ANESTHESIOLOGY & PERIOPERATIVE MEDICINE

ANNIE R. YU-SOLIVEN, MD, DPBA, FPSA

Brief History of Anesthesia  August Bier gave first deliberate spinal

 Nitrous oxide (N2O) anesthetic
• Humphrey Davy suggested use in 1800  Twentieth Century
• 1845 - Horace Wells’ public • 1900s - Intravenous anesthesia
demonstration for a dental procedure at • 1934 - Barbital, hexobarbital and
Harvard Medical School failed because it thiopental facilitated rapid more
has analgesic but no anesthetic pleasant induction of anesthesia
properties; Wells holds a place in history • John Lundy proposed thiopentone for
being the first person to recognize and induction followed by inhaled agents for
use N2O maintenance; authored first textbook on
 Diethyl ether modern anesthesia and helped found
 1842 – Crawford Long used diethyl American Board of Anesthesiology
ether to induce anesthesia • 1923 - Cyclopropane – rapid acting ,
 William Morton preferred ether more pleasant smelling; but flammability and
than N2O for dental patients because cardiac irritability limited its use
ether supports respiration and the • 1953, 1956 – Halothane – stable,
cardiovascular system at analgesic potent, volatile, not flammable most
levels, and potent enough to administer widely used fluorinated anesthetic.
in room air without hypoxia • 1972 – Enflurane
 1846 – Morton’s first public • 1981 - Isoflurane
demonstration of ether in Massachusetts • 1990s - Desflurane and Sevoflurane –
General Hospital (called Ether Dome, a low solubility, rapid onset/recovery,
registered national landmark particularly well-suited to outpatient
commemorating first public surgery.
demonstration of ether as anesthetic); • 1895 - Harvey Cushing began first
the successful surgery led to the advent anesthesia records (ether charts)
of surgical anesthesia recorded vital signs, pupillary diameter,
 First Anesthesiologists amounts of ether and drugs
 John Snow - clinical properties and administered; portable
pharmacology of ether, chloroform, and sphygmomanometer of Riva-Rocci to
other agents; improved ether measure BP and precordial stethoscope
administration and mastered clinical to monitor breath and heart sounds.
techniques of anesthesia • Endotracheal intubation pioneered by Sir
 James Simpson popularized chloroform Ivan Magill and Arthur Guedel invented
in England for labor and relieving pain cuffed endotracheal tube that merged
during childbirth which brought with invention of mechanical ventilation
anesthesia to public awareness for use of muscle relaxants.
 Cocaine: first local anesthetic • Curare - a non-depolarizing muscle
 Ancient Incas chewed coca leaves relaxant popularized by Harold Griffith
dripping saliva into the wound allegedly revolutionized practice of anesthesia as
facilitating trephination of skull. relaxation of abdominal muscles could
 Active alkaloid synthesized in 1860 be controlled to facilitate surgery.
named cocaine by Albert Niemann; • Succinylcholine - a depolarizing muscle
benumbs the nerves of the tongue, relaxant introduced in 1949.
depriving sensation.
 Sigmund Freud studied properties and General Anesthesia - Triad of three major and
wrote famous monograph “Uber Coca” separate effects: unconsciousness (and amnesia),
in 1884; also attempted use to treat analgesia, and muscle relaxation.
morphine addiction.
 Freud and Karl Koller experimented with Intravenous Agents:
effects on muscle strength; noted Unconsciousness and Amnesia
numbness of tongue when swallowed.  Barbiturates: thiopental, thiamylal,
 Koller first instilled cocaine into his methohexital
cornea and reported its use as local  Act at – aminobutyric acid (GABA)
anesthetic. receptor to inhibit synaptic transmission
 William Halstead and Richard Hall  Produce rapid, smooth induction within
injected cocaine intradermally and first 60 secs; wear off about 5 mins
used it for regional blocks.  Cause hypotension, myocardial
 Halsted et al. became addicted to depression at higher doses and patients
cocaine; toxicity led for search of local with intravascular depletion
anesthetics (procaine synthesized in  Act as anticonvulsants for
1905 and lidocaine in 1943) neuroprotection by reducing cerebral
 Leonard Corning published first textbook metabolism
on local anesthesia; intradurally injected  Propofol – alkylated phenol
cocaine into a patient, termed spinal  Inhibits synaptic transmission through
anesthesia. GABA
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 ANESTHESIOLOGY & PERIOPERATIVE MEDICINE
ANNIE R. YU-SOLIVEN, MD, DPBA, FPSA

 Short duration, rapid recovery, low • Naloxone and longer acting naltrexone –
incidence of nausea/vomiting ideal for pure opioid antagonists used to reverse
ambulatory/minor surgery side effects of opioid overdose
 Bronchodilator properties advantageous (respiratory depression) but analgesic
for asthmatics and smokers effects of the opioid will also be
 Caution in hypovolemia and/or CAD due reversed.
to hypotension  Nonopioid analgesics
 For sedation in the ICU setting Acetaminophen (paracetamol) – analgesic
 Irritating causing pain on injection and antipyretic of moderate potency; site of
action is CNS, as part of postoperative
 Benzodiazepines – diazepam, lorazepam, analgesia reduces amount of opioids
midazolam required
 Reduce anxiety and produce amnesia • Weak inhibitor of the synthesis of
 Peripheral vasodilatation and hypotension prostaglandins
but minimal effects on respiration when • Mechanism of action includes peripheral
used alone (COX inhibition), and central (COX,
 Synergistic reaction with opioids cause serotonergic descending neuronal
respiratory depression pathway, L-arginine/NO pathway,
 Only rarely cause allergic reactions cannabinoid system)
 Etomidate – imidazole derivative • A component of a multimodal analgesic
 Acts on GABA receptor regime; works in synergy combined with
 Rapid almost complete hydrolysis to inactive a number of other agents and generally
metabolite results in rapid awakening considered to have useful opioid-sparing
 Painful on injection effects (reduction in opioid
 Little or no effect on cardiac output and HR; consumption)
less reduction in BP  Non-steroidal anti-inflammatory medicines
 More nausea and vomiting than thiopental (NSAIDs, COXIBs)
or Propofol • NSAIDs (ketorolac, aspirin, and
 Ketamine –acts on N-methyl-D-aspartate indomethacin, ibuprofen, diclofenac,
receptor etc.) inhibit both COX-1 and COX-2
 Produces analgesia and amnesia which cause major side effects of gastric
 Dissociative anesthetic with cataleptic gaze bleeding, platelet dysfunction and
and nystagmus hepatic and renal damage
 May have delirium and hallucinations while • COX-2 selective inhibitors (parecoxib,
regaining consciousness celecoxib, etoricoxib) produce analgesia
 Increase HR and BP that may cause and reduces inflammation without GIT
myocardial ischemia in patients with CAD bleeding or platelet dysfunction
 Useful in acutely hypovolemic patients to
maintain BP via sympathetic stimulation but Neuromuscular Blocking Agents
direct myocardial depressant when  No amnestic, hypnotic, or analgesic
catecholamines are depleted properties; patients must be properly
 Bronchodilator effects useful for asthmatic anesthetized before and in addition to the
patients administration of these agents
 Rarely associated with allergic reactions.  Depth of blockade best monitored with a
 Significant sedation and amnesia; peripheral nerve stimulator to ensure
 Supports respiration; can be combined with immobility intra-operatively and confirm
opioids; dysphoric effects must be masked lack of residual paralysis post-operatively
with simultaneous use of sedatives  No effect on either nerves or muscles but
(benzodiazepines) act primarily on the neuromuscular
 Dexmedetomidine – α-2 adrenergic agonist junction.
with sedative and analgesic properties; dose
spares opioids  Depolarizing NMB
• Succinylcholine binds on acetylcholine
Analgesia (Ach) receptors on the post-junctional
 Opioid analgesics membrane in the neuromuscular
Morphine, codeine, oxymorphone, junction causing depolarization of
meperidine, fentanyl and analogues muscle fibers
• Act centrally on - receptors in the brain  Rapid onset <60 secs, rapid
and spinal cord effect 5-8 mins ideal for
• Main side effects: euphoria, sedation, management of airway but total
constipation and respiratory depression body muscle fasciculation can
• Differing potencies with equianalgesic cause post-operative aches and
doses result in equal degrees of pains; elevation in serum K and
respiratory depression thus no increase in intraocular and intra-
completely safe opioid analgesic gastric pressures

