GERD and PEPTIC ULCER Flashcards by Iseoluwa Ojo

Different Parts : Upper1/3; middle1/3; lower 1/3

Muscularis
mucosae (smooth
muscle)

Submucosal
glands

Muscularis
externa

Absent in beginning; longitudinal; Inner
circular & outer Longitudinal

Absent; Absent; present

Skeletal muscle ; Skeletal & smooth muscle ; smooth muscle

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Diseases of the oesophagus

Congenital- oesophageal ________, __________ fistula, vascular _____, ———,———

Diverticuli- ________

___________

atresia; tracheoesophageal; ring

webs, duplication

Achalasia

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Diseases of the oesophagus

 Inflammatory-_____ disease, ___________, candidiasis, ________ disease

 Neoplasm- ____________ ca, ___________

Reflux; Barrett’s oesophagus

Crohn’s

Squamous cell ; Adenocarcinoma

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Zenker’s diverticulum, also known as ___________ diverticulum, is a type of diverticulum that forms in the _______, specifically in the area called the __________.

It is a _____-like protrusion that develops as a result of ___________ within the pharynx during swallowing.

pharyngoesophageal

pharynx; Killian triangle

pouch; increased pressure

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In achalasia, the _____________, a ring of muscle at the bottom of the esophagus, ________________ during swallowing, leading to difficulty in _______________________

lower esophageal sphincter (LES)

fails to relax properly

moving food and liquid from the esophagus into the stomach.

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Oesophagitis- Causes

Lacerations-________ syndrome

Chemical- alcohol, corrosive acids
or alkalis, heavy cigarette smoking,
drugs, radiation therapy

Infection: ________ virus, ________,
Fungal(_________)

Mallory-Weiss

Herpes simplex; CMV; candida

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Oesophagitis- Causes

 ____________ ——- disease
 ______ disease
 _______ oesophagitis
 ______ oesophagitis

Pemphigoid skin

Crohn

Eosinophilic

Reflux

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most common cause of Oesophagitis is ??

Reflux oesophagitis

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Mallory-Weiss syndrome refers to a condition characterized by a _______ or ______ in the mucous membrane lining the ____________________.

This typically occurs as a result of severe or prolonged _______ or _________.

tear or rupture

junction of the esophagus and stomach

vomiting or retching

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Pemphigoid is a group of ________ _______ diseases characterized by the formation of ______ and ______ on the skin and mucous membranes.

autoimmune blistering skin

blisters; erosions

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Gastro-oesophageal Reflux Disease(GERD or GORD)

• Reflux refers to a condition in which _________ content moves _____________

• It becomes a disease when _____________ causing ____________ and patient experiences symptoms

acidic stomach; up into the oesophagus.

it occurs frequently ; irritation of the lining

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GERD is defined as any symptomatic condition or histopathologic _______________________ resulting from ___________________

alteration of the oesophageal mucosa

episodes of gastro-oesophageal reflux.

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Occasionally, everyone experiences
regurgitation of acidic gastric content into the lower oesophagus

T/F

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Reflux disease

Reflux disease occurs in any of these scenarios:

 When there is exposure of oesophageal mucosa to PH
<____ for more than ____% of 24hrs

 When ______ causes damage or when

 Patient becomes __________

4.0; 4.5

regurgitation

symptomatic

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Epidemiology of GERD

Prevalence of GERD is largely unknown in Africa.

T/F

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Epidemiology of GERD

____-_____ % -Western world

<___% in Asia this was lower

10–20

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Mechanisms that Protect oesophageal
Mucosa against damaging effect of acid

_______ secretion from ______ glands

______ present in ________

 Constant ____________________prevents reflux

Mucin; submucosal

HCO3; saliva

lower oesophageal sphincter tone

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Mechanisms that Protect oesophageal
Mucosa against damaging effect of acid

_________ and __________→ neutralize acid

HCO3 and submucosal mucin

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Conditions that decrease _____ or increase __________ lead to GERD

LES

abdominal pressure

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Predisposing factors for GERD

Factors that decrease LES:

________
________
 _______
 Delayed __________
 Certain foods/drinks (e.g, _____,_______)→decrease LES pressure
 Drugs- ______________,
nitrates, _______ ,________
→decrease LES pressure

Pregnancy; Diabetes

Hiatus hernia; gastric emptying

coffee, alcohol

calcium channel blockers

beta-blockers, progesterone

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Predisposing factors for GERD

__________
________
__________

Cigarette smoking

Connective tissue disorders, such as
_______

_______________

Obesity

Alcohol

Asthma

scleroderma

Zollinger-Ellison syndrome

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Zollinger-Ellison syndrome (ZES) is a (common or rare?) condition characterized by the development of ________-secreting tumors called _______.

