PHARMACOTHERAPY

OF AUTONOMIC
SYSTEM DISORDERS
Joyce Ann Medina, RPh
 CLINICAL PHARMACY

•Essential Outcome
Demonstrate understanding in applying in-depth knowledge
of pharmacology, pharmacotherapy, pathophysiology, and
the clinical signs, symptoms, and natural history of diseases
and/or disorders under autonomic nervous system.
 CLINICAL PHARMACY

•Learning Objective/s
To identify factors that may induce or
01 potentiate the Autonomic Nervous
System disorders
To describe the clinical presentation of
02 the disorder, including diagnostic and
laboratory tests, evaluate the
therapeutic outcomes and create
appropriate medication interventions in
a simulated clinical pharmacy situation
 CLINICAL PHARMACY

• GLAUCOMA & MYASTHENIA GRAVIS

• PHYSIOLOGY
• PATHOPHYSIOLOGY
• CLINICAL MANIFESTATIONS
• DIAGNOSIS
• TREATMENT
• Pharmacologic
• Non – pharmacologic
• Algorithm

OUTLINE
CLINICAL PHARMACY

GLAUCOMA
Ocular disorders that lead to an optic
neuropathy characterized by changes
in the optic nerve head (optic disc)
that is associated with loss of visual
sensitivity and field.
 CLINICAL PHARMACY

GLAUCOMA

PHYSIOLOGY OF AQUEOUS HUMOR FLOW

• Aqueous Humor
• A clear water fluid filling the anterior chamber
and poster chamber of the eyeball
• Functions
• It maintains a proper intraocular pressure
• It keeps the globe of the eye inflated
• It also plays an important role in providing
nutrients in a form of amino acids and glucose
 CLINICAL PHARMACY

GLAUCOMA

PHYSIOLOGY OF AQUEOUS HUMOR FLOW

• Key Players
• Ciliary bodies
• Intraocular pressure
• Trabecular mesh work
• INFLOW = OUTFLOW
 CLINICAL PHARMACY

GLAUCOMA

PATHOPHYSIOLOGY

• Imbalances between the inflow and

outflow of aqueous humor may lead to
ocular disorder
• The drainage canal is partially or
completely block Increase IOP
Intraocular pressure
 CLINICAL PHARMACY

GLAUCOMA

PRIMARY OPEN-ANGLE GLAUCOMA

• Cause by partial blockage of the

drainage canal.
• The angle between the cornea and the
iris is OPEN meaning the entrance to
the canal is clear but the flow of
aqueous humor is slower than the
normal
• IOP greater than 21 mm Hg (2.8 kPa)
 CLINICAL PHARMACY

GLAUCOMA

CLOSED-ANGLE GLAUCOMA

• Caused by a sudden or complete

blockage of aqueous humor drainage
• The pressure within the eye rises
rapidly and may lead to total vison loss
quickly
• IOP 40–90 mm Hg (5.3–12 kPa)
 CLINICAL PHARMACY

GLAUCOMA

CLINICAL MANIFESTATIONS
 CLINICAL PHARMACY

GLAUCOMA

DRUG INDUCED: OPEN-ANGLE GLAUCOMA

 GLAUCOMA

DRUG INDUCED: CLOSED-ANGLE

GLAUCOMA
 GLAUCOMA
DIAGNOSIS

SLIT LAMP & GONIOSCOPY

• A gonioscopy lens may be used to view the

drainage angle
 CLINICAL PHARMACY

GLAUCOMA
DIAGNOSIS

TONOMETRY

• Procedure eye care professionals perform to

determine the intraocular pressure
• Normal pressure range is 12 to 22 mm Hg
 CLINICAL PHARMACY

GLAUCOMA
DIAGNOSIS

OPHTHALMOSCOPY

• Eye drops may be placed in the eyes to dilate

the pupils
• Special magnifying lenses are used to examine
the retina and optic nerve for damage
 CLINICAL PHARMACY

GLAUCOMA
PHARMACOLOGIC TREATMENT

OPEN-ANGLE GLAUCOMA

• Frist line treatment:

• β-blockers
• Prostaglandin analogs
• Brimonidine and topical CAIs
• Third line treatment:
• Prodrug of epinephrine
• Last resort treatment:
• Topical cholinesterase inhibitors
• Oral CAIs
 CLINICAL PHARMACY

GLAUCOMA
PHARMACOLOGIC TREATMENT FOR OPEN-ANGLE GLAUCOMA
 CLINICAL PHARMACY

GLAUCOMA
PHARMACOLOGIC TREATMENT FOR OPEN-ANGLE GLAUCOMA
 CLINICAL PHARMACY

GLAUCOMA
TREATMENT ALGORITHM FOR OPEN-ANGLE GLAUCOMA
 CLINICAL PHARMACY

GLAUCOMA
TREATMENT ALGORITHM FOR OPEN-ANGLE GLAUCOMA
 CLINICAL PHARMACY

GLAUCOMA
PHARMACOLOGIC TREATMENT FOR OPEN-ANGLE GLAUCOMA

CLOSED-ANGLE GLAUCOMA

• Iridectomy
• Treatment producing a hole in the iris that
permits aqueous humor flow to move
directly from the posterior to the anterior
chamber
• β-blocker, α2-agonist, latanoprost, or CAI
• Osmotic agents
• Glycerin, 1 to 2 g/kg
• Orally, and mannitol, 1 to 2 g/kg IV
• Topical corticosteroids
 CLINICAL PHARMACY

GLAUCOMA
SURGICAL TREATMENT

TRABECULOTOMY

• A partial thickness incision is made in the

sclera and further section of sclera is removed
to produce an opening for aqueous humor
outflow under the conjunctiva, creating a
filtering bleb
 CLINICAL PHARMACY

GLAUCOMA
SURGICAL TREATMENT

TRABECULAR STENT BYPASS

• A tiny tube is placed into your eye to increase

the drainage of fluid
 CLINICAL PHARMACY

GLAUCOMA
SURGICAL TREATMENT

SCLEROTOMY

• A partial thickness incision is made in the

sclera and one or more openings are made
with a punch. The top flap of sclera is closed
over the punched holes.
 CLINICAL PHARMACY

GLAUCOMA
LASER TREATMENT

LASER TRABECULOPLASTY

• A laser is used to open up the drainage tubes

within your eye, which allows more fluid to
drain out and reduces the pressure inside
 CLINICAL PHARMACY

GLAUCOMA
LASER TREATMENT

CYCLODIODE LASER TREATMENT

• Application of a freezing probe to the sclera

over the Ciliary body that destroy some of the
Ciliary processes, results in the reduction of
the amount of aqueous humor produced
 CLINICAL PHARMACY

GLAUCOMA
LASER TREATMENT

LASER IRIDOTOMY

• A laser is used to create holes in your iris to

allow fluid to drain from your eye
 CLINICAL PHARMACY

GLAUCOMA
NON-PHARMACOLOGIC TREATMENT

EAT A HEALTHY DIET

EXERCISE SAFELY

LIMIT YOUR CAFFEINE

SIP FLUIDS FREQUENTLY

SLEEP WITH YOUR HEAD ELEVATED

TAKE PRESCRIBED MEDICINE

CLINICAL PHARMACY

MYASTHENIA GRAVIS
Autoimmune neuromuscular disorder
that causes weakness in the skeletal
muscles, which are the muscles your
body uses for movement
 CLINICAL PHARMACY

MYASTHENIA GRAVIS

PHYSIOLOGY OF MUSCLE CONTRACTION

• Key Players
• Motor nerves
• Acetylcholine
• Skeletal muscles
• In order for the motor nerve to communicate with
muscle cells they need to release acetylcholine and
this needs to bind to receptors on the postsynaptic
membrane Neuromuscular junction

Skeletal muscles cells

 CLINICAL PHARMACY

MYASTHENIA GRAVIS

PATHOPHYSIOLOGY
• Key Players
• Acetylcholine antibodies
• Thymoma type of tumor or growth in the
thymus gland
• Immune system

Muscle contraction
 CLINICAL PHARMACY

MYASTHENIA GRAVIS

CLINICAL MANIFESTATIONS
 CLINICAL PHARMACY

MYASTHENIA GRAVIS
DIAGNOSIS

CHEST X-RAY

• Chest CT scan is mandatory to identify

thymoma
 CLINICAL PHARMACY

MYASTHENIA GRAVIS
DIAGNOSIS

LAB STUDIES

• Acetylcholine receptor (ACh-R) antibodies

• Muscle-specific kinase (MuSK) antibodies
• LRP4 (low-density lipoprotein receptor-related
protein 4) antibodies
 CLINICAL PHARMACY

MYASTHENIA GRAVIS
DIAGNOSIS

EDROPHONIUM TEST (TENSILON TEST)

• Edrophonium is a short acting Acetylcholine

Esterase Inhibitor
• 0.1ml of a 10 mg/ml edrophonium solution is
administered as a test
 CLINICAL PHARMACY

MYASTHENIA GRAVIS
PHARMACOLOGIC TREATMENT

REVERSIBLE ACETYLCHOLINESTERASE
INHIBITORS
• Pyridostigmine bromide (Mestinon)
• Starts working in 30-60 minutes and lasts 3-6
hours
• Individualize dose
• Adult dose:
• 60 – 960 mg/d PO
• 2mg IV/IM q2-3h (Administer as slow IV push)
• Caution
• Check for cholinergic crisis
• Others: Neostigmine Bromide
 CLINICAL PHARMACY

MYASTHENIA GRAVIS
PHARMACOLOGIC TREATMENT

CORTICOSTEROIDS

• Prednisone
• No single dose regimen is accepted
• Used in conjunction with immune globulin IV
or plasma exchange
• Usual dose range: 60 to 80 mg daily
• Some start low and go high
• Clearance may be decreased by estrogens or
digoxin
• Patients taking concurrent diuretics should be
monitored for hypokalemia
 CLINICAL PHARMACY

MYASTHENIA GRAVIS
PHARMACOLOGIC TREATMENT

IMMUNOSUPPRESSANTS
• Azathioprine (Azasan, Imuran)
• Initial: 50 mg/day; increase by 50 mg increments
every 1 to 2 weeks to a target dose of 2.5 to 3
mg/kg/day
• Mycophenolate mofetil (Cellcept)
• Initial: 500 mg twice daily
• Cyclosporine (Sandimmune)
• Dose: 4 -10 mg/kg/day divided in 2-3 doses
• Methotrexate (Trexall)
• 17.5 mg/week
• Tacrolimus (Astrograf XL, Prograf)
• Initial: 3 to 5 mg/day or 0.1 mg/kg/day, in one or
two divided doses
• Side effects: Increased risk of infection and liver or
kidney damage, can be serious.
CLINICAL PHARMACY

MYASTHENIA GRAVIS
TREATMENT ALGORITHM
 CLINICAL PHARMACY

MYASTHENIA GRAVIS
TREATMENT

PLASMAPHERESIS

• Your blood is routed through a machine that

removes the antibodies that block
transmission of signals from your nerve
endings to your muscles' receptor sites.
 CLINICAL PHARMACY

MYASTHENIA GRAVIS
TREATMENT

THYMECTOMY

• An open surgery or as a minimally invasive

surgery. In open surgery, your surgeon splits
the central breastbone (sternum) to open your
chest and remove your thymus gland.
 CLINICAL PHARMACY

MYASTHENIA GRAVIS
TREATMENT: NON-PHARMACOLOGIC

ADJUST YOUR EATING ROUTINE

USE SAFETY PRECAUTIONS AT HOME

USE ELECTRIC APPLIANCES AND POWER

TOOLS

WEAR AN EYE PATCH

CLINICAL PHARMACY

REFERENCES:
DiPiro, J. T. (2008). Pharmacotherapy: A pathophysiologic
approach. New York: McGraw-Hill Medical.
Katzung, B. G., Masters, S. B., & Trevor, A. J. (2012). Basic &
clinical pharmacology. New York: McGraw-Hill Medical.
Chicago
Snell, R. S. (1995). Clinical anatomy for medical students.
Boston: Little, Brown.
www.lexicomp.com
PHARMACOTHERAPY
OF NEUROLOGIC
NERVOUS SYSTEM
DISORDERS
Joyce Ann Medina, RPh
 CLINICAL PHARMACY

•Essential Outcome
Demonstrate understanding in applying in-depth knowledge
of pharmacology, pharmacotherapy, pathophysiology, and
the clinical signs, symptoms, and natural history of diseases
and/or disorders under autonomic nervous system.
 CLINICAL PHARMACY

•Learning Objective/s
To identify factors that may induce or
01 potentiate the Autonomic Nervous
System disorders
To describe the clinical presentation of
02 the disorder, including diagnostic and
laboratory tests, evaluate the
therapeutic outcomes and create
appropriate medication interventions in
a simulated clinical pharmacy situation
 CLINICAL PHARMACY

PARKINSON’S DISEASE

Parkinson’s disease (PD) is a chronic,

progressive neurodegenerative
condition resulting from the loss of
the dopamine-containing cells of the
substantia nigra, and its prevalence
increases with age.

OUTLINE Parkinson's disease (PD) is a common

neurodegenerative disease.
 Parkinson’s disease

Aka (SHAKING PALSY)

chronic progressive disease of the nervous
system characterized by the cardinal features of
rigidity, bradykinesia , tremor and postural
instability.
REFERENCE: (2018, June 30). Parkinson's disease. Retrieved from
https://www.mayoclinic.org/diseases-conditions/parkinsons-disease/diagnosis-treatment/drc-2
0376062
PATHOPYHSIOLOGY

There is depletion of the

pigmented dopaminergic
neurons in the substantia
nigra, atrophic changes in
the substantia nigra&
depletion of neurons in the
locus coeruleus.