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 ANESTHESIOLOGY & PERIOPERATIVE MEDICINE
ANNIE R. YU-SOLIVEN, MD, DPBA, FPSA

 Use in burns or traumatic tissue  their closed state preventing action

injuries may result in elevated potentials
serum K to produce arrhythmias  Toxicity results from absorption into the
and cardiac arrest bloodstream or inadvertent direct
 Effects cannot be reversed but intravascular injection; manifests first in
rapidly hydrolyzed by plasma the more sensitive CNS and then the
cholinesterase cardiovascular system.
(pseudocholinesterase)  CNS toxicity – restlessness, tinnitus,
 Succinylcholine is the only IV slurred speech, seizures and
triggering agent of malignant unconsciousness; administer
hyperthermia benzodiazepine or thiopental
 CVS toxicity – hypotension,
 Non-depolarizing NMBs increased P-R intervals, bradycardia
 All non-depolarizers reversibly bind to and cardiac arrest
the postsynaptic terminal in the  Bupivacaine more cardiotoxic compared to
neuromuscular junction and prevent others; direct effect on ventricular muscle;
acetylcholine from depolarizing the more lipid soluble than lidocaine; binds
muscle; muscle blockade occurs tightly to Na+ channels (fast-in, slow-out
without fasciculation local anesthetic); inadvertent intravascular
 Longest-acting – Pancuronium, injection cause profound hypotension,
excreted almost completely ventricular tachycardia and fibrillation and
unchanged by the kidney complete A-V heart block extremely
 Intermediate acting – refractory to treatment
vecuronium and rocuronium  Toxic dose of lidocaine is approximately
metabolized by kidneys and 5mg/kg; bupivacaine approximately 3
liver; atracurium and cis- mg/kg.
atracurium undergo breakdown  Epinephrine reduces local bleeding,
in plasma (Hofmann molecules of the local anesthetic remain in
elimination) proximity to the nerve for a longer time;
 Shortest duration – mivacurium onset of block is faster; quality of block
– the only non-depolarizer improved; duration of block longer and less
metabolized by plasma local anesthetic absorbed into the
cholinesterase bloodstream reducing toxicity.
 Reversal of neuromuscular blockade  Although epinephrine 1:200,000
is reversal of the effect using (5g/ml) added to a local anesthetic
neostigmine, edrophonium or for infiltration will greatly lengthen
pyridostigmine. time of analgesia, epinephrine-
containing solutions should not be
Inhalational Agents injected into body parts with end-
 Minimum alveolar concentration (MAC) – arteries (toes or fingers) to avoid
measure of anesthetic potency; dose ischemia or loss of a digit.
required to block a response to a painful • NaHCO3 added will raise the pH favoring
stimulus in 50% of subjects; the higher the non-ionized uncharged form of the
MAC, the less potent as agent is. molecule; speeds onset of block especially in
 The potency and speed of induction of local anesthetics mixed with epinephrine.
inhaled agents correlate with their lipid
solubility (Meyer-Overton rule).  Amides
 N2O has a low solubility and is a weak • Lidocaine, bupivacaine, mepivacaine,
anesthetic agent but has the most rapid prilocaine, and ropivacaine
onset and offset. • 95% metabolized in the liver, 5%
 The potent gases (desflurane, sevoflurane, excreted unchanged by kidneys
enflurane and halothane) are more soluble • Amide linkage between a benzene
in blood than N2O and can be given in ring and a hydrocarbon chain
lower concentrations but have longer attached to a tertiary amine
induction and emergence characteristics. • Benzene ring confers lipid solubility
 Sevoflurane and desflurane have relatively for penetration of nerve membranes
lower tissue and blood solubility; induction • Tertiary amine attached to the
and recovery are more rapid than with hydrocarbon chain making the
isoflurane or enflurane. anesthetics water soluble.
 All potent inhalational agents as well as the • Lidocaine has more rapid onset and
depolarizing agent succinylcholine trigger shorter acting than bupivacaine
malignant hyperthermia. • Ropivacaine – most recently
introduced; clinically similar to
Local Anesthetics bupivacaine with slow onset and
 Reversibly block transmission of neural long duration but less cardiotoxic.
impulses by stabilizing sodium channels in
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 ANESTHESIOLOGY & PERIOPERATIVE MEDICINE
ANNIE R. YU-SOLIVEN, MD, DPBA, FPSA

