L5 GI Disorders Flashcards
1
Q
Upper Gi
A
ingestion and digestion of food
mouth to duodenum
2
Q
Lower GI
A
small intestine to anus
small = digestion and nutrient absorption
large = absorption of water and electrolytes
3
Q
Red Flags of Systemic Pathology
A
nausea/vomiting
diarrhea
malaise
fever
night sweats
pallor/diaphoresis
dizziness
4
Q
Nausea/Vomiting
A
irritation of nerves, pain, GI disorders, ADR of meds
5
Q
Diarrhea
A
abnormal frequency or volume of watery stools
tube feeding, antibiotics, increased caffeine intake
6
Q
Constipation
A
infrequent bowel movements b/c they are too hard. Decreased fiber, dehydration, low PA
7
Q
Anorexia
A
aversion to food. Cancer, chemotherapy
8
Q
Dysphagia
A
obstruction in esophagus neuro condition
9
Q
Achalasia
A
failure of esophageal spinchter to relax leads to dysphagia. neuro disease, stress, anxiety
10
Q
Heartburn/dyspepsia
A
midline burning pain. Esophageal reflux
11
Q
GI Bleeding
A
Hematemesis = vomiting blood, esophagus + up
Melena = black tarry stools. stomach to rectum
Hematochexia = bright red blood in stool. Local bleeding
12
Q
Fecal incontinence
A
unable to hold poop. CNS injury
13
Q
Pain in GI
A
T4-T12 depends on structure
14
Q
RUQ
A
liver and gallbladder
duodenum
transverse and ascending colon
1/2 pancreas
15
Q
LUQ
A
left liver lobe
stomach
1/2 pancreas
transverse and descending colon
16
Q
RLQ
A
cecum
appendix
ascending colon
17
Q
LLQ
A
sigmoid colon
portion of descending colon
18
Q
Normal aging effects on GI system
A
appetite depression
vitamins, macronutrients due to slow absorption
decreased gastric acid
Decrease in intrinsic factor production, can lead to anemia
19
Q
B12
A
needed for RBC, neurons, DNA. HCL breaks B12 bond so it can be used. then it is bound to intrinsic factor so it can be used
20
Q
Gastroesophageal reflux disease (GERD)
A
Chronic heartburn >2x a week
lower esophageal sphincter does not close properly and stomach contents reflux into the esophagus.
21
Q
Epidemiology GERD
A
Extremely common in american adults, 2/3 will experience it
peaks at 50 years of age
75% of individuals experience reoccurrence
22
Q
RF of GERD
A
decreased pressure of lower esophageal sphincter
increased gastric pressure, pushes food back up
gastric contents near gastroesophageal junction
23
Q
Common heartburn triggers
A
fatty/fried foods, alcohol, carbonated drinks, spicy foods, garlic, NSAIDs, caffeine, chocolate, etc
24
Q
GERD Patho and Dx
A
Patho: acidic gastric contents contact the walls of the esophagus causing inflammation in mucosal walls
Dx: usually by history
25
CP of GERD
heartburn, midline burning pain
dysphagia
coughing wheezing
bending over, laying down makes it worse
antacids, standing, fluids make it better
26
GERD Referral of Pain
can present without heartburn
symptoms could include excessive clearing of throat, change in voice, problems swallowing
27
TX GERD
Lifestyle modifications --> avoid caffeine/personal triggers, remain upright 3 hours after eating, eat small meals, drink fluids between meals
Drugs to decrease acid--> antacids, histamine blockers, proton pump inhibitors
surgery
28
Sleeping positions for GERD
1. put risers under bedposts at head of bed
2. use bolster for reading
3.Left sidelying is better b/c is kinks the esophageal sphincter
29
Exercise-related GERD
strenuous exercise inhibits gastric emptying
condition is more common in athletes who have non-exercise tendency for GERD
Advice: eat smaller meals before training, dilute sports drinks, avoid exercises that increases abdominal pressure
30
Hiatal Hernia Pathogenesis
b/c of enlarged lower esophageal spinchter, the stomach moves into and past the diaphragm. Pressure on sphincter is reduced, allowing sphincter to open at the wrong time, causing stomach contents and acid to flow into esophagus
31
Hiatal hernia
lower esophageal sphincter becomes enlarged, allowing stomach to pass through diaphragm into thoracic cavity
relatively common, incidence increases with age. More common in female
32
DX of Hiatal Hernia
barium x-ray
endoscopy
33
RF of Hiatal Hernia
anything that weakness the diaphragm
increases in intra-abdominal pressure
(lifting, forceful cough, pregnancy, obesity)
34
CP of Hiatal hernia
heartburn 30-60 min after meals, exacerbated with tight clothing or supine position