Rare; gastrin; gastrinomas

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Zollinger-Ellison syndrome (ZES)

These tumors usually form in the _______ or the _______.

pancreas; duodenum

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Pathogenesis

The mechanisms that result in GERD include:

_________ ———- of the _____ oesophagus to ________ and ______

____ reflux from duodenum may aggravate damage

Prolonged exposure; distal

acid and pepsin

Bile

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Pathogenesis In a minority of people with reflux disease, normal levels of reflux of acid and pepsin trigger reflux-induced symptoms.” T/F

Natural Course of GERD Reflux results in damage to the ________ epithelium and accelerated __________. The response to the reflux is two fold: Epithelial(__________ and ——————— ) and _________________ reaction

squamous; desquamation desquamation and basal cell hyperplasia Chronic inflammatory

IN GERD The microscopic changes to the oesophageal epithelium may be present even if oesophagus appears normal grossly on endoscopy T/F

Natural Course of GERD: Inflammatory response Intraepithelial infiltration by eosinophil (IEE) occurs (early or late?) • This is later followed by _________ and _______ – Healing follows with ______________ , leading to oesophageal ________ and _______ • Other complications

Early neutrophils and lymphocytes subepithelial fibrosis; stricture and narrowing

Morphology of GERD  _________ hyperplasia,_______ , ______ of the papillae and ______ of the ______________ ________________ infiltration.

Basal cell ; oedema elongation; thinning; squamous cell layer Inflammatory cell

Morphology of GERD  Intraepithelial eosinophils of ____/HPF highly suggestive of GERD _________ inflammation (non-specific)  ___________ inflammation (usually due to _______ or ___________)

<20; Lymphocytic; Neutrophilic reflux or Helicobacter gastritis

Morphology of GERD _____________ metaplasia or _________ metaplasia Dysplasia

Goblet cell intestinal Barrett’s

Symptoms of GERD _______ ______ pain Difficulty _______ ______ cough

Heartburn Chest; swallowing Dry

Symptoms of GERD _________ or ———— ___________ of food or sour liquid (acid reflux) Sensation of __________________

Hoarseness or sore throat Regurgitation a lump in the throat

Complications of GERD ________ metaplasia  Oesophageal ______ _________-__________  Haemorrhage-(presenting as ______,________)

Barrett's stricture Pseudo-diverticula haematemesis, melena

Complications of GERD  ________  ______ formation  Inflammatory _____  Adenocarcinoma

Perforation Fistula polyps

Barrett’s oesophagus  Barrett’s oesophagus is characterized by ________ within the ______ mucosa of the oesophagus

intestinal metaplasia; squamous

Barrett’s oesophagus  Wang and Sampliner, 2008 described BE as a change in the ________________ epithelium of any length that can be recognized as ________ type mucosa at _________ and is confirmed to have __________ by ______ of the tubular oesophagu

distal oesophageal columnar; endoscopy intestinal metaplasia; biopsy

Barrett Oesophagus Patients with BE have ——— folds increase in risk of developing adenocarcinoma of the oesophagus However only ______% of Barrett’s progress to cancer

20; 1-5

Barrett Oesophagus Types: • Long segment- =/>____ • Short segment BE- <_____ If _______ is present, its classified as ________ or _______

3cm; 3cm dysplasia low or high grade

Peptic ulcer is defined as a ___________ of the G.I.T which extends through the _________ into the ———— or deeper and produced by the action of __________

breach in the mucosa muscularis mucosa submucosa; gastric secretions

Common Sites of ulcer It can occur in any portion of the G.I.T tht is exposed to the aggressive action of acid-peptic juices _______________ and __________ are most common sites  __________ mucosa  ___________ of _________ Multiple sites in __________ Meckel’s diverticulum containing ____________

Distal stomach and proximal part of duodenum Barrett’s Margins of gastro-enterostomy Zoolinger-Ellison’s syndrome ectopic gastric mucosa

Normal mechanisms that protects mucosa against acid & pepsin Mucus secretion-form protective surface coat.  HCO3 secretion-neutralizes effect of acid  Tight intercellular junction between mucosal epithelial cells -prevent acid penetration • Regenerative capacity of the cells-rapidly replace damaged cells • Rich mucosal blood flow • Prostaglandins

