digestive system disorder medical surgical.pdf
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About This Presentation
digestive system disorder
Slide Content
Nursing Intervention for Patients with
Gastrointestinal Disorders
1
Medical Surgical Nursing
Gastrointestinal Disorders
1
Medical Surgical Nursing
Chapter Content
1. Diseases of mouth and
related structures
Perio-dental diseases Peri-apical abscesses Stomatitis Parotitis Gingivitis Dental decay and carries
2
2. Disorder of esophagus AchalsiaOsophagitisEosophagial
diaverticulatis
Hiatus hernia3. Gastric disordersGastritis (acute, chronic)PUDPyloric stenosis
1. Diseases of mouth and
related structures
Perio-dental diseases Peri-apical abscesses Stomatitis Parotitis Gingivitis Dental decay and carries
2
2. Disorder of esophagus AchalsiaOsophagitisEosophagial
diaverticulatis
Hiatus hernia3. Gastric disordersGastritis (acute, chronic)PUDPyloric stenosis
Chapter Content cont. …
4. Disorder of lower GIT Intestinal obstruction Hernias Disorder of rectum Hemorrhoids Anal fissure Anal abscess
3
5. Acute inflammatory
intestinal disease
AppendicitisPeritonitis6. Diseases of biliary tract7. Diseases of liver
4. Disorder of lower GIT Intestinal obstruction Hernias Disorder of rectum Hemorrhoids Anal fissure Anal abscess
3
5. Acute inflammatory
intestinal disease
AppendicitisPeritonitis6. Diseases of biliary tract7. Diseases of liver
GIT Anatomy and Physiology Overview
GIT is 7- 8 m long pathwaySub-divisions:A. Digestive tract A tube extending from mouth to anus Open to environment at both ends Includes the:
Oral cavity Pharynx Esophagus Stomach Small intestine Large intestine
4
GIT is 7- 8 m long pathwaySub-divisions:A. Digestive tract A tube extending from mouth to anus Open to environment at both ends Includes the:
Oral cavity Pharynx Esophagus Stomach Small intestine Large intestine
4
GIT Anatomy and Physiology Overview…
B. Accessory organs
Teeth Tongue Salivary glands Liver Gall bladder Pancreas
5
B. Accessory organs
Teeth Tongue Salivary glands Liver Gall bladder Pancreas
5
GIT Anatomy and Physiology Overview…
6
6
Reading Assignment
Oral cavityMouthTeethEsophagusStomachParts of stomachFunctions of
stomach
Small intestineDuodenumJejunumIl
7
Large IntestineParts of large
intestine
Function of large
intestine
GIT--Blood SupplyGIT--InnervationsLiverBlood Circulation Into
and Out of Liver
Portal Venous
System
Oral cavityMouthTeethEsophagusStomachParts of stomachFunctions of
stomach
Small intestineDuodenumJejunumIl
7
Large IntestineParts of large
intestine
Function of large
intestine
GIT--Blood SupplyGIT--InnervationsLiverBlood Circulation Into
and Out of Liver
Portal Venous
System
Function of Digestive System
To break down food particles To absorb small molecules into bloodstream To eliminate undigested and unabsorbed
foods and other waste products from body
8
To break down food particles To absorb small molecules into bloodstream To eliminate undigested and unabsorbed
foods and other waste products from body
8
Function of Digestive System …
Digestive Processes Ingestion Peristalsis Digestion Absorption Defecation
9
Digestive Processes Ingestion Peristalsis Digestion Absorption Defecation
9
Assessment & Physical Examination of GIT
AssessmentHealth history Identify c/c It is also important to determine: When health problems or symptoms were
started
Past and current medication used Any previous diagnostic studies Treatment and surgery It is also important to asking about the use of
tobacco and alcohol.
10
AssessmentHealth history Identify c/c It is also important to determine: When health problems or symptoms were
started
Past and current medication used Any previous diagnostic studies Treatment and surgery It is also important to asking about the use of
tobacco and alcohol.
10
Clinical Manifestations
Anorexia, nausea,
and vomiting
Regurgitation Vomitus smellingHematemesisHeartburnDysphagiaOdynophagia
11
Diarrhea Melena Hematochezia Jaundice Constipation Obstipation Risk factors for liverdiseases
Anorexia, nausea,
and vomiting
Regurgitation Vomitus smellingHematemesisHeartburnDysphagiaOdynophagia
11
Diarrhea Melena Hematochezia Jaundice Constipation Obstipation Risk factors for liverdiseases
Health Hx & C/M cont’d…
Abdominal Pain Character, duration, pattern, location,
distribution of referred pain and time of pain
vary greatly depending on underlying cause.
Three categoriesVisceral painParietal painReferred pain
12
Abdominal Pain Character, duration, pattern, location,
distribution of referred pain and time of pain
vary greatly depending on underlying cause.
Three categoriesVisceral painParietal painReferred pain
12
Visceral pain
Occurs when hollow abdominal organs such as
the intestine, liver or biliary tree contract
unusually forcefully or when they are distended
or stretched.
Characteristics
Difficult to localize May be gnawing, burning, cramping or aching When it becomes severe, it may be associated
with sweating, pallor, nausea, vomiting and
restlessness.
13
Occurs when hollow abdominal organs such as
the intestine, liver or biliary tree contract
unusually forcefully or when they are distended
or stretched.
Characteristics
Difficult to localize May be gnawing, burning, cramping or aching When it becomes severe, it may be associated
with sweating, pallor, nausea, vomiting and
restlessness.
13
Parietal pain
Originate in the parietal peritoneum and is caused
by inflammation.
Characteristics
It is steady aching pain Usually more severe than visceral pain More precisely localized over involved structure Typically aggravated by movement or coughing Patients with this type of pain usually prefer to lie
14
Originate in the parietal peritoneum and is caused
by inflammation.
Characteristics
It is steady aching pain Usually more severe than visceral pain More precisely localized over involved structure Typically aggravated by movement or coughing Patients with this type of pain usually prefer to lie
14
Referred pain
Felt in more distant sites, which are innervated
at approximately same spinal levels.
It may be felt superficially or deeply but is
usually well localized.
Pain may also be referred from abdomen to
chest, spine, or pelvis.
Pain of duodenal or pancreatic origin may be
referred to back
Pain from biliary tree radiate to right shoulder
or right posterior chest.
Pain from acute myocardial infarction may be
referred to upper abdomen.
15
Felt in more distant sites, which are innervated
at approximately same spinal levels.
It may be felt superficially or deeply but is
usually well localized.
Pain may also be referred from abdomen to
chest, spine, or pelvis.
Pain of duodenal or pancreatic origin may be
referred to back
Pain from biliary tree radiate to right shoulder
or right posterior chest.
Pain from acute myocardial infarction may be
referred to upper abdomen.
15
Common sites of referred abdominal
pain
16
pain
16
Physical Examination
Sequence of examining Gastrointestinal System 17
Sequence of examining Gastrointestinal System 17
Inspection
Scars Dilated veins Rashes and lesions Umbilicus PulsationsSymmetry of abdomen Bulging of flank Asymmetry due to enlarged organ or mass Lower abdominal mass- ovarian/uterine tumor
Respiratory movement
18
Scars Dilated veins Rashes and lesions Umbilicus PulsationsSymmetry of abdomen Bulging of flank Asymmetry due to enlarged organ or mass Lower abdominal mass- ovarian/uterine tumor
Respiratory movement
18
Auscultation
Used to determine bowel motilityBowel sound frequency and characteristics
Frequency of 5 to 34 per minute Normally, consists & gurgle sound Borborygmi:- long prolonged gurgles of hyper-peristalsis
Bruit:- may be heard over diseased aorta (by
aneurysm of aorta, renal artery stenosis)
19
Used to determine bowel motilityBowel sound frequency and characteristics
Frequency of 5 to 34 per minute Normally, consists & gurgle sound Borborygmi:- long prolonged gurgles of hyper-peristalsis
Bruit:- may be heard over diseased aorta (by
aneurysm of aorta, renal artery stenosis)
19
Sites of bruit auscultation
20
20
Percussion
Amount and distribution of gas in the abdomen Estimate size of liver and spleen Possible masses that are solid or fluid filled Distribution of tympany and dullness Protuberant abdomen that is tympanic
throughout
Intestinal obstruction Large dull areas Pregnant uterus, ovarian tumor, distended
bladder, large liver or spleen
Shifting dullness Ascites
21
Amount and distribution of gas in the abdomen Estimate size of liver and spleen Possible masses that are solid or fluid filled Distribution of tympany and dullness Protuberant abdomen that is tympanic
throughout
Intestinal obstruction Large dull areas Pregnant uterus, ovarian tumor, distended
bladder, large liver or spleen
Shifting dullness Ascites
21
Palpation
A. Light Palpation
To identify:Abdominal tendernessMuscular resistanceSome superficial organs and MassesReassure and relax patient
22
A. Light Palpation
To identify:Abdominal tendernessMuscular resistanceSome superficial organs and MassesReassure and relax patient
22
Palpation cont’d…
B. Deep palpationTo describe abdominal masses by their: Size, location, shape, consistency,
tenderness
Pulsations Any mobility with respiration or with examining hand Assessment for Peritoneal Inflammation Rebound tenderness
23
B. Deep palpationTo describe abdominal masses by their: Size, location, shape, consistency,
tenderness
Pulsations Any mobility with respiration or with examining hand Assessment for Peritoneal Inflammation Rebound tenderness
23
Palpation cont’d…
24
24
Diagnostic Evaluation
Stool tests for
Consistency and color Occult (not visible) blood Fecal fat, nitrogen, parasites, pathogens, food residues, and other
substances
Abdominal UltrasonographyImaging Studies MRI CT scans x-rayEndoscopic ProceduresLiver Function Tests
25
Stool tests for
Consistency and color Occult (not visible) blood Fecal fat, nitrogen, parasites, pathogens, food residues, and other
substances
Abdominal UltrasonographyImaging Studies MRI CT scans x-rayEndoscopic ProceduresLiver Function Tests
25
Reading AssignmentManagement of Patients with OralDisordersTooth decayDental plaque and cariesDento-alveolar abscess or peri-apical abscess
26
26
Dental Plaque and Caries
Tooth decay
An erosive process that begins with the action
of bacteria on fermentable carbohydrates in
mouth
Produces acids that dissolve tooth enamelBacteria produce acids from the breakdown of
sugars contained in food within 30 minutes after
eating
27
Tooth decay
An erosive process that begins with the action
of bacteria on fermentable carbohydrates in
mouth
Produces acids that dissolve tooth enamelBacteria produce acids from the breakdown of
sugars contained in food within 30 minutes after
eating
27
Dental Plaque and Caries …
Tooth decay …
The extent of damage to teeth depends on
following:
Presence of dental plaque Strength of acids and ability of saliva to
neutralize them
Length of time that acids are contact with
teeth
28
Tooth decay …
The extent of damage to teeth depends on
following:
Presence of dental plaque Strength of acids and ability of saliva to
neutralize them
Length of time that acids are contact with
teeth
28
Dental Plaque and Caries …
Dental Plaque Gluey, gelatin-like substance consisting of: Bacteria (lactobacilli and streptococcus mutans) Saliva and Epithelial cells that adheres to the teeth.
29
Dental Plaque Gluey, gelatin-like substance consisting of: Bacteria (lactobacilli and streptococcus mutans) Saliva and Epithelial cells that adheres to the teeth.
29
PP of Dental Caries30
31
Dental Plaque and Caries …32
Dental Plaque and Caries …33
Treatments
Common treatments
Removal of the softened and infected hard
tissues
FillingsDental implantsExtractions
34
Common treatments
Removal of the softened and infected hard
tissues
FillingsDental implantsExtractions
34
Prevention of Dental Carries
A. Mouth CareNormal mastication (chewing)- normal flow of
saliva
Brushing and flossing every dayWiping the teeth with a gauze padSwishing the mouth with an antiseptic
mouthwash several times before expectorating
35
A. Mouth CareNormal mastication (chewing)- normal flow of
saliva
Brushing and flossing every dayWiping the teeth with a gauze padSwishing the mouth with an antiseptic
mouthwash several times before expectorating
35
Prevention of Dental Carries …
B. Diet
Decreasing the amount of sugar and starch in
the diet
Snacks --less cariogenic alternativesFruitsVegetablesCheeses
36
B. Diet
Decreasing the amount of sugar and starch in
the diet
Snacks --less cariogenic alternativesFruitsVegetablesCheeses
36
Prevention of Dental Carries …
C. FluoridationPublic water supplies Applying a concentrated gel or solution to the teeth Adding fluoride to home water suppliesUsing fluoridated toothpaste or mouth rinseUsing sodium fluoride tablets, drops, or lozengesD. Pit and Fissure Sealants Applying a special coating to fill and seal pits and
fissures which last up to 7 years
E. Controlling diabetes
37
C. FluoridationPublic water supplies Applying a concentrated gel or solution to the teeth Adding fluoride to home water suppliesUsing fluoridated toothpaste or mouth rinseUsing sodium fluoride tablets, drops, or lozengesD. Pit and Fissure Sealants Applying a special coating to fill and seal pits and
fissures which last up to 7 years
E. Controlling diabetes
37
Dento-alveolar Abscess or Peri- apical Abscess
An abscessed tooth, involve collection of pus in the
apical dental perio-steum and tissue surrounding
the apex of the tooth.
