Case 1 - Trudy Baxtor - (PUD)b

8/6/2019 Case 1 - Trudy Baxtor - (PUD)b

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TRUDY BAXTOR GIT#1

TRUDY BAXTOR GIT #1

1 Describe the nine regions and four quadrants of the abdominopelvic cavity and list the organs they contain.

2 Describe the macroscopic anatomy of the pharynx and oesophagus.

3 Review the microscopic organization of GIT (from Year 1) and describe the histological structure of oesophagus in relation to its

function.

4 Describe the mechanisms of swallowing, reflux and vomiting.

5 Describe the basic macroscopic anatomy of the stomach. Include blood supply, innervation and important immediate relations.

6 Describe the mechanism of pain from gastric pathology (including referred pain).

7 Describe briefly the development of the GIT and explain common developmental anomalies of the GIT. Include the development andorganization of the peritoneal reflections and compartments of the abdominal cavity.

8 Describe the components of gastric juice, the cell types responsible for secreting its components and indicate the imp ortance of each

component in stomach activity.

9 Describe the mechanisms of production of gastric acid by oxyntic cells in the gastric mucosa, including the major ionic mecha nisms

(especially the K+/H+ ATPase)

10 Describe the neural and hormonal regulation of gastric acid secretion.

11 Describe the mechanisms of gastrointestinal motility.

12 Describe the neural and hormonal regulation of gastric emptying.

13 Describe the the major mechanisms that protect the stomach from self digestion and the leakage of gastric juice into the peritoneum.

14 Describe the role of Helicobacter pylori (H. pylori), non -steroidal anti inflammatory drugs, and smoking in the formation of ulcers.

15 Describe the utility and limitations of imaging techniques, H. pylori tests, endoscopy and biopsy in the diagnosis of oesophageal disease,

peptic ulcer disease (PUD) and malignancy.

16 Outline the principles of management of ulcers including antacids, H2 antagonists, acid pump inhibitors, H. pylori eradicatio n and

surgical approaches (the last in only the most intractable cases).

17 Describe the pathology of diseases of the oesophagus, including achalasia, varices, oesophagitis and tumours; and pathology o f diseases

of the stomach, including gastritis, ulcer and gastric tumours.

18 Outline the indications for use and mechanism of action of antifungal drugs.

19 Review the concept of negligence and consider how it applies to this case in terms of:

y the conditions that create a "duty of care"

y types of medical mistakes which may lead to an action in negligence

y how the Bolam Principle can be applied in a potential negligence case

y provisions in the Civil Liability Act (Qld) 2003 that apply to cases of negligence

y the various elements of negligence that need to be satisfied for a successf ul action.

20 Demonstrate competence in exploring a patient's experience of important gastrointestinal presentations (abdominal pain, chang ed

appetite, unintentional weight change, nausea, vomiting, heartburn, reflux, dyspepsia, dysphagia, odynophagia, ha ematemesis,

melaena or rectal bleeding) [REVISION] including: the cardinal characteristics of the symptom and its time course; relevant a ssociated

symptoms; the patient's understanding of, and concerns about, what they are experiencing.

21 Demonstrate appropriate infection control manoeuvres prior to and after physical examination of a patient [REVISION].

22 Prepare a patient appropriately for examination of the abdomen, in relation to appropriate explanation, confirmation of conse nt andpatient positioning.

23 Describe the anatomy of the abdomen and pelvis relevant to the performance of abdominal examination.

24 Demonstrate competence in the physical examination of a patient for the assessment of presentations where abdominal signs may

occur, including inspection, palpation, percussion and auscultation of the abdomen, as well as the identification of organomegaly or

abnormal masses, elicitation of tenderness and signs of peritonism, then discuss the significance of any abnormal findings.



TRUDY BAXTOR GIT#1

1. DESCRIBE THE NINE REGIONS AND FOUR QUADRANTS OF THE ABDOMINOP ELVIC CAVITY AND L IST THE ORGANS THEY CONTAIN.



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TRUDY BAXTOR GIT#1

2 . DESCRIBE THE MACROSCOPIC ANATOMY OF THE P HARYNX AND OESOPHAGUS.

Pharynx

Goes from the base of the skull CVI

Tonsils

1. Pharyngeal tonsil (adenoids when enlarged) is in the midline on the roof of the nasopharynx;

2. Palatine tonsils are on each side of the oropharynx between the palatoglossal and palatopharyngeal arches just

posterior to the oropharyngeal isthmus;

3. Lingual tonsil refers collectively to numerous lymphoid nodules on the posterior one -third of the tongue

Constrictors narrow the

pharyngeal cavity,

when they contract

sequentially they move

a bolus from pharynx

oesophagus.

All constrictors

innervated by the

pharyngeal branch of

the vagus (X)

There are 3 more

longtitudinal muscles

that elevate thepharyngeal wall and

pull the pharynx up and

over a bolus of food

y stylopharyngeus

(IX)

y salpingopharynx (X)

y palatopharyngeus

(X)

Oesophagus

y Begins @ inferior border of the cricoid cartilage (C VI) and ends at the cardiac

opening of the stomach (TXI).

y 27cms long

y Nerves = motor via Vagus (CNX)

y HISTO = stratified squamous (nk), thick muscularis mucosa, mucous gla nds in

mucosa and submucosa



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TRUDY BAXTOR GIT#1

3 . REVIEW THE MICROSCOPIC ORGANIZATION OF GIT (FROM YEAR 1) AND DESCRIBE THE HISTOLOGICAL STRUCTURE

OF OESOPHAGUS IN RELATION TO ITS FUNCTION.

Specific Variations

Mucosa = epithelium + lamina propria (vessels,

glands, lymphoid nodules) + muscularis mucosa

Submucosa = ct +

submucosal plexus +

vessels

Muscularis Propria =

circular + myogenic

Adventitia (retroperitoneal) or

Serosa (intraperitoneal) =

Pharynx Stratified squamous in oropharynx and

laryngopharynx

Respiratory mucosa in nasopharynx

Oropharynx lacks MM, but has glands in LM

Oropharynx lacks

submucosa

skeletal Oral cavity = adventitia

Oesophagus Stratified squamous (n.k.)

scattered glands in LP of upper and loweresophagus

MM is thick

glands in SM for mucous

secretion

Upper

skel m

middle

= skel + sm

Thoracic = adventitia + retro

Peritoneal = serosa + intra

Stomach

longitudinal

folds = rugae

Mucosa is thick and has numerous tubular

glands

MM is thick and in places there is 3 layers of sm

Gastric glands extend below into the LP into

invaginations called gastric pits. There are 3

types:

I. cardiac - small in number, secrete mainly

mucin

II. fundic and body - highest in number and

secrete the acidic juice

III. pyloric glands - secrete mucous

No glands 3 layers: oblique + c + l

Pyloric sphincter =

thickening of circular layer

Serosa

Duodenum plicae circulares, villi, and microvill i. Brunners glands -

branched tubuloalveolar

glands that produceglycoproteins and HCO3

-.

Serosa + adventitia

Jejuno-ilium Jejunum - plicae circulares (valves of Kerckring, valvulae conniventes) - core

of submucosa and the overlying mucosa. They have a semilunar, circular or

spiral form and extend about one-half to two-thirds around the

circumference of the lumen. Although they may be present in the duodenum

and ileum, they are not as large and are not a s ignificant feature in those

regions.

