Segment 3 Diseases
Chiaia
 Pituitary gland tumors-commonly found in chromophobes of pars distalis
 Pituitary dwarfism-deficiency of GH during development, long bones do not
grow
 Pituitary gigantism-overproduction of GH during development (may be due
to GH secreting tumors), prolongs bone growth into adulthood, individuals
have enormous stature
 Acromegaly-overproduction of GH in adulthood (after epiphyseal plate
closes), results in increased bone production and overgrowth in extremities
(i.e. ankles, hand, face)
 Thyroid gland atrophy-loss of plasma TSH (hypophysectomy)
 Hyperthyroidism-increased or overproduction of plasma TSH (pituitary
tumor)
 Thyroidectomy (loss of T3 and T4)-increase in thyrotrophs, increase in TSH
 Thyroid dysfunction
o Hypothyroid-mentally and physically sluggish, low BMR, mental
retardation, decreased glucose absorption in GI tract, weak heart beat
 Cretinism-occurs during development, stunting of physical and
mental development
 Myxedema-occurs in adulthood, characterized by lethargy and
mental deficiency
 Hashimoto’s disease-autoimmune destruction of follicular cells
(thyroglobulin)
o Hyperthyroid-restless, irritable, anxious, elevated BMR, mentally
alert, increased glucose absorption in GI tract, tachycardia
 Goiter-enlargement of thyroid gland due to hypertrophy and hyperplasia of
follicular cells, can occur for a couple reasons:
o Iodine deficiency (leads to decreased T3/T4 output, signals an
increase of TSH production and thus compensatory follicular cell
hypertrophy)
o Graves disease-direct stimulation of follicular cells by IgG, secondary
symptom is exopthalmos-protrusion of eyeballs
 Hypercalcemia-elevated plasma Ca2+ (can occur over time), develop ectopic
calcification of soft tissues and kidney stones
 Hypocalcemia-decreased plasma Ca2+, develop hyperexcitability of neurons,
prolong skeletal muscle contractions (tetany), and aberrant cardiac muscle
contraction and rhythmicity
 Diabetes mellitus-characterized by hyperglycemia, glucosuria, polyuria
o Type 1-early onset, usually associated with reduced beta cell secretion
o Type 2-adult onset, due to defect in insulin receptors (cannot detect
insulin)
 Adrenogenital syndrome-occurs in females, increase in adrenal androgens by
tumor secretion leads to androgenization of genitalia and development of
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male secondary sexual characteristics, in extreme casespseudohermaphroditism
Adrenal cortex dysfunction
o Addison’s disease-hypoadrenalism, idiopathic atrophy of adrenal
cortex, weakness and drowsiness due to low blood glucose, increased
ACTH secretion, decreased BP due to decreased extracellular fluid,
decreased absorption of ions in kidneys
 Fatigue, weakness, low BP, darkening of skin
o Cushing’s disease-hyperadrenalism (adrenal cortical tumors), can be
due to excessive synthetic glucocorticoid use, moon faceredistribution of fat around neck and face, wasting of limb
musculature and thinning of bones, thinning of skin and loss of fat
(shows vessels through skin), hyperglycemia
Glaucoma-blockage of aqueous drainage, results in increased intraocular
pressure, decreases blood flow and causes ischemia of the retina, leads to
blindness
Presbyopia-lens fibers harden with age, lens loses ability to change shape,
results in need of reading glasses or bifocals
Cataracts-lens becomes semi-opaque with age, results in blurred vision
Detached retina-RPE and photoreceptor layers separate following head
trauma, results in slow death of photoreceptors if layers are not reattached
Diabetic retinopathy-one of leading causes of blindness in USA, uncontrolled
plasma glucose in tunics of eye causes vascular edema and altered retinal
and choroidal vasculature, from blood in retina can develop scar tissue which
can induce retinal detachment (and thus vision loss)
Otitis media-auditory tube connects middle ear to nasopharynx, is a common
route for infection within middle ear
Disorders of the ear
o Neural dysfunction-loss of hearing due to destruction of hair cells or
8th nerve fibers, fixation or calcification of ossicle, rupture or puncture
of tympanic membrane, or tumors of 8th nerve or its ganglion
 Hair cells are sensitive to antibiotics, diuretics, and salicylates,
as well as chronic exposure to loud sounds can result in
excitotoxicity of hair cells and nerve fibers