It could be acute and chronic. Acute periapical abscess is usually secondary to
supporative pulpitis that arises from an infection
extending from dental caries.
38
An abscessed tooth, involve collection of pus in the
apical dental perio-steum and tissue surrounding
the apex of the tooth.
It could be acute and chronic. Acute periapical abscess is usually secondary to
supporative pulpitis that arises from an infection
extending from dental caries.
38
39
Peri-apical Abscess ...
Chronic dento alveolar abscess is slowly progressive
infectious process. Which eventually leads to “blind
dental abscess,”
Clinical ManifestationsDull, gnawing, continuous pain, often with a
surrounding cellulitis and edema
Gum opposite the apex of the tooth is usually swollen
on the cheek side
In well-developed abscesses, there may be a systemic
reaction fever and malaise.
40
Chronic dento alveolar abscess is slowly progressive
infectious process. Which eventually leads to “blind
dental abscess,”
Clinical ManifestationsDull, gnawing, continuous pain, often with a
surrounding cellulitis and edema
Gum opposite the apex of the tooth is usually swollen
on the cheek side
In well-developed abscesses, there may be a systemic
reaction fever and malaise.
40
41
Peri-apical Abscess ...42
Management
Warm salt-water rinses may be soothing.Antibiotics may be given to fight infectionNeedle aspiration an opening into pulp
chamber to relieve tension and pain and to
provide drainage
After the inflammatory reaction has subsided,
the tooth may be extracted
43
Warm salt-water rinses may be soothing.Antibiotics may be given to fight infectionNeedle aspiration an opening into pulp
chamber to relieve tension and pain and to
provide drainage
After the inflammatory reaction has subsided,
the tooth may be extracted
43
Stomatitis
An inflammation of mucous lining of any
structures in mouth
Causes
Poor oral hygienePoorly fitted denturesMouth burns from hot food or drinksConditions that affect entire body like
medications, allergic reactions, infections
Chronic irritation by tobacco:- called Nicotine
stomatitis
Dietary deficiencies of iron
44
An inflammation of mucous lining of any
structures in mouth
Causes
Poor oral hygienePoorly fitted denturesMouth burns from hot food or drinksConditions that affect entire body like
medications, allergic reactions, infections
Chronic irritation by tobacco:- called Nicotine
stomatitis
Dietary deficiencies of iron
44
Stomatitis …
Clinical manifestation
Redness,Swelling,Bleeding (Occasional)Excessive salivationHalitosis (Stale or foul smelling breathing)Sore of mouth
45
Clinical manifestation
Redness,Swelling,Bleeding (Occasional)Excessive salivationHalitosis (Stale or foul smelling breathing)Sore of mouth
45
Stomatitis …
Management
Removal or treatment of causeOral hygiene with soothing solutionsTopical medicationsSoft bland dietCorrecting any vitamin B
12
, iron, or folate deficiencyCessation of tobacco use
46
Management
Removal or treatment of causeOral hygiene with soothing solutionsTopical medicationsSoft bland dietCorrecting any vitamin B
12
, iron, or folate deficiencyCessation of tobacco use
46
Parotitis
An inflammation of parotid gland which are
large salivary glands located in front of each
ear
Causative agentsBacterial infection of Staphylococcus
aureus for adults
Virus:-epidemic(mump)forpediatrics
47Disorders of Salivary Glands
An inflammation of parotid gland which are
large salivary glands located in front of each
ear
Causative agentsBacterial infection of Staphylococcus
aureus for adults
Virus:-epidemic(mump)forpediatrics
47Disorders of Salivary Glands
Parotitis …
Sign and symptoms
Pain on gland and ear, Fever, Gland swollen and becomes tense or tender Swollen gland interferes swallowing, Swelling increase rapidly and becomes red
48
Sign and symptoms
Pain on gland and ear, Fever, Gland swollen and becomes tense or tender Swollen gland interferes swallowing, Swelling increase rapidly and becomes red
48
Parotitis …
Management Maintaining adequate nutritional & fluid
intake,
Good oral hygiene, Discontinuing medications (diuretics) that
can diminish salivation
Antibiotic therapy Analgesics to control pain If antibiotic therapy is not effective, gland
may need to be drained by surgical
procedure known as parotidectomy.
49
Management Maintaining adequate nutritional & fluid
intake,
Good oral hygiene, Discontinuing medications (diuretics) that
can diminish salivation
Antibiotic therapy Analgesics to control pain If antibiotic therapy is not effective, gland
may need to be drained by surgical
procedure known as parotidectomy.
49
Disorder of Esophagus
50
50
Achalasia
Absent or ineffective peristalsis of smooth muscle layer of distal esophagus (2/3
rd
of lower):-muscular ability to move food down to
esophagus
Accompanied by failure of esophageal
sphincter to relax in response to swallowing
Also known as
Esophageal achalasia Achalasia cardiae Cardiospasm Esophageal a peristalsis
51
Absent or ineffective peristalsis of smooth muscle layer of distal esophagus (2/3
rd
of lower):-muscular ability to move food down to
esophagus
Accompanied by failure of esophageal
sphincter to relax in response to swallowing
Also known as
Esophageal achalasia Achalasia cardiae Cardiospasm Esophageal a peristalsis
51
Etiology
Cause is unknown
Degeneration of nerve cells in muscular layer
of esophagus
Characterized by incomplete LES (lower esophageal
sphincter) relaxation
A peristalsis of esophagus in the absence of other
explanations like cancer or fibrosis
People 40 years of age or older
52
Cause is unknown
Degeneration of nerve cells in muscular layer
of esophagus
Characterized by incomplete LES (lower esophageal
sphincter) relaxation
A peristalsis of esophagus in the absence of other
explanations like cancer or fibrosis
People 40 years of age or older
52
Clinical Manifestations
Difficulty in swallowing both liquids and
solids
A sensation of food sticking in lower
portion of esophagus
Food regurgitation Complaint of chest pain & heart burn
(pyrosis)
53
Difficulty in swallowing both liquids and
solids
A sensation of food sticking in lower
portion of esophagus
Food regurgitation Complaint of chest pain & heart burn
(pyrosis)
53
Diagnosis
X-ray studies show esophageal dilation above
narrowing at GEJ (Gastro esophageal Junction)
CT scan Endoscopy Barium swallow Manometry
54
X-ray studies show esophageal dilation above
narrowing at GEJ (Gastro esophageal Junction)
CT scan Endoscopy Barium swallow Manometry
54
Management
Eating slowly and drinking fluids with mealsCalcium channel blockers and nitrates to
decrease esophageal pressure and improve
swallowing
Balloon (pneumatic) dilationSurgery: - esophago - myotomy
55
Eating slowly and drinking fluids with mealsCalcium channel blockers and nitrates to
decrease esophageal pressure and improve
swallowing
Balloon (pneumatic) dilationSurgery: - esophago - myotomy
55
Balloon (pneumatic) dilation56
Hiatal Hernia/ hiatus hernia
Normally, all part of stomach is below diaphragm
and completely being in abdomen
The muscle fibers in diaphragm around lower
esophagus help sphincter to keep esophagus closed
to prevent reflux of acid and food
It is protrusion (herniation) of upper part of stomach
into thorax through tear or weakness in diaphragm
It is also called diaphragmatic hernia or esophageal
hernia
57
Normally, all part of stomach is below diaphragm
and completely being in abdomen
The muscle fibers in diaphragm around lower
esophagus help sphincter to keep esophagus closed
to prevent reflux of acid and food
It is protrusion (herniation) of upper part of stomach
into thorax through tear or weakness in diaphragm
It is also called diaphragmatic hernia or esophageal
hernia
57
Types of hiatal hernia
1. Sliding Hernia
The upper stomach and GEJ are displaced
upward and slide in and out of thorax
Is the most common type (90%)58
1. Sliding Hernia
The upper stomach and GEJ are displaced
upward and slide in and out of thorax
Is the most common type (90%)58
2. Para-esophageal Hernia
The GEJ remains fixed in its normal location and
pouch of stomach is herniated (forming pocket)
beside GEJ through esophageal hiatus
59
The GEJ remains fixed in its normal location and
pouch of stomach is herniated (forming pocket)
beside GEJ through esophageal hiatus
59
Etiology
Actual cause not knownContributing factorsStructural changes like weakening of muscles in diaphragm
around GEJ
Increased age, traumaCongenital weaknessIncreased intra-abdominal pressure by:ObesityPregnancy
60
AscitesTumors
Actual cause not knownContributing factorsStructural changes like weakening of muscles in diaphragm
around GEJ
Increased age, traumaCongenital weaknessIncreased intra-abdominal pressure by:ObesityPregnancy
60
AscitesTumors
Clinical manifestations
S/S may be similar to that of:GERD,Peptic ulcer, andAnginaHeartburn/ burning painRegurgitationDysphagiaAt least 50% of patients are asymptomaticReflux in Sliding hiatal herniaFeeling sense of fullness after eating in
para-esophageal hernia
61
S/S may be similar to that of:GERD,Peptic ulcer, andAnginaHeartburn/ burning painRegurgitationDysphagiaAt least 50% of patients are asymptomaticReflux in Sliding hiatal herniaFeeling sense of fullness after eating in
para-esophageal hernia
61
Diagnosis
Barium swallow Esophagoscopy with biopsy X-ray studies Bronchoscopy62
Barium swallow Esophagoscopy with biopsy X-ray studies Bronchoscopy62
Management
A. Conservative management
Frequent, small feedingsAvoiding to recline for1 hour after eatingElevating head of bed on10-20cm blocksAnti-acids and anti-secretory agentsAvoidance of lifting and strainingElimination of alcohol and smokingWeight reduction if patient is obese
63
A. Conservative management
Frequent, small feedingsAvoiding to recline for1 hour after eatingElevating head of bed on10-20cm blocksAnti-acids and anti-secretory agentsAvoidance of lifting and strainingElimination of alcohol and smokingWeight reduction if patient is obese
63
Management
B. Surgical interventions
FundoplicationInvolves “wrapping” fundus of stomach
around lower portion of esophagus in varying
degrees (360,720,…)
64
360-degree wrap
B. Surgical interventions
FundoplicationInvolves “wrapping” fundus of stomach
around lower portion of esophagus in varying
degrees (360,720,…)
64
360-degree wrap
Gastro-esophageal Reflux Disease
(GERD)
GERD is not disease, it is syndrome
produced by condition that result in reflux
(back-flow) of gastric or duodenal secretions
in to esophagus
Stomach lining protects stomach from this
effects since its own acid production but
esophagus can’t protect itself then producing
S/S
65
(GERD)
GERD is not disease, it is syndrome
produced by condition that result in reflux
(back-flow) of gastric or duodenal secretions
in to esophagus
Stomach lining protects stomach from this
effects since its own acid production but
esophagus can’t protect itself then producing
S/S
65
GERD--Predisposing conditions
Incompetent LES Conditions resulting in gastric
contents near to GEJ
Bending down Hiatal hernia Certain drugs that interfere LES
function
Ingestion of alcohol Tobacco smoking
gastric
pressure
Dietary habits Fatty foods Chocolate Caffeinated Carbonated
beverages
Pyloric stenosis
66
Incompetent LES Conditions resulting in gastric
contents near to GEJ
Bending down Hiatal hernia Certain drugs that interfere LES
function
Ingestion of alcohol Tobacco smoking
gastric
pressure
Dietary habits Fatty foods Chocolate Caffeinated Carbonated
beverages
Pyloric stenosis
66
Clinical manifestations
PyrosisDyspepsia (indigestion)RegurgitationDysphagiaOdynophagiaHypersalivationEsophagitis
67
PyrosisDyspepsia (indigestion)RegurgitationDysphagiaOdynophagiaHypersalivationEsophagitis
67
Diagnosis
Barium swallow Esophagoscopy:- determine incompetence
of LES and extent of inflammation
Biopsy and cytologic analysis pH monitoring Motility (manometry) studies Bilirubin monitoring
68
Barium swallow Esophagoscopy:- determine incompetence
of LES and extent of inflammation
Biopsy and cytologic analysis pH monitoring Motility (manometry) studies Bilirubin monitoring
68
Management
A. Patient education
Low-fat dietAvoid caffeine, tobacco, beer, milk, foods, and
carbonated beverages which increase gastric
secretion
Encourage eating/ drinking 2 hrs. before
bedtime
Maintain normal body weightAvoid tight-fitting clothesElevateheadofthebedon15-20-cmblocks
69
A. Patient education
Low-fat dietAvoid caffeine, tobacco, beer, milk, foods, and
carbonated beverages which increase gastric
secretion
Encourage eating/ drinking 2 hrs. before
bedtime
Maintain normal body weightAvoid tight-fitting clothesElevateheadofthebedon15-20-cmblocks
69
GERD-- Mgt Cont’d…
B. Drugs
Antacids:- 1 to 2 hrs. after meals and at bed
time
Histamine receptor blockersProton pump inhibitors like omeprazoleMetoclopramide:- to increase LES pressure
and gastric emptying
70
B. Drugs
Antacids:- 1 to 2 hrs. after meals and at bed
time
Histamine receptor blockersProton pump inhibitors like omeprazoleMetoclopramide:- to increase LES pressure
and gastric emptying
70
Complications
Esophageal irritation and inflammationCorrosion to the esophagusScar tissue formation and decreased
dispensability secondary to inflammation and
irritation
Aspiration
71
Esophageal irritation and inflammationCorrosion to the esophagusScar tissue formation and decreased
dispensability secondary to inflammation and
irritation
Aspiration
71
1.2.
