PROBLEM 1

VIVIAN SAPUTRA
405140126
 LEARNING OBJECTIVE
1. Describe the anatomy, histology, physiology, and biochemistry of the
upper GIT
2. Describe the etiology & epidemiology of swallowing difficulty
3. Describe the terminology and pathophysiology of dysphagia and
odynophagia
4. Describe the sign and symptoms of swallowing difficulty
5. Describe the therapeutic management of swallowing difficulty
6. Describe the complication and prognosis of swallowing difficulty
7. Describe the prevention and health education for swallowing difficulty
LO 1
DESCRIBE THE ANATOMY, HISTOLOGY, PHYSIOLOGY,
AND BIOCHEMISTRY OF THE UPPER GIT
ANATOMY
 ORAL CAVITY :
OVERVIEW

1. Hard palate
2. Soft palate
3. Uvula
4. Palatopharyngeal arch
5. Palatoglossal arch
6. Palatine tonsil
7. Oral part of tongue (anterior two thirds)
8. Posterior wall of oropharynx
ORAL CAVITY: FLOOR

1. M. Genioglossus
2. M. Mylohyoid
3. M. Hyoglossus
• The mylohyoid muscles together form a muscular diaphragm that defines
the inferior limit of the floor of the oral cavity.
• The genioglossus and hyoglossus muscles are extrinsic muscles of the
tongue. The function of the genioglossus muscle is used to test the
function of the hypoglossal nerve.
 Oral Cavity : Tongue

1. Anterior two thirds (oral part) of tongue

2. Palatoglossus muscle
3. Styloglossus muscle
4. Posterior third (pharyngeal part) of tongue
5. Hyoglossus muscle
6. Genioglossus muscle
• All muscles of the tongue (intrinsic and extrinsic) are innervated by the
hypoglossal nerve (XII)  except the palatoglossus muscle, which is
innervated by the vagus nerve (X) through the pharyngeal plexus.
• General sensation from the oral part of the tongue is by the lingual branch
of the mandibular nerve (V3).
• Special sensation from the oral part of the tongue is by the facial nerve
(VII) via the chorda tympani branch that joins the lingual nerve in the
infratemporal fossa.
• General and special sensation from the pharyngeal part of the tongue is
by the glossopharyngeal nerve (IX).
Oral Cavity :
Teeth
ORAL CAVITY: SOFT PALATE
(OVERVIEW)

