Upper GI 2 Flashcards

1
Q

hiatal hernia - more common in who?

A

Most common abnormality found on upper GI x-ray
■ More common in older adults and women

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

2 types of hiatal hernia (hernias slide in pairs)

A

sliding and Paraesophageal or rolling

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

sliding hernia (the slide goes down)

A

slides into stomach when pt is lying down

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

Paraesophageal or rolling hernia

A

Fundus and greater curvature of stomach roll up through diaphragm, forming a pocket alongside the esophagus

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

Acute paraesophageal hernia is a (a cute para needs a paramedic)

A

medical emergency

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

hiatal hernia - causes (big)

A

Structural changes occur with aging
▪ Weakening of muscles in diaphragm ▪ Increased intraabdominal pressure
▪ Obesity
▪ Pregnancy
▪ Heavy lifting

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

hiatal hernia - symptoms (Hernia - H)

A

May be asymptomatic
▪ Symptoms include
▪ Heartburn
▪ After meal or when lying supine
▪ Dysphagia

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

hiatal hernia - complications

A

■ GERD
■ Esophagitis
■ Hemorrhage from erosion
■ Stenosis
■ Ulcerations of herniated portion
■ Strangulation of the hernia
■ Regurgitation with tracheal aspiration
■ Increased risk of respiratory problems

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

hiatal hernia - diagnostics (the only 2 you know)

A

Esophagogram (barium swallow) and endoscopy

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

hiatal hernia - management - conservative therapy (and what meds?)

A

ConservativeTherapy
▪ Lifestyle modifications
▪ Eliminate alcohol
▪ Elevate head of bed
▪ Smoking cessation
▪ Avoid lifting/straining
▪ Reduce weight, if appropriate
▪ Use antisecretory agents and antacids

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

esophageal diverticula (divert the zinc w/ traction and epinephrine)

A

Occur in 3 main areas
1. Zenker’s diverticulum
▪ Most common location
▪ Above the upper esophageal sphincter 2. Traction diverticulum
▪ Near esophageal midpoint 3. Epiphrenic diverticulum
▪ Above the LES

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

Esophageal Diverticula Clinical Manifestations (same a gerd)

A

■ Dysphagia
■ Regurgitation
■ Chronic cough
■ Aspiration
■ Weight loss

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

Esophageal Diverticula Complications (the MAP diverts up)

A

■ Malnutrition
■ Aspiration
■ Perforation

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

Esophageal Diverticula Diagnostic Studies (the same 2)

A

■ Endoscopy
■ Barium studies

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

Esophageal Diverticula Interprofessional Care (touch neck)

A

■ Applying pressure at a point on neck to empty pocket of food
■ Diet may need to be limited to foods that are blenderized
■ Treatment may be necessary if nutrition disrupted
■ Surgery
▪ Endoscopic or open approach (associated w/ morbitidy - usually older ppl)
▪ Most serious complication is esophageal perforation

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

Esophageal Strictures - over long or short time?

A

Usually develop over a long time

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

Esophageal Strictures - causes - most common? (Gerdie is #1 strict)

A

▪ GERD: most common cause
▪ Ingestion of strong acids or alkalis ▪ External beam radiation
▪ Surgical anastamosis
▪ Trauma

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

Esophageal Strictures - manifestations (DRW has strictures)

A

▪ Dysphagia
▪ Regurgitation
▪ Weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Esophageal Strictures - treatment

A

▪ Dilated endoscopically ▪ Surgical excision
▪ Patient may have a temporary or a permanent gastrostomy (opening in stomach)

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

Achalasia (atcha is paralyzed)

A

▪ Rare, chronic disorder
▪ Exact cause is unknown
▪ Peristalsis is absent in lower 2/3 of esophagus
LES pressure ↑

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

Achalasia - manifestations (atcha can’t swallow w/ a lump in her throat)

A

▪ Dysphagia
▪ Most common symptom
▪ Liquids and solids
▪ Globus sensation (lump in throat)
▪ Substernal chest pain
▪ During/after a meal

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

Achalasia Diagnostic Studies

A

▪ Esophagogram (barium swallow)
▪ Manometric studies of lower esophagus
▪ Endoscopy

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

Achalasia - treatment - Endoscopic pneumatic dilation (atcha needs balloons)