Normal mechanisms that protects mucosa against acid & pepsin ______ secretion ______ secretion ____________ junction _________ capacity of the cells • Rich mucosal _______ • Prostaglandins

Mucus HCO3 Regenerative Tight intercellular blood flow

Normal mechanisms that protects mucosa against acid & pepsin Mucus secretion-form _______________  HCO3 secretion- ______________  Tight intercellular junction between mucosal epithelial cells - _____________ • Regenerative capacity of the cells- _______ replace _______ cells

protective surface coat. neutralizes effect of acid prevent acid penetration rapidly replace damaged

Other risk factors for peptic ulcers  _____ and other \______  _____________  Alcohol-  ___________  In some patients too rapid ___________  Personality and psychological stress  Dietary habit.

Aspirin ; NSAIDS Cigarette smoking Corticosteroids gastric emptying

Other risk factors for peptic ulcers  aspirin and other NSAIDS [suppress ________ synthesis] which is protective.  Cigarette smoking- impairs ________ and _________  Corticosteroids-in (low or high?) dose

prostaglandin mucosal blood flow and healing. High

Genetic predisposition to peptic ulcers  1st degree relative of DU patients have ____x increased risk  blood group ____  High circulating pepsinogen I→5xs higher risk of DU  Familial ________ of _______

3; O hyperfunction of G cells

Diseases that have been associated with Peptic ulcer 1.Chronic ———— 2.Alcoholic _____, 3.____________disease 4.______parathyroidism 5.Liver _______ increase risk

renal failure cirrhosis Chronic obstructive airway Hyper; cirrhosis

Diseases that have been associated with Peptic ulcer 6.___________ syndrome 7.Chronic _________ 8.Hereditary endocrine syndrome- MEN type ____ due to associated ______ 9 ____________ deficiency -probably due to unopposed proteolytic activity

Zollinger-Ellison pancreatitis I; gastrinoma .Alpha 1 anti-trypsin

Helicobacter pylori and PUD H. pylori is a ______, _________, gram- ________bacterium.and, are the only known reservoir,

spiral; microaerophilic negative

Helicobacter pylori and PUD Spreads  _________ and ___________

oral-oral  faeco-oral route

Pathogenesis of Helicobacter pylori associated Peptic Ulcer Disease H. pylori also plays a significant role in PUD. A. It produces Urease, Protease, phospholipase •Urease breaks down _____ to _____. This reduces acidity creating _____________ and allows it to survive •Protease breaks down the __________________________________ leading to damage to the ______________ •Phospholipase which ________ the __________

urea; NH3 an alkali medium around the organism glyco-protein in gastric mucus protective mucus layer damages the surface epithelium

Pathogenesis of Helicobacter pylori associated Peptic Ulcer Disease H. pylori also plays a significant role in PUD. A. It produces ______,______,_______ B. Produces ______ and ______ C. H. Pylori releases ——— agents (_______)

Urease, Protease, phospholipase adhesins & toxins chemotactic; leukotrienes

Pathogenesis of Helicobacter pylori associated Peptic Ulcer Disease H. pylori also plays a significant role in PUD. Produces adhesins & toxins Flagella-for ———- within _______ Adhesins-makes _________ to ________ easy Toxins-_______,_______

motility within surface mucous adherence to surface epithelium CagA, vac A

Pathogenesis of Helicobacter pylori associated Peptic Ulcer Disease H. pylori also plays a significant role in PUD. H. Pylori releases chemotactic agents (leukotrienes)  These attract ______ and causes  Mucosal ________ and then __________

WBC inflammation ulceration

Pathogenesis of H.pylori PUD  Mucosal inflammation→  reduces ______________→  hypo________ & low ____ secretion →  favours ________ →  continued inflammation, mucosal epithelial cell proliferation and increased risk of genetic mutation

acid secretion chlorhydria; pepsin bacterial growth

Morphology of Peptic Ulcer  Site – 98% - ______,_________,________and first part of duodenum

lesser curvature, antrum, prepyloric region

Morphology of Peptic Ulcer  Duodenum –______ wall >_____ wall  Stomach– predominantly along ________ around the ———- > _________  usually single but can be multiple in 10-20%  Size- 2-10cm

ant; post lesser curvature ; antrum greater curvature

Gross morphology of PUD Shape-_______ to _______ punched out defect with ______ walls  Margins-at ___________________

round to oval ; straight level with the surrounding mucosa.