Is inflammation of gastric or stomach
mucosa
Is the result of breakdown in normal gastric
barrier (mucosa), which normally protects
stomach tissue from auto-digestion by acid
TypesAcute GastritisChronic Gastritis
72Gastritis
1.2.
Is inflammation of gastric or stomach
mucosa
Is the result of breakdown in normal gastric
barrier (mucosa), which normally protects
stomach tissue from auto-digestion by acid
TypesAcute GastritisChronic Gastritis
72Gastritis
Etiology-- Acute Gastritis
Drugs:Steroidal & NSAIDsAlcoholRadiationHelicobacter pyloriStaphylococcus
organisms
Bile and pancreatic
secretions
Physiology stress: shock,
sepsis, and burns
Psychologic stressSpicy, irritating foodsIngestion of strong acid or
alkali
Trauma: naso-gastric suction,
large hiatal hernia, endoscopic
techniques
73
Drugs:Steroidal & NSAIDsAlcoholRadiationHelicobacter pyloriStaphylococcus
organisms
Bile and pancreatic
secretions
Physiology stress: shock,
sepsis, and burns
Psychologic stressSpicy, irritating foodsIngestion of strong acid or
alkali
Trauma: naso-gastric suction,
large hiatal hernia, endoscopic
techniques
73
Etiology-- Chronic Gastritis
Repeated episodes of acute gastritisBenign or malignant ulcers of stomachBacteria Helicobacter pyloriDietary factors such as caffeineUse of medications like NSAIDsChronic alcohol abuseSmokingReflux of intestinal contents into stomach
74
Repeated episodes of acute gastritisBenign or malignant ulcers of stomachBacteria Helicobacter pyloriDietary factors such as caffeineUse of medications like NSAIDsChronic alcohol abuseSmokingReflux of intestinal contents into stomach
74
PP of Gastritis
Chronic Inflammation chronic alterations in protective mucosal barrier Progressive gastric atrophy Eventual death of chief and parietal cells Decreased number of acid-secreting parietal
cells
75
Hypochlorhydria Or
Achlorhydria
Chronic Inflammation chronic alterations in protective mucosal barrier Progressive gastric atrophy Eventual death of chief and parietal cells Decreased number of acid-secreting parietal
cells
75
Hypochlorhydria Or
Achlorhydria
Clinical Manifestation
Acute gastritisAnorexia, nausea and vomiting, hiccuppingEpigastric tendernessFeeling of fullness and abdominal discomfortHemorrhage associated with alcohol abuseHeadache usually self-limited lasting from few
hours to few days
76
Acute gastritisAnorexia, nausea and vomiting, hiccuppingEpigastric tendernessFeeling of fullness and abdominal discomfortHemorrhage associated with alcohol abuseHeadache usually self-limited lasting from few
hours to few days
76
C/Ms Cont’d…
Chronic gastritisS/S are similar to that of acute gastritisAnemia because of atrophy of cells producing
intrinsic factor
77
Chronic gastritisS/S are similar to that of acute gastritisAnemia because of atrophy of cells producing
intrinsic factor
77
Diagnosis
Endoscopic examination with biopsyComplete blood count (CBC)Stool exam for occult bloodSerologic test for H. pylori
78
Endoscopic examination with biopsyComplete blood count (CBC)Stool exam for occult bloodSerologic test for H. pylori
78
Management
Gastric mucosa is capable of repairing itself
after gastritis in1 day
Acute GastritisBed restRefraining from alcohol and food until
symptoms subside
Parentral fluid:- if symptoms persistNeutralizationAnti-acids like aluminum hydroxide if caused
by ingestion of strong acids
Diluted lemon juice if caused by strong alkali
79
Gastric mucosa is capable of repairing itself
after gastritis in1 day
Acute GastritisBed restRefraining from alcohol and food until
symptoms subside
Parentral fluid:- if symptoms persistNeutralizationAnti-acids like aluminum hydroxide if caused
by ingestion of strong acids
Diluted lemon juice if caused by strong alkali
79
Mgt Acute Gastritis Cont’d…
Anti-emetis for nausea and vomitingAnti-acidsHistamine antagonistsBlood transfusion and fluid replacement if
gastritis is hemorrhagic
Emergency surgery:Partial GastrectomyVagotomy
80
Anti-emetis for nausea and vomitingAnti-acidsHistamine antagonistsBlood transfusion and fluid replacement if
gastritis is hemorrhagic
Emergency surgery:Partial GastrectomyVagotomy
80
Mgt: Chronic Gastritis
Dietary & life styles modification reducing stressPromoting restInitiating pharmacotherapyAntibiotics:- to treat H. pyloriProton pump inhibitorBismuth saltsRegular injections of VitB12:- for patients with V-12 deficiency
anemia
81
Dietary & life styles modification reducing stressPromoting restInitiating pharmacotherapyAntibiotics:- to treat H. pyloriProton pump inhibitorBismuth saltsRegular injections of VitB12:- for patients with V-12 deficiency
anemia
81
Peptic Ulcer DiseaseGastric and Duodenal Ulcers
82
82
Definition
PUD is an excavation (hollowed-out area) that
forms in mucosal wall of stomach, duodenum,
pylorus, or esophagus
Results from digestive action of HCl & pepsinMore common in people b/n 40 & 60 yearsIncidenceRelatively uncommon in women childbearing
age
Almost equal to that in men after menopauseCan occur without excessive acid secretionUlcers are defined as breaks in mucosal surface
>5 mm in size, with depth to submucosa
83
PUD is an excavation (hollowed-out area) that
forms in mucosal wall of stomach, duodenum,
pylorus, or esophagus
Results from digestive action of HCl & pepsinMore common in people b/n 40 & 60 yearsIncidenceRelatively uncommon in women childbearing
age
Almost equal to that in men after menopauseCan occur without excessive acid secretionUlcers are defined as breaks in mucosal surface
>5 mm in size, with depth to submucosa
83
Damage of gastric mucosa from irritants84
Types of PUDa.b.
Depending on degree of mucosal involvementi. Acute PUDAssociated with superficial erosion & minimal
inflammation
ii. Chronic PUDLong duration, eroding through muscular wall with
formation of fibrous tissue
Present continuously for many months or
intermittently throughout person’s life
Is at least four times as common as acute erosionDepending on location of erosionGastric ulcer (GU)Duodenal ulcer (DU)
85
Depending on degree of mucosal involvementi. Acute PUDAssociated with superficial erosion & minimal
inflammation
ii. Chronic PUDLong duration, eroding through muscular wall with
formation of fibrous tissue
Present continuously for many months or
intermittently throughout person’s life
Is at least four times as common as acute erosionDepending on location of erosionGastric ulcer (GU)Duodenal ulcer (DU)
85
Cause
Infection with H. pylori Excessive secretion of HCl in stomach
because of:
Psychological stress e.g. anxiety and
physiological stress (like burn, shock, &
surgery)
Ingestion of milk and caffeinated beveragesIngestion of hot, rough, or spicy foodsAlcoholSmoking
86
Infection with H. pylori Excessive secretion of HCl in stomach
because of:
Psychological stress e.g. anxiety and
physiological stress (like burn, shock, &
surgery)
Ingestion of milk and caffeinated beveragesIngestion of hot, rough, or spicy foodsAlcoholSmoking
86
Cause …
Ulcerogenic drugsTumors like Zollinger-Ellison syndrome
(ZES): produce excessive amount of
hormone gastrin
GERD:- resulting esophageal ulcerFamilial tendency:- genetic link those with
blood type O
Pregnancy appears to protect women from
dlil
87
Ulcerogenic drugsTumors like Zollinger-Ellison syndrome
(ZES): produce excessive amount of
hormone gastrin
GERD:- resulting esophageal ulcerFamilial tendency:- genetic link those with
blood type O
Pregnancy appears to protect women from
dlil
87
Pathophysiology88
Acids, bile salts, aspirin, ischemia, H. pyloriBreakdown of gastric mucosal barrierAcid back-diffusion into mucosaDestruction of mucosal cells Acid & Pepsin release
Further mucosal erosionDestruction of B/VsBleeding
Histamine release
from damaged
mucosa
Vasodilation Capillary
permeability
Loss of plasma
proteins into gastric
lumen
Mucosal edemaULCERATION
Acids, bile salts, aspirin, ischemia, H. pyloriBreakdown of gastric mucosal barrierAcid back-diffusion into mucosaDestruction of mucosal cells Acid & Pepsin release
Further mucosal erosionDestruction of B/VsBleeding
Histamine release
from damaged
mucosa
Vasodilation Capillary
permeability
Loss of plasma
proteins into gastric
lumen
Mucosal edemaULCERATION
Clinical Manifestations
Symptoms may last for few days, weeks, or
months and may disappear only to reappear
without identifiable cause
Dull, gnawing pain or burning sensation in
mid epigastrium or in the back
89
Symptoms may last for few days, weeks, or
months and may disappear only to reappear
without identifiable cause
Dull, gnawing pain or burning sensation in
mid epigastrium or in the back
89
C/Ms…
Pain of duodenal ulcer origin Burning” or “cramping”Often located in
mid-epigastrium region
beneath xyphoid process
Back pain Usually relieved by eating
Pain of gastric ulcer origin Located highly in epigastrium Occurs about 1 to 2 hours after
meals
Can be burning” or “gaseous”
90
Pain of duodenal ulcer origin Burning” or “cramping”Often located in
mid-epigastrium region
beneath xyphoid process
Back pain Usually relieved by eating
Pain of gastric ulcer origin Located highly in epigastrium Occurs about 1 to 2 hours after
meals
Can be burning” or “gaseous”
90
C/Ms…
Sharply localized tenderness Around epigastrium or Slightly midline to right Pyrosis (heartburn) Emesis often containing undigested food
eaten many hours earlier
Bleeding – melana stools Epigastric tenderness Abdominal distention
91
Sharply localized tenderness Around epigastrium or Slightly midline to right Pyrosis (heartburn) Emesis often containing undigested food
eaten many hours earlier
Bleeding – melana stools Epigastric tenderness Abdominal distention
91
Emergency Complications
1.2.3.
3 major emergency complicationsHemorrhagePerforationGastric outlet obstruction92
1.2.3.
