Reporting Guide
Reporting Guide
Reporting Guide
Background:
Information from: Habif's Clinical Dermatology - 7th Edition - Elsevier
SLIDE 3:
Hives often appears as a raised, itchy rash. There can be many causes, including
exposure to an allergen, a physical trigger, such as pressure from tight clothing, or
an underlying health condition. Urticaria, ultimately, is caused by mast cell activation
in the superficial dermis.
Mast cells, when they degranulate, release histamine, which is why it's very pruritic,
and they release a variety of vasodilators. And that's what causes the localized
swelling and these classic raised flat lesions.
SLIDE 4:
There's 2 main ways in which mast cell activation occurs.
There's the IgE-mediated type and then the non-IgE mediated type.
Let's talk about IgE first. So, the IgE-mediated type is essentially a type 1 immediate
allergic reaction in which the patient has previously been exposed to some trigger,
has developed antibodies, and those antibodies are now binding to mast cells in the
skin. When that patient is then re-exposed to that allergen, the IgE immediately
recognizes it, triggers the mast cell, and massive degranulation occurs very readily.
The most common allergens or drugs, like beta-lactams, food allergies can do this,
insect bites like from Hymenoptera, mosquitoes, etc., infections like viruses,
mycoplasma, and parasites. What you'll typically see on physical exam is a very
asymmetric distribution of lesions, and they are abrupt in onset, intensely pruritic --
again, due to all that histamine -- with very well demarcated, erythematous papules
with central pallor.
SLIDE 5:
Next up, we're going to talk about the non-immune mediated causes of urticaria.
Essentially, mast cells are still involved, but IgE is not part of the equation.
So specific medications can do this. NSAIDs, particularly, COX inhibitors, can block
prostaglandin synthesis, which allows mast cells to degranulate.
Opioids and vancomycin actually directly stimulate mast cell activation in some
circumstances. And then ACE inhibitors are acting via inhibition of kinin metabolism.
In addition, there are some physical conditions that can lead to urticaria to form in
susceptible hosts. Certain physical stimuli, like cold, vibration, or pressure, can lead
to urticaria's emergence.
SLIDE 6
So, urticaria is our classic type 1 hypersensitivity reaction. We also call it "hives".
These lesions will be anywhere from 1 mm to 10 cm large. They can be huge or
small. These lesions are profoundly itchy, and they're stimulated by skin contact,
which means the more you scratch them, the more they itch.
What you'll notice about them is that they sort of "come and go" even before your
eyes.
You may walk in, see a patient with hives, and before you're done with your
conversation, the one you were looking at on the leg is gone, and there's a new one
on the arm.
They may be associated with angioedema, which is another type of type 1
hypersensitivity reaction.
SLIDE 7
What's key is that these are acute and generally short-lived.
Patients usually only have this reaction for maybe days to maybe a week out, from
when they first encountered that antigen, and had a response to it, which would be
the second time they encountered the antigen.
Alternatively, occasionally they can become chronic.
These are when hives last longer than 6 weeks.
This can really be problematic when it happens.
TYPE 2
Similar to type 1, type 2 hypersensitivity reactions also involve antibodies. In fact, type 2 and type 3
hypersensitivity both result from the same class of antibody, called IgG. The difference between them
lies in the form of antigens that generate a response. Additionally, type 2 can also involve IgM
antibodies. Type 2 hypersensitivity causes cytotoxic reactions, meaning that healthy cells die as they
respond to the antigens. This can cause long-term damage to cells and tissues, resulting in conditions
such as:
TYPE 3
In type 3 hypersensitivity, antigens and antibodies form complexes in the skin, blood vessels, joints,
and kidney tissues. These complexes cause a series of reactions that lead to tissue damage. Causes
of a type 3 hypersensitivity reaction can include:
● serum sickness
● lupus
● rheumatoid arthritis
● small-vessel vasculitis
TYPE 4
Unlike the other types, type 4 hypersensitivity reactions are cell-mediated. Instead of antibodies, white
blood cells called T cells control type 4 hypersensitivity reactions. Experts can further subdivide these
reactions into type 4a, type 4b, type 4c, and type 4d based on the type of T cell involved and the
reaction it produces. This type also differs from the other three in that it causes a delayed reaction.
Risk Factors:
Information from: Harrison's Principles of Internal Medicine, Twentieth Edition
SLIDE 8:
According to Harrison’s:
Acute or chronic urticaria can occur at any point in the life span with the third to fifth
decades the most common for chronic disease. Women are affected more often than
men with a slight predominance for those with a history of atopy. Acute urticaria is
most often the result of exposure to a food, environmental, or drug allergen or viral
infection, while chronic urticaria is often idiopathic. More than two-thirds of new-onset
urticaria cases are ultimately diagnosed as acute.
SLIDE 9
There are many things that can trigger urticaria such as foods, medicine and
environmental factors
SLIDE 10
Foods, especially food additives, include legumes, tree nuts, seafood, eggs, dairy,
shellfish, berries. These are all very common.