Serosa

Ileum - Peyers patches

Colon Asc + desc colon = adventitia

Transverse + sigmoid = serosa

rectum Adventitia



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TRUDY BAXTOR GIT#1

4 . DESCRIBE THE MECHANISMS OF SWALLOWING, REFLUX AND VOMITING.

Swallowing:

1.

food bolus moved down by tongue (XII) to oropharynx.

2. Nasopharynx closes via soft palate elevation and superior constrictor ( X)

3. Auditory tube opens

4. Pharynx and larynx move up to hyoid (happens before bolus arrives) via longtitudinal muscles in pharynx

a. Stylopharyngeus (IX)

b. Salpingopharngeus (X)

c. Palatopharngeus (X)

d. Inferior constrictor (X)

5. Oropharynx closed by palatopharngeus (X), i ntrinsic muscles of tongue (XII), styloglossus (XII)

6. Larynx closes

a. Epiglottis flaps

b. Cords close

7. Hyoid elevates bringing pharynx, larynx up more via stylohyoid (VII)

8. Hypopharynx opens due to relaxation of cricopharyngeus and upper oesophagus

9. Hyoid, larynx and pharynx move down together due to elastic recoil

10. Larynx and pharynx move down from hyoid due to further elastic recoil11. Peristalsis involving striated and then later sm

Dysphagia

Caused by either:

1. a problem with the strength or coordination of the muscles required to move material from the mouth to the stomach.

Oropharyngeal swallowing mechanism + 1 and 2 peristaltic contractions usually transport food t o stomach in 10 secs. If this fails

the accumulation of food distends the esophageal lumen and causes discomfort interpreted as dysphagia.

o in the elderly low-amplitude 1 or 2 peristaltic activity that is insufficient to clear the esophagus

o 1 or 2 motility disorder that grossly disturbs the orderly contractions of the esophageal body

2. Fixed obstruction somewhere between the mouth and the stomach . Mechanical narrowing may interrupt passage of bolus.

Symptoms vary with the degree of luminal obstruction, associated esophagitis, and type of food ingested.

y Minimally obstructing lesions cause dysphagia only with large, poorly chewed boluses of foods such as meat and dry bread



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TRUDY BAXTOR GIT#1

y Completely obstructing lesions cause dysphagia with solids and liquids.

o GERD may produce dysphagia related to an esophageal stricture, esophagitis

3. Abnormal sensory perception in the esophagus may lead to the perception of dysph agia, even when the bolus has c leared the

esophagus

Reflux

y Necessary by-product of the LOS not being a 1 way valve, it must be capable of releasing gas (burp), emesis etc.

y On inspiration LOS tone s as diaphragm contracts

y Distention of the lower oesophagus causes relaxation of LOS due to enteric reflexes and ANS control.

y Irritation of lower oesophagus leads to LOS tone

y Reflux is a result of unanticipated abdominal P on full stomach causing transient opening of the sphincter

y The body protects oesophagus by returning chyme via 2 peristalsis

Vomiting;

Stimulus:

stretch in stomach, sml intestine, substances acting on chemoreceptors in intestinal wall, brain; P in skull, rotating mvmts on skull (motion

sickness), intense pain, tactile stimuli applied t o back of throat

Sent to:

vomiting centre in the medulla emetic centre via mostly PSNS afferents in GIT but via somatic sensory afferents in mouth.

Acts via: ANS various nerves

Effect Prodrome : salivation, sweating, HR, pallor, nausea

Acts via: spinal, phrenic and vagus nerves

Effect Vomit:

1. deep inspiration, closure of glottis, elevation of soft palate.

2. Abdominal muscles contract abdominal P stomach P

3. LOS relaxes

4. contents forced into oesophagus

5.

further

P causes UOS to open and expel stomach contents.

6. Vomiting is accompanied by strong contractions of upper sml

intestine contents back into stomach expelled via vomit

bile may be present in vomitus



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y angular incisure = bend on the lesser curvature)

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TRUDY BAXTOR GIT#1

Lymphatics: Nerves

6 . DESCRIBE THE MECHANISM OF PAIN FROM GASTRIC PATHOLOGY ( INCLUDING REFERRED PAIN). UNDERSTAND

INNERVATION OF THE G ASTROINTESTINAL TRACT AND MECHANISMS OF GIT PAIN.

Salivary glands

1. Efferents for Submandibular and sublingual glands

a. PSNS (chorda tympani a branch of t he facial nerve) major instigator of salivation, also involved in exocytosis and protein

secretion, myoepithelial contraction, and vasodilation. Output: large amount of low protein saliva

b. SNS (T1-3) weak mobilise of salivation but additive effects with PSNS. Causes high levels of protein s ecretion,

myoepithelial contraction and maintenance of vasotone. Output: small am ount of high protein saliva

2. Efferents for Parotid

a. PSNS (glossopharyngeal nerve)

b. SNS (T1-3)

c. No inhibitory nerve supply to the gland

Oesophagus

1. Afferents

a. Parasympathetic (vagal) have :

i. mechanoreceptors in the muscularis propria that detect distention

ii. polymodal (detect chemo, thermo, osmo, mechano) afferents in the mucosa

iii. In general these dont play a role in visceral pain but can transmit pressure sensations into pain sen sations.

b. Sympathetic (spinal) have

i. Mechanosensitive receptors in the muscularis propria and adventitia

ii. intraepithelial nerve endings detect acid induced pain



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TRUDY BAXTOR GIT#1

iii. These nerves are most important for visceral pain transmission.

2. Efferent

a. Motor via the vagus which controls UOS, skeletal muscle and the LOS and smooth muscle.

b. PSNS (vagus) regulates glandular secretion and motor innervation to the muscularis propria

c. SNS (cervical and thoracic sympathetic chain T1 -10) controls blood vessel constriction, esophageal sphincters contractions,

relaxation of the muscular wall, and s in glandular and peristaltic activity.

3. Intrinsic

a. Myenteric plexus regulates muscularis propria

b. Submucosal plexus regulates glandular secretion and peristaltic contractions of the muscularis mucosa

Stomach

1. Afferents2. Efferents

a. Parasympathetic (vagus) preganglionic nerves penetrate stomach

wall to synapse with postganglionic cells which are a component of

the enteric nervous system. These then secrete ACh which acts on:

i. Smooth muscle M3 receptors to cause d gastic motility

ii. Gastric gland M1 receptors to cause gastric gland

secretion

b. Sympathetic (celiac ganglion) postganglionic nerves release N E onto

the targets:

i. Gastric arteries 1 receptors to blood flow

ii. Pyloric sphincter 1 receptors to tighten sphincter and

thus the passage of food from stomach to sml intestine

iii. Preganglionic parasympathetic nerve terminals 2

receptors which the subsequent release of ACh from

these terminals

iv. Circulating E binds to 2 receptors on the sm to gastric motility (inhibitory effect)

v. blood borne NE and E do same thing

3. Enteric and afferents

Stretch receptors imbedded in the GIT detect distention and relay the msg to

surrounding muscles which causes these to their motility. These same receptors send

signals to CNS t hat then returns stimulatory nerve signals (via PSNS) to the stomach/GIT

wall to reinforce motility.

