indigestion
74
Q

primary sclerosis cholangitis labs

A

elevated alk phos

low serum albumin (d/t malabsorption)

75
Q

primary sclerosis cholangitis dx

A

ERCP, MRI

Liver Bx - periductal fibrosis “onion skinning” - histology and antibody studies to look for autoimmune disease

76
Q

primary sclerosis cholangitis complications

A

-cholangocarcinoma (Cancer of the common bile duct - very poor prognosis)

  • gallstones
  • cholecystitis
  • gallbladder polyps
  • gallbladder carcinoma
77
Q

primary sclerosis cholangitis tx for acute bacterial

A

cipro 750mg BID - high dose

78
Q

chronic primary sclerosis cholangitis tx

A

Balloon dilatation or stenting (keeps duct open)

resection of dominant stricture

UC pts - colorectal screening to reduce colon cancer

cirrhosis + primary sclerosis cholangitis -> need liver transplant

79
Q

cirrhosis + primary sclerosis cholangitis pts need what tx?

A

liver transplant

80
Q

what type of organ is the pancreas?

A

retroperitoneal

81
Q

what does the sphincter of oddi do?

A

smooth muscle sphincter present around the common channel of the pancreatic duct and common bile duct

prevents reflux of duodenal juices into the pancreatic duct and CBD

82
Q

function of the pancreas?

A

part of the endocrine and digestive system

make endocrine hormones - insulin, glucagon, somatostatin

digestive - assists in digestion and absorption of nutrients in the small intestine; helps breakdown carbs, proteins, lipids

83
Q

what is the pathogenesis of pancreatitis?

A

not well understood

may include edema or obstruction of the ampulla of Vater or reflux of bile into pancreatic duct
(bile that is supposed to dump into small intestines is backed up and goes back into pancreatic duct)

84
Q

acute pancreatitis

A

occurs suddenly and may result in life-threatening complications

interstitial vs necrotic, 80% recover

85
Q

recurrent pancreatitis

A

25% will have a recurrence

most often d/t alcohol or cholelithiasis

86
Q

acute pancreatitis most common what?

A

most common inpatient GI dx

87
Q

most common causes of acute pancreatitis?

A

gallstone and chronic alcohol abuse account for 2/3 or more cases in US

88
Q

older age = what for acute pancreatitis?

A

worse prognosis

89
Q

what are the 2 most common occurrences of acute pancreatitis?

A

interstitial pancreatitis occurs most commonly
-acute inflammation of the pancreas and peri-pancreatic tissues W/OUT TISSUE NECROSIS

necrotizing pancreatitis
-inflammation associated w/pancreatic parenchymal necrosis and or peri-pancreatic necrosis and PANCREATIC BLOOD SUPPLY IS INTERRUPTED

90
Q

2 most common causes of acute pancreatitis?

A

GALLSTONES - MOST COMMON!!!

Alcohol

91
Q

acute pancreatitis complications

A

Multisystem Organ Failure - 30% mortality, after 48hrs increases to 50%

Ileus - large & small intestines stop moving

Pseudocyst - low incidence

Pancreatic necrosis - 17% mortality risk, may need percutaneous aspiration, abx, debridement
-pancreas starts digesting itself

92
Q

what are s/sx’s of Multisystem Organ Failure for acute pancreatitis?

A

Renal Failure - pre renal azotemia, may require dialysis in severe cases

Acute Respiratory Distress Syndrome - fluid not from cariogenic source, intravascular leakage of fluids in pancreatic bed and lungs

93
Q

acute pancreatitis sx’s

A

mid epigastric pain - abrupt onset, relieved with sitting forward -> HALLMARK

  • pain radiates to back
  • N/V are common
94
Q

what is the hallmark sx of acute pancreatitis?