In fact, among children who have type 1 hypersensitivity reactions to food about 85%
of them are to food when we know what the allergen is.
Still, remember, at least a third of the time we have no idea what triggers the allergy.
SLIDE 11
Also, patients can be allergic to medications.
Probably penicillins and sulfas are the most common, but they could also be allergic
to salicylates to certain vaccines or to anaesthetics.
SLIDE 12
Also patients can have environmental allergies.
Bee stings and wasp stings are particularly problematic.
Patients may be allergic to temperature changes to exercise, to latex.
Clinical Manifestation:
Slide 13
History of exposure to triggering agents for acute and chronic:
Many substances can trigger hives, such as:
1. Some food (especially peanuts, shellfish, fish, eggs, milk, chocolates)
2. Medications, such as antibiotics (especially penicillin and sulfa), aspirin and
ibuprofen
3. Insect stings or bites
4. Physical stimuli, such as pressure, cold, heat, exercise or sun exposure
SLIDE 14
ADDITIONAL:
SYMPTOMS
1. Itchiness.: When the patient has an allergic reaction to a substance, the body releases
histamine and other chemicals into the blood.
This causes itching, swelling, and other symptoms.
2. Swellings on the skin (wheals) are a frequent reaction. Persons with other allergies, such
as hay fever, frequently get hives. When swelling or welts occur around the face, especially
the lips and eyes, it is called angioedema.
Swelling can also happen around the hands, feet, and throat.
a. Raised itchy bumps, either red or skin-colored
b. Swelling of the surface of the skin into red- or skin-colored welts (called wheals) with
clearly defined edges.
c. Wheals may get bigger, spread, and join together to form larger areas of flat, raised skin.
d. Wheals can also change shape, disappear, and reappear within minutes or hours.
e. The patient knows the patient have hives when the patient press the center of a wheal, it
turns white. This is called blanching.
f. The rash is typically itchy and appears rapidly as localized red swelling on the skin
measuring a few mm to more than 10 cm in size in different shapes.
g. The swelling can also occur on eyelids, lips, palms and soles.
Pathophysiology:
YT LINK: Urticaria (Hives) and Angioedema – Pediatrics | Lecturio - YouTube
Slide 16.
*** SUPPLEMENTAL:
Slide 17.
In this diagram we will focus on non-immunologic urticaria or the non-IgE dependent
mast cell activation.
(Sa pharmaco management na ‘to) Now let’s discuss the drugs that block the action
of HISTAMINE.
Diagnosis:
SLIDE 18
ACUTE:
● Careful history to identify potential triggers — ask for atopic disease, known
allergies, drug intake, signs of infection
● Physical examination (BP, PULSE, Lung auscultation)
● If no causes identified from history, no further investigation needed due to self
limiting nature with this type of urticaria
CHRONIC:
● Infection- culture, and sensitivity, serology
● Autoreactivity- serum skin test, cellular activation test (ex: Serum induced
histamine release, thyroid auto abs, antinuclear antibodies
● Non allergic Hypersensitivity– consider triggering by aspirin/Nsaids, in rare
cases—do allergen low diet test
Slide 19:
CBC with differential: A measure of the number of red blood cells, white blood
cells, and platelets in the blood, including the different types of white blood cells
(neutrophils, lymphocytes, monocytes, basophils, and eosinophils)
*erythrocyte sedimentation rate (ESR), is a blood test that can reveal inflammatory
activity in your body
*C-reactive Protein (CRP) test measures the amount of CRP in the blood to detect
inflammation due to acute conditions or to monitor the severity of disease in chronic
conditions
Thyroid function test: looks at levels of thyroid-stimulating hormone (TSH)
and thyroxine (T4) in the blood.
*antinuclear antibody(ANAs) test checks to see if you have an autoimmune
disorder, a condition where the immune system attacks healthy cells
*Autologous serum skin test (ASST) is a rapid, in-vivo clinical test to detect
functional autoantibodies in patients with chronic spontaneous urticaria
Slide 36-39
● In urticaria, in which histamine is the primary mediator, the H1 antagonists are
the drugs of choice and are often quite effective if given before exposure
(katzung 14th pg 283)
● H1-receptor antagonist antihistamines- these are the drugs of choice for
urticaria, or the first line treatment.
There are two kinds of h2 receptor antagonists. 1st generation and second
generation. The older members of the first-generation agents, typified by
diphenhydramine, are highly sedating agents with significant autonomic
receptor-blocking effects. The second-generation H1 blockers, typified by cetirizine,
fexofenadine, and loratadine, are far less lipid soluble than the first-generation
agents and have greatly reduced sedating and autonomic effects. All H1 blockers
are active by the oral route. Several are promoted for topical use in the eye or nose.