• EMLA - Eutectic Mixture of Local • Epidural needles are larger in diameter

Anesthetic for venipuncture, lumbar than spinal needles (17 or 18 gauge) and
puncture, arterial cannulation accidental dural puncture more often
results in severe headache.
 Esters
• Cocaine, procaine, chloroprocaine, Anesthesia Management
tetracaine and benzocaine Preoperative Evaluation and Preparation
 Hydrolyzed in the blood by • Detailed medical history includes previous
pseudocholinesterase; some anesthesia and family history of problems
metabolites (PABA) have greater with anesthesia; history of atopy
allergic potential • Current drug therapy; -blocker, anti-
 Ester linkage between a benzene ring hypertensive and antiasthma medications
and a hydrocarbon chain attached to should be continued even in the morning
a tertiary amine. of surgery
 Cocaine was first used clinically, • Complete physical examination targeted
produces vasoconstriction, and primarily CNS, CVS, and respiratory
releases norepinephrine from nerve system
terminals resulting in hypertension • Laboratory and diagnostic tests
and highly addictive.
Risk Assessment
Regional Anesthesia: Peripheral vs. Central  American Society of Anesthesiologists
 Peripheral Nerve Blocks – local Physical Status Classification System
anesthetic injected peripherally near a large PS 1 A normal healthy patient
nerve or plexus to provide anesthesia to a PS 2 A patient with mild systemic disease
larger region of the body; ex. brachial PS 3 A patient with severe systemic disease
plexus, ankle, intercostal, cervical plexus, PS 4 A patient with severe systemic disease
etc. that is a constant threat to life
 Central Nerve Blocks: local anesthetic PS 5 A moribund patient who is not
injected centrally near the spinal cord; expected to survive without the operation
bathes spinal nerves as they exit the dura, PS 6 A declared brain-dead patient whose
producing sensory, motor and sympathetic organs are being removed for donor
blockade. purposes
 Spinal anesthesia
• Mechanism: Local anesthetic injected Evaluation of the Airway
directly into dural sac surrounding the  Identifies patients in whom management of
spinal cord; level of injection below L1 - the airway and conventional endotracheal
L2; direct injection into the CSF intubation may be difficult
surrounding the spinal cord requires only  Mallampati Classification –
a small dose, onset rapid and blockade Class 1: soft palate, fauces, uvula, pillars
thorough; block wears off naturally via Class 2: soft palate, fauces, and portion of
drug uptake by CSF, bloodstream or uvula
diffusion into fat. Class 3: soft palate, base of uvula
• Complications – hypotension, high spinal Class 4: hard palate only
block and postdural puncture headache;  Other predictors of difficult intubation –
Cauda equina syndrome is injury to the obesity, immobility of neck, interincisor
nerves emanating distal to the spinal cord distance <4 cm in an adult, large overbite,
resulting in bowel and bladder inability to shift lower incisors in front of
dysfunctions and lower extremity sensory upper incisors; thyromental distance <6.5
and motor loss. cm
 Epidural Anesthesia (extradural)
• Mechanism: Local anesthetic injected into Intraoperative Management
the epidural space surrounding the dural Induction of Anesthesia
sac of the spinal cord; much greater  Most critical component of anesthesia as
volumes of anesthetic required and onset majority of catastrophic anesthetic
of block is longer (10-15 mins). complications occur
• Complications similar to spinal anesthesia;  IV induction is smooth and addition of
inadvertent injection into a dural tear will opioids will blunt response to laryngoscopy
result into high block (unconsciousness, and intubation
severe hypotension and respiratory  With full stomach, goal of rapid sequence
paralysis) induction is to achieve secure protection of
• Indwelling catheters are placed through the airway with a cuffed endotracheal tube
introducers into the epidural space  Proceed only after airway evaluation
allowing intermittent or continuous predicts uncomplicated intubation
technique as opposed to single-shot of  Preoxygenate the patient
spinal anesthesia.  Rapidly introduce IV induction agent

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 ANESTHESIOLOGY & PERIOPERATIVE MEDICINE
ANNIE R. YU-SOLIVEN, MD, DPBA, FPSA

 Assistant presses firmly down on the cricoid Pain

cartilage to block any gastric contents from  Definition: an unpleasant experience An
being regurgitated unpleasant sensory and emotional
 Muscle relaxant injected experience associated with actual or
 Quick intubation of trachea potential tissue damage, or described in
 Inflate tube and confirm position terms of such damage.
 Mechanisms: Nociceptive, Neuropathic
Recovery from Anesthesia • Nociceptive - (physiological) -
• Reversal of neuromuscular blockade inflammatory pain due to chemical,
(anticholinesterases: neostigmine, mechanical and thermal stimuli at
pyridostigmine, and edrophonium) to the nociceptor
resume neuromuscular transmission • Neuropathic - (pathological) initiated
• Postanesthesia Care Unit Concerns or caused by a primary lesion or
 Postop nausea/vomiting dysfunction in the nervous system);
 Airway support acutely occurs after trauma and
 Hypotension surgery
 Abnormal bleeding
 Hypertension  Phases of Nociception
 Dysrhythmia • Transduction - translation of noxious
 Myocardial infarction stimuli into electrical energy
 Altered mental status • Transmission - propagation of impulse
 Pain as fifth vital sign (Multimodal from nociceptors through the CNS
Analgesia) • Modulation - alteration of nociceptive
 Malignant Hyperthermia information to attenuate/amplify the
• Hereditary, life-threatening, signal.
hypermetabolic, acute disorder • Perception - sensory discrimination
during or after general anesthesia /localization of nociceptive information in
(1:12,000 in children and 1:40,000 the thalamus/cortex resulting into the
in adults) emotional & physical pain experience.
• Genetic predisposition
pharmacologically triggered by  Pain Pathway
volatile anesthetics and • Periphery
succinylcholine that cause a rise in  Tissue injury releases
the myoplasmic calcium resulting in chemicals “inflammatory
persistent muscle contractions soup”
• An autosomal dominant disorder  Signal travels along Aδ and C
associated with the ryanodine through DRG to dorsal SC
receptor gene RYRI • Spinal Cord
• Diagnosed with caffeine-contracture  “1st relay station”
halothane test (muscle biopsy)  2nd-order neurons
• Classic MH crisis: tachycardia, cross/decussate
elevation of end-tidal CO2 in the • Brain
face of constant minute ventilation;  Thalamus “2nd relay station”
acidosis and muscle rigidity, connects to other parts
rhabdomyolysis, arrhythmias, • Modulation
hyperkalemia, and sudden cardiac  Pain signals can be altered in
arrest; rise in temperature often a the SC or Brain
late sign  Descending pathway from BS
• Treatment: to SC – inhibits pain signals
1. Call for help
2. Stop all inhalational anesthetics
and give 100% O2
3. Hyperventilate 3x calculated
volume
4. HCO3 to treat acidosis if
dantrolene is ineffective
5. Treat hyperkalemia (insulin,
glucose, calcium)
6. Avoid calcium channel blockers
7. Begin dantrolene sodium infusion
2.5 mg/kg IV; repeat at 1 mg/kg
every 6-8 hrs
8. Monitor in an ICU

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 ANESTHESIOLOGY & PERIOPERATIVE MEDICINE
ANNIE R. YU-SOLIVEN, MD, DPBA, FPSA

Choose the best answer: ______9. Correct statement regarding morphine:

A. It is a weak acid.
______1. How many minutes after IV injection does B. B. Approximately 95% is protein-
the brain concentration of thiopental peak? bound in the plasma.
A. 1 C. It is more water soluble than many of
B. 5 the other commonly used opioids.
C. 10 D. It does not cross the placental barrier.
D. 15
______10. Which of the following opioids is NOT an
______2. A sedative-hypnotic of short duration and agonist-antagonist?
rapid recovery used as Total Intravenous Anesthetic: A. Butorphanol
A. Ketamine B. Nalbuphine
B. Propofol C. Pentazocine
C. Barbiturate D. Meperidine
D. Etomidate
______11. Which of the following statements
______3. All of the following decrease CBF, CMRO2 concerning fentanyl is TRUE?
and ICP, EXCEPT: A. Approximately 20% protein bound at
A. Thiopental physiological pH
B. Ketamine B. Analgesic potency approximately 10
C. Propofol times that of morphine
D. Midazolam C. Highly lipid soluble
D. Causes significant histamine release
______4. All of the following tend to cause pain
upon injection, EXCEPT: ______12. Which statement is true of
A. Etomidate succinylcholine?
B. Propofol A. Prolonged onset and duration of action
C. Ketamine B. Side effects include tachycardia,
D. Diazepam hypokalemia and decreased IOP
C. Relatively contraindicated in children
______5. Amnesia for uncomfortable procedures D. Reversed by anticholinesterases
such as awake intubation, insertion of central
venous catheters, long operations under regional ______13. Which of the following statements
anesthesia, or when a patient asks not to recall concerning side effects after succinylcholine
events (anterograde amnesia) is best reliably administration is TRUE?
produced by: A. Succinylcholine typically decreases ICP.
A. Diazepam B. Serum K increases by 1.5 to 2.5 mEq
B. Meperidine /l after injection in normal patients.
C. Nalbuphine C. IOP increases 5-10mmHg for <30 sec
D. Midazolam D. Succinylcholine-induced bradycardia is
more likely upon repeat dosing.
______6. A dissociative anesthetic producing
profound analgesia and beneficial in patients with ______14. Which is a feature of nondepolarizing
hypovolemia and reactive airways? muscle relaxants?
A. Midazolam A. Molecularly resemble acetylcholine
B. Etomidate B. Enter synaptic cleft and attach to
C. Ketamine receptor to cause depolarization of NMJ
D. Dexmedetomidine C. Bind receptor but do not depolarize
motor endplate instead interfere with
______7. Which of the following does not affect neuromuscular transmission
GABAnergic transmission? D. Acute onset due to redistribution and
A. Thiopental metabolism by plasma
B. Ketamine pseudocholinesterase
C. Midazolam
D. Propofol ______15. Which is a feature of nondepolarizing
muscle relaxants?
A. Molecularly resemble acetylcholine
______8. Which of the following opioid receptors is B. Enter synaptic cleft and attach to
most likely responsible for spinal analgesia? receptor to cause depolarization of NMJ
A. Mu1 C. Bind receptor but do not depolarize
B. Kappa motor endplate instead interfere with
C. Mu2 neuromuscular transmission
D. Sigma D. Acute onset due to redistribution and
metabolism by plasma
pseudocholinesterase

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 ANESTHESIOLOGY & PERIOPERATIVE MEDICINE
ANNIE R. YU-SOLIVEN, MD, DPBA, FPSA
______16. The pKa of most local anesthetics is
between:
A. 3.0 and 4.5
B. 4.5 and 6.0
C. 6.0 and 7.5
D. 7.5 and 9.0

______17. The most likely common mechanism of

action of local anesthetics is:
A. Alteration of resting membrane
potential
B. Inhibition of sodium influx
C. Prevention of potassium efflux
D. Prevention of potassium influx

______18. Which statement is FALSE?

A. Seizures may be preceded by tinnitus
and numbness of the tongue.
B. The CVS is more sensitive than the
CNS.
C. Hypotension is due to negative
inotropy and vasodilation.
D. Seizures require immediate treatment
with thiopental.

______19. Which of the following has the fastest

rate of systemic absorption?
A. Caudal
B. Epidural
C. Intercostal block
D. Axillary block

______20. Structures traversed by a properly placed

needle in the subarachnoid space via the midline
approach include all the following EXCEPT:
A. Supraspinous ligament
B. Ligamentum flavum
C. Posterior longitudinal ligament
D. Dura mater

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 OTORHINOLARYNGOLOGY
JOEL ROMUALDEZ, MD

OTORHINOLARYNGOLOGY Symptoms / Signs

 Often indistinguishable from bacterial
Ear  OE
- Consists of the auricle and EAM  Pruritus deep within the ear
- Skin-line apparatus  Dull pain
- Approximately 2.5 cm in length  Hearing loss (obstructive)
- Ends at tympanic membrane  Tinnitus
- Auricle - is mostly skin-lined cartilage  Canal erythema
 Mild edema
A. External auditory meatus  White, gray or black fungal debris
- Cartilage: ~40%
- Bony: ~60% Otomycosis: Treatment
- S-shaped  Thorough cleaning and drying of canal
- Narrowest portion at bony-cartilage junction  Topical antifungals
- Squamous epthelium
- Bony skin – 0.2mm Complications of Otitis Media
- Cartilage skin
- 0.5 to 1.0 mm  Extracranial
- Apopilosebaceous unit o Mastoiditis, subperiosteal abscess
o Petrositis
B. Acute Otitis Externa (AOE) o Labyrinthitis
- “swimmer’s ear” o Facial nerve palsy
- Pre-inflammatory stage
- Acute inflammatory stage  Intracranial
- Mild o Meningitis
- Moderate o Epidural abscess
- Severe o Lateral sinus thrombosis
o Brain abscess
 Most common pathogens: P. aeruginosa and o Subdural abscess
S. aureus o Focal otitis encephalitis
o Otitic hydrocephalus
 Four principles
o Frequent canal cleaning  Treatment:
o Topical antibiotics - Amoxicillin 40-80 mg/kg/day 10-14 days
o Pain control 24-48 hr.
o Instruction for prevention - Supportive treatment

Furunculosis OTITIS MEDIA WITH EFFUSION

- Acute localized infection
- Lateral 1/3 of posterosuperior canal - Characterized by a non-purulent effusion of
- Obsructed apo-pilosebaceous unit the middle ear that may be either mucoid or
- Pathogen: S. aureus serous.
- Furunculosis: Symptoms / Signs
- Localized pain - Typically, do not involve pain or fever can
- Pruritus occur during the resolution of AOM once the
- Hearing loss (if lesion occludes canal) acute inflammation has resolved
- Edema
- Erythema Etiology
- Tenderness  Eustachain tube obstruction
- Occasional fluctuance o -URI / sinusitis
o -Adenoid hypertrophy
Treatment o -CA nasopharynx
 Local heat  AOM
 Analgesics  Otitis barotrauma
 Oral anti-staphylococcal antibiotics  Allergy
 Incision and drainage reserved for
localized abscess Treatment:
 IV antibiotics for soft tissue extension  NON-Pharmacologic
o Life style modification
Otomycosis o Avoiding secondhand smoke
o Breastfeeding whenever possible
- Fungal infection of EAC skin o Avoiding feeding, either by breast or
- Primary or secondary bottle, while completely supine
- Most common organisma: Aspergillus and o Avoiding exposure to a large
Candida number of children, particularly in
daycare centers
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 OTORHINOLARYNGOLOGY
JOEL ROMUALDEZ, MD