When stretch receptors in t he small intestine are excited they send stimulatory signals to

nearby muscles to motility but inhibitory signals to the stomach. This feedback loop

decreases stomach motility until food moves further down the small intestine.

H+

receptors operate the same way, when H+

is detected in the small intestine, inhibitory

signals are sent to the stomach and stimulatory signals are sent to adjoining cells.

Small intestines and Colon

1. Afferent/enteric see above

2. Efferent

a. Parasympathetic (vagus for small intestines and most of colon, pelvic

Splanchnic nerve for Desc. Colon) releases ACh onto terminal ganglia

scattered between the muscle layers. ACh is then released from these

enteric nerves to bind to M3 receptors on smooth muscle to motility

b. Sympathetic postganglionic neurons (superior mesenteric for small

intestine, inferior m esenteric for large intestine) release NE which binds to:

i. 2 receptors on postganglionic parasympathetic terminals which

s subsequent ACh release a nd thus limit sm stimulation.ii. Gastric arteries 1 receptors to blood flow

iii. blood borne NE and E do same thing

iv. Blood borne E binds with inhibitory 2 receptors on intestinal sm

to reduce motility



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TRUDY BAXTOR GIT#1

Referred Pain:

Referred pain = pain distant from place of nociceptive receptor

stimulation because of the existence of common central points of convergence of nociceptive afferent inputs from the viscera and

somatic structure.

Sensory information from rest of GIT travels via SNS and PSNS n erves.

Visceral afferents send signals to hypothalamus where some pain

sensation is processed and also to centres controlling swallowing,

vomiting, BP, HR and other ANS functions. Afferent nerves use

substance P and calcitonin gene related peptide as transmitters.

Visceral sensation is much less precise than somatic s ensation

because of low density of sensory nerves, use of non -specific naked

nerve endings that lack ability to differentiate stimuli and lack of

myelination.

Most pain of visceral origin is detected by visceral sensory fibrestravelling with sympathetics

y Pain from foregut referred to T5-9 dermatome

(epigastrium) via the greater splanchic nerve

y Small bowel problems to the peri -umbilical region via lesser

splanchnic nerves

y Large bowel to suprapubic region via least splanchic nerves.

The pain is m idline as the gut is embryologically a midline structure.

Kidneys can lateralise as they are not of midline origin.

Irritation of the peritoneum is detected by the phrenic nerve (C3,4,5)

which can be referred to the shoulder tip (C4 dermatome)

Touch, pain and temperature sensation in the mouth, tongue and

anus is similar to skin. Msges sent via afferent somatic sensory

nerves.



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TRUDY BAXTOR GIT#1

7 . DESCRIBE BRIEFLY THE DEVELOPMENT OF THE GIT AND EXPLAIN COMMO N DEVELOPMENTAL ANOMALIES OF THE

GIT. INCLUDE THE DEVELOPMENT AND ORGANIZATION OF THE PERITO NEAL REFLECTIONS AND COMPARTMENTS OF

THE ABDOMINAL CAVITY .

4th

week - lateral and ce phalocaudal folding, some of the yolk sac incorporated into embryo primitive gut. At first this is just a tube with 2

blind ends. Yolk sac is lined with eNdoderm gives rise to the epithelial lining and the parenchyma of organs. All the muscle, connective

tissue, mesentery etc are derived from the mesoderm that surrounds the primitive gut. The enteric nervous system is derived from neural

crest cells that migrate towards to primitive gut (ectoderm).

Body Cavities:

The lateral folding of the embryo also

causes the development of an intra

embryonic body cavity that later (5th

-6th

week) gets partitioned into p eritoneal

cavity, pleural cavity and pericardial cavity.

This cavity is lined with mesoderm.

The picture L is confusing because when the

intraembryonic cavity develops it is

naturally partitioned in tw o (like dissaspicture next page L). The ventral

mesentery then degenerates in most places

to form the single chamber (like L).



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TRUDY BAXTOR GIT#1

The peritoneum and mesentery are derived from various subtypes

of mesoderm depending on where theyare found:

y Parietal (body wall) serosa develops from the somatic

lateral plate mesoderm

y Visceral (covers organs) serosa develops from the

splanchnic lateral plate mesoderm

Mesenteries

Growth of the liver segments the ventral mesentery into two

Growth of the spleen and kidneys segments the dorsal mesentery in

two at the level of the stomach.

Oesophagus

This is really just an elongation of the foregut. Striated muscle that is incorporated into the upper

is derived from the 6

thpharyngeal arch that

surrounds the oesophagus at this level.

ventralmesentery

lesseromentum

falciformligament

dorsalmesestery

gastrosplenic ligament

splenorenalligament



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TRUDY BAXTOR GIT#1

Stomach

Rapid outpouching of the foregut that develops in the 4 -5th

week. In the

7-8th

week the stomach rotates about 2 axis.

Rotation pulls the dorsal mesentery to the left, creating a space

behind the stomach called the omental bursa (lesser peritoneal

sac).

This elongates and forms a double layered curtain that falls from

the greater curvature of the stomach over the small intestine and

colon. Later this double layered sheet fuses into one layer, and

then some of it fuses with the visceral mesothelium of the

transverse colon, holding it in place. This sheet is known as the

greater omentum.

Common Abnormalities:

Within the foregut there are only really two common a bnormalities

both of which affect the GIT lumen

1. Atresia occlusion of the lumen ( 1/3000) associated

with tracheoesophageal fistula in >85% cases. Can result

from failure to recannulise oesophagus aft er temporary

occlusion in 8th week or from posterior movement of the

tracheoesophageal septum that would normally separate

the oesophagus from the trachea. A foetus with this

cannot swallow and dispose of am niotic fluid via mothers

blood thus resulting in polyhydramnios. When the infant

is born its healthy and just appears to drool alot.

1. Stenosis narrowing of the lumen. Can occur anyw here

but usually in distal

. Again usually results fromimcomplete recannulisation or can be from m alformation

of oesophageal blood vessels.

2. Short Oesophagus (Congenital Hiatal Hernia) failure of

oesophagus to elongate results in displacement of part of

the stomach through oesophageal hiatus in diaphragm.

Variations of esophageal atresia and/or tracheoesophageal fi stula in

order of their frequency of appearance: A . Oesophageal atresia with

distal tracheoesophageal fistula 90%; B. Oesophageal atresia 4%; C.

Tracheoesophageal fistula 4%; D. Oesophageal atresia with proximal

tracheoesophageal fistula 1%; E. Oesophageal atresia with proximal

and distal tracheoesophageal fistula 1%.



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TRUDY BAXTOR GIT#1

8 . DESCRIBE THE COMPONENTS OF GASTRIC JUICE, THE CELL TYPES RESPONSIBLE FOR SECRETING ITS COMPONENTS

AND INDICATE THE IMP ORTANCE OF EACH COMPONENT IN STOMACH ACTIVITY.

The proximal portion of the stomach secretes acid, pepsinogens, intrinsic factor, bicarbonate and m ucus, whereas the distal part releases

gastrin and somatostatin.