REFERENCE: (2018, June 30). Parkinson's disease. Retrieved

from
https://www.mayoclinic.org/diseases-conditions/parkinsons
-disease/diagnosis-treatment/drc-20376062
SIGNS & SYMPTOMS
 SIGNS & SYMPTOMS

Parkinson's has four main symptoms:

•Tremor in hands, arms, legs, jaw, or head.
•Muscle stiffness, where muscle remains contracted for
a long time.
•Slowness of movement.
•Impaired balance and coordination, sometimes leading
to falls.
EPIDEMIOLOGY
The incidence and prevalence of
Parkinson disease increase with age,
and the average age of onset is
approximately 60 years.
Parkinson disease is about 1.5 times
more common in men than in women.

REFERENCE: (2018, June 30). (2019, August 8). Parkinson Disease. Retrieved from
https://emedicine.medscape.com/article/1831191-overview#a4
DIAGNOSIS

No specific test exists to diagnose

Parkinson's disease.

REFERENCE: (2018, June 30). Parkinson's disease. Retrieved from

https://www.mayoclinic.org/diseases-conditions/parkinsons-disease/dia
gnosis-treatment/drc-20376062
 CLINICAL PHARMACY

PATHOLOGICAL HALLMARK OF PD

PRESENCE OF LEWY BODIES

NEURONAL DEATH IN THE PARS COMPACTA OF

SUBSTANTIA NIGRA

LOSS OF PIGMENTED NEURONS IN PIGMENTED

BRAINSTEM NUCLEI
 CLINICAL PHARMACY

MANAGEMENT

STRATEGY TREATMENT:
RESTORATION OF
DOPAMINE IN THE BASAL
GANGLIA AND
ANTAGONIZING THE
EXCITATORY EFFECT OF
CHOLINERGIC NEURONS
CLINICAL PHARMACY

MANAGEMENT
MANAGEMENT
MANAGEMENT
 CLINICAL PHARMACY

CASE PRESENTATION

Gail Brown is a 68 year old female. She is a retired farmer who lives at
home alone with her dog. Mrs. Brown's husband passed away 5 years
ago. She experienced a minor fall (~3 months ago) after tripping over her
dog and landed on an outstretched right hand, leading to wrist pain. She
saw her family doctor regarding her wrist, but also complained of some
recent trouble with balance and a small hand tremor. She was referred to
a neurologist and diagnosed with early stage idiopathic Parkinson’s
Disease. She received a referral for physiotherapy to perform a falls risk
assessment, maintain her functional status, and address her concerns
regarding the condition.
 CASE PRESENTATION

Examination Findings
The patient had their intake assessment on May 9th, 2020.
Subjective
•Patient Profile (PP): 68 y/o female
•History of Present Illness (HPI): Diagnosis of idiopathic Parkinson’s Disease 1 month ago,
left-hand tremor (~5 months), right hand dominant and decreased handwriting size (~5 months),
decreased balance (~1 year)
•Past Medical History: Right wrist injury (~3 months ago, resolved), Depression
•Medications: Currently none, received prescription and education for Levadopa (doesn’t feel she
needs it yet), Advil for headaches when needed
•Health Habits: Non-smoker, no longer drinks alcohol (~3 years)
•Psychosocial: The patient describes feeling lonely, isolated, and frustrated with the diagnosis.
Showing signs of depression. She has avoided going to see her friend due to feeling unsteady
and fear of falling (~3 months). The daughter lives ~2 hours away, and visits 1-2 times/month.
 CASE PRESENTATION

•Home: Bungalow, lives with dog, 4 stairs into the house with railing,10 stairs to the basement
with railing (laundry). The bathroom has a large shower/bathtub with a non-slip mat but no
railing.
•Previous Functional Status:
• Prior to the onset of PD symptoms (decreased balance and tremor): able to walk about
~200m to her friend's house, gardening, performed activities of daily
living(ADLs) independently, driving often (grocery store, recreation center)
• Prior to husband passing (~5 years ago): attended dance classes, was very active with
farm work
•Current Functional Status
• Since the onset of PD symptoms: Drives when necessary but less confident with reaction
time, less confident walking outside, no issues with dressing/bathing, no problems with
stairs, no problems with bed mobility
•Imaging: MRI scheduled for next week to rule out other causes of symptoms.
•Precautions/Contraindications: Depression, lack of social support, right wrist injury (~3
months ago)
 CASE PRESENTATION
Objective
General
Slight masked face, slight muscular deconditioning, mild dysarthria, mild
left resting hand tremor which increased while discussing history of
diagnosis
Posture: Moderate kyphotic forward head posture
Gait: Mild bradykinesia
Tone:Normal
AROM:
U/E: Limited bilateral shoulder flexion and abduction L>R
Trunk: Limited in bilateral rotation
L/E: Limited in bilateral hip extension, bilateral dorsiflexion (non-Weight
Bearing(WB)) L>R
All other ROM within normal limit (WNL)
 CASE PRESENTATION
Objective
PROM:
U/E: Limited bilateral shoulder flexion and abduction L>R
L/E: limited in bilateral dorsiflexion (non-WB) L>R
All other ROM WNL
**Some limits due to mild rigidity (cogwheel)
Strength
Grip strength: L hand 20kg, R hand 18kg
Overall strength: L 4/5, R 4+/5
Apparent weakness in antigravity muscles (back and neck extensors, hip
extensors, quads, hip flexors)
Sensation
U/E and L/E intact
Neurological testing
myotomes, dermatomes, UMN tests, reflexes: normal
 CASE PRESENTATION

Neurological testing
myotomes, dermatomes, UMN tests, reflexes: normal
Self-Reported Outcome Measures
•Patient Health Questionnaire (PHQ-9): 12
•Parkinson's Disease Questionnaire (PDQ-39): 38/156 = 24%
• Most affected areas: mobility, emotional well-being, social support
•Activities-Specific Balance Confidence Scale (ABC Scale): 65%
Outcome Measures
•Timed Up and Go (TUG): 13.2 seconds
• With cognitive task (counting backward from 100 by 3): 13.7 seconds
• With dual-motor task (carrying a glass of water in R hand): 15 seconds
•Berg Balance Scale (BBS): 40/56
• Most affected areas: tandem stance, turning 360 degrees, standing with feet
together, standing with eyes closed
 CLINICAL IMPRESSION

The patient is a 68 y/o female with idiopathic early-stage

PD. Her subjective interview indicated that she is
independent in her ADLs, but she is concerned regarding
her balance and ability to participate in some activities.
She also has a history of depression.
Major clinical findings from the objective assessment
revealed mild bradykinesia, mild deconditioning,
decreased right-hand strength (could be reflective of a
recent wrist injury), resting tremor in the left hand,
kyphotic posture, and decreased ROM (shoulders, hips,
ankles).
 CLINICAL PROBLEM

❑ Depressive symptoms
❑ Fall risk and decreased confidence
❑ Resting tremor L hand
❑ Mild bradykinesia
❑ Kyphotic posture
❑ Decreased balance
❑ Muscle deconditioning
❑ Mild dysarthria
❑ Decreased ROM
 INTERVENTION

Patient Goals
Short Term Goals: Within 4 weeks Gail will...
Improve ABC score from 65% to 75%.
Walk to friend's house (200m one way) using Nordic walking poles.
Attend dance program at the recreation center 2x/week beginning in
2 weeks.
Long Term Goals: Within 12 weeks Gail will...
Improve BBS from 40 to 47.
Walk her dog for 30 minutes around the neighborhood.
Treatment Plan
Treatment Plan
Treatment Plan
 REFERENCES
Katzung, Bertram G. ed. (2015). Basic and Clinical Pharmacology, 13th edition. New York : McGraw
-Hill.

McPherson, Richard A.. (2015). Henry's clinical diagnosis and management by laboratory methods,
22nd ed..Elsevier: Singapore.

Papadakis, Maxine A., (ed.). 2015 Current medical diagnosis & treatment. New York : McGraw-Hill.

Rees, Judith. et al. (2014). Pharmaceutical practice (5th ed.) Edinburgh : Churchill Livingstone.

World Health Organization.. Evaluation of certain food additives and sixty-ninth report of the joint
FAO/WHO Switzerland: WHO. Latest Edition
Physiopedia. Parkinson's. Available from: https://www.physio-pedia.com/Parkinson%27s (accessed 02
OCT 2022).
ACUTE PAIN

The fifth vital sign

• Identifying pain a s the fifth vital sign suggests that the assessment of pain should be as
automatic as taking a client's bp and pulse.
• Pain is the most common reason clients seeks medical advice/
• Pain is a protective mechanism or a warning to prevent injury.

PATHOPHYSIOLOGY OF PAIN -

Pain transmission

1. Nociceptors (pain detecting neurons) are also called as pain receptors are free nerve ending in the
skin that respond only to intense, potentially damaging stimuli (mechanical, thermal, or chemical)

2. The joints, skeletal muscle, fascia, tendons and cornea also have nociceptors.

3. Large internal organ do not contain nerve endings

4. Polymodal nociceptors respond to all type of stimulus

5. Histamine, bradykinin, acetylcholine, serotonin, and substance P are chemicals that increase
transmission of pain.

6. Prostaglandins are chemical substances that are believed to increase the sensitivity of pain receptors
by enhancing the pain provoking effect of bradykinin.

7. There are 2 main types of fibers involved in the transmission of nociception - Myelinated, A delta
fibers - “fast pain” - Type C fibers - “second pain”

8. Chemicals that reduce or inhibit the transmission or perception of pain include endorphins and
enkephalins.

TYPES OF PAIN

1. ACUTE PAIN - usually of recent onset and commonly associated with specify injury, lasting from
seconds to 6 months

• Acute pain is protective, has an identifiable cause, is of short duration, and has limited tissue
damage and emotional response.
• It eventually resolves, with or without treatment after an injured area heals.
• Complete pain relief is not always achievable, but reducing pain to a tolerable level is realistic.
 • Unrelieved acute pain can progress to chronic pain.

2. CHRONIC PAIN - constant or intermittent pain that persists beyond the expected healing time and
seldom attributed to a specific cause or injury; lasts for 6 months or longer.

Information About Acute Pain

Acute pain starts quickly and lasts a relatively short time. By definition, acute pain improves within the
first 1 to 3 months after its onset. Pain that outlasts 6 months is considered chronic pain, a persistent
condition that requires additional treatment from a pain specialist. The period between 3 and 6 months
is seen as a time of transition from acute pain to chronic pain. You should seek evaluation and treatment
at this stage in order to help avoid transitioning into chronic pain.

Some common examples of acute pain:

● Surgery

● Broken bones

● Sprains

● Dental work

● Burns or cuts

● Labor and childbirth

How & Why Acute Pain Develop

Pain is a sensation you experience through the nervous system (nerves, spinal cord, and brain). Reflexes
are the nervous system’s immediate response to acute pain. When you touch a hot plate it only takes
several milliseconds for your nervous system and muscles to coordinate and make you jump out of
harm’s way. In addition to reflexes, the nervous system has more sophisticated mechanisms for
processing pain. The brain releases neurotransmitters, chemicals that influence pain levels and the
appearance of depression, in response to pain.

Diagnosis for Acute Pain

Often the reason for the pain is obvious. At other times, your doctor needs to better understand your
symptoms in order to discover how the pain started.
Diagnostic tests are helpful and include:

● Blood tests

● Imaging studies (x-ray, CT, MRI, nuclear scans)

● Local anesthetic injections

● Electromyography and nerve conduction studie

Common Causes of Acute Pain

Going to the dentist

Sprains and strains of a body part

Infections on a cut

Getting burned

Giving birth

Slipping and falling

Bumping a body part against a hard surface-

Menstrual cramps-

Signs and Symptoms of Acute Pain

Acute pain tends to be of a relatively short duration (and we use this term loosely, since when someone
is in pain, a couple of days can feel like a lifetime). The most common signs and symptoms of acute pain
include:

Sharp pain- When you feel a sudden, intense spike of pain

Throbbing- is one of the symptoms of a headache. It's a pulsing, beating sensation that happens over
and over again.

Burning- A burning sensation can affect almost any part of the body. It may feel like pins and needles,
heat, or a sharp, prickly pain. It is important to seek medical advice and receive the correct diagnosis.

Dahil A burning pain can be related to nerve problems. However, there are many other possible causes.
Injuries, infections, and autoimmune disorders have the potential to trigger nerve pain and, in some
cases, cause nerve damage.

Stabbing pain- Like sharp pain, stabbing pain occurs suddenly and intensely. However, stabbing pain
may fade and reoccur many times.
Tingling- described as a prickling, burning, or “pins and needles” sensation. In addition to tingling, you
may also feel numbness, pain, or weakness in or around your hands and feet

Weakness

Numbness- loss of sensation or feeling in a part of your body.

Effects Of Acute Pain On The Body

It’s important to note that acute pain can affect much more than an injured body part. If a person is
experiencing debilitating pain, the effects will bleed into other areas of the person’s life. It’s very
common for a person who’s suffering from severe pain to be unable to get restful sleep because of it, or
lose their appetite.

Depending on the location of the pain, it can also cause breathing difficulties, and in a worst-case
scenario, could result in addiction to pain medication or even depression.