possible difficulty in swallowing
35
Tx in Hiatal Hernia
antacids and elevating head of bed
surgical repair for some cases
36
Abdominal Precautions
logrolling, avoid twisting
no lifting >10 lbs
No bending or squatting
avoid valsalva maneuver
wear abdominal binder
37
Hiatal Hernia tips for PTs
avoid supine exercises
avoid exercises that increase intra-abdominal pressure
teach proper breath control
instruct proper body mechanics
38
Peptic ulcer disease
break in mucosal lining of stomach, upper small intestine or esophagus, exposing submucosal areas to gastric secretions
1/2 million new cases a year
39
Penetrating ulcer
gone through stomach, is now penetrating another organ
40
RF for Peptic ulcer disease
Helicobacter pylori infection
Aging
Chronic use of NSAIDs
41
Pathogenesis of peptic ulcer disease
90% are caused by h.pylori (bacteria)
common cause is NSAIDs
42
CP of Peptic ulcer disease
Burning, cramping pain is most common. Near epigastric location, lasts few min-hrs
Worse when stomach is empty, common flare ups at night, can be relieved by acid reducing meds
Dx includes history or H. pylori test
43
Tx of Peptic Ulcer disease
1. ABX
2. REduce level of acid in digestive system with histamine, PPIs, antacids
3. Prevent recurrence by stopping smoking, limit alcohol, avoid NSAIDs
44
PT Tip for Peptic Ulcer Disease
many people do not report classic S/S, but present with pain after a perforation or hemorrhage
Referred pain with complications, mid thoracic region to R shoulder
45
Gastric Cancer
malignant cells form in the gastric mucosa
2nd most common cause of cancer death in the world. Significant decline in incidence over most of the century, mainly due to improved sanitation and decreased transmission of H pylori
46
RF for Gastric Cancer
chronic h pylori infection
male
>50 year old, median age at dx is 70
47
Gastric Cancer Patho and Dx
Patho: multifactorial, often begins with h. pylori infection. Duodenal reflux, decreased gastric acid secretion
Dx: upper endoscopy and biopsy
48
CP of Gastric Cancer
Early: asymptomatic, indigestion, stomach discomfort, heartburn, nausea
Later: blood in stool, bloated feeling after eating, vomiting, weight loss, stomach pain
49
Tx and Prognosis of Gastric Cancer
Tx: surgery is a treatment of choice in 1/3 of cases. Chemo therapy and radiation
Prognosis: 2/3 of patients are diagnosed in advnaced stages, with metastatic stage is incurable.
Screening helps to detect 40% of tumors early
50
Inflammatory Bowel Disease
chronic inflammatory diseases of GI tract of unknown etiology. Includes chrohns and ulcerative colitis
about 1 million cases
51
RF for IBD
15-35 years old at peak
caucasian
females
living in N. america or europe
family history
52
Pathogenesis of IBD
UC: inflammation uniformly in rectum, extends proximally and stops. Involves mucosa and submucosa
CD: inflammation is discontinuous, most often in small intestine or colon. Involves all bowel layers
Chronic inflammation causes ulcerations. The inflammation is caused by genetics and environment, NOT By diet and stress alone
53
CP of IBD
remissions and exacerbations
abdominal pain, diarrhea, bloody stools, abdominal mass, anorexia, weight loss
54
DX of IBD
medical hx
colonoscopy (very sensitive test)
55
TX of IBD
goal is to reduce inflammation that triggers S/S
drugs: anti inflammatory, ABX
surgery, resections
56
CD is
incurable, chronic, debilitating
most patients require surgery
57
UC is
curable, by colon resection
58
PT Tips and IBD
QOL is generally lower in CD b/c of recurrences
IBD takes a emotional toll
Educate pts to take a part of support groups
59
Irritable Bowl Syndrome
collection of S/S that are not attributed to identifiable bowel abnormality. IBS is a functional GI disorder
Most common disorder of GI, 1/5 american adults
60
RF for IBS
female
usually begins 20 years of age
61
CP of IBS
intermittent s/s with variable periods of remission
Diarrhea and/or constipation
abdominal pain/cramping in LLQ
bloating
gas
mucus in stool
62
Pathogenesis of IBS
no single or specific cause identified
63
IBS Dx
remains one of exclusion
use history, sigmoidoscopy, lactose intolerance test
64
TX of IBS
focus in on symptom relief
drugs--> antidepressants, antidiarrheals, antispasmodics