o Vestibular dysfunction-due to drug toxicity, overproduction of
blockage of endolymph circulation, or tumors of 8th nerve or ganglion
 Menier’s disease-intense debilitating vertigo, nausea, vomiting,
abnormal sound perception, sometimes temporary deafness
Benign Paroxysmal Positional Vertigo (BPPV)
o Common cause of dizziness, symptoms include dizziness, vertigo,
nystagmus (involuntary eye movements), imbalance, nausea, and
difficulty concentrating
o Can be caused by otoliths detaching from otolithic membrane and
collecting in semicircular canals
o 2 types-canalithiasis (affect one of the canals), cupulothiasis (affect
cupula)
Baptista
 IJV catheterization-use SCM, jugular notch, and EJV to find IJV, prefer right
side because IJV is larger and straighter, used to obtain measurements of
central venous pressure, administer meds, and provides venous access when
peripheral access is not available
 Troisier sign-sufficiently enlarged and palpable nodes, presumptive evidence
of malignant disease (can even provide evidence for gut)
 Subclavian catheterization-need puncture skin inferior to clavicle, need to
make sure do not puncture too far as may cause a pneumothorax or enter
subclavian artery
 Thyroidectomy-can damage recurrent laryngeal nerve during ligation of
inferior thyroid artery
o Parathyroid glands are also in danger-fall in blood calcium can lead to
tetany (generalized spasms)
CBC
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Epidural hematoma-increase in blood that causes dura to push away from
skull, patient does not with symptoms, can be due to lateral blow to skull,
confirm with CT
o Fix by making a hole to let blood out
Danger area of scallop-loose areolar CT of scalp-infections can flow anterior
to posterior easily, nothing is stopping them
Danger area of face-triangle lateral to nose, any local edema or inflammation
reaction can enter vein and spread to orbit area, lead to cavernous sinus
thrombosis, ultimately can affect CN III, IV, V1, and V2 (and ICA) as all run
through cavernous sinus
Bell’s palsy-transection of facial nerve, lose function in muscles of facial
expression, most associated with middle ear infection
Mumps-inflammation of parotid gland
Enlargement of pharyngeal tonsils-can block nasopharynx, patient becomes
mouth breather
Tubes in children’s’ ears-make a hole in tympanic membrane and insert a
tube to help drain middle ear of mucus (need to be careful though as to
ensure water is not entering ear while showering, etc.)
Tonsillectomy-removal of palatine tonsils, highly vascularized area (by facial
artery branches) so need to be careful post procedure
Piriform recess-food (i.e. nuts) can get stuck here, can develop into an
abscess
Anomalies of pharyngeal pouches or grooves
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o Branchial sinuses-blind pouch, internally-occurs at site of pharyngeal
pouch (usually 2nd), externally-occurs at site of pharyngeal groove
(usually 2nd)
o Branchial cysts-persistent cervical sinus/cyst
o Branchial fistulas-open canal to cervical cyst, internal-connection to
pharynx at 2nd pouch, external-open onto skin along anterior border
of SCM
Thyroglossal duct cysts-cysts that form anywhere along course of former
thyroglossal duct (in tongue, anterior neck, or anterior to laryngeal
cartilages)
Cleft lip-more common in boys than girls
o Unilateral-failure of fusion of maxillary and intermaxilary (medial
nasal process) segments to fuse
o Bilateral-failure of fusion on both sides
Cleft palate-more common in girls than boys
o Anterior (primary)-failure of primary palate to meet with secondary
palate
o Posterior (secondary)-failure of lateral palatine processes to fuse
together and with nasal septum
o Complete-most severe cleft, combination of anterior and posterior
Sinus headaches-increase pressure within sinus because sinuses are
inflammed and there is something preventing the exit of mucus,
decongestant meds stop mucus flow and vasoconstrict membrane, unblock
ducts and lets mucus drain
Chronic sinusitis can affect maxillary teeth (and vice versa-abscess from
maxillary tooth can enter maxillary sinus and cause infection)
o Can treat chronic sinusitis by poking another hole within the sinus
which allows for a different place for fluid to drain
Laukka
 Sinusitis-infection in sinus can reach orbit via small neural foramina