Most are metabolized extensively in the liver. Half-lives of the older H1 blockers vary
from 4 to 12 h. Second generation agents have half-lives of 12–24 h. (katzung 14th
ed. Page 147)
*In simpler terms diba ang nag cause ng hives is naactivate ang histamine 1
receptors ng histamines, the result of histamines is pruritus, and allergic like
reactions, so para matigil ang pag release ng histamine, kailangan natin ng h1
receptor antagonist!
1st gen
1. Hydroxyzine - Hydroxyzine is a sedating peripheral H1 receptor antagonist. It
is very effective in urticaria. Hydroxyzine also may suppress histamine activity
in the subcortical region of the CNS.(medscape)
2. Diphenhydramine is a sedating peripheral H1 receptor antagonist. It is used
for symptomatic relief of allergic symptoms caused by histamine released in
response to allergens.
Dun sa warnings kung tatanungin bakit sya dapat in caution with narrow angle
glaucoma is because pag may glaucoma ka consistent sign of glaucoma is
mydriasis, kaya may blurring of vision diba, antihistamines is like
anticholinergics that can also cause mydriasis so ma aggravate nya pa lalo
ang glaucoma.
Katzung pg 296
Pabasa nalang din po itong pic, sa moa naman nya ung drug is nagkipag compete
sya kay histamine na magbind sa h1 receptor ha,( iba ung h2 kasi pag h2 gastric
acid secretion na un) para hindi matuloy ung masamang balak ni histamine forda
person
Effects : blocks muscarinic( parasympathetic effects like watery eyes, red skin)
*Inverse agonist A drug that binds to the non-active state of receptor molecules and
decreases constitutive activity
*Constitutive activity Activity of a receptor-effector system in the absence of an
agonist ligand
Boxed warning: can cause QT prolongation due to the inhibition of repolarization
potassium channels, which leads to prolongation of the action potential and QT
interval, and the development of early after-depolarization, which triggers
TdP(Torsades de pointes). Patients at risk of developing TdP, such as those with
congenital long QT syndrome, cardiac disease, liver disease, electrolyte disturbance,
or those taking drugs that can prolong QT interval, should avoid nonsedating
antihistamines that are also capable of prolonging the QT interval.
Contraindications:
Hypersensitivity - Immediate-type hypersensitivity reactions to both
first-generation and second-generation AHs often involve acute cutaneous
manifestations, such as urticaria and angioedema, but systemic reactions
(anaphylaxis) have also been described.
Prolonged QT interval- They may occasionally cause an increase in the
pulse rate because they have an atropine-like effect. In some individuals,
the heart rate may become rapid.
Side effects:
Drowsiness,Headache,Hallucination- First-generation H1 antihistamines cross
the blood-brain barrier, and in usual doses, they potentially cause sedation
and impair cognitive function and psychomotor performance.
Dry mouth- Antihistamines used to treat allergies and asthma can also cause
dry mouth. This is because they have a similar anticholinergic effect on
your body.
WARNINGS AND MONITORING:AHs that cross the blood-brain barrier and bind to
H1 receptors in the brain suppress central nervous system (CNS) arousal and disrupt
circadian sleep-wake rhythmicity , thus impairing both cognitive function and
psychomotor performance, including attention, memory, sensorimotor coordination,&
information processing.
Monitoring:
Why hindi pwede for long term use?
- Steroid tablets taken for longer than 3 weeks can potentially
cause: increased appetite – which can potentially lead to weight
gain if you find it difficult to control what you eat.
- Long-term use of glucocorticoids can cause a loss of muscle
tissue. It can also result in Cushing's syndrome(a disorder that
occurs when your body makes too much of the hormone cortisol
over a long period of time), which can lead to: a fatty hump
between your shoulders. round face.
- Sa monitoring kailangan tignan kung may behavioral changes
na ung patient kasi its a sign na overdose na sya ng
glucocort.(prednisone) rapid mood swings and mood changes –
such as becoming aggressive, irritable and short-tempered with
people.
- Monitor for kaposi sarcoma bec. Steroids(prednisone is a
steroid) are a risk factor for Kaposi's sarcoma-immune
reconstitution inflammatory syndrome and mortality in HIV
infection
- a patient w/ kaposi sarcoma is already immunocompromised,
prednisone is an immunosuppresant drug, so therfore it can lead
to drop in immune system.
*Kaposi sarcoma is a disease in which cancer cells are found
in the skin or mucous membranes that line the
gastrointestinal (GI) tract, from mouth to anus, including
the stomach and intestines. These tumors appear as purple
patches or nodules on the skin and/or mucous membranes and
can spread to lymph nodes and lungs.
3. Omalizumab
Moa: Omalizumab binds free IgE in the serum, forming trimers and
hexamers. The drug binds to IgE at the same site that the high-affinity
IgE receptor (Fc-epsilon-RI) binds, so IgE bound to drug cannot bind its
receptor on mast cells and basophils.