3 major emergency complicationsHemorrhagePerforationGastric outlet obstruction92
Complications …
1. Hemorrhage Is the most common observed complication CauseErosion of granulation tissue found at base of
ulcer during healing
Erosion of ulcer through major blood vessels
93
1. Hemorrhage Is the most common observed complication CauseErosion of granulation tissue found at base of
ulcer during healing
Erosion of ulcer through major blood vessels
93
Complications …
2. Perforation
The 2
nd
most common complication Commonly seen in large penetrating DU Occurs with ulcer penetrating serosa surface
with spillage of either gastric or duodenal
contents in to peritoneal cavity
S/SSudden, severe upper abdominal pain that
quickly spread throughout abdomen
Shallow and rapid respirationUsually absent bowel soundsNausea and vomiting
94
2. Perforation
The 2
nd
most common complication Commonly seen in large penetrating DU Occurs with ulcer penetrating serosa surface
with spillage of either gastric or duodenal
contents in to peritoneal cavity
S/SSudden, severe upper abdominal pain that
quickly spread throughout abdomen
Shallow and rapid respirationUsually absent bowel soundsNausea and vomiting
94
Complications …
3. Gastric outlet obstruction Is the least common ulcer-related complicationCauseInflammation and edema in peri-pyloric regionS/sLong history of ulcer painPain
Short duration or completely absentMore generalized upper abdominal
discomfort that becomes worse towards
end of day
May be relieved by belching or by
self-induced vomiting
95
3. Gastric outlet obstruction Is the least common ulcer-related complicationCauseInflammation and edema in peri-pyloric regionS/sLong history of ulcer painPain
Short duration or completely absentMore generalized upper abdominal
discomfort that becomes worse towards
end of day
May be relieved by belching or by
self-induced vomiting
95
Complications …
S/s of Gastric outlet obstructionVomiting:- which is very common and
projectile
Constipation:- as result of dehydrationSwelling in upper abdomen as result of
dilation of stomach
Loud peristalsis may be heard
96
S/s of Gastric outlet obstructionVomiting:- which is very common and
projectile
Constipation:- as result of dehydrationSwelling in upper abdomen as result of
dilation of stomach
Loud peristalsis may be heard
96
Duodenal vs Gastric Ulcers97Duodenal UlcerGastric UlcerLesionSuperficial; smooth
margins; round, oval, or
cone shaped
PenetratingIncidenceAge 30–60Male: female 2–3:180% of peptic ulcersUsually 50 and overMale: female 1:115% of peptic ulcersRisk FactorsH. pylori, alcohol, smoking,
and, stress
H. pylori, gastritis,
alcohol, smoking, use
of NSAIDs, stress
margins; round, oval, or
cone shaped
PenetratingIncidenceAge 30–60Male: female 2–3:180% of peptic ulcersUsually 50 and overMale: female 1:115% of peptic ulcersRisk FactorsH. pylori, alcohol, smoking,
and, stress
H. pylori, gastritis,
alcohol, smoking, use
of NSAIDs, stress
GUs Vs DUs …
98
Signs, Symptoms, and Clinical FindingsHyper-secretion of HClMay have weight gainPain occurs 2-3 hr. after
meal
Often awakened b/n 1-2 AMIngestion of food relieves
pain
Vomiting is uncommonHemorrhage less likelyMelena more common than
hematemesis
More likely to perforate
Normal/hypo-secretion of HClWeight loss may occurPain ¹⁄ -1 hr. after mealRarely occurs at nightMay be relieved by vomitingIngestion of food does not
help
Vomiting commonHemorrhage more likelyHematemesis more
common than melena
Less likely to perforate
Malignancy PossibilityRareOccasionally
Duodenal UlcerGastric Ulcer
98
Signs, Symptoms, and Clinical FindingsHyper-secretion of HClMay have weight gainPain occurs 2-3 hr. after
meal
Often awakened b/n 1-2 AMIngestion of food relieves
pain
Vomiting is uncommonHemorrhage less likelyMelena more common than
hematemesis
More likely to perforate
Normal/hypo-secretion of HClWeight loss may occurPain ¹⁄ -1 hr. after mealRarely occurs at nightMay be relieved by vomitingIngestion of food does not
help
Vomiting commonHemorrhage more likelyHematemesis more
common than melena
Less likely to perforate
Malignancy PossibilityRareOccasionally
Duodenal UlcerGastric Ulcer
Diagnosis
Fiberoptic endoscopyTo visualize inflammatory changes, ulcers, and
lesions
To obtain biopsy from gastric mucosaUpper GI barium:- contrast studyGastric secretory studiesCBC:– determine anemia secondary to
bleeding
Urine and stool tests:– for presence of bloodSerologictestforantibodiestoHpylori
99
Fiberoptic endoscopyTo visualize inflammatory changes, ulcers, and
lesions
To obtain biopsy from gastric mucosaUpper GI barium:- contrast studyGastric secretory studiesCBC:– determine anemia secondary to
bleeding
Urine and stool tests:– for presence of bloodSerologictestforantibodiestoHpylori
99
Management1.2.3.
Aim of treatmentTo decrease amount of gastric acidityTo enhance mucosal defense mechanismsTo minimize harmful effects on mucosa
100
Aim of treatmentTo decrease amount of gastric acidityTo enhance mucosal defense mechanismsTo minimize harmful effects on mucosa
100
Mgt…
Conservative management/minimum medical
Treatment
Adequate restDietary interventionsMedicationsElimination of smokingLong-term follow-up care
101
Conservative management/minimum medical
Treatment
Adequate restDietary interventionsMedicationsElimination of smokingLong-term follow-up care
101
Mgt…
Lifestyle modifications Adequate physical and emotional rest Quite and calm environment Elimination of stress Moderate in daily activity102
Lifestyle modifications Adequate physical and emotional rest Quite and calm environment Elimination of stress Moderate in daily activity102
Mgt…
Nutritional ManagementAvoiding irritant foods and beveragesHot, spicy foods and pepperAlcoholCarbonated beveragesTea and coffee Foods high in roughage such as raw fruits and vegetables
may irritate inflamed mucosa
103
Nutritional ManagementAvoiding irritant foods and beveragesHot, spicy foods and pepperAlcoholCarbonated beveragesTea and coffee Foods high in roughage such as raw fruits and vegetables
may irritate inflamed mucosa
103
Nutritional Mgt…i.ii.
MilkMilk proteins and calcium are stimulant to
gastric acid production
Can neutralize gastric acidityContains prostaglandins and growth factors
which protect the GI mucosa from injury
NBNo specific diet seems totally appropriate in
treatment of ulcer disease
Each patient should be instructed to eat and
drink foods and fluids that do not cause and
distressing or harmful side effects
104
MilkMilk proteins and calcium are stimulant to
gastric acid production
Can neutralize gastric acidityContains prostaglandins and growth factors
which protect the GI mucosa from injury
NBNo specific diet seems totally appropriate in
treatment of ulcer disease
Each patient should be instructed to eat and
drink foods and fluids that do not cause and
distressing or harmful side effects
104
Mgt…
Pharmacologic Therapy
1. Neutralizing agents – AntacidsAre initial drugs of choiceDecrease gastric acidity and acid content of
chyme reaching duodenum
Block conversion of pepesinogen to pepsin by
raising the pH to above 3.5
Some (like Al(OH)3) can bind to bile salts and
decrease their effects on gastric mucosa
e.g. Aluminum hydroxide and magnesium
tri-silcates
105
Pharmacologic Therapy
1. Neutralizing agents – AntacidsAre initial drugs of choiceDecrease gastric acidity and acid content of
chyme reaching duodenum
Block conversion of pepesinogen to pepsin by
raising the pH to above 3.5
Some (like Al(OH)3) can bind to bile salts and
decrease their effects on gastric mucosa
e.g. Aluminum hydroxide and magnesium
tri-silcates
105
Pharmacologic Mgt…
II. Antisecretory
a. Histamine H2-receptor antagonistsInhibit action of histamine at histamine H
2
receptor cells to reduce secretion of gastric
acid and total pepsin output
Ex: cimetidine, famotidine, ranitidine, nizatidineb. Proton pump inhibitors (H+, K+-ATPase
inhibitors)
Inhibit the H+, K+-ATPase enzyme systemBlock last step of acid production Ex: Omeprazole, Lansoprazole, Rabeprazole
106
II. Antisecretory
a. Histamine H2-receptor antagonistsInhibit action of histamine at histamine H
2
receptor cells to reduce secretion of gastric
acid and total pepsin output
Ex: cimetidine, famotidine, ranitidine, nizatidineb. Proton pump inhibitors (H+, K+-ATPase
inhibitors)
Inhibit the H+, K+-ATPase enzyme systemBlock last step of acid production Ex: Omeprazole, Lansoprazole, Rabeprazole
106
Pharmacologic Mgt…
III. CytoprotectiveA. SucralfateAccelerate healingDoesn’t have acid neutralizing effectShould be given at least 30 min. before or after anti
acid
B. Misoprostol Is a synthetic prostaglandin Protects gastric mucosa s mucus production and bicarbonate levelsC. Bismuth subsalicylate Suppresses H. pylori bacteria
107
III. CytoprotectiveA. SucralfateAccelerate healingDoesn’t have acid neutralizing effectShould be given at least 30 min. before or after anti
acid
B. Misoprostol Is a synthetic prostaglandin Protects gastric mucosa s mucus production and bicarbonate levelsC. Bismuth subsalicylate Suppresses H. pylori bacteria
107
Pharmacologic Mgt…
IV. Antibiotics for H. pylori /TripleTetracycline + proton pump inhibitor + bismuth
salts
Amoxicillin + clarithromycin + proton pump
inhibitor
Metronidazole + clarithromycin + proton pump
inhibitor
Clarithromycin + proton pump inhibitor +
amoxicillin
108
IV. Antibiotics for H. pylori /TripleTetracycline + proton pump inhibitor + bismuth
salts
Amoxicillin + clarithromycin + proton pump
inhibitor
Metronidazole + clarithromycin + proton pump
inhibitor
Clarithromycin + proton pump inhibitor +
amoxicillin
108
PUD Rx– DACA - Ethiopia
I. PUD only First LineRanitidine150 mg P.O. BID OR 300 mg at bedtime for 4-6 weeks Maintenance therapy: 150 mg at bedtime.AlternativesCimetidine400 mg P.O. BID, with breakfast and at night, OR800 mg at night for 4 - 6 weeksORFamotidine 40 mg, P.O. at night for 4-6 weeksOROmeprazole 20 mg P.O. QD for 4 weeks (DU) or 8 weeks
(GU)
109
I. PUD only First LineRanitidine150 mg P.O. BID OR 300 mg at bedtime for 4-6 weeks Maintenance therapy: 150 mg at bedtime.AlternativesCimetidine400 mg P.O. BID, with breakfast and at night, OR800 mg at night for 4 - 6 weeksORFamotidine 40 mg, P.O. at night for 4-6 weeksOROmeprazole 20 mg P.O. QD for 4 weeks (DU) or 8 weeks
(GU)
109
PUD Rx– DACA - Ethiopia …
II. PUD associated with H. pylori First LineAmoxicillin 1g P.O. BIDPLUSClarithromycin 500mg P.O. BID 7-14 daysPLUSOmeprazole, 20mg P.O. BID (or 40mg QD)AlternativeAmoxicillin 1g, P.O. BIDPLUSMetronidazole 500mg, P.O. BID 7-14 daysPLUSOmeprazole 20mg P.O. BID OR 40mg QD
110
II. PUD associated with H. pylori First LineAmoxicillin 1g P.O. BIDPLUSClarithromycin 500mg P.O. BID 7-14 daysPLUSOmeprazole, 20mg P.O. BID (or 40mg QD)AlternativeAmoxicillin 1g, P.O. BIDPLUSMetronidazole 500mg, P.O. BID 7-14 daysPLUSOmeprazole 20mg P.O. BID OR 40mg QD
110
PUD Rx-- DACA-Ethiopia …1.2.3.
Surgical ManagementUsually recommended for:Patients with intractable ulcersThose fail to heal after 12-16 weeks of medical
treatment
Life-threatening hemorrhage, perforation, or
obstruction
Those with Zollinger-Ellison syndrome not responding
to medications
TypesPyloroplasty:- pylorus is cut and re-sutured to relax
muscle and widen opening into intestine
VagotomyAntrectomyGastroduodenostomyGastrojejunostomy
111
Surgical ManagementUsually recommended for:Patients with intractable ulcersThose fail to heal after 12-16 weeks of medical
treatment
Life-threatening hemorrhage, perforation, or
obstruction
Those with Zollinger-Ellison syndrome not responding
to medications
TypesPyloroplasty:- pylorus is cut and re-sutured to relax
muscle and widen opening into intestine
VagotomyAntrectomyGastroduodenostomyGastrojejunostomy
111
Surgical Management …112
Nursing Diagnosis1.2.3.
