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House AMP > GERD and PEPTIC ULCER > Flashcards

GERD and PEPTIC ULCER Flashcards

1
Q

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

Muscularis
mucosae (smooth
muscle)

Submucosal
glands

Muscularis
externa

A

Absent in beginning; longitudinal; Inner
circular & outer Longitudinal

Absent; Absent; present

Skeletal muscle ; Skeletal & smooth muscle ; smooth muscle

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2
Q

Diseases of the oesophagus

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

Diverticuli- ________

___________

A

atresia; tracheoesophageal; ring

webs, duplication

Achalasia

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3
Q

Diseases of the oesophagus

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

 Neoplasm- ____________ ca, ___________

A

Reflux; Barrett’s oesophagus

Crohn’s

Squamous cell ; Adenocarcinoma

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4
Q

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.

A

pharyngoesophageal

pharynx; Killian triangle

pouch; increased pressure

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5
Q

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

A

lower esophageal sphincter (LES)

fails to relax properly

moving food and liquid from the esophagus into the stomach.

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6
Q

Oesophagitis- Causes

Lacerations-________ syndrome

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

Infection: ________ virus, ________,
Fungal(_________)

A

Mallory-Weiss

Herpes simplex; CMV; candida

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7
Q

Oesophagitis- Causes

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

A

Pemphigoid skin

Crohn

Eosinophilic

Reflux

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8
Q

most common cause of Oesophagitis is ??

A

Reflux oesophagitis

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9
Q

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 _________.

A

tear or rupture

junction of the esophagus and stomach

vomiting or retching

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10
Q

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

A

autoimmune blistering skin

blisters; erosions

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11
Q

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

A

acidic stomach; up into the oesophagus.

it occurs frequently ; irritation of the lining

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12
Q

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

A

alteration of the oesophageal mucosa

episodes of gastro-oesophageal reflux.

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13
Q

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

T/F

A

T

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14
Q

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 __________

A

4.0; 4.5

regurgitation

symptomatic

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15
Q

Epidemiology of GERD

Prevalence of GERD is largely unknown in Africa.

T/F

A

T

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16
Q

Epidemiology of GERD

____-_____ % -Western world

<___% in Asia this was lower

A

10–20

5

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17
Q

Mechanisms that Protect oesophageal
Mucosa against damaging effect of acid

_______ secretion from ______ glands

______ present in ________

 Constant ____________________prevents reflux

A

Mucin; submucosal

HCO3; saliva

lower oesophageal sphincter tone

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18
Q

Mechanisms that Protect oesophageal
Mucosa against damaging effect of acid

_________ and __________→ neutralize acid

A

HCO3 and submucosal mucin

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19
Q

Conditions that decrease _____ or increase __________ lead to GERD

A

LES

abdominal pressure

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20
Q

Predisposing factors for GERD

Factors that decrease LES:

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

A

Pregnancy; Diabetes

Hiatus hernia; gastric emptying

coffee, alcohol

calcium channel blockers

beta-blockers, progesterone

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21
Q

Predisposing factors for GERD

__________
________
__________

Cigarette smoking

Connective tissue disorders, such as
_______

_______________

A

Obesity

Alcohol

Asthma

scleroderma

Zollinger-Ellison syndrome

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22
Q

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

A

Rare; gastrin; gastrinomas

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23
Q

Zollinger-Ellison syndrome (ZES)

These tumors usually form in the _______ or the _______.

A

pancreas; duodenum

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24
Q

Pathogenesis

The mechanisms that result in GERD include:

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

____ reflux from duodenum may aggravate damage

A

Prolonged exposure; distal

acid and pepsin

Bile

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25
Q

Pathogenesis

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

T/F

A

T

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26
Q

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

A

squamous; desquamation

desquamation and basal cell hyperplasia

Chronic inflammatory

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27
Q

IN GERD

The microscopic changes to the
oesophageal epithelium may be present
even if oesophagus appears normal
grossly on endoscopy

T/F

A

T

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28
Q

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

A

Early

neutrophils and lymphocytes

subepithelial fibrosis; stricture and
narrowing

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29
Q

Morphology of GERD

 _________ hyperplasia,_______ , ______ of the papillae and ______ of the ______________

________________ infiltration.

A

Basal cell ; oedema

elongation; thinning; squamous cell layer

Inflammatory cell

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30
Q

Morphology of GERD

 Intraepithelial eosinophils of ____/HPF highly suggestive of GERD

_________ inflammation (non-specific)
 ___________ inflammation (usually due to _______ or ___________)

A

<20; Lymphocytic; Neutrophilic

reflux or Helicobacter gastritis

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31
Q

Morphology of GERD

_____________ metaplasia or _________ metaplasia

Dysplasia

A

Goblet cell intestinal

Barrett’s

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32
Q

Symptoms of GERD

_______
______ pain
Difficulty _______
______ cough

A

Heartburn

Chest; swallowing

Dry

33
Q

Symptoms of GERD

_________ or ————

___________ of food or sour liquid
(acid reflux)

Sensation of __________________

A

Hoarseness or sore throat

Regurgitation

a lump
in the throat

34
Q

Complications of GERD

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

A

Barrett’s

stricture

Pseudo-diverticula

haematemesis, melena

35
Q

Complications of GERD

 ________
 ______ formation
 Inflammatory _____
 Adenocarcinoma

A

Perforation

Fistula

polyps

36
Q

Barrett’s oesophagus

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

A

intestinal metaplasia; squamous

37
Q

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

A

distal oesophageal

columnar; endoscopy

intestinal metaplasia; biopsy

38
Q

Barrett Oesophagus

Patients with BE have ——— folds increase in risk of developing adenocarcinoma of the oesophagus