o Avoiding exposure to children who  The middle ear mucosa visualized

are known to be affected through the perforation may be
o Avoiding known allergens edematous or even polypoid, pale,
or erythematous.
 Pharmacologic
o Antibiotic Pure tone audiometry in chronic otitis
 Amoxycillin media
 Trimethoprim-  Chronic otitis media result in a
sulfamethoxazole mixed conduction and sensorineural
 Cephalosporin deafness which indicate more
 Steroid (nasal spray) extensive disease
 Decongestant
 Valsava maneuver Complication
 Myringotomy  Safe ear
o Tympanosclesis
Surgical o Cholesterol granuloma
 Indication for doing tympanostomy
tube insertion –  Unsafe ear
o Failed medical treatment for o Extracranial: labyrinthitis,
3 months pertrous
o Permanent medical o Sinusitis
obstruction of Eustachian
tube  Intracranial: meningitis, epidural
abscess, lateral sinus
Pathogen thrombophlebitis, brain abscess,
 Bacteria otitic hydrocephalus
 Streptococcus pneumoniae
 Haemophilus influenzae Medical Treatment
 Moraxella catarrhalis  A solution of 50% peroxide and
 Steptococcus, Gr A 50% sterile water is generally
 Staphylococcus aureus painless and effective. Thirty to 40
 Miscellaneous mL of this solution can be irrigated
 Nonpathogens culture through the external auditory canal.

Chronic Suppurative otitis media Surgical treatment

 Perforation  Tympanoplasty
 Recurrent infection  Mastoidectomy
 Common organism  Radical mastoidectomy
 -P aeruginosa (48-98%)
 -S aureus (15-30%) Chronic Otitis Media
 -Klebsiella (10-21%) 1. Inadequate treatment of acute otitis
media
History 2. Chronic dysfunction of eustachain tube
 Present with a draining ear of some 3. Persistent perforation of ear drum
duration and a premorbid history of 4. Irreversible change in middle ear
recurrent AOM 5. Persistent osteomyelitis in mastoid
 Typically, they deny pain or discomfort 6. Factors: nasal allergy, malnutrition,
 Hearing loss in the affected ear. anemia
 Reports of fever, vertigo, and pain 7. Persistent disease in nose, sinuses,
should raise concern about nasopharynx
intratemporal or intracranial
complications. Acoustic neuroma
 A history of persistent CSOM after  Most common inner ear tumor
appropriate medical treament should causing hearing loss.
alert the physiscian to consider  Acoustic neuromas, also known as
cholesteatoma. vestibular schwannomas, are non-
malignant tumors of the 8th cranial
Physical: nerve
 The external auditory canal may or  Acoustic neuromas are a rare cause
may not be edematous and is of unilateral hearing loss, dizziness,
typically not tender. as well as rarely other symptoms
 The discharge varies from fetid, related to the brain
purulent, and cheese-like to clear  The best tests to diagnose acoustic
and serous. neuroma are audiometry (hearing
 Granulation tissue is often seen in testing) and MRI scanning of the
the media canal or middle ear space. head with gadolinium contrast.
UST FMS MEDICAL BOARD REVIEW 2019 2 | OTORHINOLARYNGOLOGY
 OTORHINOLARYNGOLOGY
JOEL ROMUALDEZ, MD

Presbycusis Impetigo
 Loss of hearing over time due to the  Superficial skin infection presenting as
aging mechanism in the inner ear vesicopustular formation that forms yellow
 Due to loss of hair cell and cochlear crusts
neurons.  Staph aureus
 Has two types:  Grp A Hemolytic Streptococci
o Strial presbycusis
o Neuropresbycusis Erysipelas
 “Acute inflammation of sin and
Benign Paroxysmal Position Vertigo subcutaneous tissue caused by Streptococci
 Presents with dizziness which last for second
to few minutes.  “Raised erythmatous, hot, tender lesions
 Physical examination revealed positive dix- with sharply circumscribed border, elevated
hallpike maneuver and with fatigueable from the surrounding skin
nystagmus.
 Disease is sometimes referred to as Lupus Erythematosus
cupulothiasis  Idiopathic disease causing altered immune
response
Vestibular Neuronitis  Malar or “butterfly” rash on the fae
 Presents with severe dizziness with
intractable vomiting nausea, or inability to Rhinophyma
stand or walk  “Chronic inflammatorydisease of the nose
 Hearing is usually spared. prsenting as enlarged, erythematous nasal
 Can last from days to months. tip with prominent comedones
 “Sebaceous gland gland hypetrophy,
Labyrinthitis acanthosis, telengiectasia
 May be Acute or Chronic
 Acute suppurative labyrinthitis usually Nasal Foreign Body
begins with an acute bacterial infection that  Usually seen in children
extends to the structure of the inner ear.  Presents as unilateral foul-smelling purulent
 Chances of complete loss of hearing and discharge
vestibular function are quite high  Rhinosocopy: foul nasal discharge which
 Drainage frequently masks the foreign body from
 Superior meatus examination
o Posterior ethmoid sinus  If neglected, rhinoliths may form
 Middle meatus  Tx: removal of foreign body / rhinolith
o Maxillary sinus
o Anterior ethmoid sinus Infectious rhinitis
o Frontal sinus  Viral agents or bacteria pathogens
 Inferior meatus  Viral: transient signs and symptoms which
o Nasolacrimal duct resolve after a few days
 Bacterial: may be superimposed on a
NOSE previous infection
o -More fulminant and prolonged
Furuncolosis o -Antibiotic therapy needed
 “Most common acute infection of the
external nose Allergic Rhinitis
 “Superficial abscess usually foud in the - IgE mediated hypersensitivity reaction
vicinity of the nasal vestibule around the causing release of vasoactive inflammatory
hair follicles mediators
 “Presents with marked local erythema,
swelling and pain Non allecgic Rhinitis with eosinophilia
 “Staphylococcus aureus is the usual  Rhinitis with eosinophilia but with negative
organism allegy work up
 “Tx: antibotics, warm compress, I & D  Very responsive to steroids
 “Complications: Cavernous sinus thrombosis Vasomotor rhinitis
 Essentially a diagnosis of exclusion
Vestibulitis  Increase in acetylcholine which causes an
 Excoriation and infection of the si of the increase in parasympathetic tone
nasal vestibule
 Trauma Rhinitis medicamentosa
 Projection of dislocated septum  Worsening rebound congestion following
 Foreign body prolonged use of topical decongestants
 Eczema
 Tx: local antibiotic ointment
UST FMS MEDICAL BOARD REVIEW 2019 3 | OTORHINOLARYNGOLOGY
 OTORHINOLARYNGOLOGY
JOEL ROMUALDEZ, MD