Acute pain related to effect of gastric acid
secretion on damaged tissue
Imbalanced nutrition less than body
requirement related to changes in diet
Deficient knowledge about prevention of
symptoms and management of condition
113
Acute pain related to effect of gastric acid
secretion on damaged tissue
Imbalanced nutrition less than body
requirement related to changes in diet
Deficient knowledge about prevention of
symptoms and management of condition
113
Nursing Interventions
1. Relieving PainPatient education:To take prescribed drugsTo avoid aspirin, foods, and beverages that contain caffeineTo eat meals at regularly paced intervals in relaxed settingTeaching relaxation techniques to help manage stress and
pain
Enhance smoking cessation efforts
114
1. Relieving PainPatient education:To take prescribed drugsTo avoid aspirin, foods, and beverages that contain caffeineTo eat meals at regularly paced intervals in relaxed settingTeaching relaxation techniques to help manage stress and
pain
Enhance smoking cessation efforts
114
Nursing Interventions …
2. Maintaining Optimal Nutritional StatusAssesses patient for malnutrition and weight
loss
Advise patient about importance of complying
with medication regimen and dietary
restrictions
115
2. Maintaining Optimal Nutritional StatusAssesses patient for malnutrition and weight
loss
Advise patient about importance of complying
with medication regimen and dietary
restrictions
115
Nursing Interventions …
3. Teaching Patients Self-CareFactors that will help or aggravate conditionDrug informationAvoiding foods that aggravate symptoms and
potentially acid-producing foods
Eating meals at regular times and in relaxed
setting
Avoiding overeatingIrritant effects of smoking on ulcer and
cessation of smoking
116
3. Teaching Patients Self-CareFactors that will help or aggravate conditionDrug informationAvoiding foods that aggravate symptoms and
potentially acid-producing foods
Eating meals at regular times and in relaxed
setting
Avoiding overeatingIrritant effects of smoking on ulcer and
cessation of smoking
116
Nursing Interventions …
4. Teach about S/S of complications:i. Hemorrhagecool skin, confusion, ed heart rate, ed BP,
labored breathing, and blood in stool
ii. Penetration and perforationSevere abdominal pain, rigid and tender
abdomen, vomiting, ed temp, ed HR
iii. Pyloric obstructionNausea, vomiting, distended abdomen, and
abdominal pain
117
4. Teach about S/S of complications:i. Hemorrhagecool skin, confusion, ed heart rate, ed BP,
labored breathing, and blood in stool
ii. Penetration and perforationSevere abdominal pain, rigid and tender
abdomen, vomiting, ed temp, ed HR
iii. Pyloric obstructionNausea, vomiting, distended abdomen, and
abdominal pain
117
1. Appendicitis
Acute Inflammatory Intestinal
Disorder
118
Acute Inflammatory Intestinal
Disorder
118
Introduction
Appendix
Small finger-like appendage about 10cm
(4inch) long attached to cecum just below
ileo-cecal valve
Fills with food and empties regularly into
cecum
Because it empties inefficiently and its lumen
is small, appendix is prone to obstruction and
is particularly vulnerable to infection
119
Appendix
Small finger-like appendage about 10cm
(4inch) long attached to cecum just below
ileo-cecal valve
Fills with food and empties regularly into
cecum
Because it empties inefficiently and its lumen
is small, appendix is prone to obstruction and
is particularly vulnerable to infection
119
Definition
Appendicitis is inflammation of vermiform
appendix
EtiologyObstruction of lumen by:A fecality (accumulated feces)Foreign bodiesWorms (e.g. Pinworms, ascaris)Intra-mural thickening caused by lymphoid
hyperplasia
Tumors of cecum or appendix
120
Appendicitis is inflammation of vermiform
appendix
EtiologyObstruction of lumen by:A fecality (accumulated feces)Foreign bodiesWorms (e.g. Pinworms, ascaris)Intra-mural thickening caused by lymphoid
hyperplasia
Tumors of cecum or appendix
120
PP of Appendicitis
Obstruction Distension Venous engorgement Accumulation of mucus and bacteria (pus) Gangrene Perforation
121
Obstruction Distension Venous engorgement Accumulation of mucus and bacteria (pus) Gangrene Perforation
121
Clinical Manifestations
Vague epigastric or peri-umbilical painProgressing to RLQMay be accompanied by:Low-grade feverNausea and vomitingLoss of appetiteLocal tenderness is elicited at McBurney’s
point when pressure is applied
Guarding abdominal area by lying still with
right leg flexed at knee
122
Vague epigastric or peri-umbilical painProgressing to RLQMay be accompanied by:Low-grade feverNausea and vomitingLoss of appetiteLocal tenderness is elicited at McBurney’s
point when pressure is applied
Guarding abdominal area by lying still with
right leg flexed at knee
122
McBurney’s point
123
123
C/Ms …
a. Rebound tendernessb. Rovsing’s signElicited by palpating LLQ; this paradoxically
causes pain to be felt in RLQ
124
a. Rebound tendernessb. Rovsing’s signElicited by palpating LLQ; this paradoxically
causes pain to be felt in RLQ
124
C/Ms …c. Positive Psoas Sign
2 methods
1
st
MethodPlace your hand just above patient’s right
knee
Ask patient to raise that thigh against your
hand (extending right thigh)
2
nd
MethodAsk patient to turn onto left sideThen extend patient’s right leg at hipFlexion of leg at hip makes psoas muscle
contract; extension stretches it
125
2 methods
1
st
MethodPlace your hand just above patient’s right
knee
Ask patient to raise that thigh against your
hand (extending right thigh)
2
nd
MethodAsk patient to turn onto left sideThen extend patient’s right leg at hipFlexion of leg at hip makes psoas muscle
contract; extension stretches it
125
Possible Appendicitis-- Psoas Sign …
126
126
C/Ms…
d. Positive Obturator SignFlex patient’s right thigh at hip with knee
bent and rotate leg internally at hip
This maneuver stretches internal
obturator muscle
If appendix has rupturedPain becomes more diffuseAbdominal distention developPatient’s condition worsens
127
d. Positive Obturator SignFlex patient’s right thigh at hip with knee
bent and rotate leg internally at hip
This maneuver stretches internal
obturator muscle
If appendix has rupturedPain becomes more diffuseAbdominal distention developPatient’s condition worsens
127
Possible Appendicitis-- Obturator Sign128Obturator
Intemus Muscle
Intemus Muscle
C/Ms Cont’d…
Extent of tenderness depends on location of
inflamed appendix
Pain on defecation suggests that tip of
appendix is resting against rectum
Pain in urination suggest that tip is near to
bladder
If tip is in pelvis can be elicited only on rectal
examination
129
Extent of tenderness depends on location of
inflamed appendix
Pain on defecation suggests that tip of
appendix is resting against rectum
Pain in urination suggest that tip is near to
bladder
If tip is in pelvis can be elicited only on rectal
examination
129
Acute Complications
a.
b.c.
PerforationThe most common and generally occur 24 hours after onset
of pain
PeritonitisAbscess
130
a.
b.c.
PerforationThe most common and generally occur 24 hours after onset
of pain
PeritonitisAbscess
130
Diagnosis
HistoryComplete physical examinationLab tests CBC—ed WBCs (neutrophils >75%) Serum electrolyte profileAbdominal x-ray, ultrasound study, and CT scan
131
HistoryComplete physical examinationLab tests CBC—ed WBCs (neutrophils >75%) Serum electrolyte profileAbdominal x-ray, ultrasound study, and CT scan
131
Management
Surgery if appendicitis is diagnosed Antibiotics and intravenous fluids
To correct or prevent fluid and electrolyte
imbalance and dehydration, until surgery is
performed
Used for 6 to 8 hrs. before appendectomy if
appendix has ruptured and there is evidence of
peritonitis or abscess
Analgesics after diagnosis Appendectomy
132
Surgery if appendicitis is diagnosed Antibiotics and intravenous fluids
To correct or prevent fluid and electrolyte
imbalance and dehydration, until surgery is
performed
Used for 6 to 8 hrs. before appendectomy if
appendix has ruptured and there is evidence of
peritonitis or abscess
Analgesics after diagnosis Appendectomy
132
133 Appendectomy
Nursing Management
Patient preparation for surgeryIV infusion to replace fluid loss and promote
adequate renal function
Antibiotic therapy to prevent infectionEnema is not administered because risk of
perforation
Avoid self-treatment like use of laxatives &
enema to prevent perforation
Cold compress to RLQ to decrease blood flow
to area and impend inflammatory process
Heat is never used because it may cause
appendix to rupture
134
Patient preparation for surgeryIV infusion to replace fluid loss and promote
adequate renal function
Antibiotic therapy to prevent infectionEnema is not administered because risk of
perforation
Avoid self-treatment like use of laxatives &
enema to prevent perforation
Cold compress to RLQ to decrease blood flow
to area and impend inflammatory process
Heat is never used because it may cause
appendix to rupture
134
Nursing Mgt…
Postoperative carePlacing patient in a semi-Fowler positionOpioid, usually morphine sulfateOral fluids as toleratedFood is provided as desired and tolerated on
day of surgery
Ambulation begins at day of surgery or first
day of postoperative
Discharge on first or second postoperative dayNormal activities are resumed 2 to 3 weeks
after surgery
135
Postoperative carePlacing patient in a semi-Fowler positionOpioid, usually morphine sulfateOral fluids as toleratedFood is provided as desired and tolerated on
day of surgery
Ambulation begins at day of surgery or first
day of postoperative
Discharge on first or second postoperative dayNormal activities are resumed 2 to 3 weeks
after surgery
135
2. Peritonitis
Peritoneum is:Double-layered,
semi-permeable sac
Lines abdominal cavity and
covers some of abdominal
organs
1.2.3.4.5.6.7.8.
Peritoneal organs:LiverStomachGallbladderSpleenJejunum, ileumTransverse and sigmoid colonCecumAppendix
136
Peritoneum is:Double-layered,
semi-permeable sac
Lines abdominal cavity and
covers some of abdominal
organs
1.2.3.4.5.6.7.8.
Peritoneal organs:LiverStomachGallbladderSpleenJejunum, ileumTransverse and sigmoid colonCecumAppendix
136
Definition
Is an inflammation of peritoneumCausesThe most common causative organisms: Escherichia coli Klebsiella Proteus PseudomonasOthers organisims: Streptococci spp Staphylococci Pneumococci
137
Is an inflammation of peritoneumCausesThe most common causative organisms: Escherichia coli Klebsiella Proteus PseudomonasOthers organisims: Streptococci spp Staphylococci Pneumococci
137
Cause Peritonitis …
It can result fromDiseases of GI tractFrom internal reproductive organs (females)External sourcesInjury or trauma (e.g. gunshot wound, stab wound)Extension from inflammation of retroperitoneal
organs like kidneys
AppendicitisPerforated ulcerDiverticulitisBowel perforationAbdominal surgical procedures and peritoneal dialysis
138
It can result fromDiseases of GI tractFrom internal reproductive organs (females)External sourcesInjury or trauma (e.g. gunshot wound, stab wound)Extension from inflammation of retroperitoneal
organs like kidneys
AppendicitisPerforated ulcerDiverticulitisBowel perforationAbdominal surgical procedures and peritoneal dialysis
138
Clinical Manifestations
Symptoms depend on location and extent of
inflammation
S/S include:Pain
At first diffuse typeTend to become constant, localized, and more intense near to site
of inflammation
Usually aggravated by movement
139
Symptoms depend on location and extent of
inflammation
S/S include:Pain
At first diffuse typeTend to become constant, localized, and more intense near to site
of inflammation
Usually aggravated by movement
139
C/Ms…
Affected area of abdomen becomes extremely
tender, distended, and muscles become rigid
Rebound tendernessNausea and vomitingPeristalsis is diminishedIncreased temperature and pulse rateAlmost always elevated leukocyte count
140
Affected area of abdomen becomes extremely
tender, distended, and muscles become rigid
Rebound tendernessNausea and vomitingPeristalsis is diminishedIncreased temperature and pulse rateAlmost always elevated leukocyte count
140
Diagnosis
Lab testsIncreased leukocyte count ed Hemoglobin and hematocrit blood lossSerum electrolyte studiesAbdominal x-rayCT scan of abdomenPeritoneal aspiration and culture
141
Lab testsIncreased leukocyte count ed Hemoglobin and hematocrit blood lossSerum electrolyte studiesAbdominal x-rayCT scan of abdomenPeritoneal aspiration and culture
141
Management
Administration of several litters of isotonic
solution
AnalgesicsAntiemeticsIntestinal intubation and suctionOxygen therapy by nasal cannula or mask
142
Administration of several litters of isotonic
solution
AnalgesicsAntiemeticsIntestinal intubation and suctionOxygen therapy by nasal cannula or mask
142
Mgt…
Large doses of IV broad-spectrum antibiotic
until specific organism causing infection is
identified
Third-generation cephalosporinsCefetazidine 2 g IV TIDCeftriaxone 2 g IV dailyPatients with primary bacterial peritonitis
(PBP) usually respond within 72 hours to
appropriate antibiotic therapy
Administered for at list 5 days and can be
extended to 2 weeks
143
Large doses of IV broad-spectrum antibiotic
until specific organism causing infection is
identified
Third-generation cephalosporinsCefetazidine 2 g IV TIDCeftriaxone 2 g IV dailyPatients with primary bacterial peritonitis
(PBP) usually respond within 72 hours to
appropriate antibiotic therapy
Administered for at list 5 days and can be
extended to 2 weeks
143
Mgt…
SurgeryTo remove infected material and correct
cause
Includes:Excision (i.e. appendix)Resection with or without anastomosis (i.e.
intestine)
Repair (i.e. perforation)Drainage (i.e. abscess)
144
SurgeryTo remove infected material and correct
cause
Includes:Excision (i.e. appendix)Resection with or without anastomosis (i.e.
intestine)
Repair (i.e. perforation)Drainage (i.e. abscess)
144
Complications1.2.3.4.