1. Tensor veli palatini muscle

2. Medial plate of pterygoid process
of sphenoid bone
3. Pharyngotympanic (eustachian)
tube
4. Levator veli palatini muscle
5. Musculus uvulae
6. Palatopharyngeus muscle
7. Palatine tonsil
8. Palatine aponeurosis
9. Palatoglossus muscle
10. Pterygoid hamulus
• All muscles of the palate are innervated by cranial nerve (X) via the
pharyngeal branch through the pharyngeal plexus, except for the tensor
veli palatini, which is innervated by the mandibular nerve (V3).
• The only muscle that elevates the palate from the neutral position is the
levator veli palatini.
 Esophagus
• The esophagus is a muscular tube (approximately 25 cm [10 in] long) with
an average diameter of 2 cm that conveys food from the pharynx to the
stomach.
• As seen during fluoroscopy (x-ray, using a fluoroscope), the esophagus
normally has three constrictions where adjacent structures produce
impressions:
– Cervical constriction (upper esophageal sphincter): at its beginning at
the pharyngoesophageal junction, approximately 15 cm from the
incisor teeth; caused by the cricopharyngeus muscle
– Thoracic (broncho-aortic) constriction: a compound constriction where
it is first crossed by the arch of the aorta, 22.5 cm from the incisor
teeth, and then where it is crossed by the left main bronchus, 27.5 cm
from the incisor teeth; the former is seen in anteroposterior views, the
latter in lateral views
– Diaphragmatic constriction: where it passes through the esophageal
hiatus of the diaphragm, approximately 40 cm from the incisor teeth
 The esophagus:
• Follows the curve of the vertebral column as it descends through the neck
and mediastinum
• Has internal circular and external longitudinal layers of muscle. In its
superior third, the external layer consists of voluntary striated muscle; the
inferior third is composed of smooth muscle, and the middle third is made
up of both types of muscle.
• Passes through the elliptical esophageal hiatus in the muscular right crus of
the diaphragm, just to the left of the median plane at the level of the T10
vertebra.
• Terminates by entering the stomach at the cardial orifice of the stomach to
the left of the midline at the level of the 7th left costal cartilage and T11
vertebra.
• Is encircled by the esophageal (nerve) plexus distally
HISTOLOGY
 Histologi
• Oral cavity  stratified squamous epithelium (keratinized, artially
keratinized, nonkeratinized  tergantung lokasi)
• Lapisan berkeratin  tahan terhadap kerusakan  berkembang pada
masticatory mucosa pada gingiva (gusi) dan hard plate.
• Nonkeratinized  dominan pada lapisan mucosa pada soft plate, pipi,
dasar lidah, dan pharynx
 Bibir
• Otot lurik berkembang dengan baik  dapat bergerak bebas untuk
menela, bicara, dan komununikasi.
• 3 lapisan pada bibir:
– Internal mucous surface: punya lapisan mukosa yg tebal, epitelium
nonkeratin, dan sedikit minor labial salivary gland.
– Zona vermilion  epitel squamosa bertingkat dengan keratin yg
sangat tipis  transisi antara mukosa mulut dengan kulit.  tidak
punya salivary gland, tapi tetap lembab dengan saliva dari lidah.
• Kaya akan persarafan sensorik dan kapiler  memberi warna pink
– Outer surface  kulit yg tipis, terdiri dari lapisan epidermal dan
dermal, kelenjar keringat dan banyak folikel rambut dan sebaceous
gland.
Junqueira’s basic histology text & atlas 13th ed
 Lidah
• Merupakan otot2 lurik yg dilapisi mukosa  u/ manipulasi makanan saat
mengunyah dan menelan.
• Bgn bwh lidah  smooth, with typical lining mucosa
• Perm dorsal  irregular, having hundreds of small protruding papillae of
various types pada 2/3 anterior, 1/3 posterior: lingual tonsil.
• Bgn papila dan tonsil dipisahkan o/ alur berbentuk V yg disebut sulcus
terminalis.
 Papil lidah
• Filiform papillae: jumlah banyak, berbentuk cone, sangan berkeratin
 membuat berwarna keabu2an / keputih2an. Permukaan kasar
dan membantu pergerakan makanan saat mengunyah.
• Fungiform papillae: tidak terlalu banyak, sedikit berkeratin, dan
tersebar di antara filiform papillae.
• Foliate papillae : terdiri dari beberapa alur pada pinggir lidah,
anterior dari sulcus terminalis, tetapi belum sempurna pada
manusia, tertuama org2 yg tua.
• Vallate / circumvallate papillae : papila terbesar. 8-12 vallate papilla
tersusun berdekatan dengan sulcus terminalis.
Junqueira’s basic histology text & atlas 13th ed
Junqueira’s basic histology text & atlas 13th ed
 Esophagus
• Pada orang dewasa sepanjang 25 cm.
• Mukosa esofagus: epitel squamosa bertingkat tanpa
keratin.
• Submokosa mengandung kelenjar kecil yang
mengsekresikan mukus  esophageal glands 
lubrikasi dan melindungi mukosa.
• Pada esofagus, 1/3 atas merupakan otot lurik, bagian
tengah kombinasi dari otot lurik dan halus, 1/3 bawah
merupakan otot halus.
Junqueira’s basic histology text & atlas 13th ed
Junqueira’s basic histology text & atlas 13th ed
 Lambung
• 4 major region:
– Cardia : zona transitional yg sempit. Lebar 1,5 -3 cm, terletak
antara esofagus dan lambung.
– Fundus
– Body
– Pylorus: regio berbentuk corong yg terbuka menuju usus halus.
• Cardia dan pylorus terlibat dalam produksi mukus dan secara
histologi mirip.
• Fundus dan body: indentical pada struktur mikroskopik, regio
dimana kelenjar gastrik melepas cairan asam lambung.