A

▪ Outpatient procedure
▪ Dilation of LES using balloons of progressively larger diameters
▪ Repeat dilations are often required

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

Achalasia - Symptomatic relief (drink water with meals, back atcha)

A

▪ Semisoft diet ▪ Eating slowly
▪ Drinking with meals
▪ Sleeping with head of bed elevated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Esophageal Varices (varices is varacose) what is the cause?
Dilated, tortuous veins at the lower end of the esophagus caused by portal HTN
26
Esophageal Varices - Large varices are more likely to
bleed.
27
Ruptured esophageal varices are the
the most life- threatening complication of cirrhosis and considered a medical emergency.
28
Peptic Ulcer Disease
Erosion of GI mucosa resulting from digestive action of HCl acid and pepsin
29
peptic ulcers can occur in (pepi is in the LSD)
▪ Lower esophagus ▪ Stomach ▪ Duodenum ▪ Margin of gastrojejunal anastomosis after surgical procedures
30
acute peptic ulcer - heal fast or slow?
▪ Superficial erosion ▪ Minimal inflammation ▪ Short duration: resolves quickly when cause is identified and removed
31
chronic peptic ulcer - how long? and are they common?
▪ Long duration ▪ Muscular wall erosion with formation of fibrous tissue ▪ Present continuously for many months or intermittently throughout person’s lifetime ▪ More common than acute erosions
32
peptic ulcers - patho
■ Develop only in presence of an acid environment ■ Excess HCl may not be necessary for ulcer development ■ Pepsinogen converts to pepsin in presence of HCl acid and at pH of 2 to 3 ■ pH increases to 3.5 or more when – Food or antacids neutralize the stomach acid – Drugs block acid secretion ■ Back diffusion of HCl acid into gastric mucosa results in cellular destruction and inflammation ■ Histamine is released from damaged mucosa ■ Causes vasodilation, increased capillary permeability and further secretion of acid and pepsin
33
Destroyers of mucosal barrier: - Helicobacter pylori (helicopter is ur ease)
Helicobacter pylori (2/3 of world's pop is infected) ▪ Major risk factor for PUD ▪ Produces enzyme urease ▪ Urease activates immune response ▪ Antibody production ▪ Release of inflammatory cytokines ▪ Leads to increased gastric secretions and causes damage
34
Destroyers of mucosal barrier: NSAIDs and aspirin
▪ Inhibit prostaglandin synthesis ▪ Increase gastric acid secretion ▪ Reduce integrity of the mucosal barrier ▪ Responsible for majority of non-H. pylori peptic ulcers ▪ NSAIDs in presence of H. pylori increase risk of PUD
35
Destroyers of mucosal barrier: steroids (steroids shrink)
▪ ↓ Rate of mucosal cell renewal ▪ ↓ Protective effects
36
Gastric Ulcers (gastric ulcers go everywhere in the stomach) and who gets them? (women stress)
■ Occur in any portion of stomach ■ Less common than duodenal ulcers ■ More prevalent in women ■ Peak incidence >50 years of age ■ More likely than duodenal ulcers to result in obstruction
37
gastric ulcers - risk factors (3 things) HMR (gassy hummer)
▪ H. pylori ▪ Medications ▪ Bile reflux
38
Duodenal Ulcers (duo is prevalent and young)
▪ Account for ~80% of all peptic ulcers ▪ Occur at any age and in anyone ▪ ↑ Between ages of 35 and 45 years ▪ H. pylori is found in 90% to 95% of patients ▪ Associated with increased HCl acid secretion
39
Duodenal Ulcers - Increased risk: (Dua and Zellwiger have ulcers at the door)
▪ COPD ▪ Cirrhosis of liver ▪ Chronic pancreatitis ▪ Hyperparathyroidism ▪ Chronic kidney disease ▪ Zollinger-Ellison syndrome
40
stress-Related Mucosal Disease (SRMD) (this surgery and trauma is stressing me)
■ Also called physiologic stress ulcer ■ Acute ulcers that develop after major physiologic insult ▪ Trauma or surgery
41
Gastric ulcers - manifestations- pain how long after meals?