Gross morphology of PUD Depth- varies from superficial ulcer involving only ________ to deep one having the base at the __________

mucosa muscularis propria

Morphology of PUD Base-  (smooth or rough?) and (clean or dirty?) (_____________)  may be formed by adherent pancreas, omental fat or liver if ______________ ______________ may be seen at the base  Surrounding mucosa - __________ and _________

Smooth; clean; acid digestion entire wall is penetrated. Thrombosed vein oedematous and reddened.

Microscopy of PUD Varies from stage of  _______ ———-  chronic _______  _______  associated ___________ with H.pylori may be present.

active necrosis inflammation scarring chronic gastritis

Active ulcers with necrosis has _____ zones from top to the lowest layer

zones of Active ulcers with necrosis From top to bottom: Base and margins have a (superficial or deep?) (thin or thick?) layer of ___________ Beneath this is a zone of ____________ predominantly ________ the latter is lined by an active ________ infiltrated by ______________ cells The lowermost layer is a ___________ or ____________.

superficial thin ; fibrinoid debris non-specific inflammation ; neutrophils granulation tissue ; mononuclear inflammatory solid fibrous ; collagenous scar

Clinical Presentation of PUD  It’s a ______ and ______ disease.  Age- _____ age  Affect (male or female?) , women are most often affected at or post menopausal  _______ ———— pain  Pain is referred to the ______ in _________ ulcer  Relieved by ________ or ______

remitting and relapsing middle both Male & female Burning epigastric back in penetrating ulcer alkali or food.

Clinical Presentation of PUD  Dyspepsia, intolerance to ______ food,  Abdominal ________, and _______  Can present with complications such as _______,_______,_______

fatty distension; belching hemorrhage, anemia, perforation

Clinical course- ‘Alarm’ features that should raise suspicion of sinister complication ?? malignancy  Unexplained ______  Bleeding  Anemia  Early _____  ____phagia or ____phagia  Recurrent ______  Especially if there is a family history of _______.

weight loss satiety Dys; odyno vomiting GI cancer

Complications of PUD  Bleeding  Perforation  ________ __________  ________  ________ and ______  ______ from edema or scarring, common with pyloric channel ulcer, also with DU.  Intractable pain.  ________ transformation

Peritonitis Subphrenic abscess Pyloric stenosis healing and scarring obstruction; Malignant

Diagnosis of PUD ____________ to visualize ulcer and exclude any other pathology  (______ and _______)  Test for ____  _________ for acid _______ of _______ to rule out malignancy

Upper GI endoscopy biopsy and histology Hp; Gastric analyses Cytology of aspirate

Management of PUD  If untreated, takes ————- for healing to occur Aim of treatment  _______ of _______ by use of antacid  Promotion of ______  Inhibition of _________  Treatment of ___________

several years neutralization of gastric acid mucus secretion acid secretion Hp infection

Anatomy of the Oesophagus It is a ________ tube; between ___-___cm long that connects the _____ to the ———

muscular 25-30 mouth stomach

Anatomy of the Oesophagus • It is continuous with the ______ at level of _____ vertebra and passes through an orifice in the diaphragm at about _____

pharynx C5; T12

Histology of the Esophagus _______________ epithelium (Keratinized or Non-keratinized?)

Stratified squamous Non-keratinized

GERD: Symptoms Heartburn ________, or when ______ ______sternal “burning” sensation Dysphagia ________ ———- Respiratory symptoms Asthma (______-onset)

After meals; lying flat Retro; Painful esophagitis adult

The two major contributing factors to the development of PUD are gastrointestinal infection with __________ and ____________.

H. pylori and nonsteroidal anti inflammatory drug (NSAID) use

Helicobacter pylori infection Associated with 40–70% of ______ ulcers and 25–50% of _____ ulcers

duodenal; gastric

The rate of H. pylori infection (and, therefore, the development of PUD) is ______easing.

decr

Chronic NSAID use Associated with a ______ risk of developing PUD Increases the risk for complications of PUD

fourfold

PATHOGENESIS Duodenal ulcers H. pylori inhibits _______ secretion → ↑ ______ secretion → ↑ ____ secretion → excess H+ delivery to the duodenum •Direct spread of H. pylori to the duodenum → inhibition of _________ secretion→ _______ation and insufficient _____ of duodenal contents

somatostatin; gastrin; H+ duodenal HCO3- acidific; neutralization