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Peptic Ulcer Disease: From Definition to Treatment - A Medical Student's Guide — Transcript

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0:06Welcome to clean bed compass your path
0:10to medical
0:11excellence. Today I will be guiding you
0:13through a comprehensive lecture on
0:16peptic ulcer disease simplified for
0:19clarity and deeper understanding. I am
0:23Dr. Kevin and I will be your host. If
0:26you haven't subscribed to our channel
0:28yet, please do so and don't forget to
0:31tap the notification bell to stay
0:34updated on all our new videos. So, grab
0:38a notepad and let us dive into the
0:41fascinating world of peptic ulcer
0:42disease made easy. By the end of this
0:46session, you should be able to define
0:48peptic ulcer disease, identify its major
0:52ethological agents, understand the
0:55pathogenesis, outline the diagnostic
0:58strategies and discuss treatment options
1:01as well as recognizing key
1:04complications. What is peptic ulcer
1:07disease? Pepiculsa disease refers to the
1:10focal loss of epithelial lining in parts
1:14of the gastrointestinal tract typically
1:17in the stomach or the dodenum due to the
1:21destructive action of acid and
1:24pepsin. What differentiates an ulcer
1:27from an erosion is the depth of the
1:31tissue damage. Ulcers penetrate the
1:33muscularis mucosa and often lead to
1:37scarring. Erosions on the other hand are
1:40confined above the muscularis mucosa and
1:44do not scar. Peptic ulcer disease is
1:47considered a chronic disorder
1:49characterized by frequent exacerbation
1:52and remissions. The commonest sight of
1:55peptic ulcer disease is the stomach and
1:58the doino. Other sites include
2:02esophagus, a gastrointestinal
2:05anastmosis, ectopic gastric tissue as in
2:08mecclesiculum and even in the junum in
2:11cases of zolinga syndrome. Briefly we
2:14will discuss the epidemiology of peptic
2:17ulcer disease. It affects between 5 to
2:2010% of the global population.
2:23Encouragingly the global burden is
2:26reducing largely due to effective
2:29eradication of helicoacttor pylori,
2:31improved sanitation and widespread use
2:34of proton pump
2:36inhibitors. However, in developing
2:39countries, peptic ulcer disease remains
2:42a significant challenge due to ongoing
2:45issues with poor sanitation and
2:48inadequate treatment of helicoacttor
2:50pylori infections. Poor hygiene and
2:54overcrowding increase helicoacttor
2:56pylorate
2:57transmission. PUD is said to be more
3:00prevalent in men than women. Peptic
3:03ulcer disease is most common among
3:06middle-aged and older adults with a peak
3:09incidence between the ages of 25 to 60
3:13years. Among the two major types, bodina
3:17ulcers are more frequent than gastric
3:19ulcers. In tropical regions like
3:22Nigeria, while large scale feed
3:24prevalence data is limited,
3:27hospital-based endoscopic studies in
3:29dispectic patients show that PUB is
3:33diagnosed in as many as 20 to 40% of
3:37cases. This underscores the high burden
3:40of undiagnosed or mismanaged dispsia in
3:44clinical settings. Now let us explore
3:48the major causes of peptic ulcer
3:51disease. One is helicoact pylori
3:55infection. This is the most important
3:58cause. Use of ocerogenic medications
4:02like NSAIDs and
4:04corticosteroids. Hyper secrettory states
4:07such as zolinga elisonin syndrome.
4:10Genetic
4:11predisposition. Lifesty factors such as
4:14smoking, alcohol, coffee and chronic
4:18stress. Viral infections like cytogalo
4:21virus infections, episimplex virus one
4:25particularly in ulo compromised
4:28individuals. Let's look at more details
4:30on helicoacta pylori for short h pylori.
4:34H pylori was first identified in 1983 by
4:39Warren and Marshall whose groundbreaking
4:42discovery earned them the 2005 Nobel
4:45Prize in Physiology on Medicine. It was
4:49initially called Campilobacta pyloridis.