 Pure blow out fracture-fracture to floor of orbit
o 2 areas of weaknesses-orbital plate of ethmoid bone which overlies
ethmoid sinuses and orbital floor lining over maxillary sinuses
o Sudden blow to eye – pushes intact globe back into orbit, results in
momentary increase of intraorbital pressure which fractures the thin
portions of orbital floor, may also result in fracture of medial wall into
ethmoid air sinuses, results in herniation of periorbital contents
o Clinical signs and symptoms
 Enophthalmos-recession of eyeball within orbit
 Diplopia-double vision (especially on upward gaze), due to
inferior rectus entrapment
 Hypesthesia-reduced sense of touch or sensation due to injury
of infraorbital nerve (may also have numbness of gingival and
skin of midface)
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Orbital Fat
o In starvation-lose fat, eyeballs sink in
o In hyperthyroid disease-fat increases, eyeballs protrude
Cellulitis
o Periorbital-inflammation and infection of eyelid and portion of skin
around eye, found anterior to orbital septum
o Orbital-inflammation posterior to orbital septum, due to spread of
infection from adjacent sinuses or via blood
o Signs and symptoms-pain moving eye, sudden loss of vision, bulging
of the infected eye, limited movement, redness and swelling of eyelid,
accompanied by pain, discharge, and inability to open eye
Ptosis
o Acquired (upper lid)-“drooping” eyelid, paralysis or paresis of
muscles that elevate the upper eyelid (muscles involved are levator
palpebrae superioris, superior tarsal muscle)
o Congenital ptosis-poor development of levator palpebrae superioris
(have relaxed upper lid)
Conjunctivitis (Pink Eye)
o Eye looks pink or red, may have discharge, symptoms includeburning, itching, irritation, discharge, and crusting of eyelashes
o May not always be caused by an infection (can be viral, foreign body,
allergies, etc)
Bell’s Palsy-paralysis of CN VII, lose ability to blink and unable to move
lacrimal fluid across eye
Papilledema-edema around optic nerve canal, compresses on nerve and vein,
can be due to anything abnormal that increases CSF pressure (i.e.
hydrocephalous, increase in ventricle CSF, tumor)
Optic nerve glioma-tumors arise in children (particularly those with
neurofibromatosis), often low grade in children but aggressive in adults
o Clinical presentation-decreased vision, mass effect will occur
(displace tissue), increased intracranial pressure, hydrocephalus from
distortion of midbrain
Optic neuritis-inflammation, infection or demyelination of optic nerve,
present with partial or complete vision loss, tenderness and discomfort usual
accompanies eye movement (defining characteristic of patients with MS)
Oculomotor nerve palsy-weakness in superior rectus, inferior rectus, medial
rectus, inferior oblique, levator palpebrae, and sphincter pupillae, eye is
downward and out, ptosis (eyelid droops and unable to be raised
voluntarily), pupil is dilated and no-reactive
Trochlear nerve palsy-weakness affecting superior oblique muscle, produces
extortion (outward rotation of affected eye), vertical diplopia and weakness
in downward gaze
o Chief complaint-visual difficult when going down stairs (compensate
by tilting head)
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Sixth nerve palsy-ipsilateral lateral rectus paresis and ipsilateral gaze palsy
to same side, inability to abduct results in convergent strabismus (one or
both eyes turned inward)
o Chief complaint-diplopia (double vision), not always experienced in
children but if it does, can lead to poor visual development
Horner syndrome-aka oculosympathetic palsy, interruption of sympathetic
innervation to head and neck
o Clinical presentation-miosis (paralysis of dilator pupillae, pupil is
constricted), partial ptosis (drooping eyelid, paralysis of both tarsal
muscles, narrowed palpebral fissure), facial anhidrosis, lack of
sympathetic innervation to sweat glands, flushing (facial vasodilation,
due to lack of sympathetic vasoconstrictive innervation)
Corneal reflex-stimulate cornea by touching with cotton wisp, observe blink
response to stimulation, checks ophthalmic nerve (V1 branch, sensory) and
facial nerve (motor)
Papillary light reflex-stimulate pupil with ophthalmoscope and observe
papillary constriction, checks optic nerve (sensory) and oculomotor nerve
(motor)