Hormonal rhinitis o Lateral: optic nerves, cavernous

 Increased level of estrogen causes an sinuses, internal carotid artery
inrease in parasympathetic tone
 Treat symptomatically with decongestant or  The primary symptom or initial presentation
steroids depends on the site affected:
o Glottic: Hoarseness
Atrophic rhinitis o Supraglottic: Dysphagia
 Chronic inflammation of the nose with o Subglottic: Dyspnea
progressive atrophy of the nasal mucosa
and turbinates rsulting in widened nasal  Clinical Division of Larynx
passages, excessive crusting, foul odor and o Supraglottic Area - tip of the
anosmia epiglottis to 1 cm below the
laryngeal ventricles
 Tx: Nasal douche with alkaline solution, o Glottic Area - laryngeal ventricles to
application of 25% glucose in glycerine plus 1 cm below true vocal cords
regular removal of crusts and discharge o Subglottic Area - 1 cm below the
true vocal cords to inferior border of
Following sinuses are already present at birth the cricoid
– Ethmoid and Maxillary
 What is the only laryngeal structure
Maxillary Sinus consisting of elastic cartilage? – Epiglottis
 a.k.a. Antrum of Highmore
 Pyramidal in shape located in the maxillery  The larynx is primarily composed of 6
bone cartilages:
 Large paranasal sinus o Epiglottis
 Volume: 15 ml each o Arytenoids
 Present at birth o Cricoid
 Floor is formed by the alveolar process of o Cuneiform
the maxilla o Thyroid
 Drain at the middle meatus o Corniculate
o 1 bone – Hyoid Bone
Ethmoid Sinus
 Bony labyrinth of small air cells Abductors
 Between the medial wall of the orbit and the  Posterior cricoarytenoid
middle turbinate  Interarytenoid
 Present at birth  Lateral cricoarytenoid
 Develop as out-pocketings of the medial  Cricothyroid
meatus
 Quantity: 7-15 per side, 14 ml volume Tensors
 Anterior:  Cricothyroid (external)
 -Drain into middle meatus  Vocalis (intenal)
 Posterior:  Thyroarytenoid (internal)
 -Drain into superior meatus
Lymphatic Drainage OF LARYNX
Frontal Sinus
 Frontal bone  Supraglottic (superior)
 Arise from an Expansion of an anterior air o accompanies superior neurovascular
cell from the ethmoids pedicle
 Not present until -6 years of age o joins upper LN of deep cervical
 Volume: 6-7 ml per sinus chain at level of hyoid
 Drainage is via the middle meatus  Subglottic (inferior)
o goes to pretracheal nodes, lower
Sphenoid Sinus deep cervical, supraclavicular,
 Develop as excavations into the sphenoid superior mediastinal nodes
bone at around 4 months of age  Glottic
o Volume:7.5 ml per sinus o practically devoid of lymphatic’s
o Ostium opens into sphenoethmoid  Vocal Nodules
recess o Screamer’s nodules, siger’s nodes,
teacher’s nodes
 Borders: o Unilateral
o Anterior: posterior ethmoids o Results from: prolonged or imprope
o Posterior: pons and basilar artery use of the vocal cords
o Superior: optic chaisma, optic o When there is coexisting
nerves, hypophysis inflammation, the vocal cords strike
o Inferior: nasal cavity and firmly together, causing formation of
nasopharynx a polyp or nodule
UST FMS MEDICAL BOARD REVIEW 2019 4 | OTORHINOLARYNGOLOGY
 OTORHINOLARYNGOLOGY
JOEL ROMUALDEZ, MD

 Histology o Cricopharyngeus
o soft, loosely edematous tumor o Aorta/left mainstem bronchus
o firm, fibrous growth o Gastroesophageal junction
o vascular lesion w/ many small
vessels  Tonsillectomy: Indications
 Treatment
o vocal restraint Absolute:
o re-education  Tonsil or adenoid hypertrophy with sleep
o endoscopic surgery apnea syndrome

Laryngomalacia Relative:
 Exaggeration of the soft, flabby state that is
normal for newborns A – abscess (Recurrent peritonsillar abscess or
 Sx: stridor abscess extending into adjacent tissue spaces
 Swallowing is unaffected
 Cry, wt gain, and development are normal B – biopsy (Excisional biopsy for suspected
 PE: larynx fall together w/ inhalation, malignancy (lymphoma)
subglottic area is normal, stridor ceases if
the larynx is held open w/ a laryngoscope C – cor pulmonale (Development of cor pulmonale
by chronic airway obstruction)
CONGENITAL ANOMALIES
 Congenital subglottic stenosis D – dysphagia (Hypertrophy to the extent of causing
o Subglottic diameter <4mm dysphagia with associated weight loss)
o Stridor shortly after birth
o Dx: endoscopically E – episodes “Paradise Criteria”
o Tx: most require tracheotomy  7 episodes of tonsillitis in 1 year
 Growth resolves the relatives stenosis  5 episodes per year in 2 consecutive years
 Laser excision  3 episodes per year in 3 consecutive years
 Reconstructive surgery o 2 weeks absence from work or
school in any given year
 Laryngocele
o Special type of congenital cyst
 Develops as residual from a small appendix
of laryngeal ventricle
o Present at any age
o Causes bulging of false vocal cord
o Dissects along superior laryngeal
nerve
o Present as neck mass

ESOPHAGUS
 Begins at the upper esophageal sphincter
o C6 and C7
o inferior border of the cricoid
cartilage
 Terminates at the gastric cardia
o T10

3 Physiologic Constrictions
 Upper constriction
o Esophageal inlet between the cricoid
cartilage and cricopharyngeal part of
the constrictor pharyngis inferior
o Muscle
 Middle constriction
o Aortic arch crosses over the tracheal
bifurcation
 Lower constriction
o Area where the esophagus pierces
the diaphragm

Foreign Body Ingestion

 Common locations
o Tonsils
o Vallecula epiglottica
o Pyriform sinuses
UST FMS MEDICAL BOARD REVIEW 2019 5 | OTORHINOLARYNGOLOGY
 OPTHALMOLOGY
RONALD YUTANGCO, MD