Treatment For Acute Pain

If it was a minor injury, your medical provider will likely instruct you to rest, ice the injury, and maybe
keep it compressed and/or elevated. Over-the-counter medication may also help alleviate the pain.

However, when dealing with more serious injuries, the person may need stronger medications, such as
opioids, as well as physical therapy, pain management alternatives, and as a last resort, surgery.

•Resting the affected part of the body

•Application of heat or ice –

Ice is used to cool down the injured joint or tissue and reduce swelling. While Heat treatment is more
appropriate to use during recovery as you rehab back to full health

Use ice to treat acute (new) injuries that are accompanied by inflammation and swelling, such as
sprains, strains, bruises and tendinitis.

Use heat for chronic (ongoing), non-inflammatory pain or stiffness, such as from arthritis, fibromyalgia,
back or neck pain.

•Nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen, or naproxen; or

acetaminophen

•Physical therapy- is a medical treatment used to restore functional movements, such as standing,
walking, and moving different body parts
the treatment of disease, injury, or deformity by physical methods such as massage, heat treatment,
and exercise rather than by drugs or surgery.

•Exercise – jogging

•Bioelectric therapy (using local electrical stimulation to moderate pain)

- is a safe, drug-free treatment option for people in pain. It is used to treat some chronic pain and acute
pain conditions. .When you are injured, pain receptors send a message to the central nervous system
(the brain and spinal cord).

•Stress reduction- examples here are non pharmacological therapies or method such as heat and cold
applications, meditation, distraction and imagery, massage, yoga acupuncture, music therapy.

•Opioid (narcotic) medications (such as codeine or morphine)-

•Muscle relaxant medications- Metaxalone, sold under the brand name Skelaxin, is a muscle relaxant
medication used to relax muscles and relieve pain caused by strains, sprains, and other musculoskeletal
conditions

•Nerve blocks ( it is the use of local anesthetics to block nerve activity)

lidocaine, mepivacaine, prilocaine, bupivacaine, etidocaine, and ropivacaine and levobupivacaine

•Trigger point injections to treat muscle spasms- Trigger point injections are a pain management
treatment that involves injecting a local anesthetic, sometimes combined with a steroid medication, into
a trigger point to relax muscles and relieve pain.

Botulinum toxin, or Botox, is a protein that stops muscle spasms. It is injected directly into the muscle

•Steroid injections to reduce tissue inflammation- They can be used to treat problems such as joint
pain, arthritis, sciatica and inflammatory bowel disease. Steroid injections are only given by healthcare
professionals. Common examples include hydrocortisone, triamcinolone and methylprednisolone.

•Acupuncture
https://www.visitcompletecare.com/blog/acute-pain/

https://www.treatingpain.com/conditions/acute-pain/
ANXIETY DISORDER

1. Generalized anxiety disorder (GAD)- With GAD, you may feel extreme and unrealistic
worry and tension.
Most days, you may worry a lot about various topics, including yung health, work, school
and sympre relationships.

2. Panic disorder- From the word panic dito nakakaramdam ka ng intense panic anxiety or
attack. Some symptoms niya is shaking, sweating, irregular heart beat, and choke

3. Phobias- Ito very familiar sa tin ito yung fear sa certain objects or situation or may be
animals dn.

4. Separation anxiety. This condition mostly happens to children or teens, who may worry
about being away from their parents.Ako lang ba or pati kayo, yung kunwari may ginawa
kayong masayang memories with your love ones or friends then pag matatapos na then
masasad ka nanamn. So yon share ko lang

The Amygdala: Where It All Starts

Anxiety reactions are considered to begin in the amygdala, a pair of tiny, almond-shaped
clusters of neurons located close to the base of the brain. It is in charge of what your body does
when you are exposed to anxiety-inducing stimuli, but it is not in charge of what you think.The
amygdala's function is to regulate memory storage based on the intensity of the emotional
response connected to the memory. Men often have a more active right amygdala than women
do, which is the brain region principally in charge of the action. On the other hand, the left
amygdala is principally in charge of storing the specifics of traumatic experiences and stimulates
more thought than action. In both women and people, this amygdala is more active than the
right one.

The Medulla Oblongata: where’s my air?

The amygdala is the part of the brain that initiates fight or flight responses. The medulla
oblongata sends signals to the body telling it that extra air is needed for circulation. This causes
shortness of breath and hyperventilation, or coughing up blood.

The Nucleus ambiguous and hypothalamus: getting on your nerves.

The fight or flight response essentially prepares your body for anything. Your heart, lungs, and
muscles are all required to equip the body with everything it needs to move fast and effectively.
On the plus side, you really are ready to fight or to fly when you are experiencing this response -
even if it's only anxiety.

Adrenal medulla : energy plus crash

Your sympathetic nerves cause a little quantity of dopamine and the well-known hormone known
as adrenaline to be released into the body by the adrenal medulla, making the body feel better
than it otherwise would (which is known in combination as the adrenaline rush). The brain is
instructed to produce a neurotransmitter called epinephrine by the adrenaline, which raises
blood pressure and blood sugar levels. This makes blood sugar and the body's stored fatty
acids available for the muscles to use as rapid energy.
The adrenal medulla releases epinephrine, which boosts blood pressure and blood sugar. This
makes the body's stored fatty acids available to be turned into quick energy by the muscles.
Post-adrenaline rush, the body crashes, taking dopamine or reward chemical with it and making
the body tired and unhappy. What your amygdala is triggered by is a key factor in defining what
anxiety disorder you have. It may be virtually anything, from reminders of past events to
crowded spaces, to disorganization, to spiders, to triggers inside you that may not even be
known. You can conquer your anxiety and remind your body whose side it's on by using your
brain's prefrontal cortex.

Neurotransmitter in Anxiety Disorders

● Serotonin
○ Central roles in development of ADs
○ To source and systems involved: amygdala and periaqueductal gray.
○ Increased levels in the brain increase anxiety.
○ Serotonin (and melatonin) are thought to help regulate several physiologic
activities,
● Dopamine
○ mesolimbic , mesocortical, and nigrostriatal dopaminergic systems are involved
in ADs
○ Evidence of dopamine role in PDA and SAD
○ There are strong links between the serotonin and dopamine systems, both
structurally and in function. In some cases, however, serotonin may inhibit
dopamine production, which means that low levels of serotonin can lead to an
overproduction of dopamine.
● Norepinephrine and Epinephrine
○ Involved in the autonomic nervous response and directly correlated to anxiety
symptoms.
○ The locus coeruleus is the principal site for brain synthesis
 ○ These two hormones work together in stressful situations to increase blood flow
throughout your body.
● GABA
○ Inhibitory neurotransmitter
○ Meditates opening chloride ion channels down polarization
○ Induce anxiolytic effect.
○ In ADs, GABA levels decrease.
○ Inhibitory neurotransmitters like GABA block certain brain signals and decrease
nervous system activity.

Next is the Diagnosis

You may start by seeing your primary care provider to find out if your anxiety could be related to
your physical health. He or she can check for signs of an underlying medical condition that may
need treatment.

However, you may need to see a mental health specialist if you have severe anxiety. A
psychiatrist is a medical doctor who specializes in diagnosing and treating mental health
conditions. A psychologist and certain other mental health professionals can diagnose anxiety
and provide counseling (psychotherapy).

Next for the CLINICAL MANIFESTATION

ANDREA:
Common Causes:
● Stress Everyone encounters stress, but excessive or unresolved stress can
increase your chances of developing chronic anxiety.
● Genetic factorsPersonality type
● Trauma
● Life events KUNWARE NAMATAYAN GANUN OR GALING BREAK UP
● Sex
 ● Medications
● Drugs or alcohol

Sign and Symptoms:

● Feeling nervous, restless or tense
● Having a sense of impending danger, panic or doom
● Having an increased heart rate
● Breathing rapidly (hyperventilation)
● Sweating
● Trembling
● Feeling weak or tired
● Trouble concentrating or thinking about anything other than the present worry
● Having trouble sleeping
● Experiencing gastrointestinal (GI) problems
● Having difficulty controlling worry
● Having the urge to avoid things that trigger anxiety

Lastly, for the TREATMENT

ANDREA:
● Counseling and therapy
The standard treatment for anxiety disorders involves psychological counseling and
therapy This might include psychotherapy, cognitive behavioral therapy (CBT), or a
combination of different therapy modalities. This helps people manage the way they
react to certain triggers. A therapist who practices CBT can help a person develop
cognitive exercises that replace negative thoughts with positive ones.

● Medications
Medications can provide offer benefits to people with anxiety. However, a person who begins to
take medications for anxiety should be cautious about not stopping them abruptly.
● Complemental health techniques.
Mindfulness, yoga, and self-management strategies such as stress management are ways to
treat your anxiety using alternative methods.

What natural remedies are used for anxiety?

● getting enough sleep
● meditating
● staying active and exercising
● eating a healthy diet
● avoiding alcohol
● avoiding caffeine
● quitting smoking cigarettes if you smoke
Group #4
● Dungca, Justine
● Morales, Allaisa
● Nikka, Miranda
● Nacpil, Debbra

Major Depressive Disorder

❖ INTRODUCTION
● Major depressive disorder is also known as Clinical depression
● Common mental health disorder

- Major depressive disorder (MDD) related to sadness which is a natural part of the human
experience.
- Humans may feel sad or depressed when a loved one passes away or when they're
going through a life challenge.
- This feeling may be short-lived but when someone experiences continuous and intense
feelings of sadness for a long period of time, then they may have MDD. MDD, also
referred to as clinical depression.

Major depressive disorder impacts a person's

● Mood
● Cognition
● Behavior

❖ EPIDEMIOLOGY
● Women (10.4%) were almost twice as likely as were men (5.5%) to have had
depression.
● It's estimated that one-in-three women and one-in-five men have an episode of major
depression by the age of 65.
● The average age of onset for major depressive disorder is between 35 and 40 years of
age.

❖ ETIOLOGY
● Genetic cause
● Environmental factors
● Biochemical factors: Biochemical theory of depression postulates a deficiency of
neurotransmitters in certain areas of the brain (noradrenaline, serotonin, and dopamine).
● Dopaminergic activity: reduced in case of depression, over activity in mania.
● Endocrine factors
- hypothyroidism, cushing's syndrome etc
❖ PATHOPHYSIOLOGY

● Serotonin is involved with mood, happiness, anxiety, and sleep induction.

Raphe-Serotonin System normally modulates homeostasis, emotionality, and tolerance
to aversive experiences
● Norepinephrine in the brain helps regulate alertness, mood, functions in dream sleep,
and maintains arousal. It also can help in the response to stressful situations.
● Dopamine in the brain regulates reward and motivation which could explain the loss of
interest in patients with depression. Dopamine motivates people to take action toward
goals, desires, and needs, and issues a surge of reinforcing pleasure once they’ve been
accomplished

The monoamine-deficiency theory posits that the underlying pathophysiological basis of

depression is a depletion of the neurotransmitters serotonin, norepinephrine or
dopamine in the central nervous system. Serotonin is the most extensively studied
neurotransmitter in depression.

1. Pathophysiology: Genetic Predisposition and Environmental Influences

- The combination of life stressors and a potentially dysfunctional serotonin (5-HT)

system. The serotonin transporter serves in the reuptake of serotonin at the synapse and
may moderate the serotonergic response to stress. Individuals with 2 copies of the s
allele were more likely to develop major depression and have suicidal thoughts in
 response to stressors than individuals homozygous for the l allele. As well as, individuals
with 2 s alleles increased their risk for major depression episodes by twofold after
experiencing 4 or more stressful events

2. Pathophysiology: Neurochemical dysregulation

- There are antidepressant drugs that can increase neurotransmitters in the body leading
to another theory called the monoamine hypothesis of depression. In this hypothesis,
there is a deficit in the concentration of the brain norepinephrine, dopamine, and/or
serotonin resulting in depression. Antidepressant therapies focus on increasing the
monoamine neurotransmitter levels within the synapses

3. Pathophysiology: Neuroendocrine Dysregulation

There are 2 theories in the pathophysiology of depression that involve dysregulation of

the neuroendocrine system.

a. The first one focuses on stress and the hypothalamic-Pituitary-Adrenal system. The
hypothalamic-pituitary-adrenal system (HPA) plays an essential role in an individual’s
ability to cope with stress. Chronic activation of the HPA system and chronic
glucocorticoid secretion are found in 30-70% of individuals with major depression
suggesting the correlation between the dysfunctional system and depression. Chronic
cortisol release in the body results in secretion of pro-inflammatory cytokines which
causes immunosuppression and inflammation. Also, there is a Neurotrophic Hypothesis
of depression. It is thought to focus on neuronal atrophy of the hippocampus resulting in
no cell growth consequently causing in a reduction of the hippocampal brain derived
neurotrophic factor (BDNF) and has been proposed as an extension of the monoamine
hypothesis of depression.
 b. The second neuroendocrine dysregulation is in the hypothalamic-pituitary-thyroid
system. While this dysfunction is not completely understood, 20-30% cases of major
depression have shown to have an altered hypothalamic-pituitary-thyroid (HPT) system.
There is an increase in thyrotropin releasing hormone, blunted thyroid stimulating
hormone in response to TRH challenge and decreased nocturnal rise in TSH level that
normally occur. This all increases risk for relapse

4. Pathophysiology: Neuroanatomic and Function Abnormalities

- Depressed individuals post-mortem brains have shown widespread decrease in

serotonin 5-HT1 a receptor subtype binding in the frontal, temporal, and limbic cortex as
well as serotonin transporter binding in the cerebral cortex and hippocampus, reflecting a
dysfunction in the raphe-serotonin system

❖ DIAGNOSIS
● Physical exam. Your doctor may do a physical exam and ask questions about
your health. In some cases, depression may be linked to an underlying physical
health problem.
● Lab tests. For example, your doctor may do a blood test called a complete blood
count or test your thyroid to make sure it's functioning properly.
● Psychiatric evaluation. Your mental health professional asks about your
symptoms, thoughts, feelings and behavior patterns. You may be asked to fill out a
questionnaire to help answer these questions.
● DSM-5. Your mental health professional may use the criteria for depression listed
in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), published by
the American Psychiatric Association.