- Monoclonal antibodies(drug class of omalizumab) directed to IgE
binding may reduce release of mediators that provoke an allergic
response. These agents may be considered when H1-anagonists are
ineffective.
- Omalizumab is a recombinant humanized monoclonal antibody
administered by subcutaneous injection every 4 weeks. It selectively
binds to IgE and inhibits binding to IgE receptors on the surface of
mast cells and basophils. It is indicated for chronic idiopathic urticaria
in adults and children aged 12 years or older who remain symptomatic
despite H1 antihistamine treatment.
Topical products are not safe for children , strictly for adult dose only.
Safety and efficacy is not yet established in children
Boxed warning: There is also the possibility that polysorbate, one of
the formulation's excipients, is responsible for anaphylactic reactions
*polysorbate- It is utilized as a surfactant in soaps and cosmetics and
also as a lubricant in eye drops. In food or pharmaceutical products, it
can act as an emulsifier(added to drugs to prevent particular parts from
separating.). Polysorbate 80 is an excipient that is used to stabilize
aqueous formulations of medications for parenteral administration or
vaccinations.
CONTRAINDICATIONS: same as above mentioned
SIDE EFFECTS:
Hair loss- may interfere with mast cell release, and mast cells
have an influence on the hair growth cycle. They also state that
because hair loss is transient with omalizumab, treatment
should continue in patients with a positive effect.
Contraindications/ cautions
Sa contraindication part, Why contraindicated to maois?
MAOIS(Monoamine Oxidase Inhibitors) - it increases levels of doxepin
by pharmacologic synergism . maois and doxepin same silang
antidepressant drugs, pag sumobra ka naman ng antiddepressants
drugs edi sobrang saya mo na nyan? Sana all char… pag nasobrahan
sa antidepressants it can make you high, like the effects of
adrenoceptor agonist- mydriasis, tachycardia, nervousness, tremors,
insomnia, dry mouth, constipation etc. we learned all about it in the
lecture before diba?
Sa urinary retention din contraindicated bec un nga adrenergic agonist
tong drug na to so, mapapalala ang retention leading to no urine
output, and delikado ang walang urine output diba,
Sa glaucoma na part same with antihistamine explanation kanina.
Why sa MI, contraindicated- bec it can aggravate the irregular rhythm
of the heart
In hepatic failure naman, nag fail na ung liver mo, and liver is the main
organ for metabolism, so mahina na din ang metabolism mo,
mahihirapan kang ieliminate ang drug can lead to overdose, kaya pag
may hepatic failure adjusted lagi ang dose ng mga gamot nila depende
sa creatinine clearance ng patient.
Thyroid dysfunction- reduce T4 hormone levels by 11.2%(accdg to
medical news.com) , papano kung hypothyroidism ang patient edi
kawawa naman sya. For hyperthyroidic patients naman, they are
known to be grabe mag tremors, and palpitate so if you give this
antidepressant/antihistamine doxepin, it can aggravate that.
and seizure- tricyclic antidepressants (TCAs), like doxepin, should be
used with extreme caution in patients with a preexisting seizure
disorder because tricyclic antidepressants (TCAs) can lower the
seizure threshold. If seizures occur during TCA therapy, the TCA
should be discontinued (pdr.net)
A high seizure threshold means that a seizure is less likely to occur,
while a low seizure threshold means that a seizure is more likely to
occur.(epilepsyontario.org)
Side effects:
dizziness, drowsiness - Compared with other antidepressants,
doxepin has extremely high selectivity for the postsynaptic
histamine H1 receptor. Since histamine is a potent stimulating
neurotransmitter, antagonist activity predictably will produce
sedation.
Emotional changes- People taking doxepin can experience
worsening depression and suicidal thoughts or behavior. The
risk of suicidal thoughts or behavior is higher in people aged 24
years and younger with depression or other mental health
conditions.
Management:
Please indicate source of info (eg. book title, weblink)
Prevention:
Please indicate source of info (eg. book title, weblink)
CORONARY ARTERY DISEASE
Background:
We all know that cardiovascular disease is a global and local burden of a disease
and in the Philippines, cardiovascular diseases ranked among the top 10 leading
causes of morbidity and was the leading cause of mortality.
CAD is commonly due to obstruction of the coronary arteries, usually the epicardial
arteries, by atheromatous plaque.
Risk Factors:
reference:
Clinical Manifestation:
Please indicate source of info (eg. book title, weblink)
Slide 9.
Slide 10.
Angina Pectoris
Angina can range from mild discomfort to severe pain. It may feel like heaviness,
tightness, pressure, aching, burning, numbness, fullness, squeezing or a dull ache.
The discomfort may spread to your shoulder, arm, neck, back or jaw.
The typical quality of pain is that it is retrosternal in location and it may be dull or
squeezing.