Gastric Glands (fundus and body of the stomach) each gastric pit communicates with several gastric glands, which extend deep into the

underlying lamina propria. Parietal cells secrete HCl and IF. The HCO3-released by parietal cells diffuse through the ISF into the bloodstream.

When gastric glands are actively secreting, enough HCO3-enter the bloodstream to pH of the blood significantly alkaline tide. Role of HCl

1. kills most of the microorganisms ingested with food.

2. denatures proteins and inactivates most of the e nzymes in food.

3. break down plant cell walls and the connective tissues in meat.

4. activation and function of pe psin.

Chief cells are most abundant near the base of a gastric gland and secrete pepsinogen. The stomachs of newborn infants (but not of adults)

produce rennin (aka chymosin) and gastric li pase , enzymes important for the digestion of milk. Rennin coagulates milk proteins; gastric lipase

initiates the digestion of milk fats.

Pyloric Glands - produce primarily a mucous secretion, rather than enzymes or acid and have several types of enteroendocrine cells which

produce 7 hormones

1. Gastrin by G cells stimulates parietal and chief, contractions of gastric wall,

2. Somatostain by D cells inhibits G cells

3. Ghrelin by P/D1 cells lining fundus initiate hunger





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TRUDY BAXTOR GIT#1

10. DESCRIBE THE NEURAL AND HORMONAL REGULATION OF GASTRIC ACID SECR ETION.

Cephalic (reflex)

y Short (mins)

y Purpose = prepares stomach for arrival of food

1. Sensory inputs:

a. Sight and thought of food stimulate cerebral cortex which through a conditioned reflex stimulate the hypothalamus

b. Smell and taste stimulate olfactory and taste receptors which travel through efferent fibers to the hypothalamus

medulla

2. Medulla stimulates vagus nerve

a. Vagus releases ACh which stimulates parietal to secrete H

+

b. Vagus releases ACh in the lamina propria of the body of the stomach stimulates ECL (enterochromaffin like) cells to

secrete histamine (H2) stimulates parietal to secrete HCl

c. Peptidergic postganglionic PSNS vagal neurons and other ENS neurons release GR P (gastrin releasing peptide) stimulates

gastrin release from G cells

i. Gastrin binds to parietal and stimulates HCl secretion

ii. Gastrin binds to ECL H2 release parietal binding HCl

d. Vagus releases ACh which inhibits D cells in the antrum and the c orpus s release of somatostatin which would normally:

i. (Direct mechanism) Bind to parietal cells and basal H+

secretion of parietal cell

ii. (Indirect mechanism) Bind to G cells and basal gastrin release

iii. (Indirect mechanism) Inhibit release of H2 from EC L





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TRUDY BAXTOR GIT#1

Intestinal

y Long (hrs)

y Purpose: Controls rate of chyme entry into duodenum

1. and peptones in the proximal duodenum

A. Duodenal G cells to secrete entero- gastrin

B. Unknown intestinal endocrine cell secretes entero -oxyntin parietal cells

C. absorbed in the proximal part of the duodenum stimulate secretion of acid by unknown mechanism

v

11. DESCRIBE THE MECHANISMS OF GASTROINTESTINAL MOTIL ITY.

Pharynx

Swallowing reflex discussed above

Oesophagus

y Peristalsis - With deglutition, a propagated wave with a large monophasic component corresponding to a pressure of 60 -80 mm Hg,

moves sequentially along the length of the esophagus, at a rate of 3 -4 cm per second. It takes 8 10 secs. to reach the LES.

y Sphincter - Begins to relax early during deglutition, remains relaxed for 6 -8 seconds, and then closes slowly, until it achieves a

pressure of 40-50 mm Hg. The latter pressure then gradually decreases over a nother 5-6 seconds, until the sphincter reaches the

normal resting pressure (10 -30 mm H g above the fundic pressure)



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TRUDY BAXTOR GIT#1

Stomach:

Receptive relaxation - centrally mediated reflex, initiated by swallowing and resulting in inhibition of tonic contraction in the stomach

wall and consequent in intragastric volume. Receptive relaxation is a largely vagally mediated reflex. The transmitter released by

the inhibitory enteric neurons activated by the vagus is not known .

Peristalsis mediated by cells of Cajal which lie within and between the muscle layers and produce slow waves or BER (3/min for

stomach). Depolarizing starts at greater curvature by the inward flux of Ca2+

and the repolarizing efflux of K+. BER do not exceed

excitation threshold and so do not cause contraction themselves, merely set the maximum rate of contraction.

Local factors (stretch and ACh) cause spike potentials seen at the peak of depolarisation in BER and they cause initiation of

contraction. Adrenaline tends to inhibit spike potentials. Peristalsis moves bolus/chyme to pyloric antrum.

Intense Antral Peristaltic Contractions during Stomach Emptying = "Pyloric Pump."

Most of the time, stomach contractions are weak and f n

mainly to cause mixing of food

and gastric secretions.

20% of the time contractions become intense, beginning in midstomach and ending in

very tight ringlike constrictions that can cause stomach emptying.

Antral contractions are always stronger and cont ractions combined with a closed

pyloric sphincter

squeeze only 10% of

antral contents through

semi-contracted pyloric

sphincter sieve like.

Very strong antral

contractions disperselarge particles grinding.

As the stomach becomes progressively more and more empty, these

constrictions begin farther and farther up the body of the stomach,

gradually pinching off the food in the b ody of the stomach and adding

this food to the chyme in the antrum.

Stimuli mechanical (distention) and chemical (products of protein

digestion)

Pathways long (vaso-vagal) short (enteric)

Hormonal gastrin (response to...) Cholecystokinin (response to ...)

Small Intestine:

Peristalsis

Occur in all parts of intestine, faster in proximal and slower in distal. Moves and spreads the chyme. Weak and die after 3-5cm. Average

1cm/min 3-5hrs to complete journey. Stimulation via distention of wall intestinal wall, gastroenteric reflex (initiated by distention of stomach and via m yenteric plexus).

Hormones :

y Positive motility = gastrin, C CK, insulin, motilin, and serotonin.

y Negative motility = secretin and glucagon.

On reaching ileocecal valve the chyme is sometimes stopped here for hours until the person eats another meal. (gastroileal re flex)

Segmentation

Distention causes localised concentric contractions spaced @ intervals along intestine and lasting a fraction of a minute. Ma ximum

frequency is determined by BER (12 in duo 8-9 in ileum)

Colon:



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TRUDY BAXTOR GIT#1

Mixing Movements-"Haustrations."

y large circular constrictions

y about 2.5 centimeters of the circular muscle contracts near occlusive

y + longitudinal muscle (taeniae coli) contracts

y Peaks @ 30s and disappears after 60s

y Much of the propulsion in the cecum and ascending colon results from the slow but persistent haustral contractions,

requiring as many as 8 to 15 hours to move the chyme from the ileocecal valve through the colon

y Initiated by cells of Cajal producing BER and then ENS m odifying.