4:53Today it is recognized as the most
4:56common bacterial infection worldwide. In
4:59developing countries, 80 to 90% of
5:02individuals are infected by age 20.
5:06While in developed countries, prevalence
5:09is less than 20% under the age of 20,
5:13rising to 50 to 69% by the age of 70. In
5:18developing countries, most children
5:21acquire H pylori between the ages of 5
5:25and 10 years. Key risk factors include
5:28low socioeconomic status, poor hygiene
5:32and overcrowded living conditions.
5:36Transmission is by foa and orura roots
5:41occasionally through iatrogenic
5:44means beyond PUB. H pylori is also
5:48associated with gastritis, gastric
5:52adenocarcinoma and gastric malt
5:54lymphoma. It accounts for 70% of gastric
5:59ulcers and 95% of dodina ulcers. Now
6:04let's examine the biological features of
6:06helicoacta pylori. It is a gram negative
6:10spirshaped microerophilic
6:13basilus. It is slow growing and highly
6:16motile due to multiple flagagella. It
6:20produces urines enabling it to
6:22neutralize gastric acid and creates an
6:25alkaline
6:26environment. It can transform into a
6:29cocoid form in its dormat state. This
6:32facilitates it survival in adverse
6:35condition. It causes mucosa injury
6:38through chronic inflammation and urous
6:40activity which weakens the stomach's
6:43protective barrier. This is a visual of
6:48elcoacta pylori the multiple flagella
6:51spirshaped organism. Now let's shift our
6:55focus to the second major cause of
6:58peptic ulcer disease nsides and related
7:02medications. Drugs like aspirin
7:05ibuprofen and even corticosteroids
7:08compromise mucosa defenses by inhibiting
7:12proal glanding sentences. Other
7:15implicated drug classes include the
7:18selective serotonin reoptic inhibitors,
7:21tricyclic anti-depressants and
7:25bisphosphonates. NAIDs are responsible
7:27for about 30% of gastric ulcers and a
7:31smaller proportion of doina ulcers. They
7:35are currently the leading cause of
7:37mucusa injury in the western world.
7:41NSAID induced injuries ranges from
7:44superficial erosions to ulcers and to
7:48gastrointestinal bleeding. Even patients
7:51on low dose asper for cardiovascular
7:54protection can experience
7:56gastrointestinal toxicity. The severity
8:00is often those dependent. Now let's look
8:04at some less common causes of peptic
8:06disease. hyper secrettory states like
8:09zuling gaisin syndrome which involves a
8:12gastrine producing tumor
8:14gastronoma leading to excess acid
8:18production. Systemic mastocytosis and
8:21antrag cell hypoplasia can also drive
8:24increased acid
8:26production. Genetic
8:29predisposition Identical twins show 56%
8:32concordance rate. firstderee relative
8:36have a free phone increased risk.
8:39Individuals with blood group O are more
8:42susceptible. Smoking is a key modifiable
8:46risk factor. It contributes to peptic
8:49ulcer disease by increasing gastric acid
8:53secretion, decreasing mucosa blood flow,
8:57reducing protective prostag glandins,
9:00inhibiting bodena bicarbonate secretion,
9:04enhancing H pylori viral and delaying
9:07ulcer
9:08healing. Alcohol has several harmful
9:11effects on the gastric mucosa.
9:14It causes direct mucusa injury leading
9:17to erosions and
9:19irritations. It increases acid
9:22secretion, decreases mucusa and
9:25bicarbonate production. And when it's
9:28combined with ns, it significantly
9:30increases the risk of ulcer
9:34formation. Another contributor to peptic
9:37ulcer disease is stress, both emotional
9:40and physiological.