• Mukosa dan submukosa pada saat lambung kosong punya lipatan
besar yg dinamakan rugae. Saat lambung berisi makanan, rugae
menjadi rata.
Junqueira’s basic histology text & atlas 13th ed
Junqueira’s basic histology text & atlas 13th ed
PHYSIOLOGY
 Physiology of Swallowing
• Swallowing begins with a voluntary (oral) phase that includes :
– preparation during which food is masticated and mixed with saliva.
– Transfer phase during which the bolus is pushed into the pharynx by
the tongue.
• Bolus entry into the hypopharynx initiates the pharyngeal swallow
response, the net result of which is to propel food through the pharynx
into the esophagus while preventing its entry into the airway.
• To accomplish this, the larynx is elevated and pulled forward, actions that
also facilitate upper esophageal sphincter (UES) opening.
• Tongue pulsion then propels the bolus through the UES, followed by a
peristaltic contraction that clears residue from the pharynx and through
the esophagus.
• The lower esophageal sphincter (LES) relaxes as the food enters the
esophagus and remains relaxed until the peristaltic contraction has
delivered the bolus into the stomach.
• Peristaltic contractions elicited in response to a swallow are called primary
peristalsis and involve sequenced inhibition followed by contraction of the
musculature along the entire length of the esophagus.  The inhibition
that precedes the peristaltic contractionis called deglutitive inhibition
• Local distention of the esophagus anywhere along its length, as may occur
with gastroesophageal reflux, activates secondary peristalsis.
• Tertiary esophageal contractions are nonperistaltic, disordered esophageal
contractions that may be observed to occur spontaneously during
fluoroscopic observation.
• Swallowing is a complex process. Some 50 pairs of muscles and many
nerves work to receive food into the mouth, prepare it, and move it from
the mouth to the stomach.
• This happens in three stages:
– During the first stage, called the oral phase, the tongue collects the
food or liquid, making it ready for swallowing.
– The second stage begins when the tongue pushes the food or liquid to
the back of the mouth.
– The third stage begins when food or liquid enters the esophagus, the
tube that carries food and liquid to the stomach.
 Fisiologi
• 4 proses dasar dalam pencernaan:
– Motility
• Kontraksi otot yg mencampur dan mendorong makanan yang ada pada saluran
pencernaan.
– Propulsive movement : mendorong makanan ke saluran pencernaan dengan
kekuatan pendorong yang berbeda-beda sesuai kebutuhan organ.
– Mixing movement: untuk mencampur makanan dengan cairan pencernaan
(digestive juice) dan memfasilitasi penyerapan oleh usus halus.
– Secretion  sekresi cairan pencernaan oleh kelenjar eksokrin.
– Digestion  pemecahan biokimia dari makanan menjadi molekul yang lebih kecil
sehingga dapat diserap
– Absorbtion  menyerap molekul makanan yang telah di pecah bersama dengan air,
vit, dan elektrolit dari lumen usus ke pembuluh darah atau lymph.
 The digestive tract wall has four layer
• Mucosa  pada permukaan lumen sistem pencernaan, tdp 3 lapisan:
– Membran mukosa : lapisan epitel yang berfungsi untuk proteksi. Pada
bbrp bgn sudah termodifikasi untuk sekresi dan absorbsi.
– Lamia propria : lapisan tengan yang tipis. Merupakan tempat gut-
associated lymphoid tissue (GALT), yg penting sbg pertahanan dari
bakteri yang menyebabkan penyakit.
– Muscularis mucosa: lapisan otot polos yang sedikit. Merupakan
lapisan terluar dari mukosa yang berdekatan dengan lapisan
submukosa.
• Submucosa  lapisan tebal dari connective tissue yg menyediakan
elastisitas dan distensibility u/ sal pencernaan.
 The digestive tract wall has four layer
• Muscularis externa  otot halus yang melapisi saluran pencernaan yg
mengelilingi submucosa. Terdapat 2 lapisan: inner circular layer dan
longitudinal circular layer.
– inner circular layer: untuk mengecilkan diameter lumen.
– longitudinal circular layer: kontraksi otot ini dapat memperpendek
saluran.
– Kontraksi otot ini berfungsi untuk menghasilkan propulsive dan mixing
movement
• Serosa  sekresi cairan yang licin untuk mencegah pergesekan antara organ
pencernaan dan sekelilingnya.
– Mesentery : berfungsi untuk mempertahankan organ pencernaan pada
tempatnya.
Sherwood Human Physiology 7th ed.
 Regulation of digestive function
• 4 faktor yang terlibat dalam regulasi sistem pencernaan:
1. Autonomous smooth muscle function.
2. Intrinsic nerve plexuses.
3. Extrinsic nerve.
4. Gastrointestinal hormones.
 Autonomous smooth muscle function
• Sel seperti otot yg tak berkontraksi yg dikenal sebagai interstitial cells of cajal adl
sel pacemaker yg memulai slow wave activity.
• Terletak pada perbatasan antara otot polos longitudinal dan circular.
• Slow wave ini bukan aksi potensial  berfungsi untuk membawa membran
mendekati threshold potential. Jika gelombang ini mencapai treshold pada
puncak depolarisasi, aksi potensial terpicu pada setiap puncak dan
menyebabkan siklus kontraksi otot yang ritmik.
• Jika treshold tidak tercapai, aktivitas listrik terus berjalan pada otot tanpa
aktivitas kontraksi.
• Tercapainya treshold tergantung dari efek faktor mekanik, neural, dan hormon