Diagnosis of Major depressive disorder has few conditions like medical, psychiatric and other
conditions.

Medical Condition
● Neurological abnormality (e.g.,Parkinson's Disease, Huntington Disease, Multiple
Sclerosis, Dementia.
● Renal or Cardiopulmonary disease.
● Cancer (pancreatic) and gastrointestinal tumors.
● Viral illness (e.g., pneumonia, influenza, AIDS)
● Nutritional deficiency (e.g., Folic acid, B12)

Psychiatric Conditions:
 ● Anxiety disorder, Schizophrenia, Eating disorder, Somatic symptom disorder.
● Normal reaction to a life loss.
● Drug and alcohol use ( Particularly use of sedatives and withdrawal from stimulants.
● Prescription drug use (like steroids, antihypertensives, antineoplastics.

❖ CLINICAL MANIFESTATIONS

To be diagnosed with Major Depressive Disorder, requires that a number of different symptoms
are present everyday for at least two weeks. Major Depressive Disorder affects people’s lives in
many different ways.

“SIG-E-CAPS”
S- leep changes
I- nterest loss
G- uilt
E- nergy
C- ognition/Concentration
A- ppetite disturbance
P- sychomotor
S-uicide

Depression Symptoms in Children

● Sadness
● Irritability
● Clinginess
● Refusing to go to school
● Being underweight

Depression symptoms in teens

● Anger
● Feeling negative and worthless
● Poor performance or poor attendance at school
● Feeling misunderstood and extremely sensitive
● Using recreational drugs or alcohol
● Eating or sleeping too much, self harm
● Loss of interest and avoidance of social interaction

Depression symptoms in older adults

● Memory difficulties
● Physical aches or pain
● Sleep problems or loss of interest in sex- not caused by a medical condition or
medication
 ● Loss of interest in socializing or in activities
● Suicidal thinking or feelings, especially in older men

1. DIAGNOSIS OF MDD IS ALSO RELATED WITH OTHER CONDITION.

➢ Major depressive disorder has relation with a few medical conditions, psychiatric
conditions, and other conditions
➢ It is most commonly confused with Bipolar Disorder and other types of
depressive disorders previously mentioned.

2. MEDICAL CONDITIONS
➢ Neurological abnormality (e.g., Parkinson’s disease, Huntington disease, Multiple
sclerosis, Dementia).
➢ Renal or Cardiopulmunary disease
➢ Cancer (pancreatic) and gastrointestinal tumors
➢ Viral illness
➢ Nutritional defeiency (e.g,. Folic acid, B12)

3. PSYCHIATRIC AND RELATED CONDITIONS

➢ Anxiety disorder. Schizophrenoa, Eating disorder, Somatic symptom disorder
➢ Normal reaction to a life loss
➢ Drug and alcohol use (particulary use of sedatives and withdrawal from
stimulants)
➢ Prescription drug use (like steriods, antihypertensive, antineoplastics.

MMD DSM 5
A. Five or more of the following symptoms either
1. Depressed mood or
2. Loss of interest or pleasure have been present during the same 2-week period.
3. Depressed mood:
- For children and adolescents, this can also be an irritable mood.
4. Anhedonia
- Loss of interest or pleasure in almost all activities
5. Appetite disturbance
- Weight loss or gain
6. Insomnia or Hypersomnia
7. Psychomoto agitation or retardation
8. Fatigue
9. Feeling of worthlessness
10. Decreased concentration
11. Thoughts of death/suicide

B. The symptoms cause clinically significant distress or impairment in social, occupational or

other important area.
C. the episode is not attributable to the physiological effects of a substance or to another
medical condition.
D. the occurence of major depressive episode is not better expained by another disorders
E. there has never been a manic episode or hypomanic episode.

❖ TREATMENT

Treatment for depression can be long term, but there are many effective options out there.
➢ See your doctor regularly to address any other health problems that could be impacting
your mood. If your treatment includes medication, keep taking it as your doctor
prescribed, but be sure to let them know how it’s working or any side effects that you are
having.
➢ CONNECTS WITH A LICENSED THERAPIST
- In addition to medication, your doctor may also suggest talk therapy. Combining
tese 2 strategies can be very effective, so work with your doctors to create the
best treatment strategy for you.
- Finding a healthy life while living with depression takes a lot of work, but it’s so
important to keep working toward your treatment goals.
- Here’s a couple of things to keep in mind.
1. Have realistic goals
2. Spend your time with friends and family
3. Postpone any big decision during a depressive episode
4. Continue to educate yourself about the mood-related symptoms of
depression

MEDICATION OF MDD

1. Selective serotonin reuptake inhibitors (SSRIs).

➢ Are generally used. Doctors often start by prescribing an SSRI. These drugs are
considered safer and generally cause fewer bothersome side effects than other
types of antidepressants.
➢ SSRIs include Citalopram (Celexa), Fluoxetine (Prozac), Paroxetine (Paxil,
Pexeva), Sertraline (Zoloft) and Vilazodone (Viibryd).
2. Serotonin-norepinephrine reuptake inhibitors (SNRIs)
➢ Examples of SNRIs include Duloxetine (Cymbalta), Venlafaxine (Effexor XR),
Desvenlafaxine (Pristiq, Khedezla) and Levomilnacipran (Fetzima).
3. Atypical antidepressants
➢ These medications don't fit neatly into any of the other antidepressant categories.
They include bupropion (Wellbutrin XL, Wellbutrin SR, Aplenzin, Forfivo XL),
mirtazapine (Remeron), nefazodone, trazodone and vortioxetine (Trintellix).
 4. Tricyclic antidepressants
➢ Drug such as imipramine (Tofranil), nortriptyline (Pamelor), amitriptyline,
doxepin, trimipramine (Surmontil), desipramine (Norpramin) and protriptyline
(Vivactil) are very effective, but tend to cause more-severe side effects than
newer antidepressants. So tricyclics generally aren't prescribed unless you've
tried an SSRI first without improvement.
5. Monoamine oxidase inhibitors (MAOIs)
➢ MAOIs such as tranylcypromine (Parnate), phenelzine (Nardil) and isocarboxazid
(Marplan) may be prescribed, typically when other drugs haven't worked,
because they can have serious side effects. Using MAOIs requires a strict diet
because of dangerous (or even deadly) interactions with foods such as certain
cheeses, pickles and wines and some medications and herbal supplements.
➢ Selegiline (Emsam), a newer MAOI that has fewer side effects than other MAOIs
do. These medications can’t be combined with SSRIs
6. Other medications
➢ Other medications may be added to an antidepressant to enhance
antidepressant effects. Your doctor may recommend combining two
antidepressants or adding medications such as mood stabilizers or
antipsychotics
➢ Anti-anxiety and stimulant medications also may be added for short-term use.

*Other Treatment Options

1. Electroconvulsive therapy (ECT)

● Is used in depression to impact the function and effect of the neurotransmitter in
the brain.
2. Transcranial magnetic stimulations (TMS)
● Uses magnetic pulses to stimulate nerve cells in the brain that are involved in the
regulation of mood.
3. Lifestyle and Home remedies
● In addition to professional treatment.
● Stick to a treatment plan.
● Learn to pay attention to warning signs.
● Avoid taking alcohol and recreational drugs.

Mind-Body connections

● Acupuncture
 ● Relaxation techniques e.g Yoga
● Meditation session and guided imagery.
● Massage therapy.
● Art or music therapy.
● Aerobic exercises.

Schizophrenia

❖ INTRODUCTION
● Schizophrenia literally means "Fragmented MInd".
● Schizophrenia is one of the most complex, chronic and challenging of psychiatric
disorders that affects how a person thinks, feels, behaves.
● It represents a heterogeneous syndrome of disorganized thoughts, delusions,
hallucinations, and impaired psychosocial functioning.

Brain imaging shows that people with schizophrenia have less gray matter volume,
especially in the temporal and frontal lobes. These areas of the brain are important for thinking
and judgment. What's more, gray matter loss continues over time. Studies show that certain
brain chemicals that control thinking, behavior, and emotions are either too active or not active
enough in people with schizophrenia. Doctors also believe the brain loses tissue over time.

Individuals with schizophrenia have up to 25% less volume of gray matter in their brains,
especially in the temporal and frontal lobes (known to be important for coordination of thinking
and judgment). Patients demonstrating the worst brain tissue losses also tend to show the worst
symptoms.
❖ ETIOLOGY
● While many factors have been associated with developing schizophrenia—including
genetics, early environment, neurobiology, and psychological and social processes--the
exact cause of the disease is unknown.

1. Viral Infections and Immune Disorders :

● Schizophrenia may be triggered by environmental events, such as viral infections or
immune disorders.
● For instance, babies whose mothers get the flu while they are pregnant are at higher risk
of developing schizophrenia later in life. People who are hospitalized for severe
infections are also at higher risk.

2. Genetics (Heredity) :
● Scientists recognize that the disorder tends to run in families and that a person inherits a
tendency to develop the disease. Similar to some other genetically-related illnesses,
schizophrenia may appear when the body undergoes hormonal and physical changes.
● The risk of developing schizophrenia increases to approximately 10% if a first-degree
relative has the illness and to 3% if a second-degree relative has the illness. If both
parents have schizophrenia, the risk of producing a schizophrenic offspring increases to
approx 40%,

❖ EPIDEMIOLOGY
● Schizophrenia most commonly has its onset in The peak ages of onset are 20–38 years
for males and 26-32 years for females, late adolescence or early adulthood and rarely
occurs before adolescence or after the age of 40 years.
● Slightly more men are diagnosed with schizophrenia than women (on the order of 1.4:1)
and women tend to be diagnosed later in life than men

❖ PATHOPHYSIOLOGY
 - dysregulation of neurotransmitter dopamine, glutamate, GABA and serotonin

1. Dopamine Hypothesis
● Numerous Positron Emission Tomography (PET) studies have shown dopaminergic
hyperactivity in the nucleus accumbens and dopaminergic hypofunction in the fronto
temporal regions.
● PET studies using D-specific ligands provide data suggesting increased densities of D,
receptors in the nucleus accumbens
● PET studies assessing D function suggest that subpopulations of schizophrenics may
have decreased densities of D, receptors in the prefrontal cortex.
● Thus positive symptoms are thought to result from overactivity in the mesolimbic
dopaminergic pathway activating D receptors whereas negative symptoms may result
from a decreased activity in the mesocortical dopaminergic pathway where D, receptors
predominate.

2. Glutamate Hypothesis
● NMDA receptor hypofunction is thought to reduce the level of activity in mesocortical
dopaminergic neurons. This would result in a decrease in dopamine release in the
prefrontal cortex and thus give rise to negative symptoms of schizophrenia.
● On the other hand, NMDA receptor hypofunction is thought to enhance activity in the
mesolimbic dopaminergic pathway, perhaps because in this pathway the important
NMDA receptors are those located on GABAergic interneurons.
● Thus NMDA receptor hypofunction would result in reduced GABAergic inhibition
(disinhibition) of mesolimbic dopaminergic neurons and thus give rise to enhanced
dopamine release in limbic areas such as the nucleus accumbens.

3. 5-HT Hypothesis
● Serotonergic receptors are present on dopaminergic axons and it is known that
stimulation of these receptors will decrease DA release in the prefrontal cortex.
● Patients with schizophrenia with abnormal brain scans have higher whole blood 5-HT
concentrations and these concentrations are correlated with increased ventricular size.
● Atypical antipsychotics with potent 5-HT, receptor antagonist effects reverse worsening
of symptomatology induced by 5-HT agonists in patients with schizophrenia

❖ TYPES
Paranoid schizophrenia
● Common form of schizophrenia
● Prominent hallucinations and/or delusions.
● May develop at a later age than other types of schizophrenia,
● Speech and emotions may be unaffected
● At risk for suicidal or violent behavior under influence of delusions
Hebephrenic / Disorganized schizophrenia
● Behaviour is disorganised and without purpose
● Thoughts are disorganised, difficult to understand by others
● Pranks, giggling, health complaints, grimacing and mannerisms are, common
● Delusions and hallucinations are fleeting
● Usually develops between 15-25

Catatonic schizophrenia
● Rarer than other types
● At risk for malnutrition, exhaustion or self-injury
● Unusual movements, often switching between extremes of over activity and stillness
● Unable to talk (Catatonia)

Undifferentiated schizophrenia
● Some characteristics of paranoid, hebephrenic or catatonic schizophrenia, but does not
obviously fit one of these types

Residual schizophrenia
● Past History of psychosis but only having negative symptoms

❖ DIAGNOSIS

● DIAGNOSTIC CRITERIA FOR SCHIZOPHRENIA :

- It includes the criteria in the Diagnostic and Statistical Manual of Mental
Disorders (DSM-IV), published by the American Psychiatric Association.