9:42While stress may not directly cause
9:44ulcers in healthy individuals, it plays
9:46a significant role in hospitalized or
9:49critically ill patients. Two specific
9:52types of ulcers include the cushions
9:55ulcers which is associated with brain
9:58injuries or tumors. The Collins ulcers
10:01which is seen in patients with extensive
10:03bones. In cases of sepsis, hypotension
10:08or multi- trauma, mucusa eskemia impairs
10:11gastric defenses making the stomach
10:14lining more vulnerable to acid
10:17damage. Let's take a closer look at the
10:20gastric secrettory
10:23complex. In the antrum, the mucus neck
10:26cells secrete mucus and bicarbonates.
10:29The GC cells produce gastrine, a hormone
10:33that stimulates acid
10:35secretion. The D cells secrete
10:38somatine which inhibits gastrin release
10:41and provides a negative feedback. In the
10:45fundus and the body of the stomach, we
10:48find oxintic glands which contains the
10:51peral cells which secrete hydrochloric
10:55acid and the chief cells that secrete
10:58pepsinogene which is converted to pepsin
11:01in acidic environment to aid protein
11:05digestion. The stomach isn't
11:07defenseless. It has several protective
11:10mechanism to prevent self- digestion by
11:14acid. One of them is the mucus
11:16bicarbonate barrier. This forms a
11:19gel-like layer that neutralizes acid at
11:22the mucosa surface. We have the prostag
11:26glandins. This stimulate mucus and
11:28bicarbonate secretion, enhance mucosa
11:32blood flow and promote epithelial cell
11:35repair. Then the tight junctions will
11:38prevent back diffusion of hydrogen ions
11:41into the
11:43mucosa. Other protective mechanism
11:45include the mucosa blood flow which
11:49supplies oxygen and nutrients and help
11:51clears acid and toxin. Then epithelial
11:55cell turnover. This enables rapid
11:58regeneration of damaged cells. This
12:01delicate balance between injury and
12:03repair is essential for maintaining
12:06mucosa
12:08integrity. Even with the protective
12:10mechanism in the stomach, several
12:12aggressive factors threaten mucosa
12:15integrity. One is the gastric acid. This
12:19is secreted by pieta cells and
12:22stimulated by gastrine, histamine and
12:25acetylcoline. Pepsine. This is activated
12:28in low pH. It digests protein but can
12:32also damage mucosa tissues. Then in the
12:35bio salt reflux from the doden and
12:38highly irritating to gastric epithelium.
12:41Next is the helicoacta pylori salicyate
12:44and alcohol all capable of inflicting
12:48direct mucusa damage.
12:51Having discussed the protective and
12:53aggressive factors, it is important to
12:56state that ulcers will develop when
12:58there is an imbalance between the
13:00aggressive and protective factors. When
13:04damaging forces outweigh the mucosa
13:06defenses, ulcers will definitely
13:09develop. This concept is useful but it
13:12cannot explain the basis of pepicosa
13:16disease in totality.
13:18Let us look at the role of helicoacta
13:21pylori in the pathogenesis of peptic
13:23ulcer disease. Helcobacttor pylori is a
13:27master at evading defenses and promoting
13:30injury. It colonizes the mucus layer and
13:34disrupts the mucus bicarbonate barrier.
13:37It also stimulates gastric acid
13:40secretion. It produces uras which
13:42converts ura to ammonia damaging cells
13:46and neutralizing acid aiding its
13:49survival. It reduces proteasis and this
13:52contributes to mucosa degradation. H
13:55pylori exacts direct cytoatic effect
13:58also on the gastrointestinal
14:01mucosa and it gets worse. Elcobata
14:04pylori also reduces bicarabolate
14:06secretion in the doenum. It induces
14:10inflammation by activating neutr and
14:13macrofasages and releasing cytoins like
14:16interalucinate and reactive oxygen
14:18species. It also disrupts tight
14:21junctions thereby increasing acid back
14:24dusion and stimulates gastrin release
14:27which further increases output.
14:31Now let us look at the role of noise to
14:34rea anti-inflammatory drugs in the
14:36pathogenesis of peptic ulcer disease.
14:40Naid disrupt mucosa integrity through
14:42multiple mechanisms. One it inhibits
14:46cycllo oxygenase one enzyme leading to
14:48reduced proaglandine sentences.