yang mempengaruhi.
• Kekuatan dari kontraksi tergantung pada jumlah potensial aksi yg terjadi saat
slow wave potentioal mencapai treshold.
 Intrinsic nerve plexuses
• Merupakan 2 jaringan utama dari nerve fibers: submucosal plexus dan
myenteric plexus.
• The intrinsic plexuses influence all facets of digestive tract activity.
• Various types of neurons are present in the intrinsic plexuses.
• Some are sensory neurons, which have receptors that respond to specific
local stimuli in the digestive tract.
• Other local neurons innervate the smooth muscle cells and exocrine and
endocrine cells of the digestive tract to directly affect digestive tract motility,
secretion of digestive juices, and secretion of gastrointestinal hormones
• These intrinsic nerve networks primarily coordinate local activity within the
digestive tract. To illustrate, if a large piece of food gets stuck in the
esophagus, the intrinsic plexuses coordinate local responses to push the food
forward.
 Extrinsic nerve
• The extrinsic nerves are the nerve fi bers from both branches of the
autonomic nervous system that originate outside the digestive tract and
innervate the various digestive organs.
• the sympathetic and parasympathetic nerves supplying any given tissue exert
opposing actions on that tissue.
• The sympathetic system, which dominates in “fight-or-flight” situations, tends
to inhibit or slow down digestive tract contraction and secretion.
• The parasympathetic nervous system, by contrast, dominates in quiet,
“restand-digest” situations, when general maintenance types of activities such
as digestion can proceed optimally
• the parasympathetic nerve fi bers supplying the digestive tract, which arrive
primarily by way of the vagus nerve, tend to increase smooth muscle
motility and promote secretion of digestive enzymes and hormones.
 Gastrointestinal hormon
• Tucked within the mucosa of certain regions of the
digestive tract are endocrine gland cells that, on
appropriate stimulation, release hormones into the
blood.
• Th ese gastrointestinal hormones are carried through the
blood to other areas of the digestive tract, where they
exert either excitatory or inhibitory influences on smooth
muscle and exocrine gland cells.
Receptor activation alters digestive activity through
neural reflexes and hormonal pathways.
• Dinsing sal pencernaan mengandunng 2 reseptor sensorik yg merespon
pada perubahan lokal pada saluran pencernaan:
– chemoreceptors sensitive to chemical components within the lumen,
– mechanoreceptors (pressure receptors) sensitive to stretch or tension
within the wall, and
– osmoreceptors sensitive to the osmolarity of the luminal contents.
 Refleks menelan
• Proses menelan dimulai saat bolus secara volunter didorong oleh lidah ke
pharynx.
• Tekanan yg diberikan bolus menstimulasi reseptor tekanan pharyngeal yg
mengirim impuls ke pusat menelan di medulla pada stem otak.
• Pusat menelan secara refleks memulai proses menelan. Proses menelan
stelah dimulai tidak akan bisa berhenti.
• Pada saat bolus berada di orofaring, bolus harus diarahkan menuju
esofagus.
– Posisi lidah menempel ke hard plate, sehingga makanan tidak kembali ke depan.
– Uvula terangkat dan menempel ke dinding belakang tenggorokan, menutup jalan
ke nasal sehingga makanan tidak msk ke hidung.
– Makanan dicegah masuk ke trakea dengan penutupan glotis dan penutupan pita
suara. Kontraksi otot laring mensejajarkan pita suara 1 dengan yg lain sehingga
dapat menutup glotis. Kemudian bolus mendorong epiglotis kebawah sehingga
mencegah makanan masuk ke trakea.
Sherwood Human Physiology 7th ed.
• Kedua ujung esofagus terdapat sphincter. Pada esofagus atas terdapat
pharyngoesophageal spincter dan pd bgn bawah esofaus terdapat
gastroesophageal spincther.
• Kontraksi pada sphincter atas menutup saluran esofagus untuk mencegah
masuknya volume udara yg besar ke lambung saat bernapas dan mengarahkannya
ke saluran respirasi.
• Saat menelan, sphincter terbuka dan bolus masuk ke esofagus. Setelah bolus
masuk ke esofagusm pharyngoesophageal sphincter tertutup dan respirasi
berlanjut kembali.
• Saat bolus tertelan, pusat menelan memicu primary peristaltic wave yg
mendorong bolus menuju lambung. Jika bolus yg tertelan besar dan lengket gagal
dibawa ke lambung dengan primary peristaltic wave, bolus yg tertahan memberi
stimulasi tekana pada dinding esofagus, sehingga memulai gelombang peristaltic
yg lebih kuat (secondary peristaltic wave). Selain itu, tekanan pada dinding
esofagus juga meningkatkan sekresi kelenjar saliva sehingga bolus terlubrikasi
dan dapat didorong ke lambung.
Sherwood Human Physiology 7th ed.
• Pada gastroesophageal sphincter, otot polos tetap berkontraksi kuat untuk
membatasi antara esofagus dan lambung supaya mencegah refluks asam
lambung
• Saat bolus didorong ke lambung, LES relaksasi sehingga bolus dpt msk ke
lambung, setelah masuk, LES berkontraksi kembali.
BIOCHEMISTRY
 Definition
• Digestion is the chemical breakdown of large food molecules into smaller
molecules that can be used by cells. The breakdown occurs when certain
specific enzymes are mixed with the food.
Enzymes involved in Digestion
• Polysaccharides maltose glucose
• Proteins peptides amino acids
• fats fatty acids and glycerol