A

mid epigastric pain - abrupt onset, relieved with sitting forward

95
Q

acute pancreatitis signs

A
  • EPIGASTRIC TENDERNESS

- jaundice, nausea

96
Q

signs of severe pancreatitis

A

Tachypnea, hypoxemia, hypotension

Cullen’s Sign (retroperitoneal hemorrhage around the umbilicus - bruising)

Grey Turner’s sign (ecchymosis of the flanks)

97
Q

acute pancreatitis hx work-up

A
  • gallstones
  • alcohol use
  • hypertriglyceridemia
  • autoimmune diseases affecting the pancreas
  • fam hx of pancreatic d/o
  • med hx
98
Q

acute pancreatitis lab analysis

A

Amylase - 3x ULN (elevated, but short half-life so falls w/acute episode so less sensitive)

LIPASE - 3x ULN

99
Q

acute pancreatitis imaging

A

CT scan of Abdomen IV contrast

Abd US

MRI

NOT NEEDED FOR DX

100
Q

is acute pancreatitis imaging needed for dx?

A

NO!!!

CT scan is saved usually saved for when deteriorating

101
Q

pancreatitis dx ≥2 of the following…

A

≥2 of the following:

  • characteristic midepigastric and pain +/- radiation to the back
  • lipase and/or amylase 3x ULN
  • CT confirmation of pancreatitis (don’t need this)
102
Q

acute pancreatitis management

A
  • admit to hospital (b/c decompensate quickly)
  • find and treat underlying cause
  • **-NPO (give pancreas a rest)
  • IVF (Lactated Ringer’s or NS)
  • analgesia
  • repeat labs assessing BUN/Cr, HCT q8-12 hrs
103
Q

how often do you repeat labs for acute pancreatitis and why?

A

repeat labs of BUN/Cr, HCT q8-12 hrs

helps determine how severe and how quickly they are going to deteriorate

want to make sure fluid won’t go into their lungs

104
Q

acute pancreatitis severity predictor scores

A

Ranson criteria (most common)

Apache II score

SIRS (systemic inflammatory response syndrome) score

BISAP

105
Q

what is the Ranson criteria?

A

Estimates mortality from pancreatitis. Done on admission (5 tests) and after 48h (6 tests). Poor predictor but used often.

106
Q

scores of Ranson criteria for acute pancreatitis

A

1-3 = mild pancreatitis

> 3 = more severe pancreatitis

107
Q

what is the SIRS score?

A

Predict severity of pancreatitis. Easily done at bedside. Temp, HR, RR, WBC.

reliably predicts severity of pancreatitis

tells you if pt is systemically sick

108
Q

difference b/w Ranson criteria and Apache II score?

A

Apache II score can be performed daily

109
Q

what is mild acute pancreatitis?

A

w/out local complications or organ failure

self-limited, subsides in 3-7 days

110
Q

what is moderate severe acute pancreatitis?

A
  • transient organ failure (<48 hrs)
  • local systemic complications minus organ failure
  • may/may not develop a local complication such as pseudocyst
111
Q

what is severe acute pancreatitis?

A

persistent organ failure >48 hrs

CT scan to assess for necrosis recommended

112
Q

what is chronic pancreatitis?

A

irreversible damage to the pancreas as distinct from the reversible changes noted in acute pancreatitis

histologic abnormalities, including chronic inflammation, fibrosis, and progressive destruction of both exocrine and eventually endocrine tissue (atrophy)
-can be inflammatory response to its own hormones & digestive enzymes

113
Q

what is the most common cause of chronic pancreatitis?

A

alcohol abuse

114
Q

causes of chronic pancreatitis

A
  • ALCOHOL ABUSE (M/C)
  • Idiopathic
  • Cig smoking (esp if alcoholic)
  • cystic fibrosis (children)
  • genetic defects
  • autoimmune pancreatitis
115
Q

chronic pancreatitis complications

A
  • NARCOTIC ADDICTION (b/c of so much pain)
  • Diabetes/impaired glucose tolerance - b/c pancreas makes insulin and now can’t make it
  • gastroparesis (intestines stop working)
  • malabsorption
  • biliary stricture
  • pancreatic carcinoma - hereditary pancreatitis 10x incr risk of pancreatic cancer
116
Q

chronic pancreatitis sx’s

A

calcifications, steatorrhea, and DM - classic

-abd pain, anorexia, N/V, weight loss

117
Q

chronic pancreatitis signs

A

PE findings are unimpressive

tenderness over pancreas - during attacks

118
Q

chronic pancreatitis dx (labs and imaging)