Lifestyle changes--> dietary changes (increased fiber and probiotics), stress reduction
65
Diverticulitis
DIVERTICULOSIS: condition of having diverticula, small mucosal blind pouches in wall of colon
DiverticuLITIS is the inflammation of >1 diverticula
66
RF of Diverticulitis
aging
low fiber diet
67
Diverticula development
come about in weaker places in colon
most common is in sigmoid colon
often occur due to straining during bowel movements over years
68
Diverticulitis patho
diverticuli fill with fecal material, leading to infection and inflammation
localized abscess forms in limited area around wall of colon
if performation develops in a pouch, can cause fistula or peritonitis infection within abdominal caivty
69
CP of Diverticulitis
pain is severe, abrupt, localized to LLW, worsens over time
fever, nausea, vomiting
dx with enema, CT, WBC count
70
Tx of Diverticulitis
Depends on severity
MILD: ABX and liquid/low fiber diet
Recurrent/Severe: surgery. Primary bowel resection or bowel resection w/colosotomy
71
Primary bowel resection
removal of diseased segment with reconneciton to healthy segements
72
Bowel resection with colostomy
chosen if significant inflammation in colon makes it impossible to rejoin colon and rectum
opening made in abdomnal wall and unaffected part of colon is connected to stoma. Waste passes into a bag. Can be temporary or permanent
73
Referral of pain diverticulitis
LLW pain or pain in back
assess for presence of abscesses: iliopsoas muscle palpation and test, rebound tenderness
74
Exercise for Diverticulitis
avoid exercises that increase intra-abdominal pressure
aerobic exercise promotes GI motility
75
Abdominal Hernias
congenital or acquired abnormal protrusion of abdominal contents through a weak point or tear in muscular wall of abdomen
76
Types of abdominal hernias
inguinal
femoral
umbilical
incisional
77
RF for Hernias
Muscular weakness
family or personal hx
certain medical conditions and smoking
chronic constipation
excess weight
c-section/pregnancy
activities (standing for long periods)
premature birth
78
Reducible hernia
when contents of hernial sac can be replaced into abdominal cavity by manual manipulation
79
Irreducible hernia
hernias that cannot be replaced by manipulation
80
Strangulated hernia
when protruding organ is constricted to extent that circulation is impaired
81
Clinical Presentation of Hernia
initially is an intermittent or persistent bulge that may be painless and easily reducible
as pressure increases and pushes more abdominal contents out through the weakened wall, bulge size increases, accompanied by intermittent or persistent pain
pain depends on structures involved though usually localized. Sharp, aggraved by increases in pressure, relieved by cessation, radiation
82
Inguinal hernia Indirect patho
most common
herniation through inguinal ring, may protrude into scrotum
may occur at any age, more common males <1 year and 16-20 yr
pain with straining
83
Direct Inguinal Hernia
herniation above inguinal ligament where abdominal wall is slightly thinner
occurs most often in men >40 yr, rarely protrudes into the scrotum
usually painful
84
Distinguishing between direct and indirect hernia is
not that important because both are treated the same
85
Femoral hernia
herniation of abdominnal contents through enlarged femoral ring/canal, causing bluge below inguinal crease
more common in women with more children
rare, high risk of becoming irreducible and strangulated
86
Umbilical hernia
opening in abdominal wall does not close completely. Usually close 2-3 years of age, unless large and need surgery
even if closed at birth, umbilical hernias may appear later because that area remains weaker
87
Tx Options of Hernias
wait and watch for minimally symptomatic hernias
curative surgical repair
acutely irreducible need emergency tx because of risk of strangulation
if the intestinal contents of hernia have blood supply cut off, gangrenous bowel possible in 6 hr
88
Tips for PTs with Hernias
PTs may be key players in recognition of hernias
in pts with chronic cough, pregnancy ,or other RF, ask about the presence of a known hernia
PT should encourage body mechanics, postural education, weight management, encourage smoking cessation
89
Appendicitis