14:51Decreased proaglandine results in
14:54reduced mucus and bicarbonate secretion
14:56impaired blood flow and delayed healing.
15:00NSAID also cause direct epithelial
15:02toxicity and increased gastric acid
15:05secretion contributing to ulcer
15:08formation. Besides helicoacttor pylori
15:12and nidates, other contributing factors
15:15include smoking. This reduces mucosa
15:18blood flow and delays healing. Alcohol
15:22stimulates acid secretion and irritates
15:25the mucosa. Stress especially in
15:28critically ill patients impairs
15:31perfusion and suppresses protective
15:33secretions. Zoliga Ellison syndrome a
15:37hypers secrettory states it's a gastrine
15:39secretreting tumor causing profound acid
15:42hyper
15:43secretion. Let us look at the clinical
15:47manifestations. The cardinal symptom of
15:49peptic ulcer disease is abdominal pain.
15:52It is typically
15:54epigastric
15:55burning knowing or described as pepper
15:59in character. The pain is episodic and
16:03may radiate to the back especially if
16:05the ulcer penetrates the pancreas. It is
16:09worse at night and may disturb sleep.
16:13The timing of the pain helps
16:15differentiate ulcer types. In doala
16:19ulcers, pain occurs 2 to 3 hours after
16:22meals and is relieved by food or
16:26antacids. In gastric ulcers, pain
16:29worsens with meals due to acid
16:32secretion. Beyond pain, patients may
16:35also experience nausea and vomiting due
16:38to irritation of the gastric mucosa,
16:42bloating and buring especially if
16:45coexisting functional dispersia is
16:47present. Weight loss which is more
16:49common in gastric ulcer especially if
16:53eating worsening symptoms or if the
16:56ulcer is
16:57malignant. Not all cases of PUD present
17:01classically. Some patients have non
17:04uloscera disyspsia which is ulcer like
17:06symptoms without visible mucosa breaks.
17:10Elderly patients and those on nsides may
17:13present with silent ulcers diagnosed
17:16only when complications occur. These
17:19atypical presentations are dangerous as
17:22they delay diagnosis and
17:24treatment. Let us examine dina ulcers in
17:27more detail. Buggina ulcers commonly
17:31affect adults aged 25 to 75 years with a
17:35male
17:36predominance. About 90 to 95% of dural
17:40ulcers are linked to helicoacttor pylori
17:43infection. Other risk factors are
17:45smoking NCUS and family history. About
17:4990% of dural ulcers occur in the first
17:52part of the doen usually within 3 cm of
17:56the pylorus. Urina ulcers present with
17:59epigastric pain which could be burning
18:02or peppery often within 2 to 3 hours
18:05after meals or at night. The pain is
18:08typically relieved by food or antacid.
18:12Weight loss and anorexia are
18:15uncommon. For gastric ulcers the peak
18:18incidence is between 55 to 65 years.
18:23Common causes include helicoact pylori
18:26noa anti-inflammatory drugs especially
18:29when combined with
18:31corticosteroids. It presents with
18:33abdominal pain. The pain occurs shortly
18:36after meals and is less relieved by food
18:39or
18:40antacid. Eating may trigger or worsen
18:43the pain. Onethird of patients
18:45experience nighttime symptoms. Weight
18:48loss and anorexia are more common than
18:52indoor ulcers. Treatment typically
18:55requires a longer duration to ensure
18:58full healing. Now let us review the red
19:01flags which we refer to as the alarm
19:03symptoms. This may indicate
19:05complications or
19:07malignancy. The first is new onset
19:10symptoms especially in patients above 45
19:14years. anemia which could be iron
19:17deficiency, significant weight loss,
19:20recurrent vomiting, melanina or
19:22hematiteis and dysphasia. These symptoms
19:26warrant urgent endoscopy to rule out
19:29cancer or bleeding
19:32ulcers. Peptic ulcer disease can lead to
19:35serious
19:36complications. The most common being
19:38gastrointestinal bleeding. These
19:41patients will present with
19:43hematiteis, melanina, iron deficiency
19:46anemia from chronic blood loss,
19:48hypovalmic shock in cases of massive
19:51hemorrhage. Bleeding ulcers are a major
19:54cause of upper GI
19:58emergencies. Another life-threatening
20:01complication is
20:03perforation especially with anterior
20:05ulcers. may present as sudden severe
20:08abdominal pain. Signs of peritonitis
20:12including guarding aribbound
20:14tenderness. Imaging may reveal free air
20:17under the diaphragm on upright abdominal
20:20or chest X-ray. Next is
20:24penetration. Penetration occurs when the
20:26ulcers erode into nearby organs like the
20:30pancreas leading to persistent or
20:32referred pain.