▪ Pain generally high in epigastrium ▪ 1–2 hours after meals ▪ “Burning” or “gaseous” ▪ Food aggravates pain if ulcer has eroded through gastric mucosa
42
Duodenal ulcer - manifestations - pain how long after meals? (Dua is 25)
▪ Pain in midepigastric region beneath xiphoid process ▪ Back pain—if ulcer is located in posterior aspect ▪ 2–5 hours after meals ▪ “Burning” or “cramplike” ▪ Tendency to occur, then disappear, then occur again
43
Gastric ulcer - G
great pain
44
Duadenal ulcer - D
decrease pain
45
3 complications with ulcers (think if they rip off or block)
▪ Hemorrhage ▪ Perforation ▪ Gastric outlet obstruction ▪ All considered emergency situations
46
hemmorhage - does pain increase or decrease?
▪ Most common complication of PUD ▪ Dudoenal ulcers cause more UGIB (upper GI bleeds) episodes than gastric ulcers ▪ Clinical Manifestations: ▪ Changes in vital signs, ↑ in amount and redness of aspirate ▪ Signals massive upper GI bleeding ▪ ↑ Amount of blood in gastric contents ▪ ↓ Pain because blood neutralizes acidic gastric contents
47
Perforation
■ Occurs when ulcer penetrates serosal surface with spillage of contents into peritoneal cavity
48
manifestations of perforation - pain how quickly? and bowel sounds?
▪ Sudden, dramatic onset ▪ Initial phase (0–2 hours after perforation) ▪ Sudden, severe upper abdominal pain- quickly spreads throughout abdomen ▪ Pain radiates to back ▪ Rigid, boardlike abdominal muscles ▪ Shallow, rapid respirations ▪ Tachycardia, weak pulse ▪ Bowel sounds absent ▪ Nausea/vomiting
49
perforation treatment
▪ Immediate focus: ▪ Stop spillage of gastric or duodenal contents into peritoneal cavity ▪ Restore blood volume ▪ NG tube ▪ IVF ▪ pRBCs may be necessary ▪ ECG if patient has history of cardiac disease ▪ Broad-spectrum antibiotics ▪ Open or laparoscopic repair
50
Gastric Outlet Obstruction (Distal stomach and duodenum obstruction is the result...)
■ Acute and chronic PUD can result in gastric outlet obstruction ■ Distal stomach and duodenum obstruction is the result of: ▪ Edema ▪ Inflammation ▪ Pylorospasm and fibrous scar tissue formation
51
Gastric Outlet Obstruction - Clinical manifestations: (projectile vomiting at the outlet mall) and when is pain worse?
▪ Pain worsens toward end of day as stomach fills and dilates ▪ Relief obtained by belching or vomiting ▪ Vomiting is common, often projectile
52
Gastric Outlet Obstruction - treatment
▪ Decompress stomach via NGT ▪ Correct any existing fluid and electrolyte imbalances ▪ PPI or H2 receptor blocker if obstruction due to active ulcer ▪ Balloon dilation for pyloric obstruction ▪ Surgery may be needed to remove scar tissue
53
PUD - diagnostic studies
Endoscopy with biopsy ▪ Most often used as it allows for direct viewing of mucosa ▪ Tissue specimens can be obtained to identify H. pylori and rule out stomach cancer ▪ Determine degree of ulcer healing after treatment
54
PUD - diagnostic studies - non-invasive (pugs have urea on their breath)
Noninvasive tests for H. pylori ▪ Urea breath test ▪ Can determine active infection ▪ Stool antigen test ▪ Serum or whole blood antibody tests ▪ Immunoglobin G (IgG) ▪ Will not distinguish between past and current infection
55
PUD - diagnostic studies - invasive
Invasive tests for H. pylori infection ▪ Endoscopic procedure ▪ Biopsy of stomach ▪ Rapid urease testing
56
PUD diagnostic - con't
Barium contrast study ▪ Reserved for patient who cannot undergo endoscopy ▪ Not accurate for shallow, superficial ulcers ▪ Used in diagnosis of gastric outlet obstruction ▪ Gastric analysis ▪ Analysis of gastric contents for acidity and volume ▪ NG tube is inserted, and gastric contents are aspirated ▪ Contents analyzed for HCl acid
57
PUD - labs (pud needs liver tests)
Laboratory analysis ▪ CBC ▪ Liver enzyme studies ▪ Serum amylase determination ▪ Stool examination for blood