• .The most important enzymatic reaction in digestion of foodstuffs is

hydrolysis - the breaking of a chemical bond by the addition of a water
molecule.
 Proteins
• Proteins are polymers of amino acids linked together by peptide bonds.
• Chain length varies tremendously and many dietary proteins have been
modified after translation by addition of carbohydrate (glycoproteins) or
lipid (lipoprotein) moieties.
• Very short proteins, typically 3 to 10 amino acids in length, are called
peptides.
 Lipids
• Fatty acids are present in only small amounts in animal and plant tissues,
but are the building blocks of many important complex lipids.
• True fatty acids possess a long hydrocarbon chain terminating in a carboxyl
group.
• Nearly all fatty acids have an even number of carbons and have chains
between 14 and 22 carbons in length.
• The principle differences among the many fatty acids are the length of the
chain (usually 16 or 18 carbons) and the positions of unsaturated or
double bonds.
• The most abundant storage form of fat in animals and plants, and hence
the most important dietary lipid, is triglyceride.
• A molecule of triglyceride is composed of a molecule of glycerol in which
each of the three carbons is linked through an ester bond to a fatty acid.
• Triglycerides cannot be efficiently absorbed, and are enzymatically
digested by pancreatic lipase into a 2-monoglyceride and two free fatty
acids, all of which can be absorbed.
• Other lipases hydrolyse a triglyceride into glycerol and three fatty acids.
 Carbohydrates
• Monosaccharides or simple sugars are either hexoses (6-carbon) like
glucose, galactose and fructose, or pentoses (5-carbon) like ribose. These
are the breakdown products of more complex carbohydrates and can be
efficiently absorbed across the wall of the digestive tube and transported
into blood.
• Disaccharides are simply two monosaccharides linked together by a
glycosidic bond. The disaccharides most important in nutrition and
digestion are:
– lactose or "milk sugar": glucose + galactose
– sucrose or "table sugar": glucose + fructose
– maltose: glucose + glucose
 Polysaccharides
• Starch is a major plant storage form of glucose. It occurs in two forms:
alpha-amylose, in which the glucoses are linked together in straight
chains, and amylopectin, in which the glucose chains are highly branched
• Cellulose is the other major plant carbohydrate. It is the major constituent
of plant cell walls, and more than half of the organic carbon on earth is
found in cellulose.
• Glycogen is the third large polymer of glucose and is the major animal
storage carbohydrate. Like starch, the glucose molecules in glycogen are
linked together by alpha(1->4) glycosidic bonds
 Mouth
• Chewing breaks food into smaller particles so that chemical digestion can
occur faster.
• Enzymes: Salivary amylase breaks starch (a polysaccharide) down to
maltose (a disaccharide).
• Bicarbonate ions in saliva act as buffers, maintaining a pH between 6.5
and 7.5.
• Mucins (mucous) lubricate and help hold chewed food together in a clump
called a bolus
 Stomach
• The stomach stores up to 2 liters of food. Gastric glands within the stomach
produce secretions called gastric juice.
• The muscular walls of the stomach contract vigorously to mix food with gastric
juice, producing a mixture called chyme.
• Gastric juice
– Pepsinogen is converted to pepsin, which digests proteins. Pepsinogen
production is stimulated by the presence of gastrin in the blood.
– HCl
• Hydrochloric acid (HCl) converts pepsinogen to pepsin which breaks down proteins
to peptides. HCl maintains a pH in the stomach of approximately 2.0. It also
dissolves food and kills microorganisms.
• Mucous protects the stomach from HCl and pepsin.
• Secretion of Gastric Juice: Gastrin is a hormone that stimulates the stomach to
secrete gastric juice.
 Hormones Involved in Digestion
• Gastrin: The presence of food in the stomach stimulates specific receptors
which in turn stimulates endocrine cells in the stomach to secrete the
hormone gastrin into the circulatory system. Gastrin stimulates the
stomach to secrete gastric juice.
• Secretin: Secretin is produced by cells of the duodenum.
– It’s production is stimulated by acid chyme from stomach.
– It stimulates the pancreas to produce sodium bicarbonate, which
neutralizes the acidic chyme. It also stimulates the liver to secrete bile.
• CCK (cholecystokinin): CCK production is stimulated by the presence of
food in the duodenum. It stimulates the gallbladder to release bile and the
pancreas to produce pancreatic enzymes.
• GIP (Gastric Inhibitory Peptide):Food in the duodenum stimulates certain
endocrine cells to produce GIP.
– It has the opposite effects of gastrin; it inhibits gastric glands in the
stomach and it inhibits the mixing and churning movement of stomach
muscles. This slows the rate of stomach emptying when the
duodenum contains food.
LO 2
DESCRIBE THE ETIOLOGY & EPIDEMIOLOGY OF
SWALLOWING DIFFICULTY
 Description
• Dysphagia—difficulty with swallowing—refers to problems with the transit
of food or liquid from the mouth to the hypopharynx or through the
esophagus.
• Odynophagia refers to painful swallowing, typically resulting from mucosal
ulceration within the oropharynx or esophagus.
 Etiology
 Central nervous system disorders
 Muscular disorders