Mass Movements

y move faeces 1/3 to ¾ of the length of the colon

y only 1-3/day

y lasts for about 15mins during the 1st

hr after eating breakfast

y Initiated by food entering the stomach and the gastrocolic reflex, which is m ediated by gastrin, serotonin, and extrinsic

autonomic nerves

y Mediated by gastrocolic and duodenocolic reflexes. Reflexes triggered by distention of the stomach and duodenum. They

occur either not at all or hardly at all when the extrinsic ANS to the colon have been removed; therefore, the reflexes

almost certainly are transmitted by way of the ANS

y Irritation in the colon can also initiate intense mass movements. For instance, a person who has an ulcerated condition

of the colon mucosa (ulcerative colitis) frequently has mass movements that persist almost all the time.

1. C onstrictive ring occurs in response to distention or irritation, usually in the transverse

2. Distal 20 cm lose haustrations and instead contract as a unit, propelling faeces en masse further down the colon. The

contraction develops progressively more force for about 30 seconds, and relaxation occurs during the next 2 to 3 minutes.

3. Then another mass movement occurs distal to t he 1st

4. persists for 10 to 30 minutes then they cease

5. return perhaps a half day later.

6. When they have forced a mass of feces into the rectum, the desire for defecation is felt

12 . DESCRIBE THE NEURAL AND HORMONAL REGULATION OF GASTRIC EMPTYING.

Stomach emptying is promoted by intense peristaltic contractions in the stomach antrum. At the same time, emptying is opposed by varying

degrees of resistance to passage of chyme at the pylorus. Both gastric and duodenal signals play a part but duodenal > gastric

Regulation of Stomach Emptying

Gastric 1. Distension - the greater the volume of the meal in the stomach, the greater the peristaltic activity, the faster the rate of

emptying (via direct stretch, local reflexes, vago -vagal excitatory reflexes).

food volume stretch of wall myenteric NS pylorus tone + pyloric pump

2. Gastrin pyloric pump

Duodenal 1. Enterogastric inhibitory reflex

Triggers: distention, pH, or osmolality, presence of proteins and fats, irritationCauses:

ENS mediated to inhibit pyloric pump and pyloric sphincter tone

SNS afferent stimulation to prevertebral ganglia back to gastric mucosa (via SNS) to inhibit pyloric pump and pyloric

sphincter tone

Vagus afferent in small intestine to brain stem which inhibits normal vagal activity

Overall result: rate of gastric emptying

2. Hormonal Feedback

Release of CCK from mucosa of jejunum in response to fatty chyme acts as an inhibitor to block d stomach motility caused by

gastrin

Secretin released from duodenal mucosa in response to gastric acid weak inhibitor of gastric motility

GIP released from upper small intestine in response to fatty chyme limited inhibitor of gastric motility

13 . DESCRIBE THE MAJOR MECHANISMS THAT PRO TECT THE STOMACH FROM SELF DIGESTION AND THE LEAKAGE OF

GASTRIC JUICE INTO THE PERITONEUM.

y mucus secreted by surface foveolar cells forms a thin layer of mucus that prevents large food particles touching the epithelium. The

mucus layer also promotes formation of an ³unstirred´ layer that has pH 7 (due to HCO3-secretion by surface epithelial cells)

y rich vascular supply delivers O2, HCO3-and nutrients while washing away acid.

y inhibition of further acid production - H+-mediated inhibition of gastrin secretion

y secretion of proenzyme (pepsinogen)

y too harsh an environment for most pathogens to cause harm

y constant epithelial cell renewal



21

TRUDY BAXTOR GIT#1

14 . DESCRIBE THE ROLE OF HELICOBACTER PYLORI (H. PYLORI) , NON-STEROIDAL ANTI INFLAMMATORY DRUGS, AND

SMOKING IN THE FORMATION OF ULCERS.

Helicobactor Pylori injury in uremic patients and those infected with urease -secreting H. pylori may be due to inhibition of gastric HC O3-

transporters by ammonium ions. May HCl secretion.

Virulence factors =

1. Flagella motile in viscous mucus

2. urease generates ammonia from endogenous urea and thereby elevates local gastric pH

3. adhesins can adhere to surface foveolar cells

4. produce toxins, such as cytotoxin-associated gene A (CagA), that may be involved in ulcer or cancer development by poorly defined

mechanisms

NSAIDs causes direct mucosal irritation and suppresses PGE2 synthesis. PGE2 would normally stimulate mucus, HCO3-, and phospholipid

production. Many prostaglandins also mucosal blood flow and stimulate epithelial regenerative processes.

The metabolism of arachidonic acid via the enzyme COX produces mainly thromboxane (TxA2) in platelets and prostacyclin (PGI2) in the

vascular endothelium. Prostacyclin and thromboxane have a reciprocal relationship

y TxA2 causes vasoconstriction and induces platelet aggression

y PGI2 causes vasodilatation and has a platelet anti -aggregatory effect

The aspirin irreversibly inhibit s the COX enzymes. Platelet COX is more s ensitive to aspirin i nhibition and can only be regenerated with the

formation of new platelets. Aspirin can, therefore, have a selective inhibitory effect on thromboxane production and hence on platelet

aggregation.

y COX-1 is found in the GI tract, where it is involved in the production of the gastroprotective PGE2, and in platelets, where it produces

the proaggregatory vasoconstricting thromboxane.

y

COX-2 is found at sites of inflammation such as the arthritic joint.

Smoking impairs mucosal blood flow a nd healing

15 . DESCRIBE THE UTIL ITY AND L IMITATIONS OF IMAGING TECHNIQUES, H. PYLORI TESTS, ENDOSCOPY AND BIOPSY IN

THE DIAGNOSIS OF OES OPHAGEAL DISEASE, PEPTIC ULCER DISEASE (PUD) AND MALIGNANCY.

Gastroscopy/Endoscopy

Current reference standard for diagnosis of PUD. Done whilst patient is sedated.

Pros

y allows observation of any inflammation or irritation of the oesophagus, while also investigating any other abnormalities such as

stomach ulcer, Barrett's oesophagus, or malignancy

y can assess whether ulcer is chronic or acute

y Can visualise other suspicious regions (comorbid cancer)

y

for obtaining biopsy specimens, such as for histologic examination and to assess for Helicobacter pyloriy therapeutic interventions (eg haemostasis)

y 95% sensitive for peptic ulcer

Dis.

y Small gastric ulcers may be missed

y Expensive

y bleeding and gastrointestinal perforation

y diagnostic upper endoscopy and colonoscopy (<1:1000 procedures),

y Infectious complications - give prophylactic antibiotics in some patients.

y Sedation risks include respiratory depression or allergic reactions.

C ontrast radiography i.e. barium meal

Performed to examine the stomach and Duodenum. Barium is a chalky substance administered orally, it outlines the stomach lini ng on X-ray.



22

TRUDY BAXTOR GIT#1

Pros

y Ulcers may be visualised as an irregular outline of the stomach or duodenal lining

y Carcinoma may be se en as a filling defect or an irregular ulcer with rolled edges.

y Less invasive.

Dis.

y Radiation exposure.

y Inability to confirm malignancy in gastric ulcers

H. pylori tests - Non Invasive methods13C Urea breath Test

y Breath in13

C Urea urease converts to13

CO2

y requires a mass spectrometer, but is very sensitive and specific.

y Can demonstrate eradication of the organism following treatment.