20:34Peptic ulcer disease may also cause
20:37gastric outlet obstruction due to
20:40fibroic scarring, edema, active
20:43inflammation near the pyloric channel.
20:47They may present with early satiety,
20:49recurrent vomiting of undigested food,
20:52abdominal distension, visible
20:55peristasis, weight loss and dehydration.
20:58These signs suggest mechanical
21:00obstruction often requiring
21:04intervention. Although rare, malignant
21:07transformation is a serious concern with
21:10gastric ulcers. Because of this, an
21:13endoscopic biopsy is essential for any
21:17suspicious ulcer. Even ulcers that
21:20appear benign should be re-evaluated
21:23with repeat endoscopy after 6 to 8 weeks
21:27to confirm healing and exclude
21:30cancers. When a patient presents with
21:33epigastric pain or disyspsia, it is
21:36essential to consider other potential
21:39causes beyond peptic ulcer disease. This
21:43includes gastric cancer. Look for
21:46irregular ulcer margins. modularities or
21:50masses on
21:52endoscoping. Pancreatic cancer often
21:55presents with weight loss and sometimes
21:58back
21:59pain.
22:01Pancreatitis often presents with back
22:04pain and elevated amalayise or
22:08lipase.
22:09Chiccyitis especially when the right
22:12upper quadrant pain is present.
22:16Gastroosophedia reflux disease marked by
22:18heartburn and regurgitation without
22:22ulceration. Mesenteric eskeemia presents
22:25with pain out of proportion to
22:28examination findings. Functional
22:31dispsia. Epigastric discomfort with no
22:34identifiable organic cause. Biliary
22:37colic and gastritis.
22:40These are some of the differential
22:42diagnosis of peptic ulcer
22:45disease. The diagnostic process begins
22:48with a detailed history and physical
22:52examination. Important questions to ask
22:55include the nature and the timing of
22:58pain. Is it burning or knowing?
23:03Relationship to meals. Does food relieve
23:06or worsening it? Medication history,
23:10especially NSAIDs and aspirin use.
23:14Lifestyle factors such as smoking and
23:17alcohol intake. Red flag symptoms which
23:20include unexplained weight loss,
23:22persistent vomiting, dysphasia or signs
23:25of anemia. A thorough history often
23:29points towards the likely diagnosis
23:31before any testing is done.
23:35Let us look at some diagnostic tests in
23:37the evaluation of peptic ulcer disease.
23:41The gold standard for diagnosing peptic
23:43ulcer disease is upper gastrointestinal
23:47endoscopy also known as poss
23:51gastroindoscopy. Why choose endoscoping?
23:54It allows direct visualization of
23:56ulcers. It enables biopsy to assess for
24:01malignancy or helicoacttor pylorine. It
24:04has a diagnostic accuracy of up to
24:0895%. The key findings of note include
24:12ulcer sizes, location and margins.
24:16Irregularity or nodularity may suggest
24:19malignancy. Biopsy results help guide
24:22prognosis and treatment.
24:26These are endoscopic images revealing
24:29ulcers. During endoscopic, classic
24:31findings include round or over ulcers.