 Neuropathic disorders
 Endocrine disorders
 Pharmacologic causes
 Surgical causes
 Epidemiology
• Occurrence in the United States
– Neurologic swallowing disorders are encountered more
frequently in rehabilitation medicine than in most other medical
specialties. Stroke is the leading cause of neurologic dysphagia,
with the condition occurring in approximately 51-73% of
patients with stroke.
 Epidemiology
• Race- and age-related demographics
– According to the US National Medicare database, the incidence of
poststroke dysphagia is higher in Asians and other minority groups
than in whites, suggesting racial disparities in the development of
dysphagia after stroke.
– the prevalence of dysphagia increases with age, and dysphagia is a
major health care problem in elderly patients
LO 3
DESCRIBE THE TERMINOLOGY AND PATHOPHYSIOLOGY OF
DYSPHAGIA AND ODYNOPHAGIA
 Pathophysiology of Dysphagia
• Dysphagia can be subclassified both by location and by the circumstances
in which it occurs. With respect to location, distinct considerations apply
to oral, pharyngeal, or esophageal dysphagia.
• Normal transport of an ingested bolus depends on the consistency and
size of the bolus, the caliber of the lumen, the integrity of peristaltic
contraction, and deglutitive inhibition of both the UES and the LES.
• Dysphagia caused by an oversized bolus or a narrow lumen is called
structural dysphagia.
• Dysphagia due to abnormalities of peristalsis or impaired sphincter
relaxation after swallowing is called propulsive or motor dysphagia.
• Scleroderma commonly presents with absent peristalsis as well as a
weakened LES that predisposes patients to peptic stricture formation.
• radiation therapy for head and neck cancer may compound the functional
deficits in the oropharyngeal swallow attributable to the tumor and cause
cervical esophageal stenosis.
LO 4
DESCRIBE THE SIGN AND SYMPTOMS OF SWALLOWING
DIFFICULTY
 Signs and symptoms
Oral or pharyngeal dysphagia
•Coughing or choking with swallowing
•Difficulty initiating swallowing
•Food sticking in the throat
•Unexplained weight loss
•Change in dietary habits
•Recurrent pneumonia
•Change in voice or speech (wet voice)
esophageal dysphagia
•Sensation of food sticking in the chest or
throat
•Change in dietary habits
•Recurrent pneumonia
•Symptoms of gastroesophageal reflux
disease (GERD), including heartburn,
belching, sour regurgitation, and water
brash
 Diagnosis
• Transnasal esophagoscopy
• Cervical auscultation
• Blood tests: Including thyroid-stimulating hormone, vitamin B-12, and
creatine kinase; may be useful, especially in neurogenic dysphagia
• Imaging studies: May include videofluoroscopy, computed tomography
(CT) scanning, magnetic resonance imaging (MRI), and chest radiography
• Endoscopic examination
• Esophageal pH monitoring: The criterion standard for diagnosing reflux
disease
LO 5
DESCRIBE THE THERAPEUTIC MANAGEMENT OF
SWALLOWING DIFFICULTY
 Pharmacologic treatment
• Medications used in the treatment of dysphagia include the following:
• Botulinum toxin type A (BoNT-A)
• Diltiazem
• Glucagon
• Cystine-depleting therapy with cysteamine
• Nitrates
 Dietary treatment
• Dysphagia diet 1: Thin liquids (eg, fruit juice, coffee, tea)
• Dysphagia diet 2: Nectar-thick liquids (eg, cream soup, tomato juice)
• Dysphagia diet 3: Honey-thick liquids (ie, liquids that are thickened to a honey
consistency)
• Dysphagia diet 4: Pudding-thick liquids/foods (eg, mashed bananas, cooked
cereals, purees)
• Dysphagia diet 5: Mechanical soft foods (eg, meat loaf, baked beans,
casseroles)
• Dysphagia diet 6: Chewy foods (eg, pizza, cheese, bagels)
• Dysphagia diet 7: Foods that fall apart (eg, bread, rice, muffins)
• Dysphagia diet 8: Mixed textures
LO 6
DESCRIBE THE COMPLICATION AND PROGNOSIS OF
SWALLOWING DIFFICULTY
LO 7
DESCRIBE THE PREVENTION AND HEALTH EDUCATION FOR
SWALLOWING DIFFICULTY
LEUKOPLAKIA
 Definition
• Oral leukoplakia (OL) is a white patch or plaque that cannot be rubbed off,
cannot be characterized clinically or histologically as any other condition,
and is not associated with any physical or chemical causative agent except
tobacco.
 Pathophysiology
• The etiology of most cases of OL is unknown (idiopathic).
• In other cases, the initiation of the condition may depend on extrinsic
local factors and/or intrinsic predisposing factors.
• Factors most frequently blamed for the development of idiopathic
leukoplakia include tobacco use, alcohol consumption, chronic irritation,
candidiasis, vitamin deficiency, endocrine disturbances, and possibly a
virus.
 Epidemiology
• Oral leukoplakia occurs in fewer than 1% of individuals.
• Oral leukoplakia is more common in men than in women, with a male-to-
female ratio of 2:1.
• Most cases of Oral leukoplakia occur in persons in their fifth to seventh
decade of life. Approximately 80% of patients are older than 40 years.
 Sign and Symptoms
• Patches in the mouth usually develop on the tongue and on the insides of
the cheeks.
• Leukoplakia patches are:
– Most often white or gray
– Uneven in shape
– Fuzzy (oral hairy leukoplakia)
– Slightly raised, with a hard surface
– Unable to be scraped off
– Painful when the mouth patches come into contact with acidic or spicy
food
White Lesions of Oral Mucosa
Hairy leukoplakia Usual Location Usually lateral tongue, rarely elsewhere on oral mucosa