The two kinds of angina, stable and unstable, differ mainly in their onset: stable
angina usually occurs in the presence of triggers such as physical and emotional
stressors, and increased oxygen demand. (I.e. if the patient is exercising, or pagod,
or nagulat). This has predictable triggers and timing. In unstable angina, on the
other hand, chest pain occurs even when the patient is at rest, even in the absence
of triggers previously mentioned. So, timing is usually unpredictable.
Stable angina is usually relieved by rest and administration of nitrates, while unstable
angina is not.
Slide 11.
In the case of MI, there is evidence of myocardial injury or necrosis.
Chest pain is more severe and prolonged than angina and does not resolve with rest
or nitrates. Diaphoresis (excessive sweating) also occurs.
Pathophysiology:
SLIDE 12
As discussed earlier, coronary heart disease is caused by the hardening and
narrowing of the arteries caused by a buildup of plaque or what we call as
atherosclerosis. This is our main culprit in the pathogenesis of CAD. This plaque
build-up is the end product of chronic inflammatory process. Here, we should take
note that this process will not begin without endothelial injury.
SLIDE 13
Low-density lipoproteins (LDLs) then cross the damaged endothelium into the wall of
the artery. Overtime, cholesterol becomes part of the plaque where they start to
compromise circulation which ends up with a higher risk for myocardial infarction.
SLIDE 14
To make things easier, let’s take it step by step.
As said earlier, arterial injury is the first requirement for the process of plaque
build-up to begin. These may be brought about by hypertension, hyperlipidemia, or
even diabetes mellitus.
SLIDE 15
Because of this injury, fatty materials such LDLs, cholesterol, triglycerides plus the
inflammatory mediators, macrophages and WBCs infiltrate the lining of the damaged
artery.
SLIDE 16
They then recruit platelets which release growth factor at the site. These growth
factors stimulate smooth muscle to proliferate.
SLIDE 17
The lipids and other substances are trapped in the wall of the artery, which is
thickening, and blood flow becomes increasingly reduced as the opening becomes
smaller.
SLIDE 18
Over time, the fatty deposits harden and become a tough and fibrous plaque. They
can be seen on just one side or all the way around the lumen of the artery. As blood
flow decreases, the arteries will not be able to supply enough oxygen-rich blood to
meet the demands of the heart muscle which produces the different manifestations
such as angina pectoris. As the process continue, the patient usually start to
experience ischemia and has an increased risk of MI.
SLIDE 19
Here is an expanded presentation of the pathophysiology as discussed earlier.
(Pakibasa na lang yung laman ng mga boxes since same lang naman sa explanation
earlier)
SLIDE 20
HELLO MGA PHARMA! PAKI-EXPLAIN NA LANG PO :(((
Diagnosis:
Source: 2014 PHA Clinical Practice Guidelines for the Diagnosis and Management
of Patients with Coronary Artery Disease
Slide 21.
A resting 12-lead electrocardiogram (ECG) IS RECOMMENDED during initial
evaluation, and during or immediately after an episode of chest pain suspected to
indicate clinical instability.
ECG or EKG Measures the electrical activity, rate, and regularity of your
(electrocardiogra heartbeat.
m)
Echocardiogram Uses ultrasound (special sound wave) to create a picture of
the heart.
Exercise stress Measures your heart rate while you walk on a treadmill. This
test helps to determine how well your heart is working when it has
to pump more blood.
Chest X-ray Uses x-rays to create a picture of the heart, lungs, and other
organs in the chest.
Slide 22..
It IS RECOMMENDED that the following initial laboratory tests be performed to
establish CV risk factors, identify possible causes of ischemia and determine
prognosis:
1. Fasting lipid profile (total cholesterol, high density lipoprotein [HDL] cholesterol,
low density lipoprotein [LDL] cholesterol and triglyceride levels)
Prevention:
Source: Source: European Cardiology Review. Current Treatment of Familial
Hypercholesterolaemia
Slide 38:
*For the prevention of CHD, ABCDEs of primary prevention derived from American
Heart Association (AHA) provided a definition of ideal cardiovascular health using 7
metrics collectively called "Life's Simple 7".
* First is assess risk, aspirin: to assess the risk of having CHD, pooled cohort
equations should be used by the clinician to estimate 10-year CHD risk. Aspirin or
the antiplatelet therapy should be used infrequently for primary CHD prevention and
should be reserved for high risk individuals after other risk factors have been
addressed.
*2nd is blood pressure: lifestyle modification are recommended for all those with
elevated blood pressure and hypertension
*3rd is cholesterol: statins are recommended for adults 40-75 yrs old with 10 year
CHD risk of >7.5%. Diabetics, and those with >190mg/dL
*4th is cigarettes: for those who use tobacco, a combination of behavioral
intervention and pharmacotherapy should be recommended to assist quitting.
*5th is diabetes: metformin is the main first line therapy for patients with type 2
diabetes.
*6th is diet and weight: a diet rich in legumes , vegetables, nuts, wholegrains and
fish is recommended.Intake of trans and unsaturated fat should be avoided.