OPTHALMOLOGY SCLERA
 - fibrous outer covering made of collagen
I. Eye Anatomy  Continuous anteriorly with the cornea
Orbit Cornea
Openings in the Orbit:  Avascular
 Superior orbital fissures  Transparent
 Inferior orbital fissures  Richly supplied with nerves
 Optic foramen
Lens
 Orbital septum  The crystalline lens is located just behind
- barrier between the eyelids and the orbit the iris.
- anterior limit of the orbital cavity  Its purpose is to focus light onto the retina.
 30% protein 65% water
Walls: ROOF  The nucleus, the innermost part of the lens,
 a triangle formed by the lesser wing of the is surrounded by softer material called the
sphenoid and the frontal bone cortex.
 Orbital plate of the frontal bone
 Anterolateral: Lacrimal Fossa Uveal Tract
 Posterior: Lesser wing of the sphenoid.  Iris-
Contains the optic canal Ciliary body
FLOOR MoP Z Choroid
 Maxillary  Iris pars plicata - corrugated anterior
 Palatine pars plana-flat posterior
 Zygomatic
MEDIAL Wall Choroid
 Sphenoid (lesser wing)  It is composed of layers of blood vessels
 maxilla that nourish the retina
 Ethmoid bone (paper-thin)
 Lacrimal bone Aqueous
 Body of the Sphenoid - most posterior  the thin, watery fluid that fills the anterior
aspect segment
 Lacrimal Crest  It is continuously produced by the ciliary
LATERAL Wall body
 greater wing of the sphenoid  nourishes the cornea and lens
zygomatic bone- Strongest part Aqueous Humor function
 Optical transparency
Superior Orbital Fissure SOF  Nutrition
- Structures passing through  Structural integrity
Inferior Ophthalmic vein
Lateral: Superior ophthalmic vein - Vitreous: gel attached at vitreous base, optic
nerve, and macula-rich in hyaluronic acid
CN 3,4,5,6 and water
Lacrimal, Frontal and Trochlear nerves V 1 & IV - RETINA LAYERS: divided into
Medial Superior and Inferior divisions of the III  Outer RPE and Bruch’s membrane
Abducens nerve VI  Inner sensory retina
Nasociliary nerve V1  Macula (posterior pole, macula lutea, central
retina, area centralis)
 Optic Canal - Optic Nerve CN II-not in SOF o ganglion cells are reduced to a
single layer
Tear Film  Fovea (fovea centralis)
Three layers: o all cones
1. The lower mucous layer serves as an anchor
for the tear film and helps it adhere to the Optic Nerve
eye. - goblet cells  axons of cell bodies in ganglion cell layer
2. The middle layer is comprised of water- ◦ sensory receptor cells of the retina
lacrimal/accessory glands. are absent from the optic nerve
3. The upper oil layer seals the tear film and head or disc which corresponds to
prevents evaporation- meibomian gland the blind spot
 Eyeball: ave. length =24.2mm
 Three Coats Refractive Errors
 Sclera – white collagenous coat Myopia (nearsightedness)
 Uvea – red vascular coat o images are formed in front of the retina
 Retina – clear neurosensory layer

UST FMS MEDICAL BOARD REVIEW 2019 1 | OPTHALMOLOGY

 OPTHALMOLOGY
RONALD YUTANGCO, MD

o the eye is relatively too long, or the

refractive power of the eye are relatively too Hyphema
strong. Goal of treatment -Prevent the following:
o Correction of myopia: concave lens/minus 1. peripheral anterior synechiae
lens 2. severe acute glaucoma
3. corneal blood staining
Presbyopia
o Loss of accommodation that comes with 3. Cataract
aging Fluctuation of visual acuity in diabetes Sudden
o crystalline lens can no longer change its changes in blood sugar or serum electrolyte alter the
shape in accommodation/ weakening of the hydration of the lens
ciliary muscle and stiffening of the lens
o results from the natural aging 4. Vitreous Hemorrhage
process Absence of red-orange reflex
o Worse in dim light, early in the morning, Causes: Trauma
when fatigued Retinal vein occlusion
o Correction for presbyopia: plus, lens Diabetes
bifocals: far and near Subarachnoid hemorrhage
Aneurysm
Hyperopia (farsightedness)
 unaccommodated eye focuses the image 5. PRERETINAL HEMORRHAGE
behind the retina
 hypermetropia B. Retinal Disease
 Axial hyperopia-due to reduced axial length - Visual loss involving the retina will present as
 Refractive hyperopia - reduced refractive painless loss of vision.
power as seen in aphakia
 glasses are needed when accommodation is 1. Retinal detachment-
inadequate  RHEGMATOGENOUS
 Correction of hyperopia convex lens/plus  NON-RHEGMATOGENOUS- Tractional
lens and serous

Astigmatism 2. Macular disease

 the cornea isn't round. shaped like a  Age related Macular Degeneration
football, not a basketball  Diabetic retinopathy with macular edema
 the cornea has two curves:  Central Serous Retinochoroidopathy -Serous
 a steeper one, and a flatter one 90 degrees detachment of sensory retina bec of leak
away. from choriocapillaris through a defect in
 These two curves bend light entering the RPE. FA:smoke stack sign
eye, causing two images to form on the
retina. 3. Retinal vascular occlusion
 Correction of astigmatism - cylindrical lens -  Central retinal artery occlusion CRAO
may initially cause disorientation  Branch retinal artery occlusion BRAO
 Central retinal vein occlusion CRVO
II. Acute Visual Loss
Differential Diagnosis of Blurring of Vision Central retinal artery occlusion (CRAO):
• A. Media opacities  Sudden, painless loss of vision
• B. Retinal disease  Diffuse ischemia of the retina
• C. Optic nerve disease  Edema of the retina with marked decrease
• D. Visual pathway disorders in vascularity-Pallid swelling of the retina
A. Ocular Medial Opacities: cornea, aqueous, lens,  Cherry red spot at center due to choroidal
vitreous perfusion
1. Corneal edema  perifoveal edema does not extend beyond
2. Hyphema the macula because of the reduced
3. Cataract concentration of ganglion cells in the
4. Vitreous hemorrhage extramacular retina.
1. Corneal Edema  Marked pallor of the optic disc is present
- Dulling of the normal crisp reflection of incident  Assoc. w/: giant cell arteritis
light  arteriosclerosis
Ex. Acute attack of angle closure glaucoma  emboli from carotids or
Dystrophy heart
After cataract surgery  CRAO Treatment (Permanent damage in 90
Acute infection or inflammation of the cornea min)-massage, anti-glaucoma,
2. Hyphema - Blood in the anterior chamber  AC paracentesis – decrease IOP to inc.
Presence of abnormal blood vessel perfusion
UST FMS MEDICAL BOARD REVIEW 2019 2 | OPTHALMOLOGY
 OPTHALMOLOGY
RONALD YUTANGCO, MD