A

NO BIOMARKER FOR DISEASE SO HARD TO DX

Labs:

  • amylase/lipase mild-normal elevation
  • glucose may be elevated
  • secretin test: abnormal when >60% of pancreatic exocrine fxn has been lost (takes long time to occur)

Imaging:
abd CT is initial modality of choice
-not done every time pt has exacerbation, just for dx

119
Q

chronic pancreatitis tx

A

Low fat diet, no EtOH.
Abd pain=Hard to treat, try TCAs. Avoid opiates.
Steatorrhea=pancreatic enzyme

Endoscopic tx - sphincterotomy, stenting, stone extraction, drainage of pseudocyst

Whipple -> usually for tumor in head of pancreas

120
Q

what is diverticulosis?

A

a weakness in the wall of the colon resulting in outpouching (diverticula)
-mucosa and submucosa herniate thru muscle layer

-dx with colonoscopy

121
Q

what is diverticular bleed?

A

painless bleeding of diverticula

diverticula have blood supply -> so can bleed

122
Q

what is diverticulitis?

A

inflammation of diverticulum

EXTREME PAIN

123
Q

diverticulosis most common in what age? most common where in the colon? strongly correlated with what?

A
  • M/C in ppl >80 y/o
  • M/C is sigmoid diverticulosis (left side)
  • westernized diet strongly correlated
124
Q

complications of diverticula

A

they can perf and the contents are now in the peritoneal space

125
Q

diverticulosis risk factors

A
  • age
  • constipation (puts pressure on colon and causes weakness -> diverticula)
  • diet (high fat and red meat)
  • obesity
  • genetics (connective tissue disorders)
  • physical inactivity
126
Q

Complication of diverticulitis

A
  • abscess
  • obstruction
  • perforation
  • fistula (protrusion connects to bladder -> contents of the diverticula go into the bladder)
127
Q

diverticulosis dx

A

COLONOSCOPY

other studies incidental finding:
-CT, MRI, Barium Enema

128
Q

recurrent complications of diverticulitis

A

chronic abd pain; fibrosis w/strictures lead to ileum and bowel obstructions

129
Q

diverticulitis sx’s

A

Abd pain in LLQ that is CONSTANT AND LASTS SEVERAL DAYS (not colicky pain - doesn’t start/stop abruptly)

N/V, fever

Change in bowel habits
(constipation b/c of inflammation; diarrhea b/c body trying to rid infection)

130
Q

diverticulitis signs

A

Abd tenderness in LLQ - guarding, rigidity, rebound

131
Q

diverticulitis PE

A

vital signs, heart and lungs, abdomen, pelvis (female), back

132
Q

diverticulitis work-up labs

A

CBC w/diff

BMP - electrolytes can be off w/diarrhea

Urinalysis - looking for translocation of bacteria into the bladder

133
Q

diverticulitis work-up imaging

A

ABD CT/PELVIS WITH IV CONTRAST +/- PO CONTRAST
-hard for pt to swallow so do IV if can’t do PO

Abd and CXR - good for ileum, pneumoperitoneum (free air)

Can also do KUB - kidney urinary bladder Xray to see if any perforations

134
Q

diverticulitis management options - medical vs complicated

A

If complicated - ADMIT

Medical: acute uncomplicated can be treated non-operatively

Acute Complicated:

  • Micro perf = medical management
  • Abscess = may require IR drainage
  • Free perf = EMERGENCY SURGERY
  • Significant obstruction = Urgent to Emergent surgery
135
Q

acute diverticulitis medical management

A

Antibiotics - cover for enterobacteriaciae & gram neg anaerobe (B. Frag)
-Cipro & Flagyl

IVF (admitted)
Analgesia & antiemetics PRN (IV vs PO)
NPO vs Clear Diet vs normal diet

136
Q

acute diverticulitis goal of surgical management

A

to restore intestinal continuity if possible

137
Q

when do you do emergent surgery for diverticulitis?