*7th is exercise: clinicians should encourage adults to engage in atleast 150
minutes of moderate-intensity exercise or 75 minutes of vigorous-intensity exercise
weekly.
*Ratio for doses for drugs with extended release(ER), sustained release, or
controlled release drugs: Time-release drugs use a special technology to release
small amounts of the medication into a person's system over a long period of time.
This is also referred to as sustained release, extended release, or controlled release.
These tend to come in pill form and are simply made to be more potent but dissolve
slowly.
Coat release: Enteric coating is a useful strategy for the oral delivery of drugs which
rapidly degrade in the stomach, as it prevents the drug being released in the acidic
conditions of the stomach before reaching the intestine.
Beta blockers—
MOA: decrease sympathetic stimulation particularly in the heart..
Decrease din ang HR and contractility which in turn decrease myocardial oxygen
demand
—Adults bisoprolol
Metoprolol is used alone or in combination with other medications to treat high blood
pressure. It also is used to prevent angina (chest pain) and to improve survival after
a heart attack. Metoprolol is in a class of medications called beta blockers. It works
by relaxing blood vessels and slowing heart rate to improve blood flow and decrease
blood pressure.
Bisoprolol is used alone or together with other medicines to treat high blood pressure
(hypertension). High blood pressure adds to the workload of the heart and arteries. If
it continues for a long time, the heart and arteries may not function properly. This can
damage the blood vessels of the brain, heart, and kidneys, resulting in a stroke,
heart failure, or kidney failure. High blood pressure may also increase the risk of
heart attacks. These problems may be less likely to occur if blood pressure is
controlled .This medicine is a beta-blocker. It works by affecting the response to
nerve impulses in certain parts of the body, like the heart. As a result, the heart beats
slower and decreases the blood pressure. When the blood pressure is lowered, the
amount of blood and oxygen is increased to the heart .
—----
SIDE NOTES:
WHY DO WE NOT STOP TAKING BETA BLOCKERS SUDDENLY? Do not stop
taking a beta blocker suddenly without consulting your doctor. This is important
because when you take a beta blocker regularly, your body becomes used to it.
Stopping it suddenly could cause problems such as palpitations, a recurrence
of angina pain or a rise in blood pressure.
****Some of the more common medicines that can interact with beta-blockers
include:NSAIDS(aspirin)– it will cause hypotensive
Side effects: because they drop the HR, if you drop HR, the amount of blood that
the heart is pumping forward may also drop creating symptoms of fatigue,
impotence, drowsiness. Also it can cause DOB bec they block the sympathetic
effects of Beta 2 receptors that causes bronchodilation, in contrast they can cause
bronchoconstriction.
Contraindications: some people are allergic to amlodipine and its constituents like
microcrystalline cellulose, dibasic calcium PO4 anhydrous, sodium starch glycolate,
and magnesium stearate that causes allergy to some people. In severe hypotension
it is contraindicated bec. It can aggregate the drop in blood pressure, if your Bp gets
too low it can cause dizziness, fainting or death. Do not use nicardipine in patients
with advanced aortic stenosis because of the afterload reduction effect of
nicardipine. Reduction of diastolic pressure in these patients may worsen rather than
improve myocardial oxygen balance.
Calcium channel blockers do not reduce the risk of initial or recurrent infarction
or death when given routinely to patients with acute myocardial infarction or
unstable angina.
ACE inhibitors
MOA: The ACE inhibitors lower blood pressure by reducing peripheral vascular
resistance without reflexively increasing cardiac output, heart rate, or contractility.
These drugs block the enzyme ACE which cleaves angiotensin I to form the potent
vasoconstrictor angiotensin II ACE is also responsible for the breakdown of
bradykinin, a peptide that increases the production of nitric oxide and prostacyclin
by the blood vessels. Both nitric oxide and prostacyclin are potent vasodilators.
Vasodilation of both arterioles and veins occurs as a result of decreased
vasoconstriction (from diminished levels of angiotensin II) and enhanced vasodilation
(from increased bradykinin). By reducing circulating angiotensin II levels, ACE
inhibitors also decrease the secretion of aldosterone, resulting in decreased sodium
and water retention. ACE inhibitors reduce both cardiac preload and afterload,
thereby decreasing workload on the heart.
Uses: ACE inhibitors are medications used to treat and manage hypertension, which is
a significant risk factor for coronary disease, heart failure, stroke, and a host of other
cardiovascular conditions
—-moa: Angiotensin II causes direct vasoconstriction of precapillary arterioles and
postcapillary venules, inhibits the reuptake of norepinephrine, stimulates the release of
catecholamines from the adrenal medulla, reduces urinary excretion of sodium and water,
stimulates synthesis and release of aldosterone, and stimulates hypertrophy of both vascular
smooth muscle cells and cardiac myocytes.