● MEDICAL HISTORY :
- A thorough medical history is the first step in the diagnosis of schizophrenia. This
may be done to find other problems that could be causing symptoms and to
check for any related complications.

● BLOOD TESTS & IMAGING :

- A Complete Blood Count (CBC) test is helpful to monitor general health and rule
out other conditions that may have been responsible for the symptoms. A blood
test can provide accurate information about the involvement of recreational
drugs. In some cases, certain imaging techniques such as Magnetic Resonance
Imaging (MRI) or Computed Tomography (CT) scan may aid in the diagnosis.

● PSYCHIATRIC EVALUATION :
- A doctor or mental health professional checks mental status by observing
appearance, demeanor and asking about thoughts, moods and awareness. A
person may be diagnosed if they have at least 2 of the following symptoms
usually over a month :
 ● Delusions
● Hallucinations
● Disorganised behaviour
● Disorganised speech and thought processes
● Catatonic behaviour, presenting as strong daze or hyperactivity
● Negative symptoms, impaired normal function

❖ CLINICAL MANIFESTATIONS

Positive Symptoms
DELUSION: False beliefs that are not based in reality
HALLUCINATION: Involving seeing or hearing things that don't exist
DISORGANIZED SPEECH & THINKING : Effective communication can be impaired and
answers to questions may be partially or completely unrelated
CATATONIA : Purposeless abnormal motor activity or aggressive, behavior

Cognitive Symptoms
POOR EXECUTIVE FUNCTIONING : Unability to understand information to make decisions
POOR WORKING MEMORY : Unability to use information immediately after learning

Negative Symptoms
FLAT EFFECT : Reduced expression of emotions via facial expression or voice tone
ALOGIA : Reduced speech
AVOLITION : Inability to begin & sustain activities
ANHEDONIA : Inability to experience pleasure

❖ TREATMENT
● There is no known cure for Schizophrenia. Fortunately, there are effective treatments
that can reduce symptoms, decrease the likelihood that new episodes of psychosis will
occur, shorten the duration of psychotic episodes, and in general, offer the majority of
people the possibility of living more productive and satisfying lives.
● With the proper medications and supportive counseling, the ability of schizophrenic
persons to live and function relatively well in society is excellent.
● Medications are the cornerstone of schizophrenia treatment, and antipsychotic
medications are the most commonly prescribed drugs. They're thought to control
symptoms by affecting the brain neurotransmitter dopamine.
● The goal of treatment with antipsychotic medications is to effectively manage signs and
symptoms at the lowest possible dose. The psychiatrist may try different drugs, different
doses or combinations over time to achieve the desired result. Other medications also
may help, such as antidepressants or anti-anxiety drugs. It can take several weeks to
notice an improvement in symptoms.
➢ Second-generation antipsychotics
- These newer, second-generation medications are generally preferred because
they pose a lower risk of serious side effects than do first-generation
antipsychotics.

Common second-generation antipsychotics include:

● Aripiprazole
● Asenapine
● Brexpiprazole

➢ First-generation antipsychotics
These first-generation antipsychotics have frequent and potentially significant
neurological side effects, including the possibility of developing a movement disorder
(tardive dyskinesia) that may or may not be reversible.

Common First-generation antipsychotics include:

● Chlorpromazine
● Fluphenazine
● Haloperidol

These antipsychotics are often cheaper than second-generation antipsychotics,

especially the generic versions, which can be an important consideration when long-term
treatment is necessary.

➢ Long-acting injectable antipsychotics

- Some antipsychotics may be given as an intramuscular or subcutaneous
injection. They are usually given every two to four weeks, depending on the
medication. The physician will provide more information on injectable
medications. This may be an option if someone has a preference for fewer pills
and may help with adherence.

Common medications that are available as an injection include:

● Aripiprazole (Abilify Maintena, Aristada)
● Fluphenazine decanoate
● Haloperidol decanoate

➢ Psychosocial interventions
Once psychosis recedes, in addition to continuing on medication, psychological and
social (psychosocial) interventions are important. These may include:
 ● Individual therapy. Psychotherapy may help to normalize thought patterns. Also,
learning to cope with stress and identify early warning signs of relapse can help
people with schizophrenia manage their illness.

● Social skills training. This focuses on improving communication and social

interactions and improving the ability to participate in daily activities.

● Family therapy. This provides support and education to families dealing with
schizophrenia.

● Vocational rehabilitation and supported employment. This focuses on helping

people with schizophrenia prepare for, find and keep jobs.

➢ Hospitalization
During crisis periods or times of severe symptoms, hospitalization may be necessary to
ensure safety, proper nutrition, adequate sleep and basic hygiene.

➢ Electroconvulsive therapy
For adults with schizophrenia who do not respond to drug therapy, electroconvulsive
therapy (ECT) may be considered. ECT may be helpful for someone who also has
depression.

References:
https://www.slideshare.net/Dryogeshcsv/major-depressive-disorder-mdd-ppt
https://u.osu.edu/majordepressioncasestudy2018/pathophysiology/
https://www.slideshare.net/rahulbs89/depression-35571974
https://www.slideshare.net/Dryogeshcsv/major-depressive-disorder-mdd-presentation
https://www.mayoclinic.org/diseases-conditions/schizophrenia/diagnosis-treatment/drc-2035444
9
https://www.slideshare.net/RuchitaBhavsar/schizophrenia-74881247
https://pt.slideshare.net/silky1/schizophrenia-29590580/11
https://youtu.be/98iuc4ift9I
 CLINICAL PHARMACY
(Group 1)
Members:
Acenas, Patricia Ysabel
Baldemor, Paul
Bagas, Kate
Cabrera, Keisha Lee
Visda, Mariel

TOPICS: Epilepsy, Headache, Migraine, and Tension type

Objectives: Pathophysiology, Diagnosis, Clinical manifestations (Signs and symptoms) and,

Treatment

EPILEPSY - is sometimes called a seizure disorder, is a disorder of the brain. A person is

diagnosed with epilepsy when they have had two or more seizures. A seizure is a
shortchange in normal brain activity. Seizures are the main sign of epilepsy. Some seizures
can look like staring spells.

Pathophysiology
➢ The clinical manifestation of epilepsy is a seizure. This is caused by excessive
neuronal firing and the rapid diffusion of these impulses throughout the brain. Thus,
in the pathophysiology of a seizure, there are two phenomena: hyper-excitability of
a neuron. Hyper synchronization

Diagnosis
➢ The specialist may recommend an electroencephalogram (EEG) test to monitor your
brain activity or a brain scan to search for any problems in your brain. However,
even if these tests come out negative, you might still have epilepsy and be diagnosed
based only on your symptoms.

Clinical Manifestation
➢ Temporary confusion.
➢ A staring spell.
➢ Stiff muscles.
➢ Uncontrollable jerking movements of the arms and legs.
➢ Loss of consciousness or awareness.
➢ Psychological symptoms such as fear, anxiety or deja vu.

Treatments
➢ medicines called anti-epileptic drugs (AEDs)
➢ surgery to remove a small part of the brain that's causing the seizures.
➢ a procedure to put a small electrical device inside the body that can help control
seizures.
➢ a special diet (ketogenic diet) that can help control seizures.
Headache - is the symptom of pain anywhere in the region of the head.

Types of headaches: Cluster headache, Tension headache, and Migraine

Pathophysiology
➢ The brain parenchyma does not have nociceptors, and thus, headache is typically
the result of pain originating in surrounding structures, such as blood vessels,
meninges, muscle fibers, facial structures, and cranial or spinal nerves.

Diagnosis
➢ Location
➢ Onset
➢ Duration
➢ Character
➢ Severity
➢ Radiation
➢ Exacerbating or Alleviating Factors
➢ Associations

Labs and Tests

➢ There are no specific laboratory tests for identifying primary headache disorders.
To evaluate your general health and rule out potential causes of secondary
headaches, such as infection, dehydration, diabetes, and thyroid conditions, you may
undergo blood and urine tests. Imaging
➢ If you have symptoms that suggest a structural cause for your headaches, your
doctor may order imaging tests even though they are not typically part of a
headache workup.

Clinical Manifestation
➢ Deep and constant pain in the cheekbones, forehead, or bridge of the nose. Pain that
gets worse with sudden head movement or straining. Pain along with other sinus
symptoms, like nasal discharge, a feeling of fullness in the ears, fever, and facial
swelling.

Treatments
➢ Rest in a quiet, dark room.
➢ Hot or cold compresses to your head or neck.
➢ Massage and small amounts of caffeine.
➢ Over-the-counter medications such as ibuprofen (Advil, Motrin IB, others),
acetaminophen (Tylenol, others) and aspirin.

Tension-type headache (TTH) - is generally a mild to moderate pain that's often

described as feeling like a tight band around the head. Tension headaches are the most
common type of headache, yet its causes aren't well understood.

There are two types: * Episodic tension headaches * Chronic tension headaches
Pathophysiology
➢ Increased excitability of the central nervous system generated by repetitive and
sustained pericrania myofascial input may be responsible for the transformation of
episodic tension-type headache into the chronic form. Studies of nitric oxide (NO)
mechanisms suggest that NO may play a key role in the pathophysiology of tension-
type headache and that the antinociceptive effect of nitric oxide synthase inhibitors
may become a novel principle in the future treatment of chronic headache

Diagnosis
➢ Diagnosed based on the symptoms you report. There are two common tests that can
be used to image your brain include: Magnetic resonance imaging (MRI)
Computerized tomography (CT)

Clinical Manifestation
➢ Dull, aching head pain
➢ Head usually hurts on both sides
➢ Muscle aches
➢ Pain is usually mild to moderate, but not severe

Treatments
Acute medications Preventive medications Supplements

Migraine - is a complex neurological disease symptom well beyond a headache. Which can
also impact the entire nervous system. Which means people may experience symptoms in
various parts of the body.

Types of Migraine
Episodic and Chronic Migraine
Episodic Migraine- migraine who have 0 to 14 headache days per month
Chronic Migraine - Is characterized by 15 or more headache days per month

Migraine with Aura

Aura- is a temporary sensory disturbance before or during the headache. And about 25-
30% of people experience migraine with aura.

Some examples of common auras:

➢ Visual Disturbance
➢ Phantom smells
➢ Ringing in the ears
➢ Dizziness

Pathophysiology
➢ is a primary brain disorder most likely involving an ion channel in the aminergic
brain stem nuclei (←), a form of neurovascular headache in which neural events
 result in dilation of blood vessels aggravating the pain and resulting in further nerve
activation.

Diagnosis
Patient must have had at least 5 headache attacks that lasted 4 to 72 hours.
And headache should have had at least 2 Characteristics
➢ One sided head pain
➢ Pulsating Sensation
➢ Moderate or severe pain intensity
➢ Aggravation by physical activity

Clinical Manifestation
➢ Nausea
➢ Vomiting
➢ Light Sensitivity
➢ Sound Sensitivity
➢ Confused thinking
➢ Ear pain
➢ Dizziness

Treatments
Drug Treatment’s for Migraine
➢ Analgesics
➢ NSAID’s (Nonsteroidal Anti- Inflammatory Drug)
➢ Triptans
➢ Gepants

References:
https://www.cdc.gov
https://www.new-medical.net
https://www.nhs.uk
https://www.mayoclinic.org
https://www.webmd.com
https://www.ncbi.nlm.nih.gov
 WRITTEN REPORT
GROUP 3

Alzheimer’s Disease
&
Bipolar Disorder

MEMBERS:

DIZON, IRYL
GARCIA, TRISHA IVY
LAYAG, MA. KHRISNA
MANALANG, PATRICIA
WANDAG, TRISHA KATE

1
 ALZHEIMER’S DISEASE

What is Alzheimer’s Disease?

- In terms of dementia, Alzheimer's disease is the most prevalent. This disease is progressive,
starting with mild memory loss and potentially progressing to the loss of communication and
environmental awareness. The brain regions that are responsible for thought, memory, and
language are affected by Alzheimer's disease. It can significantly impair a person's capacity to
carry out daily tasks.

The 3 types of Alzheimer’s Disease are:

● Early-Onset
● Late-Onset
● Familial

Early-Onset Alzheimer’s
- People in their 30s or 40s may develop early-onset Alzheimer's disease. It has an impact
on behavior, thinking, and memory. Up to 5% of all Alzheimer's patients rarely have
early-onset dementia. People with Down syndrome are more likely to develop it.

Late-Onset Alzheimer’s
- Progressive episodic memory loss is a hallmark of late-onset Alzheimer's disease, with
varied involvement of other cognitive functions. Other medial temporal lobe-related
neurodegenerative conditions can also result in progressive memory impairment.

2
Familial Alzheimer’s
- is a type of Alzheimer's disease that has a known genetic basis, according to medical
professionals. Members of at least two generations have suffered the illness in affected
families. Less than 1% of all instances of Alzheimer's are caused by FAD. The majority
of those with early-onset Alzheimer's have FAD.

PATHOPHYSIOLOGY
Alzheimer’s Disease affects the 3 processes that keep neurons healthy: communication,
metabolism, and repair. Changes in AD include progressive cortical atrophy which leads to the
neurofibrillary tangles in the neurons and senile plaques. Both neurofibrillary tangles and senile
plaques are found in large numbers in the affect’s parts of the brain in which “the plaques
disrupt neural conduction containing fragments from beta-amyloid precursor protein”. Amyloid
plaques consist of abnormal proteins and fragments of nerve cells that are attached to other
nerve cells.