Sepsis:- major cause of deathShock because of septicemia or hypovolemiaIntestinal obstruction with bowel adhesion as
result of inflammatory process
Wound evisceration and abscess formation S/STender or painful abdomenFeeling as something just gave way
145
Sepsis:- major cause of deathShock because of septicemia or hypovolemiaIntestinal obstruction with bowel adhesion as
result of inflammatory process
Wound evisceration and abscess formation S/STender or painful abdomenFeeling as something just gave way
145
A partial or complete blockage of bowel that
prevents normal flow of intestinal contents
through intestinal tract
Two types:
Mechanical obstruction Functional obstruction
146Intestinal Obstruction
A partial or complete blockage of bowel that
prevents normal flow of intestinal contents
through intestinal tract
Two types:
Mechanical obstruction Functional obstruction
146Intestinal Obstruction
Types of Intestinal Obstruction …
A. Mechanical ObstructionCause:Intra-luminal obstruction orObstruction from pressure on intestinal wallsAccounts for 90% of intestinal obstructionsExamples:1. Adhesions (50%)Loops of intestine become adherent (attach)
to areas that heal slowly or scar after
abdominal surgery
May produce kinking (sticking) of intestinal
loop
147
A. Mechanical ObstructionCause:Intra-luminal obstruction orObstruction from pressure on intestinal wallsAccounts for 90% of intestinal obstructionsExamples:1. Adhesions (50%)Loops of intestine become adherent (attach)
to areas that heal slowly or scar after
abdominal surgery
May produce kinking (sticking) of intestinal
loop
147
Types of Intestinal Obstruction …
2. Hernias (15%)Protrusion of intestine through weakened
area in abdominal muscle or wall
May result incomplete obstruction of
intestinal lumen and obstruction of blood flow
to area
3. IntussusceptionOne part of intestine slips (inter) into another
part located below it
Results in narrowing of intestinal lumen
148
2. Hernias (15%)Protrusion of intestine through weakened
area in abdominal muscle or wall
May result incomplete obstruction of
intestinal lumen and obstruction of blood flow
to area
3. IntussusceptionOne part of intestine slips (inter) into another
part located below it
Results in narrowing of intestinal lumen
148
Hernia (inguinal)
Intussusception
Types of Intestinal Obstruction …
149
Intussusception
Types of Intestinal Obstruction …
149
Types of Intestinal Obstruction …
4. VolvulusBowel twists and turns on itselfResults in obstruction to intestinal lumen
and accumulation of gas and fluid in
trapped bowel
5. Others include:Neoplasm (15%)StenosisStricturesAbscesses
150
Volvulus of sigmoid colon
4. VolvulusBowel twists and turns on itselfResults in obstruction to intestinal lumen
and accumulation of gas and fluid in
trapped bowel
5. Others include:Neoplasm (15%)StenosisStricturesAbscesses
150
Volvulus of sigmoid colon
Types of Intestinal Obstruction …
B. Functional ObstructionIntestinal musculature cannot propel (push)
contents along bowel as result of neuromuscular
or vascular disorders
Examples:Paralytic ilues (most common)Amyloidosis (D/o of amyloid fibrous protein)Muscular dystrophyEndocrine disorders such as diabetes mellitusNeurologic disorders such as Parkinson's disease
151
B. Functional ObstructionIntestinal musculature cannot propel (push)
contents along bowel as result of neuromuscular
or vascular disorders
Examples:Paralytic ilues (most common)Amyloidosis (D/o of amyloid fibrous protein)Muscular dystrophyEndocrine disorders such as diabetes mellitusNeurologic disorders such as Parkinson's disease
151
PP of small Intestinal obstruction
Accumulation of fluid, gas & intestinal content proximal to
obstruction
Abdominal distention and retention of fluid Reduced absorption of fluids and stimulation of more gastric
secretions
Increased fluid in lumen Increased intraluminal pressure Decreased venous and arteriolar capillary pressure Increased capillary permeability
152
Circulating bloodHypovolemic Shock
Edema, congestion,
necrosis
Perforation of intestinal wall
Peritonitis
Fluid and electrolyte extravasation to peritoneal cavity
Accumulation of fluid, gas & intestinal content proximal to
obstruction
Abdominal distention and retention of fluid Reduced absorption of fluids and stimulation of more gastric
secretions
Increased fluid in lumen Increased intraluminal pressure Decreased venous and arteriolar capillary pressure Increased capillary permeability
152
Circulating bloodHypovolemic Shock
Edema, congestion,
necrosis
Perforation of intestinal wall
Peritonitis
Fluid and electrolyte extravasation to peritoneal cavity
Clinical Manifestations
Crampy pain that is wavelike and colickySevere, steady pain strangulationIn absence of strangulation abdomen is not
tender
Passing blood & mucus with no fecal matter
and no flatus
Unmistakable signs of dehydrationAbdominal distensionNausea and vomiting
153
Crampy pain that is wavelike and colickySevere, steady pain strangulationIn absence of strangulation abdomen is not
tender
Passing blood & mucus with no fecal matter
and no flatus
Unmistakable signs of dehydrationAbdominal distensionNausea and vomiting
153
C/Ms Cont’d…
VomitingBilious rapid projectile vomiting obstruction located high in small bowelVomiting of fecal material Obstruction below proximal colon or in ileumProgression of vomitingVomiting Stomach contentsThen bile-stained contents of duodenum &
jejunum
Finally vomiting with pain, darker, fecal-like
contents of ileum
154
VomitingBilious rapid projectile vomiting obstruction located high in small bowelVomiting of fecal material Obstruction below proximal colon or in ileumProgression of vomitingVomiting Stomach contentsThen bile-stained contents of duodenum &
jejunum
Finally vomiting with pain, darker, fecal-like
contents of ileum
154
Diagnosis
History and physical examinationAbdominal x-ray studiesCT-scanUltrasoundBiopsyLaboratory studiesCBCd WBCs Strangulation or perforation ed hemoglobin or hematocrit Bleeding from neoplasm or strangulation with
necrosis
Serum electrolyte profile
155
History and physical examinationAbdominal x-ray studiesCT-scanUltrasoundBiopsyLaboratory studiesCBCd WBCs Strangulation or perforation ed hemoglobin or hematocrit Bleeding from neoplasm or strangulation with
necrosis
Serum electrolyte profile
155
Medical Management
Decompression of bowel through naso-gastric
or small bowel
Surgical intervention
IV therapy before surgery to replace depleted
water, sodium, chloride, and potassium
Include:Repairing herniaDividing adhesionRemoving portion of affected bowelRepairing by anastomosis
156
Decompression of bowel through naso-gastric
or small bowel
Surgical intervention
IV therapy before surgery to replace depleted
water, sodium, chloride, and potassium
Include:Repairing herniaDividing adhesionRemoving portion of affected bowelRepairing by anastomosis
156
Nursing Management1.2.
3.
Major Nursing Diagnoses may Include:Pain related to abdominal distension and
increased peristalsis
Fluid volume deficit related to decrease in
intestinal fluid re-absorption and loss of fluids
secondary to vomiting
Altered nutrition less than body requirement
related to intestinal obstruction and vomiting
157
3.
Major Nursing Diagnoses may Include:Pain related to abdominal distension and
increased peristalsis
Fluid volume deficit related to decrease in
intestinal fluid re-absorption and loss of fluids
secondary to vomiting
Altered nutrition less than body requirement
related to intestinal obstruction and vomiting
157
Large Bowel Obstruction
Attributes to15% of intestinal obstructionsCommonly occur in sigmoid colonThe most common causes:CarcinomaDiverticulitisInflammatory bowel disordersBenign tumors
158
Attributes to15% of intestinal obstructionsCommonly occur in sigmoid colonThe most common causes:CarcinomaDiverticulitisInflammatory bowel disordersBenign tumors
158
Clinical Manifestations
Unlike small intestine symptoms develop and
progress relatively slowly
Obstruction in sigmoid colon or rectumConstipation in patientDistention of abdomenVisible outlining of loops of large bowel
through abdominal wall
Crampy lower abdominal painFecal vomitingSymptoms of shock may occur
159
Unlike small intestine symptoms develop and
progress relatively slowly
Obstruction in sigmoid colon or rectumConstipation in patientDistention of abdomenVisible outlining of loops of large bowel
through abdominal wall
Crampy lower abdominal painFecal vomitingSymptoms of shock may occur
159
Diagnosis
History and physical examinationAbdominal x-ray studiesCT-scanUltrasoundBiopsyLaboratory studiesCBCSerum electrolyte profileBarium enemaTo locate large intestinal obstructionNot used if perforation is suspected
160
History and physical examinationAbdominal x-ray studiesCT-scanUltrasoundBiopsyLaboratory studiesCBCSerum electrolyte profileBarium enemaTo locate large intestinal obstructionNot used if perforation is suspected
160
Management
ColonoscopyInspection of interior surface of colonTo untwist and decompress bowelCecostomy
To make surgical opening into cecum for patient
Who are poor surgical risksIn need of urgent relief from obstructionTemporary or permanent colostomysurgical procedure where portion of large intestine is
brought out abdominal wall to carry stool
Ileoanal anastomosisTo remove entire large colonRectal tubeTo decompress area that is lower in bowel
161
ColonoscopyInspection of interior surface of colonTo untwist and decompress bowelCecostomy
To make surgical opening into cecum for patient
Who are poor surgical risksIn need of urgent relief from obstructionTemporary or permanent colostomysurgical procedure where portion of large intestine is
brought out abdominal wall to carry stool
Ileoanal anastomosisTo remove entire large colonRectal tubeTo decompress area that is lower in bowel
161
A protrusion of biological tissue, structure, or part
of organ through muscular tissue or biological
membrane
CausesCondition that increases pressure of abdominal
cavity
ObesityHeavy liftingCoughingStraining
162Abdominal hernia
A protrusion of biological tissue, structure, or part
of organ through muscular tissue or biological
membrane
CausesCondition that increases pressure of abdominal
cavity
ObesityHeavy liftingCoughingStraining
162Abdominal hernia
Types of hernias
1. Inguinal hernia
Most common hernias (up to 75%)For more understanding of inguinal hernias,
much insight is needed anatomy of inguinal
canal
Inguinal hernias divided into:Indirect inguinal herniaDirect inguinal hernia
163
1. Inguinal hernia
Most common hernias (up to 75%)For more understanding of inguinal hernias,
much insight is needed anatomy of inguinal
canal
Inguinal hernias divided into:Indirect inguinal herniaDirect inguinal hernia
163
Types of hernias …
a. Indirect inguinal hernia
Affects only menA loop of intestine passes down canal from
where testis descends early in childhood into
scrotum
Increase progressively in size causing scrotum
to expand grossly
b. Direct inguinal hernia:
Affects both sexes.The intestinal loop forms swelling in inner part
of fold of groin
164
a. Indirect inguinal hernia
Affects only menA loop of intestine passes down canal from
where testis descends early in childhood into
scrotum
Increase progressively in size causing scrotum
to expand grossly
b. Direct inguinal hernia:
Affects both sexes.The intestinal loop forms swelling in inner part
of fold of groin
164
165HerniaTypes of hernias …
Indirect Versus Direct inguinal hernias
166
166
Types of hernias …
2. Femoral hernia:Affects both sexes but most often women.An intestinal loop passes down canal
containing major blood vessels to and from leg
3. Umbilical herniaUmbilical hernias are especially common in
infants
They involve protrusion of intra abdominal
contents through weak at site at Umbilical cord
These hernias often resolve spontaneously
167
2. Femoral hernia:Affects both sexes but most often women.An intestinal loop passes down canal
containing major blood vessels to and from leg
3. Umbilical herniaUmbilical hernias are especially common in
infants
They involve protrusion of intra abdominal
contents through weak at site at Umbilical cord
These hernias often resolve spontaneously
167
Inguinal Versus Femoral hernia168
Types of hernias …
4. Incisional hernia
Occurs when defect is as result of an
incompletely healed surgical wound
These can be most frustrating and difficult to
treat, b/c of repaired tissue was already
attenuated
5. Hiatal Hernia (see previous class)Clinical manifestations
Pain and swelling
169
4. Incisional hernia
Occurs when defect is as result of an
incompletely healed surgical wound
These can be most frustrating and difficult to
treat, b/c of repaired tissue was already
attenuated
5. Hiatal Hernia (see previous class)Clinical manifestations
Pain and swelling
169
Hernia …
Complication
InflammationBowel obstructionStrangulatingManagement
Repairing weak abdomen part of abdominal
wall
Hernioplasty (mesh repair)HeriniotomyHernioraphy
170
Complication
InflammationBowel obstructionStrangulatingManagement
Repairing weak abdomen part of abdominal
wall
Hernioplasty (mesh repair)HeriniotomyHernioraphy
170
171
Diseases of Anorectum
Diseases of Anorectum
Hemorrhoids
Hemorrhoidal vein: are veins draining walls of
anal canal and rectum
Hemorrhoids are dilated portions of veins in anal
canal and are very common conditions
Typesi. Internal hemorrhoidsThose above internal sphincterii. External hemorrhoidsAppear outside external sphincterOccur at anal opening and may hang outside
anus
172
Hemorrhoidal vein: are veins draining walls of
anal canal and rectum
Hemorrhoids are dilated portions of veins in anal
canal and are very common conditions
Typesi. Internal hemorrhoidsThose above internal sphincterii. External hemorrhoidsAppear outside external sphincterOccur at anal opening and may hang outside
anus
172
173
174
Causes/Risk Factors
By the age of 50, about 50% of people have
hemorrhoids to some extent
Sliding of hemorrhoidal and vascular tissues
in wall of anal canal is during
defecationDiarrheaAnal infections
175
By the age of 50, about 50% of people have
hemorrhoids to some extent
Sliding of hemorrhoidal and vascular tissues
in wall of anal canal is during
defecationDiarrheaAnal infections
175
Cause/Risk Factors ….