However only ______% of Barrett’s progress to cancer

A

20; 1-5

39
Q

Barrett Oesophagus

Types:
• Long segment- =/>____
• Short segment BE- <_____

If _______ is present, its classified as ________ or _______

A

3cm; 3cm

dysplasia
low or high grade

40
Q

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 __________

A

breach in the mucosa

muscularis mucosa

submucosa; gastric secretions

41
Q

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 ____________

A

Distal stomach and proximal part of
duodenum

Barrett’s

Margins of gastro-enterostomy

Zoolinger-Ellison’s syndrome

ectopic gastric mucosa

42
Q

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

A
43
Q

Normal mechanisms that protects
mucosa against acid & pepsin

______ secretion

______ secretion

____________ junction

_________ capacity of
the cells

• Rich mucosal _______

• Prostaglandins

A

Mucus

HCO3

Regenerative

Tight intercellular

blood flow

44
Q

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

A

protective surface coat.

neutralizes effect of acid

prevent acid penetration

rapidly replace
damaged

45
Q

Other risk factors for peptic ulcers

 _____ and other \______
 _____________
 Alcohol-
 ___________
 In some patients too rapid ___________
 Personality and psychological stress
 Dietary habit.

A

Aspirin ; NSAIDS

Cigarette smoking

Corticosteroids

gastric emptying

46
Q

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

A

prostaglandin

mucosal blood flow and healing.

High

47
Q

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 _______

A

3; O

hyperfunction of G cells

48
Q

Diseases that have been associated
with Peptic ulcer

1.Chronic ————
2.Alcoholic _____,
3.____________disease
4.______parathyroidism
5.Liver _______ increase risk

A

renal failure

cirrhosis

Chronic obstructive airway

Hyper; cirrhosis

49
Q

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

A

Zollinger-Ellison

pancreatitis

I; gastrinoma

.Alpha 1 anti-trypsin

50
Q

Helicobacter pylori and PUD

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

A

spiral; microaerophilic

negative

51
Q

Helicobacter pylori and PUD

Spreads
 _________ and
___________

A

oral-oral

 faeco-oral route

52
Q

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 __________

A

urea; NH3

an alkali medium around the organism

glyco-protein in gastric mucus

protective mucus layer

damages the surface epithelium

53
Q

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
(_______)

A

Urease, Protease, phospholipase

adhesins & toxins

chemotactic; leukotrienes

54
Q

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-_______,_______

A

motility within surface mucous

adherence to surface epithelium

CagA, vac A

55
Q

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 __________

A

WBC

inflammation

ulceration

56
Q

Pathogenesis of H.pylori PUD

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

A

acid secretion

chlorhydria; pepsin

bacterial growth

57
Q

Morphology of Peptic Ulcer

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

A

lesser curvature, antrum, prepyloric region

58
Q

Morphology of Peptic Ulcer

 Duodenum –______ wall >_____ wall

 Stomach– predominantly along ________ around the ———- > _________
 usually single but can be multiple in 10-20%
 Size- 2-10cm

A

ant; post

lesser curvature ; antrum

greater curvature

59
Q

Gross morphology of PUD

Shape-_______ to _______ punched out defect with ______ walls

 Margins-at ___________________

A

round to oval ; straight

level with the surrounding mucosa.

60
Q

Gross morphology of PUD

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

A

mucosa

muscularis propria

61
Q

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 _________

A

Smooth; clean; acid digestion

entire wall is penetrated.

Thrombosed vein

oedematous and reddened.

62
Q

Microscopy of PUD Varies from stage of

 _______ ———-
 chronic _______
 _______
 associated ___________ with H.pylori may be
present.

A

active necrosis

inflammation

scarring

chronic gastritis

63
Q

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

A

4

64
Q

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 ____________.

A

superficial thin ; fibrinoid debris

non-specific inflammation ; neutrophils

granulation tissue ; mononuclear inflammatory

solid fibrous ; collagenous scar

65
Q

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 ______

A

remitting and relapsing

middle

both Male & female

Burning epigastric

back in penetrating ulcer

alkali or food.

66
Q

Clinical Presentation of PUD

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

A

fatty

distension; belching

hemorrhage, anemia,
perforation

67
Q

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 _______.

A

weight loss

satiety

Dys; odyno

vomiting

GI cancer

68
Q

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

A

Peritonitis

Subphrenic abscess

Pyloric stenosis

healing and scarring

obstruction; Malignant

69
Q

Diagnosis of PUD

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

A

Upper GI endoscopy

biopsy and histology

Hp; Gastric analyses

Cytology of aspirate

70
Q

Management of PUD

 If untreated, takes ————- for healing to occur

Aim of treatment
 _______ of _______ by use of antacid
 Promotion of ______
 Inhibition of _________
 Treatment of ___________

A

several years

neutralization of gastric acid

mucus secretion

acid secretion

Hp infection

71
Q

Anatomy of the Oesophagus

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

A

muscular

25-30

mouth

stomach

72
Q

Anatomy of the Oesophagus

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

A

pharynx

C5; T12

73
Q

Histology of the Esophagus

_______________ epithelium

(Keratinized or Non-keratinized?)

A

Stratified squamous

Non-keratinized

74
Q

GERD: Symptoms

Heartburn

________, or when ______
______sternal “burning” sensation

Dysphagia
________ ———-

Respiratory symptoms
Asthma (______-onset)

A

After meals; lying flat

Retro; Painful esophagitis

adult

75
Q

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

A

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

76
Q

Helicobacter pylori infection

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

A

duodenal; gastric

77
Q

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

A

decr

78
Q

Chronic NSAID use

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

A

fourfold

79
Q

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

A

somatostatin; gastrin; H+

duodenal HCO3-

acidific; neutralization

House AMP (66 decks)

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