When a nerve cell dies the amyloid protein is embedded in the cell membrane and when it
breaks off a fragment of the protein is still present, and it builds up in the brain. It’s the
destruction and death of the nerve cells and the deposits of the protein on the membrane that
causes memory failure, personality changes and carrying out activities of daily living.

CLINICAL MANIFESTATIONS (Signs and Symptoms)

Clinical Manifestations of Alzheimer’s occur in cognitive changes, changes in behavior and

personality, and changes in self-management skills.

Cognitive changes
● Apraxia (inability to use objects correctly)
● Aphasia (inability to speak or understand)
● Anomia (inability to find words)
● Agnosia (loss of sensory comprehension)

Behavior and Personality Changes

● Aggressiveness, especially verbal and physical abusive tendencies
● Rapid mood swings

3
 ● Wandering and getting lost
● Paranoia, delusions, hallucinations, and depression may occur

Changes in self-management skills

● Decreased interest in personal appearance
● Selection of clothing that is inappropriate for the weather or event
● Loss of bowel and bladder control
● Decreased appetite or ability to eat

Stages of Alzheimer's disease

Generally, the symptoms of Alzheimer's disease are divided into 3 main stages.

❖ Early symptoms
In the early stages, the main symptom of Alzheimer's disease is memory lapses.
For example, someone with early Alzheimer's disease may:
● forget about recent conversations or events
● misplace items
● forget the names of places and objects
● have trouble thinking of the right word
● ask questions repetitively
● show poor judgment or find it harder to make decisions
● become less flexible and more hesitant to try new things
● There are often signs of mood changes, such as increasing anxiety or agitation, or
periods of confusion.

❖ Middle-stage symptoms
As Alzheimer's disease develops, memory problems will get worse.
● Someone with the condition may find it increasingly difficult to remember the names of
people they know and may struggle to recognise their family and friends.

Other symptoms may also develop, such as:

● increasing confusion and disorientation – for example, getting lost, or wandering and not
knowing what time of day it is
● obsessive, repetitive or impulsive behavior

4
 ● delusions (believing things that are untrue) or feeling paranoid and suspicious about
carers or family members
● problems with speech or language (aphasia)
● disturbed sleep
● changes in mood, such as frequent mood swings, depression and feeling increasingly
anxious, frustrated or agitated
● difficulty performing spatial tasks, such as judging distances
● seeing or hearing things that other people do not (hallucinations)
● Some people also have some symptoms of vascular dementia.

By this stage, someone with Alzheimer's disease usually needs support to help them with
everyday living. For example, they may need help eating, washing, getting dressed and using
the toilet.

❖ Later symptoms
In the later stages of Alzheimer's disease, the symptoms become increasingly severe and can
be distressing for the person with the condition, as well as their carers, friends and family.
● Hallucinations and delusions may come and go over the course of the illness, but can
get worse as the condition progresses.
● Sometimes people with Alzheimer's disease can be violent, demanding and
suspicious of those around them.

A number of other symptoms may also develop as Alzheimer's disease progresses, such as:
● difficulty eating and swallowing (dysphagia)
● difficulty changing position or moving around without assistance
● weight loss – sometimes severe
● unintentional passing of urine (urinary incontinence) or stools (bowel incontinence)
● gradual loss of speech
● significant problems with short- and long-term memory
● In the severe stages of Alzheimer's disease, people may need full-time care and
assistance with eating, moving and personal care.

5
 DIAGNOSIS
● Mental status testing. Your doctor may conduct mental status tests to test your
thinking (cognitive) and memory skills. Doctors use the scores on these tests to
evaluate your degree of cognitive impairment.
● Neuropsychological tests. You may be evaluated by a specialist trained in brain
conditions and mental health conditions (neuropsychologist). The evaluation can
include extensive tests to evaluate your memory and thinking (cognitive) skills.
These tests help doctors determine if you have dementia, and if you're able to safely
conduct daily tasks such as taking medications as scheduled and managing your
finances. They provide information on what you can still do as well as what you may
have lost. These tests can also evaluate if depression may be causing your
symptoms.
● Interviews with friends and family. Doctors may ask your family member or friend
questions about you and your behavior.
Doctors look for details that don't fit with your former level of function. Your family
member or friend often can explain how your thinking (cognitive) skills, functional
abilities and behaviors have changed over time.

Brain imaging tests

- Rule out other causes, such as hemorrhages, brain tumors or strokes

- Distinguish between different types of degenerative brain disease
- Establish a baseline about the degree of degeneration

6
Examples:

Magnetic resonance imaging (MRI). MRI uses radio waves and a strong magnetic field
to produce detailed images of the brain. While they may show brain shrinkage of brain
regions associated with Alzheimer's disease, MRI scans also rule out other conditions.

Computerized tomography (CT). A CT scan, a specialized X-ray technology, produces

cross-sectional images (slices) of your brain.

Positron emission tomography (PET). A PET scan uses a radioactive substance

known as a tracer to detect substances in the body. There are different types of PET
scans. The most commonly used PET scan is a fluorodeoxyglucose (FDG) PET scan.
This scan can identify brain regions with decreased glucose metabolism. The pattern of
metabolism change can distinguish between different types of degenerative brain
disease.

7
 TREATMENT
Primary treatment for Alzheimer disease:
- To enhance mood, cognition, and behavior while maximizing functional abilities
- No cure for alzheimer disease
- Drugs called cholinesterase inhibitors can cause cognitive symptoms, including memory
loss, confusion, altered thought processes, and judgment problems.

Three common drugs approved by the FDA to treat these disease of alzheimers are:
- Donepezil ( Aricept), to treat all stages
- Galantamine (Razadyne), to treat mild-to-moderate stages
- Rivastigmine (Exelon), to treat mild-to-moderate stages

Another drugs, Memantine (Namenda) to treat moderate to severe alzheimer disease

- Memantine and donepezil (Namzaric) is the first fixed-dose combination medication
approved in the US to treat mild to moderate Alzheimer's disease.

Non-cognitive Symptoms:
● Antipsychotic drugs (Olanzapine, Risperidone)
- Haloperidol 1-3mg/day

● Anticonvulsant Agent (Valproic acid)

- Carbamazepine Oral: 200-400mg/day tablet

● Antidepressant drugs (Paroxetine, Sertraline)

- Fluoxetine 10-40mg/day tablet/capsule

8
 BIPOLAR DISORDER
What is Bipolar Disorder?
- Bipolar disorder (also known as manic-depressive illness or manic depression) is a brain
disorder that causes fluctuations in a person's mood, energy, and ability to function. Bipolar
disorder patients experience emotionally intense states that typically occur over a period of days
to weeks, known as mood episodes. These mood swings are classified as manic/hypomanic
(excessively joyful or irritable mood) or depressive (sad mood). People with bipolar disorder
frequently experience periods of neutral mood. People with bipolar disorder could still enjoy
living a full and productive life if they are treated.

4 Types of Bipolar Disorder

Bipolar I
- The most common of the four types is bipolar I disorder. Bipolar I is characterized by one
or more manic episodes, with or without depressive episodes. Mania must be severe
enough to necessitate hospitalization and last at least a week or longer.

Bipolar II
- Bipolar II disorder is distinguished by the alternation of less severe hypomanic and
depressive episodes.

Cyclothymic Disorder
- Cyclothymic disorder, also known as cyclothymia, is characterized by repeated mood
swings between depressive and hypomanic states that last for more than two years. The
manic and depressive episodes do not meet the diagnostic criteria for bipolar disorder
episodes. There might be periods of normal mood, but they last no longer than eight
weeks.

Unspecified Bipolar Disorder

- When the symptoms do not fit into the other 3 types but still involve episodes of unusual
manic mood, bipolar disorder otherwise not specified is present.

9
 PATHOPHYSIOLOGY

The pathophysiology of Bipolar Disorder or manic depressive illness(MDI) has not been
determined and no objective biological markers correspond definitively with the disease state.
However, twin, family, and adoption studies all indicate that bipolar disorder has a genetic
component.

The most common cause of bipolar disorder is a family history of the disorder. Some people
have bipolar disorder because of mental health issues that started in their childhood or
adolescence.

CLINICAL MANIFESTATIONS (Signs and Symptoms)

CLINICAL MANIFESTATIONS OF BIPOLAR I DISORDER

● Defined by the occurrence of a manic episode
● The 1st episode of mania usually occurs in the early 20s
● Lifetime suicide rates range from 10% to 15%
● Very young children may present with uncontrollable giggling.
● Adolescents may present with severe anger outbursts and agitation.
● Most children with bipolar disorder have more than one relative with the same condition.

CLINICAL MANIFESTATIONS OF BIPOLAR II DISORDER

● Characterized by the occurrence of hypomania and episodes of major depression in an
individual who has never met criteria for mania or a mixed state.
● Hypomania is determined by the same symptom complex as mania, but the symptoms
are less severe, cause less impairment, and usually do not require hospitalization.
● Suicide occurs in 10% to 15% of patients (same as bipolar I)

CLINICAL MANIFESTATIONS OF CYCLOTHYMIC DISORDER

● Cyclothymic disorder is a milder form of bipolar disorder consisting of recurrent mood
disturbances between hypomania and dysthymic mood.
● A single episode of hypomania is sufficient enough to diagnose cyclothymic disorder,
although most individuals also have dysthymic periods.

10
 ● Cyclothymic disorder is never diagnosed when there is a history of mania, major
depressive episode, or mixed episode.

In bipolar disorder, the dramatic episodes of high and low moods do not follow a set pattern.
Someone may feel the same mood state (depressed or manic) several times before switching to
the opposite mood.

Symptoms of mania ("the highs"):

● Excessive happiness, hopefulness, and excitement
● Sudden changes from being joyful to being irritable, angry, and hostile
● Restlessness
● Rapid speech and poor concentration
● Increased energy and less need for sleep
● Unusually high sex drive
● Making grand and unrealistic plans
● Showing poor judgment
● Drug and alcohol abuse
● Becoming more impulsive
● Less need for sleep
● Less of an appetite
● Larger sense of self-confidence and well-being
● Being easily distracted

During depressive periods ("the lows"), a person with bipolar disorder may have:
● Sadness
● Loss of energy
● Feelings of hopelessness or worthlessness
● Not enjoying things they once liked
● Trouble concentrating
● Forgetfulness
● Talking slowly
● Less of a sex drive
● Inability to feel pleasure
● Uncontrollable crying

11
● Trouble making decisions
● Irritability
● Needing more sleep
● Insomnia
● Appetite changes that make you lose or gain weight
● Thoughts of death or suicide
● Attempting suicide

DIAGNOSIS
- To diagnose bipolar disorder, a doctor may perform a physical examination, conduct an
interview and order lab tests. While bipolar disorder cannot be seen on a blood test or
body scan, these tests can help rule out other illnesses that can resemble the disorder,
such as hyperthyroidism. If no other illnesses (or medicines such as steroids) are
causing the symptoms, the doctor may recommend mental health care.

- To be diagnosed with bipolar disorder, a person must have experienced at least one
episode of mania or hypomania. Mental health care professionals use the Diagnostic
and Statistical Manual of Mental Disorders (DSM) to diagnose the “type” of bipolar
disorder a person may be experiencing. To determine what type of bipolar disorder a
person has, mental health care professionals assess the pattern of symptoms and how
impaired the person is during their most severe episodes.

12
 TREATMENT

Non-Pharmacological treatment
- CBT ( Cognitive- behavioral Therapy)
- Interpersonal, family and group therapy
- Psychoeducation
- ECT ( Electroconvulsive therapy)

Pharmacological treatment
- Antidepressant medication can relieve depressed feelings, restore normal sleep patterns
and appetite, and reduce anxiety
- Slowly return the balance of neurotransmitters in the brain, taking one to four weeks to
achieve their positive effects.
- Some drugs are use to calm person’s manic excitement helps to stabilize the person
mood
- Used as preventive measure they help to control mood swings
- Long term medication may be required to prevent recurrent episodes.

MEDICATIONS USED FOR BIPOLAR

Mood stabilizers
● Medications are usually the first choice to treat bipolar disorder
- Lithium , Depakote
- Lithium are drug of choice for manic episode and preventing further episodes in
bipolar disorder
- 1-2 week period of lag before appreciable improvement
- Carbamazepine, Lamotrigine, Valproate
Antipsychotics
● Are called atypical antipsychotic to set them apart from earlier medications, which called
“conventional” or “first generation” antipsychotic
● Acute manic episode
● Delusional depression
- Haloperidol, Olanzapine, Risperidone,

13
Antidepressants
- Fluoxetine, Prozac

REFERENCE/S:

https://www.mayoclinic.org/diseases-conditions/alzheimers-disease/diagnosis-treatment/drc-203
50453

https://nami.org/About-Mental-Illness/Mental-Health-Conditions/Bipolar-Disorder#:~:text=To%20
be%20diagnosed%20with%20bipolar,social%20situations%20or%20at%20work.

https://www.hopkinsmedicine.org/health/conditions-and-diseases/alzheimers-disease/earlyonset
-alzheimer-disease#:~:text=Alzheimer%20disease%20commonly%20affects%20older,good%20
diet%20and%20regular%20exercise.

https://www.nhs.uk/conditions/alzheimers-disease/symptoms/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6548536/#:~:text=Late%2Donset%20Alzheimer
%20disease%20typically,affecting%20the%20medial%20temporal%20lobes.

https://www.webmd.com/bipolar-disorder/mental-health-bipolar-disorder
https://www.ashleytreatment.org/4-types-of-bipolar-disorder/
https://www.cdc.gov/aging/aginginfo/alzheimers.htm#:~:text=Alzheimer's%20disease%20is%20t
he%20most,thought%2C%20memory%2C%20and%20language.
https://www.slideshare.net/chandanashwin/bipolar-disorder-24163255https://www.slideshare.net
/SoujanyaThippabathin/pathophysiology-and-management-of-alzheimers-disease

14
 COLLEGE OF NURSING AND PHARMACY
C-PPCO1 – CLINICAL PHARMACY
First Semester | AY 2022-2023

MYOCARDIAL INFARCTION

MYOCARDIAL INFARCTION

A heart attack, also known as myocardial infarction, is a potentially fatal ailment that develops when
the blood supply to the heart muscle is suddenly interrupted, resulting in tissue damage.