Boxed warning: during gestation, taking captopril may cause fetal death,
intrauterine growth retardation, hypotension, acute renal failure, and ductus
arteriosus patency in newborn
*patent ductus arteriosus- after birth , the ductus arteriosus normally closes within
two or three days. In premature infants, the opening often takes longer to close. If
the connection remains open, it’s referred to as patent ductus arteriosus, the
abnormal opening causes too much blood to flow to the baby’s lungs and heart.
Contraindications: hypersensitivity like the case of CCBs
Side effects :
cough- The same activity that allows ACE inhibitors to lower blood pressure
can cause other substances, like bradykinin, to build up in the airways and
make a person cough a lot.
Flushing- Captopril blocks the conversion of angiotensin I to angiotensin II
and prevents the degradation of vasodilatory prostaglandins, thereby
inhibiting vasoconstriction and promoting systemic vasodilation, thus your skin
complexion will turn out reddish.
Headache- Vasodilatation explains headache induced by most cardiovascular
drugs such as calcium-channel blockers and ACE inhibitors. In these cases,
headache is a side effect
Monitoring : When you start on an ACE inhibitor, you will need blood tests to
monitor your kidney function and potassium levels. Be aware: If you take an
ACE inhibitor, keep a written log of your heart rate (pulse) and blood pressure. Track
your heart rate by taking your pulse daily.Acute renal failure has been reported
during captopril therapy of hypertension due to renal artery stenosis with a single
kidney or bilateral renal artery stenosis.(ncbi.nlm.nih.gov)
Monitoring: Low HDL-C and elevated triglycerides (TG) are both independent risk
factors for cardiovascular disease. This lipid profile helps predict your risk for
heart disease and stroke.
Contraindications:
Hypersensitivity - some people are allergic to its contents, so as
much as possible avoid taking these drugs to avoid anaphylaxis
Severe renal impairment, ESRD, px receiving dialysis- Fenofibrate
has been observed to increase serum creatinine concentrations in
patients with CKD, patients with these disease have already increased
creatinine levels, thus statins can aggravate it. High levels of creatinine
in the blood or urine can be a sign that the kidneys are not filtering the
blood effectively
active liver disease- Liver toxicity usually is signaled by an
asymptomatic increase in transaminase levels, but rare episodes of
severe hepatotoxicity and liver damage have been reported. For this
reason, statins have been contraindicated in patients with active liver
disease and persistent elevated transaminase levels.
Gallbladder disease - FIbrates can increase the concentration of
cholesterol in the gallbladder. This may lead to gallstones. Thus it can
also aggravate the disease.
Prenancy and lactation - considered under pregnancy category c
(where benefits outweigh the risk) risk of major congenital disabilities,
adverse maternal or fetal outcomes, or miscarriage-related risk
associated with this drug. Patients should not breastfeed when taking a
statin because the medicine may pass into breast milk and pose a risk
to the baby.
Warning: The simultaneous usage of HMG CoA reductase inhibitors (statins)
with gemfibrozil enhances the probability of developing rhabdomyolysis or
myopathy. Therefore, simvastatin is contraindicated, and rosuvastatin use
should be avoided while administering gemfibrozil.
Why is the dose adjusted with 1-2 month intervals? Colestipol is given 1- 2 months
only because it can cause vitamin K deficiency and can increase tendency to bleed if
injured.
Boxed warning: You should never take the granule formulation in the dry form,
because there is a choking risk. Imagine yourself swallowing 2g granules of
drug, wouldn't be that uncomfortable?
Special precautions: These drugs have the potential to cause fetal toxicity.
Side effects: bile acids in the intestine help control how much water is in your stool.
By binding to extra bile acid in the intestines, this medication may remove some
water in your stool, causing constipation. Due to constipation, feces may become
impacted, due to the difficulty of defecation leading to abdominal discomfort. In worst
cases cause blood in stool because pinipilit mong matae despite constipation.
Why it is used?
Cholesterol absorption inhibitors are used to treat high cholesterol in people who
cannot take a statin. This medicine lowers total cholesterol and LDL (bad)
cholesterol.
This medicine is used along with lifestyle changes including diet and exercise to
lower cholesterol.
NIACIN
Dosage explanation: high doses of 500 mg/day or more can cause diarrhea, easy
bruising, and can increase bleeding from wounds. Even higher doses of 3,000
mg/day or more can cause nausea, vomiting, and liver damage
Contraindications:
Hypersensitivity- alams na yan
If you have liver disease, peptic ulcer disease or severe low blood pressure
(hypotension), don't take large amounts of niacin. The supplement has been
linked with liver damage, can cause hypotension and might activate a peptic
ulcer.
Hepatic disease - Niacin can cause mild-to-moderate serum aminotransferase
elevations and high doses and certain formulations of niacin have been linked
to clinically apparent, acute liver injury which can be severe as well as fatal
Hypotension- niacin lowers bp so they can aggravate the symptoms of
hypotension
Arterial bleeding- niacin increases prothrombin time.When the PT is high, it
takes longer for the blood to clot , therefore more prone to bleeding.