24:36The surrounding area can be inflamed and
24:39sometimes you get active bleeding as
24:41indicated in one of the images. Biopsy
24:45specimens are often taken for
24:47histologology or rapid urase testing to
24:50detect elcoacta pylori.
24:54If endoscopy isn't available or
24:57feasible, a baron meal study can be an
25:00alternative. It detects ulcer in about
25:0380% of cases. Ours appear as well
25:07defined ulcer critters or niches or
25:10filling defects in the gastric or do
25:14well. However, biron meal has some
25:18limitations. They poorly detect
25:20fundalers.
25:22They do not allow for biopsy. Up to 41%
25:26of gastric ulcers that appear benign
25:29radiologically may be malignant on
25:32biopsy. So while useful berium studies
25:35are not substitute for
25:38endoscopy. These are berium study
25:41imaging. One for gastric outlet
25:42obstruction. Look at the arrow
25:44indicating the narrow and the second is
25:47for donal ulcers revealing the ulcer
25:50crater.
25:52Diagnosis of helicoacta pylori.
25:55Identifying helicoacttor pylori
25:57infection is critical in managing peptic
26:01ulcer disease. There are two main
26:03categories of diagnostic tests. One the
26:06non-invasive test and the second the
26:09invasive which requires endoscoping. We
26:12are going to explore both tests. First
26:15the non-invasive. The URA breath test is
26:18the most accurate non-invasive test for
26:21detecting active elcoacta pylori
26:25infection. It is highly sensitive and
26:28specific. How does it work? The patient
26:31swallows ura labed with carbon 13 or
26:35carbon 14. H pyloris urus enzyme breaks
26:39it down into carbon dioxide which is
26:43measured in the breath. Advantages of
26:47URA breath test. One, it is highly
26:50sensitive and specific. It is ideal for
26:53both initial diagnosis and post
26:55treatment confirmation. Note that recent
26:58antibiotic use or the use of PPI can
27:02lead to false negative
27:04results. Other non-invasive tests
27:07include H pylori cerology. This detects
27:12imoglobin G or imoglobin A antibodies
27:15against helicoacttor pylorine. The
27:18limitation here is it cannot distinguish
27:21between active and past infection. Next
27:25is the stool or the fal antigen test.
27:28This detects bacterial antigen in
27:30physics using iminoassay or polymerase
27:33chain reaction. It is useful for both
27:35initial diagnosis and post treatment
27:38confirmation.
27:40Now let us look at invasive testing. One
27:43is the rapid urase test. With endoscopy
27:46we can perform a rapid urase test also
27:49called the clo test. How does it work? A
27:52gastric biopsy is placed in a medium
27:55containing ura and a pH indicator. If H
27:59pylori is present, uras breaks down the
28:02ura into ammonia. This raises the pH and
28:06changes the color of the medium from
28:09orange or yellow to pink or red. This is
28:14simple, fast and a reliable diagnostic
28:17tool. Additional invasive test include
28:20culture. It is time consuming but
28:23remains the good standard for antibiotic
28:26sensitivity testing. Next is
28:29hisystologology allows direct
28:30visualization of elicodacta pylori using
28:34special stains like the hematoxilene and
28:37eosine or the wthing star
28:41stain. Advanced tools include polymerase
28:44chain reaction and DNA probes on biopsy
28:48samples. Urinary excretion of nitrogen
28:5215 labed ammonia.
28:54These techniques not only confirm
28:57presence but also help to assess strain
29:00type and antibiotic
29:03resistance. Other tests that can be done
29:05include the abdominal ultrasound or CT
29:07scan, the serum gastrin level in cases
29:10of zolinga elysin syndrome, stool test
29:13to detect for odor blood. Laboratory
29:16tests will include complete blood count,
29:18anemia, especially iron deficiency or
29:21inaccurate blood loss, liver function
29:23test to rule out hepatitary causes of
29:26epigastric pain, coagulation profile.