Serological Tests only good for detection

y Detect IgG Ab.

y Used in the diagnosis and epidemiological studies.

y IgG titres may take up to 1 year to fall by 50% after eradication therapy and are

therefore not useful for confirming eradic ation or the presence of a current

infection.

Stool Test

y Stool sample detect for H. Pylori proteins using engineered monoclonal

antibodies

H. pylori tests - Invasive techniques

Rapid Urease Test

y Gastric biopsies are added to a urea solution containing phe nol red. If H. pylori are present, the urease enzyme splits the urea torelease ammonia which raises the pH of the solution and causes a rapid colour change.

C ulture

y Biopsies obtained can be cultu red and sensitivities to antibiotics can be a scertained

H istology

y H. pylori can be detected histologically on routine Giemsa stained sections of gastric mucosa obtained at endoscopy.

Test Sensitivity/

Specificity

Advantages Disadvantages

Noninvasive Tests

Serum H.

pylori antibo

dies

90% to 97%

sensitivity

50% to 90%

specificity

Noninvasive test of choice when endoscopy

is not indicated and patient has not received

prior H. pylori eradication therapy.

Not affected by PPI, antibiotics, luminal

blood.

Does not confirm eradication because antibodies

to H. pylori can persist years after microbiologic

cure.

Not an option when the patient has received prior

antimicrobial therapy for H. pylori infection.

Urea breath

test

77.5% to 97%

sensitivity

90% to 99%

specificity

Simple.

Preferred for confirming cure of H.

pylori infection, but no sooner than 4 weeks

after completion of therapy.

Possibility of false-negative results s if testing is

done after Rx with PPIs, antibiotics, or bismuth

compounds.

Small radiation exposure with carbon-14 method.

Expensive.

Stool

antigen test

91% to 96%

sensitivity

89% to 95%

specificity

Can also be used to confirm cure of H. Pylori

infection.

With current tests, a positive result after 4

weeks is predictive of failed eradication.

Affected by intake of PPIs, antibiotics, and bismuth

compounds.

Older tests have shown lower accuracy in

predicting eradication.

Invasive Tests (Require Endoscopy)

Tissue

biopsy

93% to 100%

sensitivity; >95%

specificityGiemsa and Genta

stains have >95%

sensitivity and 99%

specificity

Direct confirmation of presence of H. pylori .

Can determine presence of neoplasm if

necessary.

When hematoxylin eosin stain is nondiagnostic, a

second staining method is required.

Results are dependent on the quality o f samplestaken.

Rapid

urease test

of tissue

85% to 95%

sensitivity

93% to 98%

specificity

Simple.

Rapid (once biopsy specimen has been

obtained).

Requires a minimum of 10 organisms in the sample

to give an o bservable result.

Treatment with PPIs, antibiotics, or bismuth

compounds can yield false-negative results.

Tissue

culture

100% specificity

Low sensitivity

Done after failure of appropriate

combination therapy.

Allows determination of antibiotic

susceptibility if resistance is suspected.

Not ro utinely available in hospitals.

Time consuming.

Technically difficult.

Expensive.



23

TRUDY BAXTOR GIT#1

16 . OUTLINE THE PRINCIPLES OF MANAGEMENT OF ULCERS INCLUDING ANTACIDS, H2 ANTAGONIST S, ACID PUMP

INHIBITORS, H. PYLORI ERADICATION AND SURGICAL APPROACHES (THE LAST IN ONLY THE MOST I NTRACTABLE

CASES) .

Drug Class Drug Mechanism of Action Adverse Effects Contraindication/

Caution

H2-receptor

antagonist

Cimetidine Reversibly competes with

H2 @ gastric H2 receptor

parietal cell

stimulation secretion

of HCl

Gynecomastia in male

patients, dizziness, headache,

fatigue; and confusion and

delirium (IV doses).

Cimetidine can interact with cytochrome

P450 enzymes (CYP1A2, CYP2C).

s bioavailability of of ketoconazole,

itraconazole, and ampicillin.

Pregnancy category B.

Ranitidine

Famotidine

Nizatidine

PPIs Omeprazole Irreversibly inactivates

the H+/K

+ATPase,

effectively reducing

gastric acid release into

the gastric lumen.

Nausea, diarrhea, dizziness Decreases bioavailability of ketoconazole,

itraconazole, and ampicillin.

Cytochrome P450 interactions: exercise

caution when used with warfarin,

phenytoin, and diazepam.

Pregnancy category B; pregnancy

category C (omeprazole).

Esomeprazole

Lansoprazole

Pantoprazole

Rabeprazole

Polysaccharide Sucralfate Undergoes

polymerization in acid

environment, binding to

proteins and coating

mucosal defects.

Constipation Caution in patients with renal

insufficiency, may develop aluminum

toxicity.

Pregnancy category B.

Bismuth

compound

Bismuth

subcitrate

Binds to ulcer base,

promoting bicarbonate

and mucin production.

Has intrinsic

antimicrobial effects.

Few systemic effects.

Converted by intestinal

bacteria to bismuth sulfide,

leading to black stools that

may be confused with melena.

Bismuth subsalicylate is contraindicated

in children younger than 12 years.

Use with caution in patients with renal

insufficiency.

Pregnancy category C/D

Anticholinergic

agents

Telenzepine Act as antagonists to

muscarinic receptors,

decreasing acid

secretion.

Dry mouth, blurred vision,

constipation.

Enhanced effect when used with other

drugs with antimuscarinic properties and

with monoamine oxidase inhibitors.

Antagonistic effect with

parasympathomimetics.

Pirenzipine

Antacids Al(OH)3+Mg(OH)

2

Alkali, neutralizes gastric

acid.

Belching, abdominal

distention, constipation

(aluminum- containing

compounds), d intestinal

motility (magnesium-containing compounds).

Contraindicated in patients with renal

failure.

Prostaglandin

analogue

Misoprostol Synthetic prostaglandin,

stimulates mucin and

bicarbonate production.

Abdominal pain, diarrhea,

nausea, vomiting.

Contraindicated in pregnancy; potent

abortifacient.

Pregnancy category X.

H. Pylori Eradication

All pts with gastric and duodenal ulcers have eradication therapy regardless of whether t his is an incidental finding. Standard eradication

therapies are successful in 90%. Reinfection uncommon (1%) in developed countries, more so in developed countries.

y good compliance is essential

y there is a high incidence of resistance to metronidazole, particularly in some populations

y oral metronidazole has frequent side-effects

y bismuth chelate is unpleasant to take, even as tablets.

Metronidazole, clarithromycin, amoxicillin, tetracycline and bismuth are the most widely used agents. Resistance to amoxicill in (12%) and

tetracycline (< 1%) is low. Quinolones such as ciprofloxacin, furazolidone and rifabutin are also used when standard regimens have failed(rescue therapy). Bismuth suppresses H. pylori effectively. None of these drugs is effective alone; eradication regimens th erefore usually

comprise two antibiotics given with powerful acid suppression in the form of a PPI, all given for 7 days.

Example regimes are:

y omeprazole 20 mg + clarithromycin 500 mg and amoxicillin 1 g all twice daily

y omeprazole 20 mg + metronidazole 400 mg and clarithromycin 500 mg all twice daily.