I. Pathophysiology

Step 1: One or more of the coronary

arteries becomes blocked.

Step 2: Blood can't get past that blockage

Step 3: Ischemia (lack of blood flow)

Step 4: Necrosis (tissue death)

A myocardial infarction happens when there is a block in the blood flow to the heart,
which is ischemia of the heart. Ischemia just means that there is not enough blood flow. So
when you look at the heart, there are a bunch of coronary arteries around it, so all of these
big blood vessels. They are all around the heart and run in all different directions. And these
coronary arteries are the vessels that actually provide the heart itself with blood. So as the
heart is pumping, there is some blood going to the body, and some blood going to these
coronary arteries around the heart, to give the heart blood. Most heart attacks are caused
when one of these coronary arteries become blocked, like when there's a blood clot, or if
there is fat or plaque buildup inside the vessel. So that's really the most common cause. But
it can also happen during hypertension as well.

Now during hypertension, it's kind of the same scenario, but it can be too different types:

● The blood vessel is getting too full of that plaque that's causing hypertension
● The blood can't get through, or the blood vessels are actually so constricted, which
leads to hypertension, and that constriction doesn't allow the blood flow to get
through.
 COLLEGE OF NURSING AND PHARMACY
C-PPCO1 – CLINICAL PHARMACY
First Semester | AY 2022-2023

MI can be classified into 5 types based on etiology and circumstances:

● Type 1: Spontaneous MI caused by ischemia due to a primary coronary event (eg,

plaque rupture, erosion, or fissuring; coronary dissection)
● Type 2: Ischemia due to increased oxygen demand (eg, hypertension), or decreased
supply (eg, coronary artery spasm or embolism, arrhythmia, hypotension)
● Type 3: Related to sudden unexpected cardiac death
● Type 4a: Associated with percutaneous coronary intervention (signs and symptoms of
myocardial infarction with cTn values > 5 × 99th percentile URL)
● Type 4b: Associated with documented stent thrombosis
● Type 5: Associated with coronary artery bypass grafting (signs and symptoms of
myocardial infarction with cTn values > 10 × 99th percentile URL)

Infarct location
MI affects predominantly the left ventricle (LV), but damage may extend into the right ventricle (RV)
or the atria.
● Right ventricular infarction usually results from obstruction of the right coronary or a
dominant left circumflex artery; it is characterized by high RV filling pressure, often with
severe tricuspid regurgitation and reduced cardiac output.
● An inferoposterior infarction causes some degree of RV dysfunction in about half of
patients and causes hemodynamic abnormality in 10 to 15%.
● Anterior infarcts tend to be larger and result in a worse prognosis than inferoposterior
infarcts. They are usually due to left coronary artery obstruction, especially in the anterior
descending artery; inferoposterior infarcts reflect right coronary or dominant left
circumflex artery obstruction.

II. Diagnosis
● Electrocardiogram (ECG or EKG). This first test done to diagnose a heart attack records
electrical signals as they travel through the heart. Sticky patches (electrodes) are attached to
the chest and sometimes the arms and legs. Signals are recorded as waves displayed on a
monitor or printed on paper. An ECG can show if you are having or had a heart attack.

● Blood tests. Certain heart proteins slowly leak into the blood after heart damage from a
heart attack. Blood tests can be done to check for these proteins (cardiac markers).

● Chest X-ray. A chest X-ray shows the condition and size of the heart and lungs.

● Echocardiogram. Sound waves (ultrasound) create images of the moving heart. This test
can show how blood moves through the heart and heart valves. An echocardiogram can help
identify whether an area of your heart has been damaged.
 COLLEGE OF NURSING AND PHARMACY
C-PPCO1 – CLINICAL PHARMACY
First Semester | AY 2022-2023

● Coronary catheterization (angiogram). A long, thin tube (catheter) is inserted into an

artery, usually in the leg, and guided to the heart. Dye flows through the catheter to help the
arteries show up more clearly on images made during the test.

● Cardiac CT or MRI. These tests create images of the heart and chest. Cardiac CT scans use
X-rays. Cardiac MRI uses a magnetic field and radio waves to create images of your heart. For
both tests, you usually lie on a table that slides inside a long tubelike machine. Each test can
be used to diagnose heart problems. They can help show the severity of heart damage.

III. Clinical Manifestation Signs and symptoms

● Chest pain that may feel like pressure, tightness, pain, squeezing or aching.
● Pain or discomfort that spreads to the shoulder, arm, back, neck, jaw, teeth or sometimes the
upper belly.
● Cold sweat.
● Fatigue.
● Heartburn or indigestion.
● Lightheadedness or sudden dizziness.
● Nausea.
● Shortness of breath.

IV. Treatment

First line of treatment in case of emergency

● Call 911 or your local emergency number

● Chew and swallow an aspirin
● Take nitroglycerin
● Begin CPR if the person is unconscious
● If an automated external defibrillator (AED)

Medications
Medications to treat a heart attack might include:
● Aspirin.
● Clot busters (thrombolytics or fibrinolytics).
● Other blood-thinning medications.
● Nitroglycerin.
● Morphine.
● Beta blockers
● ACE inhibitors
● Statins.
 COLLEGE OF NURSING AND PHARMACY
C-PPCO1 – CLINICAL PHARMACY
First Semester | AY 2022-2023

Surgical and other procedures

If you've had a heart attack, a surgery or procedure may be done to open a blocked artery.
Surgeries and procedures to treat a heart attack include:

● Coronary angioplasty and stenting

- This procedure is done to open clogged heart arteries. It may also be called percutaneous
coronary intervention (PCI). If you've had a heart attack, this procedure is often done during
a procedure to find blockages (cardiac catheterization).

● Coronary artery bypass surgery (CABG)

- This is open-heart surgery. A surgeon takes a healthy blood vessel from another part of the
body to create a new path for blood in the heart.

Cardiac rehabilitation

- Cardiac rehabilitation is a personalized exercise and education program that teaches ways
to improve heart health after heart surgery. It focuses on exercise, a heart-healthy diet,
stress management and a gradual return to usual activities. Most hospitals offer cardiac
rehabilitation starting in the hospital. The program typically continues for a few weeks or
months after you return home.
 COLLEGE OF NURSING AND PHARMACY
C-PPCO1 – CLINICAL PHARMACY
First Semester | AY 2022-2023

REFERENCES:

https://www.healthline.com/health/acute-myocardial-infarction#symptoms

https://www.youtube.com/watch?v=DIDE4f5PTEg

https://www.msdmanuals.com/professional/cardiovascular-disorders/coronary-artery-disease/ac
ute-myocardial-infarction-mi

https://www.mayoclinic.org/first-aid/first-aid-heart-attack/basics/art-20056679

https://www.mayoclinic.org/diseases-conditions/heart-attack/diagnosis-treatment/drc-20373112

https://www.mayoclinic.org/diseases-conditions/heart-attack/diagnosis-treatment/drc-20373112
BSP 3A
GROUP 5:
NAGUIT, MISSY ANGELINE D.
OCAMPO, JENNY ROSE L.
PINEDA, SHIELA MAE S.
RODRIGUEZ, MARILETTE ANN C.

Topic: Hemophilia A & B

Factor II, V, VII, X, and XII

Blood Coagulation Cascade

Coagulation Cascade
- Other term, secondary hemostasis
- Series of steps that occur during the formation of a blood clot after injury by activating a cascade
of proteins called clotting factors. There are three pathways: intrinsic, extrinsic, and common.
-

Hemostasis - derived from “hem-”, which means “blood”, and “-stasis”, which means “to stop.”

Note: Therefore, hemostasis means to stop bleeding. There are two phases of hemostasis.

TWO PHASE OF HEMOSTASIS

● Primary Hemostasis
● Secondary Hemostasis ( Coagulation Cascade)

Note: Primary hemostasis forms an unstable platelet plug at the site of injury.Then, the coagulation
cascade is activated to stabilize the plug, stopping blood flow and allowing increased time to make
necessary repairs. This process minimizes blood loss after injuries.

❖ The coagulation cascade involves the activation of a series of clotting factors, which are proteins
that are involved in blood clotting. Each clotting factor is a serine protease, an enzyme that speeds
up the breakdown of another protein. The clotting factors are initially in an inactive form called
zymogens.

Note: When placed with its glycoprotein co-factor, the clotting factor is activated and is then able to
catalyze the next reaction. When a clotting factor becomes activated, it is denoted with an “a” following
its respective Roman numeral (e.g. when activated, Factor V becomes Factor Va).
Name Description Function

Fibrinogen (Factor I) MW= 34,000 daltons: Adhesive protein that forms

glycoprotein the fibrin clot
 Prothrombin (Factor II) MW= 72,000 DA: Vit. Activated form is main enzyme
K-dependent serine protease of coagulation

Tissue factor (Factor III) MW= 37,000 DA: also known Lipoprotein initiator of
as thromboplastin extrinsic pathway

Calcium ions (Factor IV) Necessity of Ca++ ions for Metal cation necessary for
coagulation reaction in 19th coagulation reactions
century

Factor V (Labile Factor) MW= 330,000 DA Cofactor for activation of

prothrombin to thrombin

Factor VII (Proconvertin) MW= 50,000 DA:Vit. K- With tissue factor, initiates
dependent serine protease extrinsic pathway

Factor VIII (Antihemophilic MW= 330,000 DA Cofactor for intrinsic activation

factor) of factor X

Factor IX (Christmas factor) MW= 55,000 DA:Vit. K- Activated form is enzyme for
dependent serine protease intrinsic activation of factor X

Factor X (Stuart-Prower MW= 58,900 DA; Vit. K- Activated form is enzyme for
factor) dependent serine protease final common pathway
activation of prothrombin

Factor XI (Plasma MW= 160,000 DA; serine Activated form is intrinsic

thromboplastin antecedent) protease activator of factor IX

Factor XII (Hageman factor) MW= 80,000 DA;serine Factor that nominally starts
protease aPPT-based intrinsic pathway

Factor XIII (Fibrin stabilizing MW= 320,000 DA Transamidase that cross-links

factor) fibrin clot

High-molecular-weight MW= 110,000 DA; circulates Cofactor

kininogen (Fitzgerald, Flaujeac in a complex factor XI
or William factor)

Prekallikrein (Fletcher factor) MW= 85,000 DA; serine Activated form that
protease participates at beginning of
aPPT-based intrinsic pathway

Three Coagulation Pathways

❖ Extrinsic
❖ Intrinsic
❖ Common
Note: The extrinsic and intrinsic coagulation pathways both lead into the final common pathway by
independently activating factor X. The extrinsic pathway involves initiation by factor III (i.e., tissue
factor) and its interaction with factor VII. Whereas, factors XII, XI, IX, and VIII are utilized in the
intrinsic pathway. Then, the common pathway uses factors X, V, II, I, and XIII.

Extrinsic Pathway

- begins when there is injury to the endothelial tissue (i.e., skin tissue), exposing tissue factor
(factor III) to the blood.
Note: Tissue factor then becomes bound with calcium and factor VIIa to activate factor X. Factor VII is
present in the blood and requires vitamin K to be activated.

Intrinsic Pathway
- begins when factor XII or the Hageman factor is exposed to collagen, kallikrein, and high
molecular weight kininogen (HMWK) and is subsequently activated. Factor XIIa activates factor
XI into XIa. With a calcium ion, factor XIa activates factor IX.

Note: Factor IXa, factor VIIIa, and calcium form a complex to activate factor X. Factor VIII is
found in the blood and is often activated by thrombin (factor IIa).

Common Pathway
- may result after the activation of factor X at the end of either pathway.
- begins when factor Xa, Va, and calcium bind together, forming a prothrombinase complex. The
prothrombinase complex then activates prothrombin (factor II) into thrombin (factor IIa). Next,
thrombin cleaves fibrinogen (factor I) into fibrin (factor Ia). Afterwards, thrombin cleaves the
stabilizing factor (factor XIII) into XIIIa. Factor XIIIa binds with calcium to then create fibrin
crosslinks to stabilize the clot.

Note:
● Thrombin has several functions, including activating platelets (cell fragments involved in clot
formation) and activating factors V, VIII, and IX.
● Fibrin (factor Ia) is a long, thin protein with branches produced at the end of the
coagulation cascade when fibrinogen (factor I) is converted to fibrin, which stabilizes the
blood clot.
Diagram of pathways

Coagulation disorders
- disorders which affect the coagulation cascade and can either cause excessive or inadequate
clotting. Coagulation disorders usually involve a deficiency in at least one clotting factor, and the
most common disorders include von Willebrand disease, hemophilia, and vitamin k deficiency.