ed pressure in hemorrhoidal tissue due to:Pregnancy or giving birthStrain during bowel movementsHolding back or waiting long time before
having bowel movement
Lifting heavy weightsSitting for long time on toiletOverweightCoughing or sneezing a lot of timeSitting or standing for long timeHaving liver disease like cirrhosis
176
ed pressure in hemorrhoidal tissue due to:Pregnancy or giving birthStrain during bowel movementsHolding back or waiting long time before
having bowel movement
Lifting heavy weightsSitting for long time on toiletOverweightCoughing or sneezing a lot of timeSitting or standing for long timeHaving liver disease like cirrhosis
176
Clinical Manifestations
Common reasons for seeking health care:BleedingProtrusionAnal itchingAnal ache or pain, especially while sittingPain during bowel movements
177
Common reasons for seeking health care:BleedingProtrusionAnal itchingAnal ache or pain, especially while sittingPain during bowel movements
177
C/Ms …
External hemorrhoids are associated with severe painInternal hemorrhoids are not usually painful until they bleed
or prolapse
Bright red blood on toilet tissue, stool, or in toilet bowlOne or more hard tender lumps near anus178
External hemorrhoids are associated with severe painInternal hemorrhoids are not usually painful until they bleed
or prolapse
Bright red blood on toilet tissue, stool, or in toilet bowlOne or more hard tender lumps near anus178
Diagnosis
HistoryPhysical examinationInspection of perianal regionCareful digital examinationAnoscopy
179
HistoryPhysical examinationInspection of perianal regionCareful digital examinationAnoscopy
179
Staging Staging of HemorrhoidsStageDescription of ClassificationIEnlargement with bleedingIIProtrusion with spontaneous
reduction
IIIProtrusion requiring manual
reduction
IVIrreducible protrusion
180
reduction
IIIProtrusion requiring manual
reduction
IVIrreducible protrusion
180
Management
Relieving hemorrhoidal symptoms and
discomfort
Good personal hygieneAvoiding excessive straining during defecationHigh-residue diet that contains fruit and fiberIncreased fluid intake to soften stoolApplication of ice packs for few hours
followed by warm compresses
Sitz bathsAnalgesic ointments and suppositories,
181
Relieving hemorrhoidal symptoms and
discomfort
Good personal hygieneAvoiding excessive straining during defecationHigh-residue diet that contains fruit and fiberIncreased fluid intake to soften stoolApplication of ice packs for few hours
followed by warm compresses
Sitz bathsAnalgesic ointments and suppositories,
181
Mgt…
Bed restT-binder to hold dressing in placeBismuth subsallate, insert one suppository in
rectum BID, or use topical application BID for
five days
Hemorrhoidectomy
182
Bed restT-binder to hold dressing in placeBismuth subsallate, insert one suppository in
rectum BID, or use topical application BID for
five days
Hemorrhoidectomy
182
Hepatic DysfunctionHepatic dysfunction results from damage to
liver’s parenchymal cells by:
Directly from primary liver diseasesIndirectly from obstruction of bile flow or derangements of hepatic
circulation
183Management of Patientswith Hepatic Disorders
liver’s parenchymal cells by:
Directly from primary liver diseasesIndirectly from obstruction of bile flow or derangements of hepatic
circulation
183Management of Patientswith Hepatic Disorders
Management of Patients with Hepatic
Disorders …
1.2.3.4.
Most common and significant symptoms of
liver disease
JaundicePortal hypertension and ascitesNutritional deficienciesHepatic encephalopathy or coma
184
Disorders …
1.2.3.4.
Most common and significant symptoms of
liver disease
JaundicePortal hypertension and ascitesNutritional deficienciesHepatic encephalopathy or coma
184
Jaundice/ Icterus
Is yellowish or greenish-yellow discoloration of
body tissues, including sclerae, mucosa, and skin
as result of abnormal elevation of bilirubin
concentration in blood
Is symptom rather than diseaseBecomes clinically evident when serum bilirubin
level exceeds 2.5 mg/dl
May result from impairment of:Hepatic uptakeConjugation of bilirubinExcretion of bilirubin into biliary system
185
Is yellowish or greenish-yellow discoloration of
body tissues, including sclerae, mucosa, and skin
as result of abnormal elevation of bilirubin
concentration in blood
Is symptom rather than diseaseBecomes clinically evident when serum bilirubin
level exceeds 2.5 mg/dl
May result from impairment of:Hepatic uptakeConjugation of bilirubinExcretion of bilirubin into biliary system
185
Types of Jaundice
1.2.3.4.
HemolyticHepato-cellularObstructiveHereditary hyper bilirubinemia186
1.2.3.4.
HemolyticHepato-cellularObstructiveHereditary hyper bilirubinemia186
I. Hemolytic/ Pre-hepatic Jaundice
Results from increased destruction of red
blood cells
Flood plasma with unconjugated bilirubin so
rapidly
CausesHemolytic transfusion reactionsSickle cell crisisHemolytic anemia
187
Results from increased destruction of red
blood cells
Flood plasma with unconjugated bilirubin so
rapidly
CausesHemolytic transfusion reactionsSickle cell crisisHemolytic anemia
187
I. Hemolytic Jaundice …
If prolonged it may result in:Formation of pigment stones in gallbladder Extremely severe jaundice (>20 to 25 mg/dl)
poses risk for brain stem damage
Lab Tests ed fecal and urine urobilinogenUrine is free of bilirubin
188
If prolonged it may result in:Formation of pigment stones in gallbladder Extremely severe jaundice (>20 to 25 mg/dl)
poses risk for brain stem damage
Lab Tests ed fecal and urine urobilinogenUrine is free of bilirubin
188
II. Hepato-cellular/ hepatic Jaundice
Caused by inability of damaged liver cells to: Take up bilirubin from blood, or Conjugate, orExcrete normal amount of Cirrhosisbilirubin from bloodPatients may be mildly or severely ill189
Caused by inability of damaged liver cells to: Take up bilirubin from blood, or Conjugate, orExcrete normal amount of Cirrhosisbilirubin from bloodPatients may be mildly or severely ill189
II. Hepatocellular Jaundice …
Causes of cellular damageInfection by viral hepatitis or other virusesMedication or chemical toxicity or alcoholHepatic carcinomaLab Tests: ed unconjugated and conjugated serum
bilirubin
ed Urine urobilinogen ed AST & ed ALT levels
190
Causes of cellular damageInfection by viral hepatitis or other virusesMedication or chemical toxicity or alcoholHepatic carcinomaLab Tests: ed unconjugated and conjugated serum
bilirubin
ed Urine urobilinogen ed AST & ed ALT levels
190
III. Obstructive / Post-hepatic Jaundice
Is due to impended or obstructed flow of bileA. Intra-hepatic obstructionMay involve obstruction of small bile ducts
within liver
Can be caused byPressure on these channels from
inflammatory swelling of liver
Inflammatory exudate within ducts
themselves
191
Is due to impended or obstructed flow of bileA. Intra-hepatic obstructionMay involve obstruction of small bile ducts
within liver
Can be caused byPressure on these channels from
inflammatory swelling of liver
Inflammatory exudate within ducts
themselves
191
III. Obstructive Jaundice …
B. Extra-hepatic obstruction
Caused by occlusion of bile duct by gallstone,
inflammatory process, tumor, or pressure from
enlarged organ
192
B. Extra-hepatic obstruction
Caused by occlusion of bile duct by gallstone,
inflammatory process, tumor, or pressure from
enlarged organ
192
III. Obstructive Jaundice …
Clinical FindingsBile backup into liver substance Reabsorbed into blood Carried throughout entire body Staining skin, mucous membranes, and sclera
Deep orange and foamy urineLight or clay-colored stoolThe skin may itch intenselyIntolerance to fatty foods
193
Clinical FindingsBile backup into liver substance Reabsorbed into blood Carried throughout entire body Staining skin, mucous membranes, and sclera
Deep orange and foamy urineLight or clay-colored stoolThe skin may itch intenselyIntolerance to fatty foods
193
III. Obstructive Jaundice …
Lab tests: AST, ALT levels generally rise moderately, ed conjugated and unconjugated bilirubin ed urine bilirubin ed to no fecal or urinary urobilinogen194
Lab tests: AST, ALT levels generally rise moderately, ed conjugated and unconjugated bilirubin ed urine bilirubin ed to no fecal or urinary urobilinogen194
Portal hypertension (PHpn)
Normal pressure in portal vein is 5 to 10 mmHgPHpn is commonly associated with hepatic cirrhosisIt can also occur with non cirrhotic liver disease like thrombosis
or clotting in portal vein
195
Normal pressure in portal vein is 5 to 10 mmHgPHpn is commonly associated with hepatic cirrhosisIt can also occur with non cirrhotic liver disease like thrombosis
or clotting in portal vein
195
196
Alcohol Abuse, Infection, Drugs, Bilary ObstructionDestruction of HepatocytesReplacement of destroyed liver cells gradually by scar
tissue
Amount of scar tissue exceeds that decrease functioning liver
tissue
Fibrosis/ScarImpaired blood and lymph flow ed pressure in the venous & sinusoidal channelsFatty infiltration—fibrosis/scar
Portal HypertensionPPHepatomegallySplenomegalyEpistaxis
Jaundice
Ascites BP
Esophageal
varices
DHN
Alcohol Abuse, Infection, Drugs, Bilary ObstructionDestruction of HepatocytesReplacement of destroyed liver cells gradually by scar
tissue
Amount of scar tissue exceeds that decrease functioning liver
tissue
Fibrosis/ScarImpaired blood and lymph flow ed pressure in the venous & sinusoidal channelsFatty infiltration—fibrosis/scar
Portal HypertensionPPHepatomegallySplenomegalyEpistaxis
Jaundice
Ascites BP
Esophageal
varices
DHN
C/Ms of PHpn
GI bleeding/ VaricesSpleenomegallyAscitesHepatic encephalopathy 197
GI bleeding/ VaricesSpleenomegallyAscitesHepatic encephalopathy 197
Ascites
Ascites is accumulation of fluid in peritoneal cavityRisk factorsCirrhosis: for 80% of casesRenal factors: stimulation of RAA systemOther conditions likeCongestive heart failureNephrosis
198
Ascites is accumulation of fluid in peritoneal cavityRisk factorsCirrhosis: for 80% of casesRenal factors: stimulation of RAA systemOther conditions likeCongestive heart failureNephrosis
198
Ascites 199
Portal Hypertension/
Resistance to Blood Flow
Leakage of plasma
into liver lymphatics
Vasocongestion within
intestinal vasculature
Development of
collateral venous
vessels
liver lymph with high
protein
Transudation of plasma
into the abdominal cavity
Persistence of amine
neurotransmitters
Leakage of lymph into
abdominal cavity
Ascites
Redistribution of blood
flow: reduced renal
perfusion
Stimulation of
RAA system
Sodium and water
retention
Leakage of plasma out
of vascular space
Intravascular oncotic pressure Albumin production
Hepatocyte Dysfunction
Esophageal VaricesHemorrhoids
Portal Hypertension/
Resistance to Blood Flow
Leakage of plasma
into liver lymphatics
Vasocongestion within
intestinal vasculature
Development of
collateral venous
vessels
liver lymph with high
protein
Transudation of plasma
into the abdominal cavity
Persistence of amine
neurotransmitters
Leakage of lymph into
abdominal cavity
Ascites
Redistribution of blood
flow: reduced renal
perfusion
Stimulation of
RAA system
Sodium and water
retention
Leakage of plasma out
of vascular space
Intravascular oncotic pressure Albumin production
Hepatocyte Dysfunction
Esophageal VaricesHemorrhoids
Clinical Manifestations
ed abdominal girthBulging of flanksShifting dullnessFluid wave/trillEverted umbilicus (severe)Rapid weight gainSOBVisible striae and distended veins over the
abdominal wall
Signs of dehydrationDecreased urine output
200
ed abdominal girthBulging of flanksShifting dullnessFluid wave/trillEverted umbilicus (severe)Rapid weight gainSOBVisible striae and distended veins over the
abdominal wall
Signs of dehydrationDecreased urine output
200
Ascites
201
201
Assessing for Abdominal fluid wave202
Diagnosis
HistoryPhysical ExaminationDiagnostic paracentesis (50 to 100 mL)Fluid should be examined for its gross
appearance; protein content, cell count, and
differential cell count should be determined
Cytologic analysis
203
HistoryPhysical ExaminationDiagnostic paracentesis (50 to 100 mL)Fluid should be examined for its gross
appearance; protein content, cell count, and
differential cell count should be determined
Cytologic analysis
203
Management of Ascites
Dietary ModificationDiureticsBed restParacentesisInsertion of peritoneo-venous shunt204
Dietary ModificationDiureticsBed restParacentesisInsertion of peritoneo-venous shunt204
Hepatic Cirrhosis
Extensive degeneration and destruction of liver parenchyma
cells and by replacement of liver tissue by fibrous scar tissue
Characterized by irreversible chronic injury of hepatic
parenchyma
205
Extensive degeneration and destruction of liver parenchyma
cells and by replacement of liver tissue by fibrous scar tissue
Characterized by irreversible chronic injury of hepatic
parenchyma
205
Types of Cirrhosis or Scarring of Liver
A. Alcoholic cirrhosis
Frequently due to chronic alcoholism for decades, resulting in:Chronic inflammatoryToxic effects on liverBlocking normal metabolism of protein, fats,
and carbohydrates
Scar tissue specifically surrounds portal areasIs most common type of cirrhosis
206
A. Alcoholic cirrhosis
Frequently due to chronic alcoholism for decades, resulting in:Chronic inflammatoryToxic effects on liverBlocking normal metabolism of protein, fats,
and carbohydrates
Scar tissue specifically surrounds portal areasIs most common type of cirrhosis
206
Types of Cirrhosis …
B. Postnecrotic CirrhosisThere are broad band of scar tissue as late result of previous
bout of acute viral hepatitis (hepatitis B or hepatitis C)
C. Biliary CirrhosisScarring occurs in liver around bile ductsIs result of chronic biliary obstruction and infection
(cholangitis)
Much less common
207
B. Postnecrotic CirrhosisThere are broad band of scar tissue as late result of previous
bout of acute viral hepatitis (hepatitis B or hepatitis C)
C. Biliary CirrhosisScarring occurs in liver around bile ductsIs result of chronic biliary obstruction and infection
(cholangitis)
Much less common
207
Clinical Manifestation
Early ManifestationPalpation of liver reveals firm, lumpy, nodular,
usually enlarged liver
GI disturbance :- anorexia, nausea, vomiting, …HepatomegallyPainLate ManifestationAscites, gastro intestinal bleeding from varicesEncephalopathy, splenomegally, jaundice, skin
lesion, and anemia
Sodium and fluid retention
208
Early ManifestationPalpation of liver reveals firm, lumpy, nodular,
usually enlarged liver
GI disturbance :- anorexia, nausea, vomiting, …HepatomegallyPainLate ManifestationAscites, gastro intestinal bleeding from varicesEncephalopathy, splenomegally, jaundice, skin
lesion, and anemia
Sodium and fluid retention
208
Diagnosis
HistoryPhysical Exam.Diagnostic
Studies
Liver scans/biopsy: Detects fatty
infiltrates, fibrosis, destruction of hepatic
tissue, tumor
Esophagogastroduodenoscopy (EGD):
demonstrate presence of esophageal
varice
Electrolytes: HypokalemiaUrine urobilinogen: May/may not be
present.