29:28This helps you to assess bleeding
29:31risk. When should we test for and treat
29:34heliccoact pylorin? Some of the
29:37established indications include active
29:39peptic ulcer disease, history of peptic
29:43ulcer disease without prior eradication
29:45of helicoacttor pylori, gastric m
29:48lymphoma especially low grade after
29:51resection of early gastric cancer to
29:53prevent recurrence
29:56uninvestigated especially in high
29:58prevalence setting. In these situations,
30:01accurate diagnosis and treatment are
30:04essential.
30:06Some indications remain controversial.
30:09The benefit of treatment may be less
30:11clear in the following conditions. Non
30:14ulcer dispsia in gastroofia reflux
30:18disease in chronic nid users unexplained
30:23iron deficiency anemia and populations
30:26at risk of gastric cancer. In these
30:29cases, testing and treatment decisions
30:32should be individualized based on
30:34clinical context and regional
30:37guidelines. Treatment of peptic ulcer
30:40disease. Let us now summarize the key
30:43goals of treating peptic ulcer disease.
30:46One to relieve symptoms. Two eradicate
30:50helicoacttor pylori when present. Three
30:53is to promote complete ulcer healing.
30:56Four is to prevent recurrence and five
30:59is to avoid complications such as
31:01bleeding, perforation or obstruction.
31:05These goals guide our approach to both
31:07medication and lifestyle
31:10management. Now we'll discuss
31:12medications used for symptom relief. One
31:16is proton pump inhibitor. They
31:19irreversibly block the hydrogen
31:22potassium ATPs pump in the peral cells.
31:25Examples are a prazo, omerazo,
31:29esomerazo. Second is the histamine
31:32receptor antagonist. These ones block
31:36histamines stimulated acid secretions.
31:39Example is formotidine, cimedine,
31:42ranidine and others. In the
31:45class we have the antacids which are
31:48very popular. They neutralize existing
31:52gastric acid secretion.
31:55They could be aluminium based or
31:57magnesium based. Some of them contain
31:59other compounds like cementicum and
32:02others. Examples are aluminium
32:05hydroxide, magnesium hydroxide, calcium
32:08carbonate, sodium
32:10bicarbonate. We also have the
32:12cytorotective agents like proaglandine
32:16analoges. Example is the misoproto.
32:19This is a synthetic proagland E1 analog
32:23that enhances mucosa
32:26protection. Then we have coating agents
32:28like safet. Socrate forms a protective
32:32gel-like barrier over the era site. Then
32:37bismouth compounds which could either be
32:39bismouth subitrate or subsalicate.
32:43They coat ulcers and have mild
32:46antibacterial and anti-inflammatory
32:49properties. Other symptom relief agents
32:52that have been used previously are
32:55anti-uscarinic agents such as
32:58penzipin. Now we talk about the
33:00eradication of helicoacta pylori.
33:04Eradicating helicoacttor pylori is key
33:07to healing ulcers and preventing
33:10recurrence especially in nonaid induced
33:14ulcers. A 14-day regimen are preferred
33:18over shorter durations. Maintenance
33:21therapy is advised in patients with
33:24complicated ulcers such as bleeding or
33:27perforation.
33:30So we'll talk about the first line
33:32therapy for helicoacttor
33:35pylorication. We have the triple
33:39regimen. This is use of a proton
33:43inhibitor such as razzo merazo and
33:46others with either two of these three
33:50antibiotics flying amoxiceline or
33:54metronidazo.
33:55The duration for treatment is 10 to 14
33:58days and eradication rate is up to 70 to
34:0385%. Failure of the triple regimen can
34:07make us use the quadruple regimen. This
34:10is actually preferred in areas of high
34:13claritis resistance or when there is
34:16treatment failure. Here we use proton
34:18pump inhibitor plus bismouth metrindazo
34:22and
34:23tetracycl all for 10 to 14 days.
34:26Eradication rate in this case is up to
34:2993%.