58
PUD treatment
▪ Adequate rest ▪ Drug therapy ▪ Smoking cessation ▪ Dietary modification ▪ Long-term follow-up care
59
goal of PUD treatment
▪ Reduce degree of gastric acidity ▪ Enhance mucosal defense mechanisms
60
PUD aftercare - how quickly does the pain subside?
▪ Generally treated in ambulatory care setting ▪ Pain disappears after 3–6 days ▪ Ulcer healing requires many weeks of therapy ▪ Endoscopic examination most accurate method to monitor healing
61
PUD drug therapy
▪ PPIs ▪ H2R blockers ▪ Antibiotics ▪ Antacids ▪ Anticholinergics ▪ Cytoprotective therapy
62
Antibiotic therapy to tx H. pylori: (pylori is tough)
▪ No single agent has been effective in eliminating H. pylori ▪ Prescribed concurrently with a PPI for 14 days
63
Antacids - what do they do? (the opposite of what you think)
▪ Adjunct therapy for PUD ▪ Increase gastric pH by neutralizing HCl acid
64
Cytoprotective drug therapy - long or short term therapy?
Used for short-term treatment ▪ Protection for esophagus, stomach, and duodenum
65
Cytoprotective drug therapy ex (socrates and miso protect my stomach)
▪ Sucralfate ▪ Misoprostol
66
PUD - nutritional therapy (pugs eat anything)
■ No specific dietary modifications ■ Eat and drink foods and fluids that do not cause symptoms ■ Avoid alcohol use
67
PUD nursing management - stool?
■ PMHx ■ Medication ■ Heartburn ■ Weight loss ■ Black, tarry stools ■ Epigastric tenderness ■ Nausea and vomiting ■ Abnormal laboratory values ■ Acute pain ■ Ineffective health management ■ Nausea
68
PUD professional care
Vagotomy and Pyloroplasty
69
PUD - most common post op complications (pugs get down in the dumps w/ low blood sugar and reflux)
▪ Dumping syndrome ▪ Postprandial hypoglycemia ▪ Bile reflux gastritis
70
dumping syndrome - how many pts get it? and how long does it last?
Experienced by 20% of patients after PUD surgery. symptoms usually lasts less than 1 hour
71
dumping syndrome
see other slide
72
PUD - nutrition post op (pugs eat dry food, with low sugar after surgery)
▪ Small, dry feedings daily ▪ Low carbohydrates ▪ Restricted sugar with meals ▪ Moderate amounts of protein and fat
73
PUD - Pernicious anemia is a long-term complication
▪ After total or partial gastrectomy ▪ Due to loss of intrinsic factor (substance that helps vitamin B12 be absorbed) ▪ Patient will require cobalamin replacement therapy
74
PUD - geriatric considerations - what is the first symptom? (let's be frank, it's geriatric)
▪ ↑ Morbidity/mortality in older adults ▪ Concurrent health problems ▪ ↑ Use of NSAIDs ▪ First manifestation may be frank gastric bleeding or ↓ hematocrit ▪ Treatment similar to that for younger adults ▪ Emphasis placed on prevention
75
Gastritis
■ Inflammation of gastric mucosa ■ One of most common problems affecting the stomach ■ May be acute or chronic ■ Result of a breakdown in gastric mucosal barrier ■ Stomach tissue unprotected from autodigestion by HCl acid and pepsin
76
Gastritis - nsaids do what? (Prostie doesn’t like nsaids)
▪ Direct irritating effect on gastric mucosa ▪ NSAIDs, including aspirin and corticosteroids, inhibit prostaglandin synthesis
77
gastritis - Stomach acid and pepsin can (basically just get through)
diffuse back into the mucosa resulting in: ▪ Tissue edema ▪ Disruption of capillary walls ▪ With loss of plasma into gastric lumen ▪ Possible hemorrhage
78
Risk factors for NSAID-induced gastritis (age and gender)
▪ Being female ▪ Being over age 60 ▪ Hx of ulcer disease ▪ Anticoagulants, other NSAIDs, or ulcerogenic drugs ▪ Having a chronic debilitating disorder ▪ Diet ▪ ETOH ▪ Microorganisms ▪ H. pylori ▪ Important cause of chronic gastritis ▪ Promotes breakdown of gastric mucosal barrier ▪ Bacterial, viral, and fungal infections
79
Autoimmune atrophic gastritis - affects what area of the stomach? (atrophy in my body is fun)
▪ Affects fundus and body of stomach
80
gastritis - risk factors con't (vomiting?)
▪ Anatomic changes following surgical procedures ▪ Prolonged vomiting ▪ Intense emotional responses ▪ CNS lesions
81
acute gastritis - clinical manifestations (think of acute sickness) and common with group?
■ Anorexia ■ Nausea ■ Vomiting ■ Epigastric tenderness ■ Feeling of fullness ■ Hemorrhage ▪ Common with alcohol abuse ▪ May be only symptom
82
Chronic Gastritis Clinical Manifestations (same as acute)
▪ Symptoms are similar to those of acute gastritis ▪ Loss of intrinsic factor can occur when acid-secreting cells are lost or nonfunctioning ▪ Essential for absorption of cobalamin (vitamin B12)
83
Acute gastritis - Diagnosis most often based on (think who gets acute)
patient’s symptoms and history of drug or alcohol use
84
Chronic gastritis ▪ Diagnosis may be delayed or missed because of
nonspecific symptoms
85
gastritis - Endoscopic examination with biopsy - is it necessary?
▪ Necessary for definitive diagnosis
86
gastritis - Samples of what? (Gastritis gets every test)
Samples of breath, urine, serum, stool, and gastric tissue to determine H. pylori infection
87
gastritis - Radiologic studies
Radiologic (x-rays) studies not helpful
88
gastritis - CBC
▪ CBC ▪ Confirm presence of anemia from blood loss or lack of intrinsic factor ▪ Occult blood test ▪ Serum tests for antibody to parietal cells and intrinsic factor ▪ Tissue biopsy with cytologic examination ▪ Rule out gastric cancer
89
chronic gastritis - care (not helpful)
Focuses on evaluating and eliminating specific cause
90
UGIB - upper GI bleeding - Obvious bleeding ▪ Hematemesis (heman is fresh)
▪ Bloody vomitus ▪ Appears fresh, bright red blood or “coffee grounds”
91
UGIB - upper GI bleeding - Melena (it's in the name)
▪ Black, tarry stools ▪ Caused by digestion of blood in GI tract ▪ Black appearance—due to iron
92
UGIB - upper GI bleeding - Occult bleeding
▪ Small amounts of blood in gastric secretions, vomitus, or stools ▪ Undetectable by appearance ▪ Detectable by guaiac test
93
Esophageal origin - bleeding
– Chronic esophagitis – GERD – Mucosa-irritating drugs – Smoking – Alcohol use
94
Stomach and duodenal origin - bleeding (think ulcers)
– Peptic ulcer disease ■ Bleeding ulcers account for 40% of cases of UGI bleeding – Drugs ■ Aspirin, NSAIDs, corticosteroids
95
– Stress-related mucosal disease (SRMD) - common among who?
■ Also called physiologic stress ulcers ■ Most common in critically ill patients – Severe burns, trauma, or major surgery – Patients with coagulopathy on mechanical ventilation
96
upper GI bleed - diagnosis (you know if, and do you wash away the blood?)
Endoscopy ▪ Primary tool for diagnosing source of upper GI bleeding ▪ Before performing ▪ Lavage may be needed for clearer view ▪ NG or orogastric tube placed, and room-temperature water or saline used ▪ Do not advance tube against resistance ▪ Stomach contents aspirated through a large-bore (Ewald) tube to remove clots
97
upper GI bleed - diagostics - angiography - used when? (angie is the last resort)
Angiography ▪ Used to diagnose only when endoscopy cannot be done ▪ Invasive procedure ▪ May not be appropriate for high-risk or unstable patient ▪ Catheter placed into left gastric or superior mesenteric artery until site of bleeding is discovered
98
Emergency Assessment and Management of UGIB - ▪ Immediate physical examination with focus on (think losing too much blood)!
BP ▪ Rate and character of pulse ▪ Peripheral perfusion with capillary refill ▪ Neurologic status
99
Emergency Assessment and Management of UGIB - how often to assess output? (emergency every hour)
Indwelling urinary catheter for assessment of hourly output
100
Emergency Assessment and Management of UGIB - tele
▪ Tele/CPO ▪ Central venous pressure line for assessment of fluid volume status ▪ Supplemental oxygen
101
Emergency Assessment and Management of UGIB - abdonminal exam
▪ Presence or absence of bowel sounds ▪ Tense, rigid, boardlike abdomen: may indicate perforation and peritonitis
102
Emergency Assessment and Management of UGIB - Type and amount of fluids infused are based on physical and laboratory findings (gi bleed is bore ing)
▪ 2 large bore IVs ▪ Isotonic crystalloid- Lactated Ringers ▪ Volume replacement ▪ Whole blood, packed red blood cells, fresh frozen plasma
103
GI bleed - Endoscopic hemostasis therapy
▪ First-line therapy of upper GI bleed ▪ Goal: to coagulate or thrombose the bleeding vessel ▪ Useful for gastritis, Mallory-Weiss tear, esophageal and gastric varices, bleeding peptic ulcers, and polyps
104
GI bleed - surgical therapy
▪ Indicated when bleeding continues ▪ Regardless of therapy provided ▪ Site of bleeding identified
105
GI bleed - surgery may be needed if how much blood loss?
May be necessary when ▪ Patient continues to bleed after rapid transfusion of up to 2000 mL whole blood ▪ Remains in shock after 24 hours
106
GI bleed - acute phase -what are drugs used for? (Just 2 things)
During acute phase, used to ▪ ↓Bleeding ▪ ↓ HCl acid secretion ▪ Neutralize HCl acid that is present
107
upper GI bleeding - injection therapy
with epinephrine during endoscopy for acute hemostasis ▪ For bleeding due to ulceration ▪ Produces tissue edema → pressure on bleeding source
108
upper GI bleed - Somatostatin (inhibits gi secretions)
▪ Used for upper GI bleeding ▪ Reduces blood flow to GI organs and acid secretion ▪ Given in IV boluses for 3–7 days after onset of bleeding
109
upper GI bleed - nursing management - Signs/symptoms of shock
▪ Low BP ▪ Rapid, weak pulse ▪ Increased thirst ▪ Cold, clammy skin ▪ Restlessness
110
ulcer perforation - lethal or not? and common where?
■ Most lethal complication ■ Common in large penetrating duodenal ulcers ■ Perforated gastric ulcers often located on lesser curvature of stomach ■ Mortality rate associated with perforation of gastric ulcers is higher
111
large perforations - surgery?
■ Large perforations need immediate surgical closure ■ Small perforations may spontaneously seal themselves
112
perforation - how quickly will bacterial peritonitis occur?
▪ Bacterial peritonitis may occur within 6–12 hours ▪ Difficult to determine from symptoms alone if gastric or duodenal ulcer has perforated ▪ Manifestations of peritonitis are the same
113
PUD aftercare - how long after can you take Aspirin and nonselective NSAIDs?
▪ Aspirin and nonselective NSAIDs are discontinued for 4–6 weeks ▪ Patients receiving low dose aspirin may need long-term PPI treatment
114
antacids - how long to start working? With and without food
▪ Effects on empty stomach in 20–30 minutes ▪ If drugs taken after meals, effects may last 3–4 hours
115
antacids and sodium
▪ ↑ Sodium preparations: used cautiously in older patients and patients with ↑BP, heart failure, liver cirrhosis, or renal disease ▪ Magnesium preparations: not to be used in patients with renal failure ▪ Can enhance or decrease the absorption of some drugs
116
autoimmune atrophic gastritis - Associated with (and linked with what?) I can atrophy my cancer and h pylori
increased risk of gastric cancer ▪ May be linked to presence of H. pylori and development of autoimmune chronic gastritis`
117
atchalsia - symptoms (atcha has bad breath and can't burp)
▪ Halitosis ▪ Inability to belch ▪ GERD ▪ Regurgitation ▪ Weight loss
118
gastric outlet obstruction - symptoms (can't poop at the outlet mall)
▪ Constipation is a common complaint ▪ Dehydration ▪ Decreased dietary intake ▪ Anorexia ▪ Swelling in stomach and upper abdomen