 Inhaled carbogen 95%O2- 5%CO2 mix to

inc perfusion Age Related Macular Degeneration
 Thrombolytics into ophthalmic artery within Stages
8 hours of occlusion- risk of stroke Early- drusen, pigmentary change, RPE atrophy
Late- wet and dry AMD
 CRVO Atrophic AMD ―Dry‖
 Usu in HPN or gl increasing atrophy of the RPE and photoreceptors -
 Dilated tortuous veins drusen
 Retinal edema w/ foveal involvement causes a major reduction in
 Hemorrhages and cotton-wool spots vision.
 Secondary NEOVASCULAR GLAUCOMA in Exudative or Wet AMD
ischemic type SRNV ingrowth of new choroidal vessels through
 More in DM smokers, hyperviscosity syn, Bruch’s membrane into the subpigment epithelial
CRF, hyperlipidemia and subretinal space. Ultimately, CNV leads to
extensive fibrous scarring of the macula
C. Optic Nerve Disease Metamorphopsia is the characteristic symptom.
 Signs: decreased visual acuity, +RAPD, color
vison changes, scotoma Diabetic Retinopathy
 Optic neuritis Progressive microangiopathy: Small vessel damage
 Usually idiopathic and occlusion
 Maybe associated with multiple sclerosis
1. Reduced visual acuity ¼ of blind in developed countries
2. (+) relative afferent pupillary defect Related to duration of DM
3. Hyperemic and swollen optic disc Type 1= usu severe proliferative
 Usually young adult with monocular loss of Type 2 = usu NPDR
vision, developing from hours to days Visual loss is late in the disease and therefore
 With pain on eye movement screening is the best prevention
 Absence of ophthalmoscopic optic nerve
abnormality Pathogenesis
 Pericyte loss from endothelial basement
D. Visual Pathway Disorders membranes- due to metabollites of the
A. Hemianopsia / quadrantanopsia sorbitol pathway
 Homonymous hemianopsia –posterior to  Increased vascular permeability--Vascular
chiasm occlusion—ischemia--neovascularizatio
 Bitemporal hemianopsia- chiasm (pituitary 1. Non-Proliferative Diabetic Retinopathy
tumors) Background DR- microaneurysms; dilated
B. Cortical Blindness veins
 Also known as central or cerebral blindness Multiple hemorrhages-
 Normal pupillary light reflex, normal fundus flame- NFL
findings dot and blot- deeper retina
 Extensive bilateral damage to the cerebral Macular edema (CSME)- break of blood
visual pathways resulting in complete loss of retinal barrier
vision CSME clinically significant macular edema-
 Transient in children after subconcussive retinal thickening/hard exudates within
head trauma 500um of the macular center
-cause of visual loss in 5-15%
III. Chronic Visual Loss
2. Proliferative DR- Neovascularization of
Cataracts the disc NVD and elsewhere NVE-
 Lens opacification- age, sunlight, diabetes. late: tractional retinal
Steroids, trauma, eye –uveitis detachment
Surgery: phacoemulsification Treatment: glycemic control, panretinal
photocoagulation, anti-VEGF
Glaucoma
 An optic neuropathy with: IV. RED EYE DISORDERS:
- Optic disc cupping 1. NON-SIGHT THREATENING
- Visual field loss -arcuate scotoma to tunnel - Subconjunctival hemorrhage
vision - Conjunctivitis
- Usu. increased IOP (normal 10-22mmHg) - Dry eyes
- Blepharitis
- Glaucomatous optic atrophy: - Corneal abrasion
- Loss of disk substance - Hordeolum
- Detected as enlargement of the optic disc - Chalazion
cup
UST FMS MEDICAL BOARD REVIEW 2019 3 | OPTHALMOLOGY
 OPTHALMOLOGY
RONALD YUTANGCO, MD

2. SIGHT THREATENING Blunt trauma

- Keratitis - an injury that causes minimal signs of
- Scleritis damage to one part of the eye can cause a
- Hyphema significant injury in another part of the eye
- Iritis - Compete eye exam is mandatory
- Glaucoma - Rule out retinal tears/ commotio retinae/
- Orbital cellulitis choroidal rupture/optic nerve involvement
- Ciliary vs. Conjunctival Injection - Also examine other eye

CONJUNCTIVAL-CONJUNCTIVITIS Hyphema
- in fornix diminishing towards limbus - Goal: to prevent corneal staining
- posterior conjunctival vessels - peripheral anterior synechiae
- Constrict w/ weak vasoconstrictors - Tx: decrease IOP mod backrest
- *conjunctivitis-bacterial/viral /allergic/ Optic Nerve Damage
- compression by intrasheath hemorrhage and
CILIARY edema and
- circumcorneal or perilimbal - direct shock-wave trauma to the nerve
- deep ciliary vessels fibers
- don’t constrict with topical vasoconstrictors - Treat with IV steroids
- *involvement corneal or deeper structures
- Ex. Corneal ulcer, acute angle closure Chemical Burns
glaucoma, iritis Alkali Burns
- Most common alkalis: lime Ca OH
Danger Signs of Red Eye  lye NaOH
- Reduced visual acuity - Fast penetration potash KOH
- Ciliary Flush - Fast transit ammonia AlOH
- Corneal Opacification - Alkalis: cleaning products (ammonia), drain
- Corneal epithelial disruption cleaners (lye), cement, fireworks MgOH,
- Pupillary abnormalities airbag rupture NaOH
- Shallow anterior chamber depth - saponify cell membranes and intercellular
- Elevated IOP bridges, which facilitates rapid penetration
- Proptosis into the deeper layers and into the aqueous
- Corneal anesthesia - Herpes simplex and vitreous compartments
keratitis- steroids are contraindicated - Colliquation necrosis of an alkali burn leads
to rapid penetration of the alkali into the
- Pupillary abnormalities anterior segment of the eye.
o Iridocyclitis – miotic due to ciliary
spasm, may have posterior Acid burn
synechiae - The coagulation necrosis caused by an acid
o Glaucoma – mid-dilated pupil. burn prevents further penetration of the
Shallow anterior chamber depth acid
- Less tissue damage than alkaline solutions
Orbital cellulitis because of the buffering capacity of tissues
- External signs: redness, swelling as well as the barrier to penetration formed
- Motility impaired by precipitated protein.
- Proptosis - Acids: battery acid, bleach, glass polish,
- Chemosis vinegar, HCl
- Optic nerve- decreased vision, RAPD, disc - sulfuric, nitric, and hydrochloric acids
edema
Summary of Suggested Actions During the
- Episcleritis and Scleritis Immediate (Acute) Period
- Irrigation is critical. Use water or saline for
V. Trauma and Emergencies at least 1 to 2 hours. Check pH of fornices
Corneal abrasion: with litmus paper.
- Treatment Goals - Debridement is essential to remove residual
o Promote rapid healing caustic particles. Use speculum and topical
o Relieve pain anesthetic.
o Prevent infection - Paracentesis helps to normalize the anterior
- Treatment chamber pH more quickly.
o Cyclopentolate or tropicamide
o Topical antibiotics Other Notes:
o Pressure patch x 24-48 hours Vitamin A deficiency- Bitot spot/keratomalacia
o Oral analgesics

UST FMS MEDICAL BOARD REVIEW 2019 4 | OPTHALMOLOGY

 OPTHALMOLOGY
RONALD YUTANGCO, MD

Retinoblastoma- retinoblastoma gene-

chromosome 13q14
- leukocoria- usually in 18 mo. Old
- most common intraocular malignancy in
children

Retinopaty of Prematurity - low birth weight

(<1500g) and premature babies (<28 weeks) are at
risk of developing tractional retinal detachment.
Screening should be done at 4 to 6 weeks of age.

Amblyopia is an acquired defect in monocular

vision caused by abnormal visual experience early in
life. during the period of visual development (0-9
yrs)

- Third nerve Palsy- eye is down and out-

exotropic and hypotropic
o dilated pupil-complete:.rule out
aneurysm of post. Communicating
a.

- Ethambutol toxicity - neuropathy common in

PTB patients

UST FMS MEDICAL BOARD REVIEW 2019 5 | OPTHALMOLOGY