A

free perf, +/- bowel obstruction

138
Q

when do you do urgent surgery for diverticulitis?

A

failure of medical tx; colonic obstruction; abscess failing non-operative intervention

139
Q

when do you do elective surgery for diverticulitis?

A

persistent pain, fistula development, pt w/prior diverticulitis complication, immunocompromised pt w/prior acute diverticulitis

140
Q

diverticulitis surgery options

A

One-Stage Procedure
-colon resection w/primary anastomosis (cut out diverticula and anastomose)

Two-Stage Procedure

  • colonic resection w/end colostomy (Hartmann’s procedure)
  • primary anastomosis w/diverting ileostomy
141
Q

what criteria do surgeons use to determine which procedure (One or Two stage) for diverticulitis?

A

Hinchey Classification Systems

142
Q

diverticulitis follow-up

A

Colonoscopy - for NEW DX of diverticulitis

  • do 6 weeks post-infection unless had one in last year (NEVER IN SOMEONE W/ACTIVE DIVERTICULITIS)
  • r/o colon cancer
  • assess diverticular disease

Diet Modifications
-consumer high fiber diet or long-term fiber supplementation

143
Q

Diverticular bleeding epidemiology

A
  • hemorrhage occurs in 5% w/diverticulosis
  • M/C cause of overt (hematochezia or maroon) lower GI bleeding in adults
  • MOST STOP SPONTANEOUSLY
144
Q

Diverticular bleeding etiology

A

vasa recta recurrent injury leading to weakness and bleeding

RIGHT COLONIC DIVERTICULA = MAJOR SOURCE

145
Q

Diverticular bleeding sx’s

A

PAINLESS hematochezia

PAINLESS maroon-color mixed w/stool (blood mixed with stool)

Bloating, cramping, urge to defecate (blood increases urge)

Hemodynamically unstable: syncope, lightheadedness, postural dizziness

146
Q

Diverticular bleeding signs

A

Abd - benign

BRBPR or dark

hemodynamically unstable

hypotension, tachycardia, pallor

147
Q

diverticular bleeding dx lab

A

Hgb/Hct - normal to decreased (MCV normal)

BMP - BUN/Cr normal

148
Q

Diverticular bleeding dx imaging

A

COLONOSCOPY - when pt is stable

Nuclear scintigraphy (tagged RBCs to see where bleeding from)

Angiography

149
Q

Diverticular bleeding PE

A

Vital signs: stable or unstable

Eyes/mouth: pale conjunctiva

Heart: tacky

Abdomen: soft, non-tender, active bowel sounds

Rectal: gross blood present

Anoscopy: no hemorrhoids (make sure no hemorrhoids b/c they love to bleed)

150
Q

Diverticular bleeding management

A

Resuscitation

  • two large bore IVs - need to put in fluid quickly
  • IVF NS
  • Type and Cross for blood - if Hct is dropping
  • Transfuse PRBCS pro

+/- NGT to r/o UGI
-if blood is dark and difficult to differentiate melena

Intervention if needed:
-bleeding often self-limited

151
Q

Diverticular bleeding surgery

A

COLONOSCOPY
-treat active bleeding w/submucosal epinephrine or endoscopic tamponade (makes blood vessels constrict and stop bleeding)

Angiography - alternative to colonoscopy, infuse vasoconstrictors

152
Q

when do you do surgery for Diverticular bleeding?

A
  • hemodynamically unstable
  • endoscopic or angiographic therapy unsuccessful
  • pts w/ recurrent episodes of bleeding
153
Q

what pts are more likely to get gallstones?

A

pts w/sickle cell anemia are more likely to get gallstones b/c have chronically elevated bile

154
Q

what is Courvoiser’s sign?

A

seen in acute cholecystitis

a palpable gallbladder on PE b/c gallbladder dilates d/t obstruction of common bile duct

155
Q

when is unconjugated bilirubin found in urine?

A

only with renal disease

Clin Med 3 (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions