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Cholecystitis
http://mbbshelp.com
Definition
Cholecystitis is defined as inflammation of the
gallbladder that occurs most commonly because of
an obstruction of the cystic duct from
cholelithiasis. Ninety percent of cases involve
stones in the cystic duct (ie, calculous cholecystitis),
with the other 10% of cases representing
acalculous cholecystitis.
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Etiology
 Bacterial infection
 From:upper airway infection, urogenital inf, infect
dis of intestine, viral hepatitis
 Transmission of inf to GB:
 Hematogenous on the liver arteries
 Ascending from intestine due to Oddi's sphincter
failure, gastric hypo secretion
 Lymphogenous
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Infectious agent
 Enterococcus, Escherichia coli, Staf-k,
streptococcus, fungus
 10% HVB HVC
 Parasites –opistorhosis, ascaridosis
 Duodenobiliary reflux
 Allergy
 Chronic GIT diseases
 Acute chol-s
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Predisposing factors
1. Cholestasis due to
 bile-excreting ductus dyskinesis
 Obesity, pregnancy due to ↑intra-abdominal
pressure and bile-excreting difficulty
 Stress due to bile-excreting ductus dyskinesis
 dietary habits disturbance- rare eating promote
cholestasis, fatty and fried food provoke Oddi's
sphincter spasm
 If little use cellulose, appears bed dilution of bile
 Hypokinesis
 Congenital GB anomalies
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 Due to inflam GITD – reflexes way
 Dysbacteriosis
 Dysbolism
 Promote phys-chem behaviour of bile
 Heredidy problem
Bile is bactericidal.
Inflamation developed if
bacteria+discholia+↓immunity+ GB wall pr
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Patogenetic factors:
 Neurodistrophic changes of GB wall
 Neuroendocrine abnormalities
 ↑Symp s-m and hormone (cholecyctokinine, pancreasimine,
hastrine, glucagon, insulin, secretin): provoke weakening of
GB and ↑tone of Oddi's sphincter, after accumulate GB
 Parasymp s-m and hormone (neurotensine, enkefaline,
thyreoid h, anticholecyctokinin): spastic contraction of GB,
weakening Oddi's sphincter and bile evacuated
 Cholestasis and Discholia
 GB wall pr
 Allergy
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Classification
1. Etiologic:
 Bacterial
 Viral
 Parasitical
 Nomicrobial
 Alergical
 Enzymal
 Unknow
2.Clinical
 Acalculeus
 Calculeous
3.Type of diskinesis
 Hypokinetic
 Hyperkinetic
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Clinical current
 Rare recidiving
 Rarely recidiving
 Permanent
 Atypical
Phase of D
 Exacerbation or decompensation
 subcompensation
 compensation
Severity
 Light
 Moderate
 severe
Complication
 Reactivity
pancreatitis
 Reactivity
hepatitis
 Pericholecyctitis
 Duodenitis
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CP
Pain
 pain begins in the epigastric region and then localizes
to the right upper quadrant (RUQ).
 Although the pain may initially be described as
colicky
 radiating to the tip of the right scapula, clavicle,
shoulder.
 ↑pain after plentiful eating, fatty, spice, fried, hot,
cold food, aerated water, alcohol, stress, phys activity
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 Dyspepsia
(↓appet, vomit, belching, to feel bitterness,
meteorism, diarrhea)
 Itchy skin or biliary pruritus due to
irritation of skin’s nerve endings by bile
acid
 Fever
 Psychological disturbance (depression,
fatigue, emotional lability, irritability,
fatiguability)
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Physical
 Jaundice may be noted in approximately 15% of
patients.
 Kera s-m: local soreness in the GB projection
 Murphy sign, which is specific but not sensitive for
cholecystitis, is described as tenderness and an
inspiratory pause elicited during palpation of the
RUQ.
 Physical examination may reveal fever,
tachycardia, and tenderness in the RUQ or
epigastric region, often with guarding or rebound.
 A palpable gallbladder or fullness of the RUQ is
present in 30-40% of cases.
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Phys s-m of GB
 There are 3 group s-ms
1. Segmentary reflexity s-s showed
exacerbation of diseases
2. Reflexity points showed expansion of
irritation beyond segmentary innervation
3. S-s of irritation GB
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Segmentary reflexity s-s showed exacerbation of diseases
assesment when pressing
 Makkensi’s soreness point - at the
intersection of lateral border of abdomen
straight muscle and right rib arch
 Boas’s soreness point level of Th X-XI on
paravertebral line
 Zaharina Geda’s zone – zones of soreness
and hypersensitivity from upper 2 point
expansion
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Reflexity points showed expansion of irritation beyond
segmentary innervation showed recidiving processes
Appears soreness in palpation this points
 Bergman’s point- intraupper border of orbita
 Ionash’s Occipital point
 Mussi-georgievsk’s point-between right sterncl
mast branches
 Chariton’s intrascapular p – centre of horizontal
line over the centreof right scapula
 Lapinsk’s femoral p – centre of internal border
right femor
 Right poplitea p
 Plantar p – back of right foot
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S-s of irritation GB
 Kera’s s-m: local soreness when deep palpation of GB
 Murphy’s sign - tenderness and an inspiratory pause
elicited during palpation
 Gausman’s s-m- appears soreness when blow on right
hypochondrium in inspiration
 Ortner’s s-m- soreness when tapotement on the right rib
arch
 Aisenberg’s s-m – in standing position pts to rise on one's
toes, after that get down appears soreness
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Investigation
Normal Ultrasound parameters of GB:
 pear-shaped, ovoid or cilindrical configuration
 N size- L=6-9.5cm x 3-3.5cm
 Wall – homogeneous, thin line, with moderate, ↑echogenicity
 Wall thickness = 2mm
 Contour is uniform, accurate
Before U
 12h no eating
 Before 1-2h no eat black bred, pea, bean, milk, sauerkraut, grapes
 Enzyme drugs 1-2 x 3 pd, activated carbon before sleep
http://mbbshelp.com
Ultrasound parameters of CH CHol:
 Thickening of GB wall
 Consolidation of GB wall
 Deformation and uneven contour of GB
 No mowing GB in breathing
 No homogenous contents of GB
 Soreness when pressing with by US sensor
 ↑or ↓ size of GB
 ↓stretchability of GB
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X-ray:
 delayed emptying
 deformation of GB
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Severity
 Light – 1-2t per year execerb, 2-3 weeks,
no intensive pain, liver function normally,
no complic
 Moderate - 5-6t per year execerb, more 2-
3 weeks, intensive pain, liver function
abnormalities, complic
 Severe - 1-2t per mounth execerb,
prolonged, intensive pain, liver function
abnormalities, complic
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Calculeous cholecyctitis
Metabolic diseases of hepatobiliary
system, characterized with formation
of gall-stone.
http://mbbshelp.com
Etiology
 Inflammatory processes of HB system
 Metabolic changes of cholesterol and bilirubine (DM,
HLipidemia, gout, obesity)
 Genetic
 Malnutrition – more fatty food, purified carbohydrates
(promote acid reaction of bile,that ↓dilution of cholesterol)
 A hypovitaminosis
 Female sex
 Certain ethnic groups
 Drugs (especially hormonal therapy in women)
 Pregnancy
 Increasing age
http://mbbshelp.com
Differential Diagnoses
 Abdominal Aortic Aneurysm Gastritis, Acute
 Acute Mesenteric Ischemia Gastroesophageal Reflux Disease
 Amebic Hepatic Abscesses Hepatitis, Viral
 Appendicitis Myocardial Infarction
 Biliary Colic Nephrolithiasis
 Biliary Disease Pancreatitis, Acute
 Cholangiocarcinoma Peptic Ulcer Disease
 Cholangitis Pneumonia, Bacterial
 Choledocholithiasis Pregnancy and Urolithiasis
 Cholelithiasis Pyelonephritis, Acute
 Gallbladder Cancer Renal Disease and Pregnancy
 Gallbladder Mucocele Renal Vein Thrombosis
 Gallbladder Tumors
 Gastric Ulcers
http://mbbshelp.com
Treatment
 Diet
 Acute exacerb: 1-2 day warm drinking
(tea, juice etc) 3-6 glasses per day
cracker
 After , grinded foot (soup, semolina,
boiled rice, porridge, kissel,
 After curd, boiled fish, milled meat
 5-6 times per day
;
http://mbbshelp.com
Recommended fasting days
 Curd-kefir days 900gr kefir, 300gr curds
 Rice- stewed fruit – 1/5l compote, boiled
rice (50gr rice)
 Watermelon or grapes – 2kg
 Fruit 1.5-2 kg apple
 No use meat broth, adipose, yolk, spicy,
fried, broiled foot
,
http://mbbshelp.com
Treatment
 Arresting pain (platiphillin, papaverin,
NTG, analgin, baralgin, promedol, droperidol
i/v
 Antibacter treatment: eritromycin,
oxacillin, rifampicine, ampicillin,
tetracyclin, furosolidon, wefalosporin,
aminoglicosids
 Choleretics: chologon 0.2 1-2 tbx3,
Decholin 5-10 ml x 1 pd, allochol 1-2 tb x
3-4, festal 1-2 tb x 3-4,
 Cholekinetiks: kcilit 50-100 ml 2-3pd,
corbit 50-100 ml
http://mbbshelp.com
Calculeous
http://mbbshelp.com
Treatment
 For acute cholecystitis, initial treatment includes bowel rest, intravenous
hydration, analgesia, and intravenous antibiotics. For mild cases of acute
cholecystitis, antibiotic therapy with a single broad-spectrum antibiotic is
adequate. Some options include the following:
 The current Sanford guide recommendations include piperacillin/tazobactam
(Zosyn, 3.375 g IV q6h or 4.5 g IV q8h), ampicillin/sulbactam (Unasyn, 3 g IV
q6h), or meropenem (Merrem, 1 g IV q8h). In severe life-threatening cases, the
Sanford Guide recommends imipenem (500 mg IV q6h).
 Alternative regimens include a third-generation cephalosporin plus Flagyl (1 g IV
loading dose followed by 500 mg IV q6h).
 Bacteria that are commonly associated with cholecystitis include E coli and
Bacteroides fragilis and Klebsiella, Enterococcus, and Pseudomonas species.
 Emesis can be treated with antiemetics and nasogastric suction.
 Because of the rapid progression of acute acalculous cholecystitis to gangrene
and perforation, early recognition and intervention are required.
 Supportive medical care should include restoration of hemodynamic stability and
antibiotic coverage for gram-negative enteric flora and anaerobes if biliary tract
infection is suspected.
 Daily stimulation of gallbladder contraction with intravenous CCK has been
shown by some to effectively prevent the formation of gallbladder sludge in
patients receiving TPN.
http://mbbshelp.com

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Cholesystitis

  • 2. Definition Cholecystitis is defined as inflammation of the gallbladder that occurs most commonly because of an obstruction of the cystic duct from cholelithiasis. Ninety percent of cases involve stones in the cystic duct (ie, calculous cholecystitis), with the other 10% of cases representing acalculous cholecystitis. http://mbbshelp.com
  • 3. Etiology  Bacterial infection  From:upper airway infection, urogenital inf, infect dis of intestine, viral hepatitis  Transmission of inf to GB:  Hematogenous on the liver arteries  Ascending from intestine due to Oddi's sphincter failure, gastric hypo secretion  Lymphogenous http://mbbshelp.com
  • 4. Infectious agent  Enterococcus, Escherichia coli, Staf-k, streptococcus, fungus  10% HVB HVC  Parasites –opistorhosis, ascaridosis  Duodenobiliary reflux  Allergy  Chronic GIT diseases  Acute chol-s http://mbbshelp.com
  • 5. Predisposing factors 1. Cholestasis due to  bile-excreting ductus dyskinesis  Obesity, pregnancy due to ↑intra-abdominal pressure and bile-excreting difficulty  Stress due to bile-excreting ductus dyskinesis  dietary habits disturbance- rare eating promote cholestasis, fatty and fried food provoke Oddi's sphincter spasm  If little use cellulose, appears bed dilution of bile  Hypokinesis  Congenital GB anomalies http://mbbshelp.com
  • 6.  Due to inflam GITD – reflexes way  Dysbacteriosis  Dysbolism  Promote phys-chem behaviour of bile  Heredidy problem Bile is bactericidal. Inflamation developed if bacteria+discholia+↓immunity+ GB wall pr http://mbbshelp.com
  • 7. Patogenetic factors:  Neurodistrophic changes of GB wall  Neuroendocrine abnormalities  ↑Symp s-m and hormone (cholecyctokinine, pancreasimine, hastrine, glucagon, insulin, secretin): provoke weakening of GB and ↑tone of Oddi's sphincter, after accumulate GB  Parasymp s-m and hormone (neurotensine, enkefaline, thyreoid h, anticholecyctokinin): spastic contraction of GB, weakening Oddi's sphincter and bile evacuated  Cholestasis and Discholia  GB wall pr  Allergy http://mbbshelp.com
  • 8. Classification 1. Etiologic:  Bacterial  Viral  Parasitical  Nomicrobial  Alergical  Enzymal  Unknow 2.Clinical  Acalculeus  Calculeous 3.Type of diskinesis  Hypokinetic  Hyperkinetic http://mbbshelp.com
  • 9. Clinical current  Rare recidiving  Rarely recidiving  Permanent  Atypical Phase of D  Exacerbation or decompensation  subcompensation  compensation Severity  Light  Moderate  severe Complication  Reactivity pancreatitis  Reactivity hepatitis  Pericholecyctitis  Duodenitis http://mbbshelp.com
  • 10. CP Pain  pain begins in the epigastric region and then localizes to the right upper quadrant (RUQ).  Although the pain may initially be described as colicky  radiating to the tip of the right scapula, clavicle, shoulder.  ↑pain after plentiful eating, fatty, spice, fried, hot, cold food, aerated water, alcohol, stress, phys activity http://mbbshelp.com
  • 11.  Dyspepsia (↓appet, vomit, belching, to feel bitterness, meteorism, diarrhea)  Itchy skin or biliary pruritus due to irritation of skin’s nerve endings by bile acid  Fever  Psychological disturbance (depression, fatigue, emotional lability, irritability, fatiguability) http://mbbshelp.com
  • 12. Physical  Jaundice may be noted in approximately 15% of patients.  Kera s-m: local soreness in the GB projection  Murphy sign, which is specific but not sensitive for cholecystitis, is described as tenderness and an inspiratory pause elicited during palpation of the RUQ.  Physical examination may reveal fever, tachycardia, and tenderness in the RUQ or epigastric region, often with guarding or rebound.  A palpable gallbladder or fullness of the RUQ is present in 30-40% of cases. http://mbbshelp.com
  • 14. Phys s-m of GB  There are 3 group s-ms 1. Segmentary reflexity s-s showed exacerbation of diseases 2. Reflexity points showed expansion of irritation beyond segmentary innervation 3. S-s of irritation GB http://mbbshelp.com
  • 15. Segmentary reflexity s-s showed exacerbation of diseases assesment when pressing  Makkensi’s soreness point - at the intersection of lateral border of abdomen straight muscle and right rib arch  Boas’s soreness point level of Th X-XI on paravertebral line  Zaharina Geda’s zone – zones of soreness and hypersensitivity from upper 2 point expansion http://mbbshelp.com
  • 16. Reflexity points showed expansion of irritation beyond segmentary innervation showed recidiving processes Appears soreness in palpation this points  Bergman’s point- intraupper border of orbita  Ionash’s Occipital point  Mussi-georgievsk’s point-between right sterncl mast branches  Chariton’s intrascapular p – centre of horizontal line over the centreof right scapula  Lapinsk’s femoral p – centre of internal border right femor  Right poplitea p  Plantar p – back of right foot http://mbbshelp.com
  • 17. S-s of irritation GB  Kera’s s-m: local soreness when deep palpation of GB  Murphy’s sign - tenderness and an inspiratory pause elicited during palpation  Gausman’s s-m- appears soreness when blow on right hypochondrium in inspiration  Ortner’s s-m- soreness when tapotement on the right rib arch  Aisenberg’s s-m – in standing position pts to rise on one's toes, after that get down appears soreness http://mbbshelp.com
  • 18. Investigation Normal Ultrasound parameters of GB:  pear-shaped, ovoid or cilindrical configuration  N size- L=6-9.5cm x 3-3.5cm  Wall – homogeneous, thin line, with moderate, ↑echogenicity  Wall thickness = 2mm  Contour is uniform, accurate Before U  12h no eating  Before 1-2h no eat black bred, pea, bean, milk, sauerkraut, grapes  Enzyme drugs 1-2 x 3 pd, activated carbon before sleep http://mbbshelp.com
  • 19. Ultrasound parameters of CH CHol:  Thickening of GB wall  Consolidation of GB wall  Deformation and uneven contour of GB  No mowing GB in breathing  No homogenous contents of GB  Soreness when pressing with by US sensor  ↑or ↓ size of GB  ↓stretchability of GB http://mbbshelp.com
  • 20. X-ray:  delayed emptying  deformation of GB http://mbbshelp.com
  • 21. Severity  Light – 1-2t per year execerb, 2-3 weeks, no intensive pain, liver function normally, no complic  Moderate - 5-6t per year execerb, more 2- 3 weeks, intensive pain, liver function abnormalities, complic  Severe - 1-2t per mounth execerb, prolonged, intensive pain, liver function abnormalities, complic http://mbbshelp.com
  • 22. Calculeous cholecyctitis Metabolic diseases of hepatobiliary system, characterized with formation of gall-stone. http://mbbshelp.com
  • 23. Etiology  Inflammatory processes of HB system  Metabolic changes of cholesterol and bilirubine (DM, HLipidemia, gout, obesity)  Genetic  Malnutrition – more fatty food, purified carbohydrates (promote acid reaction of bile,that ↓dilution of cholesterol)  A hypovitaminosis  Female sex  Certain ethnic groups  Drugs (especially hormonal therapy in women)  Pregnancy  Increasing age http://mbbshelp.com
  • 24. Differential Diagnoses  Abdominal Aortic Aneurysm Gastritis, Acute  Acute Mesenteric Ischemia Gastroesophageal Reflux Disease  Amebic Hepatic Abscesses Hepatitis, Viral  Appendicitis Myocardial Infarction  Biliary Colic Nephrolithiasis  Biliary Disease Pancreatitis, Acute  Cholangiocarcinoma Peptic Ulcer Disease  Cholangitis Pneumonia, Bacterial  Choledocholithiasis Pregnancy and Urolithiasis  Cholelithiasis Pyelonephritis, Acute  Gallbladder Cancer Renal Disease and Pregnancy  Gallbladder Mucocele Renal Vein Thrombosis  Gallbladder Tumors  Gastric Ulcers http://mbbshelp.com
  • 25. Treatment  Diet  Acute exacerb: 1-2 day warm drinking (tea, juice etc) 3-6 glasses per day cracker  After , grinded foot (soup, semolina, boiled rice, porridge, kissel,  After curd, boiled fish, milled meat  5-6 times per day ; http://mbbshelp.com
  • 26. Recommended fasting days  Curd-kefir days 900gr kefir, 300gr curds  Rice- stewed fruit – 1/5l compote, boiled rice (50gr rice)  Watermelon or grapes – 2kg  Fruit 1.5-2 kg apple  No use meat broth, adipose, yolk, spicy, fried, broiled foot , http://mbbshelp.com
  • 27. Treatment  Arresting pain (platiphillin, papaverin, NTG, analgin, baralgin, promedol, droperidol i/v  Antibacter treatment: eritromycin, oxacillin, rifampicine, ampicillin, tetracyclin, furosolidon, wefalosporin, aminoglicosids  Choleretics: chologon 0.2 1-2 tbx3, Decholin 5-10 ml x 1 pd, allochol 1-2 tb x 3-4, festal 1-2 tb x 3-4,  Cholekinetiks: kcilit 50-100 ml 2-3pd, corbit 50-100 ml http://mbbshelp.com
  • 29. Treatment  For acute cholecystitis, initial treatment includes bowel rest, intravenous hydration, analgesia, and intravenous antibiotics. For mild cases of acute cholecystitis, antibiotic therapy with a single broad-spectrum antibiotic is adequate. Some options include the following:  The current Sanford guide recommendations include piperacillin/tazobactam (Zosyn, 3.375 g IV q6h or 4.5 g IV q8h), ampicillin/sulbactam (Unasyn, 3 g IV q6h), or meropenem (Merrem, 1 g IV q8h). In severe life-threatening cases, the Sanford Guide recommends imipenem (500 mg IV q6h).  Alternative regimens include a third-generation cephalosporin plus Flagyl (1 g IV loading dose followed by 500 mg IV q6h).  Bacteria that are commonly associated with cholecystitis include E coli and Bacteroides fragilis and Klebsiella, Enterococcus, and Pseudomonas species.  Emesis can be treated with antiemetics and nasogastric suction.  Because of the rapid progression of acute acalculous cholecystitis to gangrene and perforation, early recognition and intervention are required.  Supportive medical care should include restoration of hemodynamic stability and antibiotic coverage for gram-negative enteric flora and anaerobes if biliary tract infection is suspected.  Daily stimulation of gallbladder contraction with intravenous CCK has been shown by some to effectively prevent the formation of gallbladder sludge in patients receiving TPN. http://mbbshelp.com