34:32For patients who failed the first line
34:34therapy, you consider the second line
34:36therapy and this include level fluxin
34:40based regimen where you combine a PPI
34:44leveline and amoxiceline for 10 to 14
34:47days would also be refutin based which
34:51we use a PPI fabine and amoxiceline for
34:55about 10 days to 14 days still or a
34:58frazzolin based therapy where you Use a
35:01PPI porazolidine and ambosine for same
35:06duration. We should tailor therapy based
35:09on local resistance pattern and prior
35:12antibiotic exposure.
35:15Then we have the sequential therapy
35:18where we use PPI and amoxiceline for 5
35:22to 7 days followed by PPI
35:26fitroycine tinidazu or metroindazu for 5
35:30to 7 days. Then we have the
35:32conccommittant therapy where all four
35:35drugs the PPI amoxicylene clitroycin
35:39metindaz tinidazone we use them for 10
35:43days. These regimens are especially
35:46useful in high resistance area.
35:50Surgery is rarely first line but it
35:54becomes essential in
35:57perforation, refractory ulcers,
36:00uncontrolled bleeding, gastric outlet
36:03obstruction, suspected malignancy or any
36:07complication or responsive to medical
36:10therapy.
36:12Surgical procedures include
36:14vigottomy,
36:16pyloroplasty, gasterectomy and tractomy
36:19and overswing of
36:22perforation. General measures include
36:24important lifestyle modifications such
36:26as avoiding NSAID, aspirin,
36:29corticosteroids unless they are
36:32necessary, limiting alcohol and caffeine
36:35use, stop smoking, educating patients on
36:39medication adherence, and encourage
36:42stress reduction and psychological
36:44support.
36:46Briefly on managing complications for
36:49bleeding, endoscopic heostasis, blood
36:52transfusion if needed, for perforation,
36:56emergency surgery like the use of omea
36:58patch for gastric outlet obstruction and
37:01theoscopic dilation or surgical
37:04resection. Early recognition and
37:06intervention are
37:08critical. Few words on peptic ulcer
37:11disease and diet. Let us bust some of
37:14the myths. Drink milk to suit ulcers.
37:17This is false because milk stimulates
37:20acid. Avoid all forms of spices. This
37:24has no solid evidence. Don't eat fried
37:27foods. Even though greasy food may
37:29worsen symptom, but they don't cause
37:32ulcers. Current evidence suggests that
37:34stress spicy food they are actually in
37:37significant risk. Frequent injection of
37:40milk like we said initially is
37:42associated with increased acid
37:45production. Prevention is key. Test and
37:49treat H pylori in all ulcer patient.
37:53Confirm eradication of helicoacttor
37:56pylori after 4 to 6 weeks using the
38:00stool antigen test and ura breath test.
38:03Cerological tests are not reliable post
38:07treatment. Post eradication followup is
38:10important. Repeat endoscopy at 6 to 8
38:14weeks for gastric ulcer. Long-term use
38:17of PPI may be needed in chronic naid
38:20users, elderly and patients with
38:24previous complications. Lifetime
38:26modification as previously stated no
38:29smoking, alcohol reduction and stress
38:32management are important.
38:36Key takeaway from this
38:38presentation. Peptic ulcer disease
38:41results from an imbalance between mucosa
38:44defenses and aggressive factors.
38:47Helicoacta pylori and nsid are the main
38:50causes of peptic uler. Alarm symptoms
38:54warrant prompt
38:55endoscopy. Eradication of helicoacta
38:58pylori is critical for cure.
39:01Complications such as bleeding and
39:03perforation are life-threatening.
39:06Followup is crucial for gastric ulcers
39:09and recurrent
39:11disease. Thank you for watching. I hope
39:14this strengthened your clinical graphs
39:16of peptic ulcer disease. If this was
39:19helpful, like this video, subscribe to
39:23Clement Compass, share with your
39:25colleagues, comment below with your
39:27thoughts or topic request. We simplify
39:30internal medicine one lecture at a time.
39:34I am Dr. Kevin. Stay focused, keep
39:37learning and always follow your compass
39:40to clinical excellence. See you in the
39:43next video.

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