inflammatio of vermiform appendix (blind ended tube that connects to cecum)
occurs with 7% of US population, mainly from 15-20 yrs of age
90
Pathogenesis of Appendicitis
1/2 of all cases have no known cause
obstruction of appendix lumen leads to distension of appendix b/c of fluid accumulation
ineffective drainage allows bacterial invasion of wall of appendix
in advanced cases, perforation and spillage of infected fluid into peritoneal cavity can occur
91
Perforation
can occur in 24 to 48 hr and causes peritonitis, which is an emergency
92
CP of Appendicitis
Anorexia, periumbilical pain, nausea, RLQ pain, vomiting
migration of pain from periumbilical area to RLQ is the most discriminating feature of pts history
OLDER ADULTS frequently have few to no symptoms until perforation occurs
93
Dx of Appendicitis
careful history to rule out ectopic prevnancy, right sided ovarian cysts, kidney stone, Crohns disease
palpate mcburney's point, pinch an inch test
WBC count
94
Appendicitis and PT
there may be non-classic history of appendicitis pain
perform palpation exam
positive cough test (deep cough causes pain)
if appendicitis is suspected, immediate MD attention is necssary
95
Appendicitis Tx and Prognosis
Tx: removal of appendix asap
Prognosis: usually good with surgery. If untreated, appendix can perforate, leading to serious complications. Greater likelihood of perforation in <2 yr old and >60yr
96
Colorectal Cancer
adenocarcinoma of colon or rectum
3rd most common cancer in USA
rate of new cases decreasing due to screening and changes in risk factors
in people <50, rates increasing since mid 90s
97
Risk Factors Colorectal Cancer
increasing age >50 year of age comprise >90% of those with CRC
overweight/obesity
sedentary lifestyle
alcohol use
98
Pathogenesis of Colorectal cancer
Preinvasive: exaggerated growth may cause precancerous polyps in intestinal lining. The polyps can metaastasize to nearby lymph nodes.
99
Colonoscopy
screening for prevention of CRC by identifying and removing any polyps
100
CP of CRC
change in bowel habits like diarrhea, constipation, narrow stools
-blood in stool
-frequent gas pains
-unintended weight loss
-may be asymptomatic
101
Dx and Tx of Colorectal Cancer
Dx: physical exam, blood test, biopsy
Tx: surgery is the most common, chemotherapy, radiation, rehab
102
CRC Prognosis and Prevention
Prognosis: survival related to stage at diagnosis, most present with advanced disease. Higher survival rate if limited to the bowel
Prev.: *increase activity level, lose excess weight, decrease alcohol intake, decrease consumption of red meat and processed meat*
103
CRC Screening
people of average risk should start screening at AGE 45 and continue until 76
average risk means no family hx, personal hx, IBD, pain radiation
104
How often should a colonscopy happen?
every 10 years
(sigmoid is every 5 yrs)
105
Functions of the liver
carbohydrate metabolism
protein metabolism
lipid metabolism
metabolism of drugs
removal of waste
storage of glycogen, fats, vitamins
Activation of Vit D
phagocytosis
endocrine functions
aids blood clotting
digestive functions
106
Common S/S of hepatic disease
GI S/S
RUQ pain
edema
dark urine
skin changes
neuro involvement
musculoskeletal pain
heaptic osteodystrophy
107
Ascites
edema within the peritoneal cavity
108
Jaundice
yellow color in skin, mucous membranes and/or eyes
yellow pigment is from bilirubin, a byproduct of old RBCs
109
Hepatitis
acute or chronic liver inflammation caused by a virus, chemical, drug reaction, or alcohol abuse
hepatitis from ANY cause produces similar symptoms
alcohol and drug intake can make any liver disease worse
110
Vaccine availability for viral hepatitis
A: yes
B: yes
C: NO
D: no
E: yes
111
Hepatitis A
liver disease caused by hep A virus
waves both in the nation and within communities. 1/3 of americans have a evidence of past infection
Usually spread by putting the mouth that has been contaminated with stool
112
RF of Hep A
household or sexual contact with infected person
living in ares with high HAV rates
persons traveling to countries where HAV is common
homosexual men who are active sexually
illicit drug users
113
Prev of Hep A
active vaccine is best
immune globulin can be given for short term
hand washing!