Fecal urobilinogen: Decreased.
209
HistoryPhysical Exam.Diagnostic
Studies
Liver scans/biopsy: Detects fatty
infiltrates, fibrosis, destruction of hepatic
tissue, tumor
Esophagogastroduodenoscopy (EGD):
demonstrate presence of esophageal
varice
Electrolytes: HypokalemiaUrine urobilinogen: May/may not be
present.
Fecal urobilinogen: Decreased.
209
Diagnosis …
Increased Serum bilirubinIncreased Serum ammonia: because of inability
to convert ammonia to urea.
Decreased Serum glucose: impaired
glycogenesis
Decreased Serum albuminCBC: Hb/Hct and RBCs may be decreased
because of bleeding
Increased BUN: indicates breakdown of blood/
protein
IncreasedLiverenzymes
210
Increased Serum bilirubinIncreased Serum ammonia: because of inability
to convert ammonia to urea.
Decreased Serum glucose: impaired
glycogenesis
Decreased Serum albuminCBC: Hb/Hct and RBCs may be decreased
because of bleeding
Increased BUN: indicates breakdown of blood/
protein
IncreasedLiverenzymes
210
Medical Management
Symptomatic managementAntacids—to decrease gastric distress and
minimize the possibility of GI bleeding.
Vitamins and nutritional supplementsPotassium-sparing diuretics (spironolactone,
triamterene)--to decrease ascites
Avoidance of alcohol
211
Symptomatic managementAntacids—to decrease gastric distress and
minimize the possibility of GI bleeding.
Vitamins and nutritional supplementsPotassium-sparing diuretics (spironolactone,
triamterene)--to decrease ascites
Avoidance of alcohol
211
Nursing Diagnoses1.2.3.4.
5.
Activity intolerance related to fatigue, general
debility, muscle wasting, and discomfort
Imbalanced nutrition, less than body requirements,
related to chronic gastritis, decreased GI motility,
and anorexia
Impaired skin integrity related to compromised
immunologic status, edema, and poor nutrition
Fluid Volume excess related to compromised
regulatory mechanism (decreased plasma proteins,
malnutrition) or excess sodium or fluid intake as
evidenced by edema, weight gain
Knowledge, deficient regarding condition,
prognosis, treatment, self-care, and discharge
212
5.
Activity intolerance related to fatigue, general
debility, muscle wasting, and discomfort
Imbalanced nutrition, less than body requirements,
related to chronic gastritis, decreased GI motility,
and anorexia
Impaired skin integrity related to compromised
immunologic status, edema, and poor nutrition
Fluid Volume excess related to compromised
regulatory mechanism (decreased plasma proteins,
malnutrition) or excess sodium or fluid intake as
evidenced by edema, weight gain
Knowledge, deficient regarding condition,
prognosis, treatment, self-care, and discharge
212
Hepatic Encephalopathy and Coma
Hepatic encephalopathyIs life-threatening complication of liver
disease occurring with profound liver failure
May result from accumulation of ammonia
and other toxic metabolites in blood
Can occur in any condition which liver damage
causes ammonia to enter in systemic
circulation without liver detoxification
Hepatic coma: represents most advanced stage
of hepatic encephalopathy
213
Hepatic encephalopathyIs life-threatening complication of liver
disease occurring with profound liver failure
May result from accumulation of ammonia
and other toxic metabolites in blood
Can occur in any condition which liver damage
causes ammonia to enter in systemic
circulation without liver detoxification
Hepatic coma: represents most advanced stage
of hepatic encephalopathy
213
Hepatic Encephalopathy …
Normally, liver convert ammonia in to glutamine,
which is stored in liver and later converted to urea
and excreted via kidneys
Blood ammonia rises when liver cells are unable to
perform this conversion due to liver cell damage and
necrosis
C/m From mild mental confusion like, unresponsiveness, forgetfulness, trouble
concentrating, or changes in sleep habits to deep
coma
Simple tasks, such as handwriting become difficult
214
Normally, liver convert ammonia in to glutamine,
which is stored in liver and later converted to urea
and excreted via kidneys
Blood ammonia rises when liver cells are unable to
perform this conversion due to liver cell damage and
necrosis
C/m From mild mental confusion like, unresponsiveness, forgetfulness, trouble
concentrating, or changes in sleep habits to deep
coma
Simple tasks, such as handwriting become difficult
214
Hepatic Encephalopathy …
DxAsterixis or “liver flap”, patient is asked to hold
arm out with hand held upward (dorsiflexed).
Within few seconds, hand falls forward
involuntarily and then quickly returns to
dorsiflexed position
Lab-results show elevated blood ammonia
215
DxAsterixis or “liver flap”, patient is asked to hold
arm out with hand held upward (dorsiflexed).
Within few seconds, hand falls forward
involuntarily and then quickly returns to
dorsiflexed position
Lab-results show elevated blood ammonia
215
Hepatic Encephalopathy …
Medical ManagementPrinciples of intervention in hepatic
encephalopathy.
Reduce protein in intestinePrevent gastro-intestinal bleedingReduce bacterial production of NH
3
by neomycinHigh cleansing enema to decrease bacteriaEliminate infectionIntravenous administration of glucose to minimize
protein breakdown
216
Medical ManagementPrinciples of intervention in hepatic
encephalopathy.
Reduce protein in intestinePrevent gastro-intestinal bleedingReduce bacterial production of NH
3
by neomycinHigh cleansing enema to decrease bacteriaEliminate infectionIntravenous administration of glucose to minimize
protein breakdown
216
Cholelithiasis
It is presence or formation of calculi in
gallbladder
Usually form in gallbladder in from of solid
constituents of bile:
CholesterolBile saltsBilirubinCalciumProteinThey vary greatly in size, shape, and
217
It is presence or formation of calculi in
gallbladder
Usually form in gallbladder in from of solid
constituents of bile:
CholesterolBile saltsBilirubinCalciumProteinThey vary greatly in size, shape, and
217
218
Cholelithiasis…
Cholelithiasis…
Types: There are two major types
A. Cholesterol stonesPredominantly composed of cholesterolIs insoluble in waterIts solubility depends on bile acids and
lecithin (phospholipids) in bile
B. Pigment stonesPrimarily composed of pigmentWhen unconjugated pigments in bile
precipitate to form stone
Account for about one third of cases in USCannot be dissolved and must be removed
surgically
219
A. Cholesterol stonesPredominantly composed of cholesterolIs insoluble in waterIts solubility depends on bile acids and
lecithin (phospholipids) in bile
B. Pigment stonesPrimarily composed of pigmentWhen unconjugated pigments in bile
precipitate to form stone
Account for about one third of cases in USCannot be dissolved and must be removed
surgically
219
Risk Factors
Long –term parenteral nutrition, which results
in decrease gal bladder motility
Cirrhosis of liverChronic hemolytic disorders, which result in
increased bile pigments
Obesity
220
Long –term parenteral nutrition, which results
in decrease gal bladder motility
Cirrhosis of liverChronic hemolytic disorders, which result in
increased bile pigments
Obesity
220
Clinical Manifestations
Gallstones may be silentPain, tenderness, and rigidity of upper right
abdomen that may radiate to midsternal area or
right shoulder
Pain and biliary colicBleeding tendency as result of vitamin
deficiency
Changes in urine and stool colorVery dark color urineUrine become foamy when shakenClay-colored fecesJaundice
221
Gallstones may be silentPain, tenderness, and rigidity of upper right
abdomen that may radiate to midsternal area or
right shoulder
Pain and biliary colicBleeding tendency as result of vitamin
deficiency
Changes in urine and stool colorVery dark color urineUrine become foamy when shakenClay-colored fecesJaundice
221
Management
Nutritional and Supportive TherapyRest, intravenous fluids, nasogastric suction,
analgesia, and antibiotic agents
Low-fat foodsHigh protein and carbohydratesCooked fruits, rice, lean meats, mashed
potatoes, bread, coffee, or tea may be taken
Remind the patient that fatty foods may bring
on an episode
222
Nutritional and Supportive TherapyRest, intravenous fluids, nasogastric suction,
analgesia, and antibiotic agents
Low-fat foodsHigh protein and carbohydratesCooked fruits, rice, lean meats, mashed
potatoes, bread, coffee, or tea may be taken
Remind the patient that fatty foods may bring
on an episode
222
Management ….
Pharmacologic TherapyDrugs to dissolveUrsodeoxycholic acid (UDCA)Chenodeoxycholic acid (chenodiol or CDCA)
223
Pharmacologic TherapyDrugs to dissolveUrsodeoxycholic acid (UDCA)Chenodeoxycholic acid (chenodiol or CDCA)
223
Management ….
Non-surgical ManagementsDissolving gallstones by infusion of solventLithotripsy- uses repeated shock waves directed
at gallstones in gallbladder or common bile duct
Surgical InterventionsCholecystostomy- removal of gallbladderCholecystectomy- gallbladder is surgically
opened, then stone and bile or purulent drainage
are removed
Choledochostomy- an incision into common duct,
usually for removal of stones
224
Non-surgical ManagementsDissolving gallstones by infusion of solventLithotripsy- uses repeated shock waves directed
at gallstones in gallbladder or common bile duct
Surgical InterventionsCholecystostomy- removal of gallbladderCholecystectomy- gallbladder is surgically
opened, then stone and bile or purulent drainage
are removed
Choledochostomy- an incision into common duct,
usually for removal of stones
224
225Thanks for yourtime &attention
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