Surgery

y Hardly ever done - 90% of all ulcer operations are interventions for hemorrhage, perforation, or obstruction

y Endoscopic therapy remains the procedure of choice for the majority of patients with rebleeding. However, emergency surgery i s

preferred among patients with hypotension and with a large ulcer siz e (> 2 cm diameter).



TRUDY BAXTOR GIT#1

17 . DESCRIBE THE PATHOLOGY OF DISEASES OF THE OESOPHAGUS, INCLUDING ACHALASIA, VARIC ES, OESOPHAGITIS AND TUMOUR

STOMACH, INCLUDING GASTRITIS , ULCER AND GASTRIC TUMOURS.

PATHOLOGY MORPHOLOGY

Achalasia

LOS tone b/c of impaired sm relaxation.

Failure of inhibitory neuron release of NO and VIP during swallowing

1 = idiopathic, 2 = degenerative (Chagas dx = infective destruction), diabetic neuropathy, malignancy, amyloidosis, carsoidosis, polio, surge

Triad of symptoms

(i) incomplete LES relax(ii) LES tone

(iii) aperistalsis of the esophagus

Varices

Caused by portal HTN and development of collateral channels

Detected via venogram - torturous dilated veins in SM of distal oesophagus

After rupture ulceration and necrosis

Rupture via inflammatory erosion, tension, hydrostatic pressure

Oesophagitis

Lacerations - Mallory Weiss tear

y Near gastrooesophageal junction

y Severe retching + vomiting

y 2 to alcoholism and failure of normal vomiting reflex (that induces relaxation of MM)

pressure tear

Chemical

y Alcohol, corrosive acids/bases, hot fluid, heavy smoking, pills that lodge and dissolve (pill

induced oesophagitis)y Iatrogenic chemo, radiation, graft vs host

Lye, acid, detergent necrosis

Radiation causes intima proliferatio

vessels

Infection

y HSV, CMV, fungal (candidiasis, mucormycosis, aspergillosis)

Candidiasis may cause gray-while p

HSV punched out ulcers

Reflux Oesophagitis

y CF: adult > 40 dysphagia, heartburn, sour taste

y Oesophagus protected from trauma but not acid

y Protection = LOS + submucosal glands (mucin and HCO3-)

y +ve pressure gradient draws food up

y Pathogenesis either

o Loss of LOS - Alcohol, smoking, depressed CNS, hiatus hernia

o abdo P obesity, pregnancy

o Hiatus hernia

Hyperaemia

Eosinophils in mucosa

PMNs

Elongation of LP papilla

Barretts

Oesophagus

Intestinal metaplasia

RF: white, male, 40-60

>= 1 tongue or patch of red, velvety

segment (<3cm)

Diagnosis requires endoscope and

Tumours

Squamous Papilloma

y Sessile lesion

y Central core ct

y Hyperplastic papilliform sq mucosa

Leiomyoma

y Sm origin



TRUDY BAXTOR GIT#1

Adenocarcinoma

RF = barretts, smoking, GORD, o besity, prior radiation, H Pylori, 7M:1F, western country

RP = fresh fruit and veg

CF = pain, dysphagia, wt loss, hematemesis, chest pain, vomit

Distal 1/3 + may invade gastric card

Initially flat or raised patches

Barretts present next to Ca

Produce mucin and form intestinal

Squamous Cell carcinoma

RF: alcohol, smoking, poverty, caustic injury, achalasia, hot liquid, previous radiation, >45, 4M:1F,

6black:1white

CF: dysphagia, odynophagia, obstruction, wt loss, trachea -oesophageal fistula

Lymphatic spread

50% in middle 1/3

Begins as in-situ lesion (squamous

Looks small gray-white plaque

Later on tumous mass or polypoidy May be ulcerative or may

luminal narrowing

y May invade adjacent stru

Gastritis

ACUTE

Cause: disruption of normal protective mechanisms

y Decrease mucin synthesis in elderly

y NSAIDs PGE2 or HCO3- secretion

y Uremia and H. Pylori infection urea NH4+ secretion inhibits HCO3 - transporters

y Ingestion of toxins, alcohol, radiation, chemo

Moderate oedema in LP

Surface epithelium intact

PMNs above basement membrane

Erosion = loss of superficial epithel

CHRONIC

Cause: H. Pylori, autoimmune (pernicious anemia), toxic (alcohol, smoking), postsurgical , motor and

mechanical, radiation, granulomatous conditions

Presence of cx m ucosal inflam mucosal atrophy + intestinal metaplasia usu. In the absence of

erosion

Epithelial s may be dysplastic adenocarcinoma

CF: nausea, vomit, UL/RQ pain, hypoCl-

H. Pylori

May cause expression of pro-inflam cytokines (IL-6,8, TNF) + directly injures epithelial cells.

Do not invade mucosa and are absent from areas of intestinal metaplasia.

2 patterns:

(i) antral + acid + duodenal ulcer

(ii)pan gastritis multifocal atrophy + acid + risk of adenocarcinoma

Virulence

y Motility

y Urease

y Bacterial adhesions

y Bacterial toxinsTests:

y Serologic Ab

y Fecal bacterial detection

y Urea breath tests

y Gastric biopsy

Antral mucosa or antral-body-fund

flattened

inflam infiltrate of lymphocytes + p

1. Regenerative change p

2. Metaplasia intestinal

3. Atrophy loss of glandul

cells

4. Dysplasia carcinoma in







TRUDY BAXTOR GIT#1

histoplasmosis, Scedos porium

spp.

-ve inotropic effect

CF or gastric acid

absorption poor

Miconazole candidiasis

FLUCYTOSINE Converted to active form in fungal cells

then inhibits DNA synthase and is

incorporated into fungal RNA to affect

protein synthesis

Limited range (mainly yeast)

Drug resistance is common

during course so hardly ever

given alone

Cryptococcal infections (with

amphotericin)

C aution in bone marrow

de pression,

myelosu ppressive drugs,

radiation treatment, AIDS

b/c of blood dyscrasias

Renal impairment s risk of haematological toxicity

Rx nephrotoxic drugs

may renal excretion and

the risk of toxicity

pregnancy

Common or infrequent

anaemia, leucopenia, thromboc

diarrhoea, nausea, vomiting, ele

Infrequent or rare

hepatic necrosis, agranulocytos

necrolysis, seizures, confusion,

TERBINAFINE

Oral or IV

Selectively inhibits enzyme involved in

sterol formation

Accumulation of inactive enzyme is

toxic to cell

tinea Psoriasis may worsen

Caution in renal f n

Contra in severe liver

failure

Common

nausea, vomiting, diarrhoea, ab

liver enzymes, arthralgia, myalg

Infrequent

taste disturbance (usually rever

Rare

hepatitis, hepatic failure, neutr

pancytopenia, Stevens-Johnson

lesions, worsening of psoriasis,

anaphylactoid reactions, dizzine

Aspergillosis Blastomycosis C andidiasis -

Vulvovaginal To pical

C andidiasis -

Systemic

C andidemia C andidiasis -

urinary

C occidioidomycosis C ry ptococcosis

AMPHOTERICIN Y y y y y Y

NYSTATIN

GRISEOFULVIN

ECHINOCANDINS Y (2° ) y

AZOLES y y Y y y Y Y Y (2° )

FLUCYTOSINE Y (2° ) y

TERBINAFINE

Oral or IV



29

TRUDY BAXTOR GIT#1

Fungal infections: 4 main types

y yeasts (e.g. Cryptococcus neoformans)

y yeast-like fungi that produce a structure resembling a mycelium (e.g. Candida albicans)

y filamentous fungi with a true mycelium (e.g. Aspergillus fumigatus)

y 'dimorphic' fungi that, depending on nutritional constraints, may grow as either yeasts or filamentous fungi (e.g. Histoplasma

capsulatum).