Types of Coagulation disorder

● Von Willebrand disease
- most common bleeding disorder
- deficiency in von Willebrand factor due to an autosomal dominant genetic mutation
Note: The von Willebrand factor is mostly involved in primary hemostasis where it helps platelets stick
together. The factor also plays a role in secondary hemostasis by helping stabilize factor VIII.

● Vitamin K deficiency
- a sufficient amount of vitamin K is not absorbed from foods or when not enough foods
with vitamin K are consumed (e.g., leafy dark green vegetables like spinach).
Notes: Vitamin K is a cofactor required to make factors II, VII, IX, and X functional. Therefore, vitamin
K deficiency affects all three pathways.

● Hemophilia
- Hemophilia A is a deficiency in factor VIII
- Hemophilia B is a deficiency in factor IX
- Hemophilia C is a deficiency in factor XI
HISTORY OF HEMOPHILIA
- Best known of the hereditary bleeding disorders since 2nd century AD, (almud Jewish rabbinical
Tradition and Laws manuscripts).
- First coined by Schonlein in the 1820s.
- Originally termed "Haemorraphilia"i.e. love for haemorrhages but over time contracted to
Henophila.
- Hemophilia is often called the disease of kings, because it was carried by many members of
Europe's royal families. Queen Victoria I of England was a carrier of hemophilia.

INHERITANCE OF HEMOPHILIA

- Hemophilia A and Hemophilia B are inherited in an X-linked recessive pattern. The genes
associated with these conditions are located on the X chromosome, which is one of the two sex
chromosomes. In males (who have only one X chromosome), one changed copy of the gene in
each cell is sufficient to cause the condition. In females (who have two Xchromosomes), a
mutation would have to occur in both copies of the gene to cause the disorder.

Note: Because it is unlikely that females will have two changed copies of this gene, it is very rare for
females to have hemophilia. A characteristic of X-linked inheritance is that fathers cannot pass X-linked
traits to their sons.

- In X-linked recessive inheritance, a female with one changed copy of the gene in each cell is
called a carrier. Carrier females have about half the usual amount of clotting factor VIll or clotting
factor IX, which is generally enough for normal blood clotting.

Note: However, about 10 percent of carrier females have less than half the normal amount of one of
these clotting factors; these individuals are at risk for unusual bleeding, particularly after an injury,
surgery, or tooth extraction.

Hemophilia A

- Also known as classic hemophilia or Factor VIII Deficiency

- People with this type of hemophilia have low levels of a blood clotting factor called factor 8
(FVII). It's the most common.
- Mild Hemophilia A: Do NOT have spontaneous bleeding but unusual bleeding occurs with
surgery and tooth extractions. People are usually diagnosed with this in later life.
- Moderate Hemophilia A: spontaneous bleeding, delayed oozing after minor injury, and usually
diagnosed before they are 5 to 6 years old.
- Severe Hemophilia A: Spontaneous joint or deep muscle bleeding. Usually diagnosed within the
first two years of life.
Hemophilia B

- Also known as Christmas disease or Factor lX Deficiency

- People with this type of hemophilia have low levels of a blood clotting factor called factor 9
(FIX).

Note:The two different types of hemophilia are caused by permanent gene changes (mutations).
Mutations in the FVIll gene cause Hemophilia A. Mutations in the FIX gene cause Hemophilia B.

Pathophysiology

Hemophilia is a rare, inherited hemorrhagic disorder that results from the deficiency or dysfunction of
coagulation protein factors.1,2 Factor VIII (FVIII) and factor IX (FIX) deficiencies and dysfunctions are
the pathological basis of hemophilia A and hemophilia B, respectively.

Clinical Manifestation: Signs and Symptoms

Signs and Symptoms - HEMOPHILIA A

People with hemophilia A bleed longer than other people. Bleeds can occur internally, into joints and
muscles, or externally, from minor cuts, dental procedures, or injuries. How often a person bleeds and the
severity of those bleeds depends on how much FVIII a person produces naturally.

Normal levels of FVIII range from 50% to 150%. Levels below 50% – or half of what is needed to form a
clot – determine a person’s symptoms.

• Mild hemophilia A: 6% up to 49% of FVIII factor 8 in the blood. People with mild hemophilia A
generally experience bleeding typically only after serious injury, trauma, or surgery. In many cases, mild
hemophilia is not diagnosed until an injury, surgery or tooth extraction results in prolonged bleeding. The
first episode may not occur until adulthood. Women with mild hemophilia often experience heavy
menstrual bleeding, and can hemorrhage (bleed extensively) after childbirth.

• Moderate hemophilia A: 1% up to 5% of FVIII in the blood. People with moderate hemophilia A

tend to have bleeding episodes after injuries.

• Severe hemophilia A: <1% of FVIII in the blood. People with severe hemophilia A experience
bleeding following an injury and may have frequent spontaneous bleeding episodes – bleeds that occur
without obvious cause – often into their joints and muscles. Many males with severe hemophilia are
diagnosed due to bleeding after circumcision.
Signs and Symptoms - HEMOPHILIA B

Severity of symptoms can vary. Prolonged bleeding is the main symptom. It is often first seen when the
infant is circumcised. Other bleeding problems usually show up when the infant starts crawling and
walking.

Mild cases may go unnoticed until later in life. Symptoms may first occur after surgery or injury. Internal
bleeding may occur anywhere.Symptoms may include:

● Bleeding into joints with associated pain and swelling

● Blood in the urine or stool
● Bruising
● Gastrointestinal tract and urinary tract bleeding
● Nosebleeds
● Prolonged bleeding from cuts, tooth extraction, and surgery
● Bleeding that stats without cause

TREATMENT

The best way to treat hemophilia is to replace the missing blood clotting factor so that the blood can clot
properly. This is typically done by injecting treatment products, called clotting factor concentrates, into a
person’s vein.Often the best choice for care is at a comprehensive hemophilia treatment center (HTC). An
HTC provides patients with the care and education to address all issues related to the disorder. The team
consists of physicians (hematologists or blood specialists), nurses, social workers, physical therapists, and
other healthcare providers who are specialized in the care of people with bleeding disorders.

There are several treatments available to help control bleeding in people with factor XIII deficiency.

➢ Factor XIII concentrate

➢ Cryoprecipitate
➢ Fresh frozen plasma (FFP)

Excessive menstrual bleeding in women with factor XIII deficiency may be controlled with hormonal
contraceptives (birth control pills) or antifibrinolytic drugs.

Treatment Medications
 ● FACTOR CONCENTRATES When they are available, factor concentrates are the ideal and
safest treatment for rare bleeding disorders. Unfortunately, individual concentrates are available
only for factors I, VII, VIII, XI, and XIII. Factor concentrates for rare bleeding disorders are
usually made from human plasma and are treated to eliminate viruses like HIV and hepatitis B
and C. Recombinant factor VIII and recombinant factor VIIa are also available. They are made in
the laboratory and not from human plasma, so they carry no risk of infectious disease. Factor
concentrates are administered intravenously.

● PROTHROMBIN COMPLEX CONCENTRATE (PCC) This concentrate is made from

human plasma and contains a mixture of clotting factors, including factors II, VII, IX, and X
(however, some products do not contain all four factors). PCC is suitable for individual
deficiencies of factor II and X as well as inherited combined deficiency of the vitamin
K-dependent clotting factors (VKCFD). It is treated to eliminate viruses like HIV and hepatitis B
and C. Some PCCs have been reported to cause potentially dangerous blood clots (thrombosis).
PCC is administered intravenously

● Cryoprecipitate Cryoprecipitate is a substance that comes from thawing fresh frozen plasma. It
is rich in factor VIII (8), and was commonly used to control serious bleeding in the past.

● FRESH FROZEN PLASMA (FFP) Plasma is the portion of blood that contains all the clotting
factors, as well as other blood proteins. FFP is used to treat rare bleeding disorders when
concentrates of the specific factor that is missing are not available. FFP is the usual treatment for
factor V deficiency. However, it usually does not undergo viral inactivation, so the risk of
transmission of infectious diseases is higher. Viral-inactivated FFP is available in some countries
and is preferable. Circulatory overload is a potential problem with this treatment: since the
concentration of each coagulation factor in FFP is low, a large volume of it must be given over
several hours in order to achieve an adequate rise in factor level. This large amount of FFP
needed can overload the circulatory system and stress the heart. Other complications of treatment
with FFP can occur, particularly allergic reactions or lung problems (transfusion-related lung
injury [ TRALI ] ). What are rare clotting factor deficiencies? 23 problems are much less common
if viral-inactivated pooled FFP is used. FFP is administered intravenously

HEMOPHILIA A TREATMENT

● Hemlibra® (also known as ACE 910 or emicizumab)

- Hemlibra® works by replacing the function of factor VIII (8), rather than replacing the missing
clotting factor VIII directly. It can be used to either prevent or reduce the frequency of bleeding
episodes in people with hemophilia A. This treatment product can be given by injection under the
skin.

● DDAVP® or Stimate® (Desmopressin Acetate)

 - DDAVP® and Stimate® are medications that are similar to a hormone that occurs naturally in
the body. The medications release factor VIII (8) from where it is stored in the body tissues.

● Amicar® (Epsilon Amino Caproic Acid)

- Amicar® is a medication that can be given through a vein or by mouth (as a pill or a liquid). It
prevents blood clots from breaking down, resulting in a firmer clot.

● Cryoprecipitate
- Cryoprecipitate is a substance that comes from thawing fresh frozen plasma. It is rich in factor
VIII (8), and was commonly used to control serious bleeding in the past.

HEMOPHILIA B TREATMENT

● Recombinant factor IX therapy is the recommended treatment for individuals with hemophilia B.
In the U.S., the currently available recombinant factor IX products are BeneFIX, Rixubis,
Ixinity, Alprolix Idelvion, and Rebinyn.

DIAGNOSIS

HEMOPHILIA A
❖ CBC (complete blood count) Test
❖ Screening Coagulation Test
❖ Measurement of the level of specific Factor (e.g. factor VIII)
❖ Clotting activity assay
❖ Molecular genetic testing

NOTES:
Complete Blood Count (CBC)
- Common test measures the amount of hemoglobin (the red pigment inside red blood cells that
carries oxygen), the size and number of red blood cells and numbers of different types of white
blood cells and platelets found in blood. The CBC is normal in people with hemophilia.

Screening Coagulation Test

- Screening tests are blood tests that show if the blood is clotting properly. Clotting factor tests,
also called factor assays, are required to diagnose a bleeding disorder. This blood test shows the
type of hemophilia and the severity.
- Screening coagulation tests that measure how long it takes the blood to clot include the activated
partial thromboplastin time (aPTT) and prothrombin time (PT). Typically, the PT is normal,
whereas the aPTT is prolonged in hemophilia A when the factor VIII level is less than 30% of
 normal. In such cases, a diagnosis of hemophilia A must be confirmed through a clotting activity
assay.

Clotting activity assay

- This assay can determine whether the cause of the abnormal aPTT is deficiency of factor VIII
(hemophilia A), factor IX (hemophilia B) or another blood clotting factor deficiency. This
specific test will also determine the severity of the factor VIII deficiency. Even if an aPTT test is
normal this does not rule out mild cases of hemophilia A because of the relative insensitivity of
the test.

Molecular genetic testing

- Molecular genetic testing, which can identify mutations in the factor VIII gene, is available on a
clinical basis. Understanding the specific F8 gene mutation can also be helpful in identifying
female carriers in the family as well as in the prenatal diagnosis of hemophilia A, which is not
only feasible, but is also available and encouraged in most Western and developing countries.

HEMOPHILIA B

❖ Complete blood count (CBC).

❖ Prothrombin time (PT) and activated partial thromboplastin time (PTT).
❖ Factor VIII and factor IX tests.

NOTES:
In the first 6 months of life, babies don’t fall or get hurt often, so an early diagnosis is rare. You may start
noticing issues once your baby becomes more active. As they begin to crawl, they may get bumps and
raised bruises. There may be bleeding in the joints. Bruising and long-lasting bleeding from even small
injuries may cause a doctor to suspect hemophilia.The doctor will also ask about your family’s medical
history to find out if anyone had a problem with bleeding or blood clotting.
To get the diagnosis, doctors will test your child's blood to find out how long it takes to clot and to see if
it's missing any clotting factors. This often includes:

● Complete blood count (CBC). It gives important information about the kinds and numbers of
cells in your blood.
- measures the amount of hemoglobin (the red pigment inside red blood cells that carries oxygen),
the size and number of red blood cells and numbers of different types of white blood cells and
platelets found in blood. The CBC is normal in people with hemophilia.
● Prothrombin time (PT) and activated partial thromboplastin time (PTT). Both test how long
it takes blood to clot.
 - This test measures how long it takes for blood to clot. It measures the clotting ability of factors
VIII (8), IX (9), XI (11), and XII (12). If any of these clotting factors are too low, it takes longer
than normal for the blood to clot
● Factor VIII and factor IX tests. These measure levels of those clotting factors.
- Doctors order the factor IX and factor VIII activity test to help diagnose or monitor the treatment
of hemophilia A and B. The test also can help find the reason for an abnormal result on other
clotting tests, such as prothrombin time (PT) or partial thromboplastin time (PTT).

REFERENCES:

https://medlineplus.gov/ency/article/000539.htm
https://www.cdc.gov/ncbddd/hemophilia/facts.html
https://www.osmosis.org/answers/coagulation-cascade
https://www.slideshare.net/HelaoSilas/haemophilia-76369646
https://onlinelibrary.wiley.com/doi/pdf/10.1002/clc.1990.13.s6.5