Clinical Features White areas ranging from small and flat to extensive
accentuation of vertical folds; found in HIV carriers
in all risk groups for AIDS
Course Due to EBV; responds to high-dose acyclovir but recurs; rarely
causes discomfort unless secondarily
infected with Candida
Smoker’s Usual Location Any area of oral mucosa, sometimes related to
leukoplakia location of habit
Clinical Features White patch that may become firm, rough, or red-fissured and
ulcerated; may become sore and painful but usually painless

Course May or may not resolve with cessation of habit; 2%

develop squamous cell carcinoma; early biopsy essential
 Prevention
• Stop smoking or using other tobacco products.
• Do not drink alcohol, or limit the number of drinks you have.
• Have rough teeth treated and dental appliances repaired right away.
Ludwig’s angina
 Definition
• Ludwig’s angina is a rare skin infection that occurs on the floor of the
mouth, underneath the tongue.
• This bacterial infection often occurs after a tooth abscess, which is a
collection of pus in the center of a tooth. It can also follow other mouth
infections or injuries.
• This infection is more common in adults than children.
 Symptoms of Ludwig’s angina
• The symptoms include swelling of the tongue, neck pain, and breathing
problems.
• Ludwig’s angina often follows a tooth infection or other infection or injury
in the mouth. The symptoms include:
– pain or tenderness in the floor of your mouth,
– difficulty swallowing
– drooling
– problems with speech
– neck pain
– swelling of the neck
– weakness
– tongue swelling that causes your tongue to push against your palate
– a fever
 Causes of Ludwig’s angina
• Ludwig’s angina is a bacterial infection. The bacteria
Streptococcus and Staphylococcus are common causes.
• The following may also contribute to developing Ludwig’s angina:
– poor dental hygiene
– trauma or lacerations in the mouth
– a recent tooth extraction
 Diagnosing Ludwig’s angina
• Contrast-enhanced MRI or CT images can confirm swelling on the floor of
the mouth.
• test fluid cultures from the affected area to identify the specific bacterium
that’s causing the infection.
• the basis for diagnosis of Ludwig’s angina:
– Your head, neck, and tongue may appear red and swollen.
– You may have swelling that reaches to the floor of your mouth.
– Your tongue may have extreme swelling.
– Your tongue may be out of place
 Treatment for Ludwig’s angina
• Clear the airway
• Drain excess fluids
• Fight the infection
• Get further treatment
 Complications
• a blocked airway
• sepsis, which is a severe reaction to bacteria or other germs
• septic shock, which is an infection that leads to dangerously low blood
pressure
 Prevention
• You can decrease your risk of developing Ludwig’s angina by:
– practicing good oral hygiene
– having regular dental checkups
– seeking prompt treatment for tooth and mouth infections
– If you’re planning on getting a tongue piercing, make sure it’s with a
professional using clean, sterile tools.
– You should brush your teeth twice every day and use mouthwash with
antiseptic liquid once per day.
Glossitis
• Glossitis is a problem in which the tongue is swollen and changes color,
often making the surface of the tongue appear smooth.
• Glossitis is often a symptom of other conditions, such as:
– Allergic reactions to oralcare products, foods, or medicine
– Dry mouth due to Sjogren syndrome
– Infection from bacteria, yeast or viruses (including oral herpes)
– Injury (such as from burns, rough teeth, or bad-fitting dentures)
– Skin conditions that affect the mouth
– Irritants such as tobacco, alcohol, hot foods, spices, or other irritants
– Hormonal factors
– Certain vitamin deficiencies
 Symptoms
• Symptoms of glossitis may come on quickly or develop over time. They
include:
– Problems chewing, swallowing, or speaking
– Smooth surface of the tongue
– Sore, tender, or swollen tongue
– Pale or bright red color to the tongue
– Tongue swelling
• Rare symptoms or problems include
– Blocked airway
– Problems speaking, chewing, or swallowing
 The Types of Glossitis
• Acute Glossitis
– an inflammation of the tongue that appears suddenly, and it often has
severe symptoms.
– typically develops during an allergic reaction.

• Chronic Glossitis
– an inflammation of the tongue that continues to recur.
– This type may begin as a symptom of another health condition.
 The Types of Glossitis
• Idiopathic Glossitis
– also known as Hunter’s glossitis
– affects the muscles of the tongue.
– In this condition, a significant amount of papillae can be lost. The
cause of idiopathic glossitis is unknown.