Fungi of Medical Importance 1. Yeasts a. C andida species:

C. albicans C. glabrata C. krusei C. para psilo psis C. tro picalis C. lusitaniae

b. Cryptococci C. neoformans var grubii C. neoformans var gattii

c. Trichos poron species

2. Molds: a. As pergillus b. F usarium c. Pseudallescheria boydii (Scedos porium a pios permum) d. Z ygomycetes: Rhizo pus, Mucor , others

19 . REVIEW THE CONCEPT OF NEGLIGENCE AND CONSIDER HOW IT APPLIES TO THIS CASE IN TERMS OF:

y THE CONDITIONS THAT CREATE A "DUTY OF CARE"

y TYPES OF MEDICAL MISTAKES WHICH MAY LEAD TO AN ACTION IN NEGLIGENCE

y HOW THE BOLAM PRINCIPLE CAN BE APPLIED IN A POTENTIAL NEGLIGENCE CASE

y PROVISIONS IN THE CIVIL L IABIL ITY ACT (QLD) 20 03 THAT APPLY TO CASES OF NEGLIGENCE

y THE VARIOUS ELEMENTS OF NEGLIGENCE THAT NE ED TO BE SATISFIED FOR A SUCCESSFUL ACTION.

DoC :

obligation to take reasonable care to ensure that they do not through their actions cause another person to suffer harm.

y Donahue v Stevenson (1932) neighbour principle c losely and directly affected

y Roger v Whitaker automatic DoC for D r Pt relationship

y Duty of care to spouse of pt.

Medical Mistakes:

Failure to

y Attend

y Take history

y Diagnose



30

TRUDY BAXTOR GIT#1

y Provide advice

y Disclose risk

y Lack of knowledge or reasonable care

y Refer on

y Train medical staff

y Keep confidentiality

Bolam:

y Judged by peers in relation to negligence of diagnosis or treatment

y Case: pt had clinical depression, ECT, fracture, failure to use relaxant drugs, constraints , warn of risk not upheld

y Standard of care standard of the ordinary skilled man exercising and professing to have a special skill .

R v W

y The Dr is under a DoC to warn of

o material risks that a reasonable person would be likely to attach significance to

o risks that the Dr knows or ou ght to know this pt would attach significance to

CLA (2003)

y Sec 21 = r v Whitaker

y Sec 22 = bolam

y Sec 11 = requirement for negligence

y Sec 12 = onus of proof

Negligence:

1. There exists a DoC

2. DoC was breeched

a. Bolam for diagnosis and Rx.

b. R v W says advice is judged by judge.

3. Breeched caused damage4. Damage was foreseeable and is now quantifiable

20. DEMONSTRATE COMPETENCE IN EXPLORING A PATIENT'S EXP ERIENCE OF IMPORTANT GASTROINTESTINAL

PRESENTATIONS (ABDOMINAL PAIN, CHANGED APPETITE, UNINTENTIONAL WEIGHT CHANGE, NAUSEA, VOMITING, HEARTBURN,

REFLUX, DYSPEPSIA, DYSPHAGIA, ODYNOPHAGIA, HAEMATEMESIS, MELAENA OR RECTAL BLEEDING) [REVISION] INCLUDING: THE

CARDINAL CHARACTERISTICS OF THE SYMPTOM AND ITS TIME COURSE; RELEVANT ASSOCIATED SYMPTOMS; THE PATIENT'S

UNDERSTANDING OF, AND CONCERNS ABOUT, WHAT THEY ARE EXPERIENCING.

21. DEMONSTRATE APPROPRIATE INFECTION CONTROL MANOEUVRES PRIOR TO AND AFTER PHYSICAL EXAMINATION

OF A PATIENT [REVISION].

22 . PREPARE A PATIENT APPROPR IATELY FOR EXAMINATION OF THE ABDOM EN, IN RELATION TO APPROPRIATEEXPLANATION, CONFIRMATION OF CONSENT AND P ATIENT POSITIONING.

23 . DESCRIBE THE ANATOMY OF THE ABDOMEN AND PELVIS RELEVANT TO THE PERFOR MANCE OF ABDOMINAL

EXAMINATION.



31

TRUDY BAXTOR GIT#1

24 . DEMONSTRATE COMPETENCE IN THE PHYSICAL EXAMINATION OF A PATIENT FOR THE ASSESSMENT OF

PRESENTATIONS WHERE ABDOMINAL S IGNS MAY OCC UR, INCLUDING INSPECTION, PALPATION, PERC USSION AND

AUSCULTATION OF THE ABDOMEN, AS WELL AS THE IDENTIFICATION OF ORGANOMEGALY OR ABNORM AL MASSES,

EL ICITATION OF TENDERNESS AND SIGNS OF PERITONISM, THEN DISCUSS THE S IGNIFICANCE OF ANY ABNORMAL

FINDINGS.



32

TRUDY BAXTOR GIT#1



33

TRUDY BAXTOR GIT#1

10. UNDERSTAND THE IMPORTANC E OF HELICOBAC TER PYLORI (H. PYLORI), NON- STEROIDAL AN TI INFL AMM ATORY

DR UGS, AND SMOKING AND THEIR POSSIBL E UNDER LYI NG MECHA N ISMS IN RELA TI O N TO THE FORMATI ON OF ULCERS.

Helicobactor Pylori

y Present in almost all duodenal ulcers and the ma jority of individuals with gastric ulcers or chronic gastritis (907

of c8

antrum

gastritis)

y Have 4 main virulence factors: adhesions, produce urease from endogenous urea to pH, flagellate to move, produce toxin which

may have some aff ect on ulceration. They can invade mucosabut not re9

uired for ulceration

y Inf ection causes HCl + gastric def ence mechanisms

NSAIDs

y direct chemical irritationy block COX1 found on ... which would normally produce gastro-protective prostaglandins which would :

PGE2

EP1 y GI tract smooth muscle contraction

EP2 y GI tract smooth muscle relaxation

y vasodilatation

EP3

y gastric acid secretion

y gastric mucus secretion

y GI tract smooth muscle contraction

y platelet response to their agonists and

atherothrombosis

Smoking

y impairs mucosal blood flow and healing

Corticosteroids

y suppress prostaglandin synthesis and impair healing

Duodenal ulcers are more fre@

uent in individuals with alcoholic cirrhosis,COPD, chronic renal failure, and hyperparathyroidism. In the latter2

conditions, hypercalcemia stimulates gastrin production and therefore s acid secretion. Finally, self -imposed or exogenous psychologic stress

may gastric acid production.



Documents

Case 1 - Trudy Baxtor - (PUD)b