Side effects:
Flushing and pruritus- The flush happens when niacin causes the small
capillaries in your skin to dilate, which increases the flow of blood to the
surface of the skin. Niacin flush is a very common side effect, with almost
everyone who takes large doses of niacin experiencing the reddening. Niacin
flush is a common side effect of taking high doses of niacin supplements. It's
uncomfortable, but it's harmless. It appears as a flush of red on the skin,
which may be accompanied by an itching or burning sensation
PCSK9-
MOA—is an enzyme circulating in the blood that binds to LDL receptors on the
surface of liver cells and promotes their degradation in other words the activity of
PCSK9 reduces the removal of LDL from the circulation
—now the PCKS9 inhibitors are monoclonal antibodies that bind to and inactivate
PCSK9 in the absence of PCSK9 there’s more LDL receptors available to bind and
clear LDL from the circulation leading to decreased levels of LDL cholesterol
‘’Pag walang inhibitor ng PCSK9, DADAMI ANG LDL SA KATAWAN’’
(Proprotein convertase subtilisin/kexin type 9 is an enzyme encoded by the PCSK9
gene in humans on chromosome 1. It is the 9th member of the proprotein convertase
family of proteins that activate other proteins. )
Dosage : Long-lasting drugs, which your doctor may call long-acting injectables,
improve symptoms the same way as daily pills. They stay longer in your body so
they are given every 2-4 weeks( monthly).
CONTRAINDICATIONS: Hypersensitivity
SIDE EFFECTS: inj site reactions, The most common kinds of reactions reported in
Repatha's studies were discoloration, pain, and bruising at the injection site.
Monitoring: PCSK-9 inhibitors also cause hepatocyte damage, presenting as
elevation in serum transaminases. PCSK-9 can enhance the liver injury in patients
with risk factor of liver injury like hepatic steatosis.
Nitroglycerin
MOA: Organic nitrate which causes systemic venodilation, decreasing preload
Cellular mechanism: enters vascular smooth muscle and is converted to nitric oxide
(NO) which induces synthesis of cGMP and vasodilation
Relaxes smooth muscle via dose-dependent dilation of arterial and venous beds to
reduce both preload and afterload, and myocardial O2 demand
Also improves coronary collateral circulation. Lower BP, increased HR, occasional
paradoxical bradycardia
Questions
10 mcq on CAD
1. What drugs are recommended if you cant take beta blockers or beta blockers
don’t work?
A. ARBS
B. CCB
C. ACE INHIBITORS
- Calcium channel blockers relax blood vessels and lower your blood
pressure. These medications can reduce your heart's workload, help
coronary arteries open, and relieve and control angina.
- They work by preventing calcium from entering the cells of the heart
and arteries.
- Calcium causes the heart and arteries to squeeze (contract) more
strongly. By blocking calcium, calcium channel blockers allow blood
vessels to relax and open.
2. Why should you always monitor the blood pressure of a patient taking drugs
for hyperlipidemia?
Answer : D
-One of the most important things you can do to manage high blood pressure is to
track it every day to measure the success off your treatment and to spot trends
that may indicate complications(ex: to reduce cardiac events) .
Coat release: Enteric coating is a useful strategy for the oral delivery of drugs which
rapidly degrade in the stomach, as it prevents the drug being released in the acidic
conditions of the stomach before reaching the intestine.
5. Which among the following drug has a boxed warning due to cognitive
impairment including memory loss:
A. Cholestyramine
B. Ezetemibe
C.Fenofibrate
D.Atorvastatin
Answer: D–
Drugs (statins) that lower blood levels of cholesterol may impair memory and other
mental processes by depleting brain levels of cholesterol as well. In the brain, these
lipids (cholesterol, glycosphingolipids (GSLs and phosholipids) are vital to the
formation of connections between nerve cells — the links underlying memory and
learning.
Answer : D
Answer: A
a. Diphenhydramine
b. Loratadine
c. Cetirizine
d. All of the above
Ans: D
6. Why should you not take the drug with fruit juices?
a. Becuase they can irritate the stomach and cause hyperacidity leading to
decreased absorption of the drug
b. Fruit juices like grapefruit juice is an enzyme inhibitor
c. Bec the taste is not pleasant
d. Taking drugs with fruit juices can make you vomit
- answer b: do not take with fruit juices esp grapefruit juice because it
is an enzyme (cyp450) inhibitors, this cyp 450 is an enzyme for
metabolism, so ang ginagawa ng grapefruit juice iniinhibit nya ang
further metabolism( metabolism is a preparation for a drug to be
excreted) so matatagalan ngaun ang excretion ng drug sa katawan, na
memetabolize sya lalo, mag accumulate ang dose then can lead to
overdosage na naman.
Answer: A
a. Dopamine
b. Dobutamine
c. Norepinephrine
d. Epinephrine