114
CP of Hep A
jaundice, fatigue, loss of appetite, abd pain
nausea, diarrhea, fever
115
Tx and Long Term Effects of Hep A
Tx: primarily symptomatic, bed rest
Long term: once you have it, you can't get it again. Most heal within 1-2 months
116
Hep B
can cause lifelong infection, cirrhosis of liver, liver CA, liver failure, death
1.25 million americans are chronically infected
Transmitted through blood/bodily person
117
RF and PRevention of Hep B
RF: multiple sex partners, sexually active homosexual men, injecting drugs, work in healthcare
Prevention: Hep B vaccinne is the best production
118
CP and TX of Hep B
CP: jaundice, fatigue, loss of appetite, abd pain, nausea, vomiting, joint pain
TX: alpha interfern and lamivudine are 2 drugs that can be used
119
Hep C
liver disease caused by hep C virus, can lead to liver failure, cirrhosis, liver cancer
accounts for 60 to 70% of chronic hepatitis. Infections are increasing after a period of downfall
120
Transmission and Prevention of Hep C
Trans: BLOOD BORNE route
Prevention: No vaccine available!!! Use standard precautions and don't share personal hygiene items
121
CP of Hep C
80% have NO S/S
jaundice, fatigue, loss of appetite, abdominal pain, nausea, dark urine
122
TX of Hep C
possible pill
liver transplant
PX: chronic infection will develop if untreated, and can increase risk of liver cancer
123
Pancreatitis
inflammation of pancreas due to alcohol abuse (40%), gallstone (40%), idiopathic causes (20%), can be acute or chronic
124
Acute pancreatitis
abrupt onset, lasts for a few days
can have repeated episodes and recover fully
125
Chronic Pancreatitis
gradual development and persists over years
destroys pancreas and nearby tissues, although it may be years before S/S appear
less common than acute
126
RF for Pancreatitis
Heavy alcohol use
gallstones
male, black american
127
Pathogenesis of Pancreatitis
primary causes are heavy alcohol ingestion and gallstones
END RESULT: pancreatic digestive enzymes move into pancreas itself, causing potentially severe damage
128
Alcohol and pancreatitis
causes digestive ensymes to be released sooner
increased permeability of ducts, allows digestive enzymes to leak into pancreatic tissue
leads to formation of protein plugs that block parts of pancreatic duct
129
Gallstones and Pancreatitis
leave gallbladder and lodge/obstruct pancreatic duct
130
Exocrine Pancreas
most cells in pancreas
releases enzymes though ducts
131
CP Of Pancreatitis
Mild to severe mid epigastric and LUQ pain that is nearly constant
1/2 of patients have pain radiating to back
pain aggravated by eating, alcohol, walking, lying supine
severe: dehydration, low BP, internal bleeding shock
Chronic: weight loss, oily stools, diabetes
132
Dx and Tx of Pancreatitis
DX: Blood test, increased WBC, increased liver enzymes, stool test, endscopic test
TX: pain control, IV fluids, NPO. Removal of gallstones, decrease alcohol dependency
133
PT Tips and Pancreatitis
PT may be consulted for pain relief
position for comfort like sidelying, fetal position
Relaxation techniques
134
Cholelithiasis
gallstones, which are deposits of cholesterol or caclium salts
135
Cholecystitis
inflammation of gallbladder or cystic duct, due to impaction of gallstone in cystic duct
136
Epidemiology of Cholecystitis/Cholelithiasis
Gallstones are VERY common
incidence increases with age
most common in obese females >40 yr of age
137
RF of Cholecystitis/Cholelithiasis
Increasing age
female
high bile cholesterol
high fat diet
decreased PA
138
Pathogenesis of Cholecystitis/Cholelithiasis
1.Gallstones form when bile in gallbladder becomes oversaturated with cholesterol
2. high cholesterol and decreased gallbladder motility results in production of cholesterol crystals and formation of gallstones
3. If obstruction of cystic duct occurs, gallbladder distends, while muscles in duct wall contract to expel stone
139
CP of Cholecystitis/Cholelithiasis
30% cause symptoms
Biliary colic or gallbladder attack
RUQ abdominal pain, pain may radiate between scapulae, right shoulder or neck
pain frequently abrupt onset and gradually subsides
nausea, vomiting, anxiety, fear
140
Dx and TX of Cholecystitis/Cholelithiasis
Dx: ULTRASOUND
Tx: ERCP to remove stones, cholecystectomy, bile salt tablets
141
PTs and Cholecystitis/Cholelithiasis
in treating patients for MSK pain between scapulae, right shoulder, neck associated with RUQ pain
GI screaning questions, should contact MD
Cholecystitis may occur without formation of gallstones
142
Increasing levels of PA activity ____ the risk of _____ cancers and other conditions
LOWERS, 13
Endometrial, breast, colon, rectum
Diverticulitis, gallstones