• Atrophic Glossitis
– Atrophic glossitis occurs when a large number of papillae are lost,
resulting in changes to the tongue’s color and texture.
– This type of glossitis typically turns the tongue dark red.
 Treatment
• Good oral care. Brush your teeth thoroughly at least twice a day and floss
at least once a day.
• Antibiotics or other medicines to treat infection.
• Diet changes and supplements to treat nutrition problems.
• Avoiding irritants (such as hot or spicy foods, alcohol, and tobacco) to ease
discomfort.
Candidiasis
 Description
• Oral thrush occurs when a yeast infection develops on the inside of your
mouth and on your tongue. This condition is also known as oropharyngeal
candidiasis.
• The Candida albicans fungus causes oral thrush.
• Oral thrush most often occurs in infants and toddlers. It causes
white bumps to form on the inner cheeks and tongue.
• Oral thrush is typically a mild infection that rarely causes complications.
 Symptoms of Oral Thrush
• In its initial stages, oral thrush may not cause any symptoms. However, as
time passes and the fungus continues to grow, the following symptoms
may develop:
– creamy white bumps on the tongue, inner cheeks, gums, or tonsils
– slight bleeding when the bumps are scraped
– pain at the site of the bumps
– dry, cracked skin at the corners of the mouth
– difficulty swallowing
 Risk Factors
• have HIV, AIDS, diabetes, or anemia
• have an illness that causes dry mouth
• take antibiotics or corticosteroids
• use chemotherapy, radiation, or drugs to treat cancer
• wear dentures
• smoke cigarettes
• recently had an organ transplant
 Medical treatment for oral thrush
• fluconazole, which is an oral antifungal medication
• a clotrimazole lozenge, which is an antifungal medication that you leave in
your mouth until it dissolves
• nystatin, which is an antifungal mouthwash that you swish around in your
mouth and then swallow
• itraconazole, which is an oral antifungal medication used for people who
are resistant to initial treatments or who have HIV or AIDS
• amphotericin B, which is a drug used to treat severe infections
 Management
• brushing your teeth with a soft toothbrush to avoid scraping the lesions
• replacing your toothbrush every day until the infection goes away
• not using mouthwashes or sprays
• using a saltwater mixture to rinse your mouth
• maintaining appropriate blood sugar levels if you have diabetes
• eating unsweetened yogurt to help restore and maintain healthy levels of
good bacteria
Esophageal atresia
 Description
• Esophageal atresia is a disorder of the digestive system in which the
esophagus does not develop properly.
• Causes :
– Esophageal atresia (EA) is a congenital defect. There are several types.
In most cases, the upper esophagus ends and does not connect with
the lower esophagus and stomach.
– Most infants with EA have another defect called tracheoesophageal
fistula (TEF). This is an abnormal connection between the esophagus
and the windpipe (trachea).
 Symptoms
• Symptoms of EA may include:
• Bluish coloration to the skin (cyanosis) with attempted feeding
• Coughing, gagging, and choking with attempted feeding
• Drooling
• Poor feeding
 Exams and Tests
• Before birth, a mother's ultrasound may show too much amniotic fluid.
This can be a sign of EA or other blockage of the baby's digestive tract.
• The disorder is usually detected shortly after birth when the infant tries to
feed and then coughs, chokes, and turns blue.
• An x-ray is then done and will show any of the following:
– An air-filled pouch in the esophagus.
– Air in the stomach and intestine.
– If a feeding tube has been inserted before the x-ray, it will appear
coiled in the upper esophagus.
 Possible Complications
• The infant may breathe saliva and other fluids into the lungs,
causing aspiration pneumonia, choking, and possibly death.
• Other complications may include:
– Feeding problems
– Reflux (the repeated bringing up of food from the stomach)
after surgery
– Narrowing (stricture) of the esophagus due to scarring from
surgery
Achalasia
 Description
• Achalasia is a primary esophageal motility disorder characterized by the
absence of esophageal peristalsis and impaired relaxation of the lower
esophageal sphincter (LES) in response to swallowing.

Signs and symptoms

• Symptoms of achalasia include the following:
– Dysphagia (most common)
– Regurgitation
– Chest pain
– Heartburn
– Weight loss
 Pathophysiology
• LES pressure and relaxation are regulated by excitatory (eg, acetylcholine,
substance P) and inhibitory (eg, nitric oxide, vasoactive intestinal peptide)
neurotransmitters.
• Persons with achalasia lack nonadrenergic, noncholinergic, inhibitory
ganglion cells, causing an imbalance in excitatory and inhibitory
neurotransmission.
• The result is a hypertensive nonrelaxed esophageal sphincter.
 Epidemiology
• In the USA, The incidence of achalasia is approximately 1 per 100,000
people per year.
• The incidence of esophageal dysmotility appears to increased in patients
with spinal cord injury (SCI).
• In a retrospective study (1990-2013) from the Netherlands, the mean
incidence of achalasia in children was 0.1 per 100,000 people per year .
• The male-to-female ratio of achalasia is 1:1.
• Achalasia typically occurs in adults aged 25-60 years. Less than 5% of cases
occur in children.
Reflux Esophagitis
 Definition
• Reflux esophagitis is an esophageal mucosal injury that occurs secondary
to retrograde flux of gastric contents into the esophagus.
• Clinically, this is referred to as gastroesophageal reflux disease (GERD).
• Typically, the reflux disease involves the distal 8-10 cm of the esophagus
and the gastroesophageal junction. The disease is patchy in distribution.
• The American College of Gastroenterology has defined GERD as “chronic
symptoms or mucosal damage produced by the abnormal reflux of gastric
contents into the esophagus
 Definition
• The morphologic features of reflux esophagitis in the distal esophagus are
variable and nonspecific, and they include
– basal cell hyperplasia,
– elongation of vascular papillae,
– intercellular edema,
– presence of intraepithelial eosinophils,
– intraepithelial lymphocytosis,
– ballooning degeneration of squamous cells and ulceration/erosions.