CALCIUM CHANNEL BLOCKERS

Calcium Channel Blockers:

1.  Phenylalkylamines (Verapamil) 

2.  Benzothiazipines (Diltiazem)

3.  Dihydropyridines 

     First Generation:  Nifedipine

    Second Generation:  Isradipine

                                      Nicardipine

                                      Felodipine

Third Generation:  Amlodipine

(source: rniam143)

RENIN ANGIOTENSIN ALDOSTERONE SYSTEM (RAAS)

Cardiovascular Drugs

Angiotensinogen a hormone released in the liver. It will encounter an enzyme called RENIN. Renin’s job is to find Angiotensinogen and cleave off part of the protein and form an inactive hormone called ANGIOTENSIN l. From there, a different enzyme called Angiotensin Converting Enzyme or ACE will convert the Angiotensin l to the active hormone Angiotension ll. It is active and will go to the kidney and activate the ANGIOTENSIN 1 RECEPTOR or AT1R then

ANGIOTENSIN ll tells the kidney to:
- increase Na+ retention
- increase H20 retention
- increase Aldosterone
(they all causes increase blood pressure)

It is good for people who have low blood pressure but for people who have normal blood pressure too much of it will cause their blood pressure to be high.

RAA SYSTEM DRUG TARGETS:
1. It blocks the conversion of Angiotensin l to Angiotensin ll. It is called ACE l
2. This drug prevent Angiotensin ll from working on the kidney by blocking the receptor that Angiotensin relies on. It is called Angiotensin ll Receptor Blocker or ARBS

MOST COMMON ACE INHIBITOR DRUGS (ending in “pril”):
- Lisinopril (Prinivil, Zestril)
- Lininopril/HCTZ is a combination product with Thiazide (Prinzide, Zestroetic)
- Enalapril (Vasotec)
- Ramipril (Altace) most commonly used

ANGIOTENSION l RECEPTOR BLOCKER DRUGS or ARBS (ending in “sartan”):
- Losartan (Cozaar)
- Olmesartan (Benicar)
- Valsartan (Diovan)

Clinical use of ACE l and ARBS:
- HYPERTENSION
- HEART FAILURE esp following a heart attack
- Hypertension that causes kidney problem like Proteinuria which the kidney spills protein into the urine as the result of kidney damaged caused by high blood pressure

ADVERSE EFFECTS OF ACE l AND ARBS:
1. Symptoms of low blood pressure (orthostasis)
- that is why we advice patient not to get up or rise quickly
2. Hyperkalemia
- it happens because if we block the Angiotensin ll the Na+ can’t be reabsorbed which means the K+ will stay in the blood causing K+ level in our blood to be high.
3. Acute Kidney Injury
- Serum Crea in your blood will increase. This is because the Angiotension ll is very important hormone to regulate blood flow to the kidney AND if we block the effect of Angiotensin ll we prevent the kidney’s ability to maintain its own blood flow which can cause damage to the kidney
4. Angioedema (very rare)
- most common with ACE l than ARB’s

5. Dry Cough (why it happened)
- ACE l does not only involve in converting Angiotensin l to ll but it also involve in breaking down BRADYKININ into PROTEIN. So if we are taking ACE inhibitor, we are blocking the conversion of Angiotensin l and ll, and we are also blocking the conversion of Bradykinin causing the Bradykinin to increase and thus cause Dry Cough.

Quick facts about Bradykinin:
The activation of the kinin system-bradykinin is particularly important in blood pressure regulation and in inflammatory reactions, through bradykinin ability to elevate vascular permeability and to cause vasodilatation in some arteries and veins. The biological effects of kinins are mediated by specific receptors called B1 and B2.The activation of this system is particularly important in blood pressure regulation and in inflammatory reactions, through bradykinin (BK) ability to elevate vascular permeability and to cause vasodilatation of arteries and veins of the gut, aorta, uterus and urethra. The kinin system is involved in many clinical situations including respiratory allergic reactions, septic shock, hypertension and its treatment, hypotensive transfusion reactions, heart diseases, pancreatitis, hereditary and acquired angioedema, Alzheimer disease and liver cirrhosis with ascites.
Apart from being a pro-inflammatory mediator, bradykinin is now recognized as a neuromediator and regulator of several vascular and renal functions.
Bradykinin (BK) has multiple pathophysiologic functions such as induction of vascular permeability and mitogenesis, and it triggers the release of other mediators such as nitric oxide in inflammatory and cancer tissues. (from nlm)

WHO SHOULD NOT TAKE ACE-l and ARB’s?
1. Those with high K+ level
2. Angioedema
3. Pregnant women (category D)
4. Acute Kidney Injury
5. Bilateral Renal Artery Stenosis (the body can’t regulate the blood flow to the kidney)

SOURCE: Sean P. Kane (ClinCalc Academy)

Visit his YouTube channel for more info about drugs

emtgoingonrn:

image

image

Have a request for an infographic? Need something explained? Submit a request!

_______________

Works Cited

"Endocrine and Hematologic Emergencies." Emergency Care and Transportation of the Sick and Injured. Ed. Andrew N. Pollak, MD, FAAOS, Leaugeay Barnes,…

(via nclexstudyguide)

dieselotherapy:

Ventricular Tachycardia (V-Tach) 
Ventricular Tachycardia is a dysrhythmia that usually originates from a single site within the ventricles at a rate greater than 100 bpm. The QRS complex is wide, bizarre and >0.12 seconds. As the heart rate increases, the ventricles do not have the opportunity to completely empty and refill. Therefore, cardiac output is decreased and adequate amounts of blood are not circulated to vital organs. Once the heart rate exceeds 160 impulses per minute, there is usually no effective pumping action of the heart and the patient presents with PULSELESS V-Tach. This patient requires immediate defibrillation. It is possible to have a pulse with V-Tach, however this will degrade into a life threatening dysrhythmia if left untreated.
 
Ventricular Fibrillation (V-Fib) 
With V-Fib there are many impulses initiated from many locations within the ventricles. As a result the cardiac output is nonexistent and the patient will not have a pulse. The fibrillation may be fine or course waves. As the amplitude of fibrillation waves decreases so does the chance of successful defibrillation and reorganization of a viable perfusing rhythm. 
dieselotherapy:

Ventricular Tachycardia (V-Tach) 
Ventricular Tachycardia is a dysrhythmia that usually originates from a single site within the ventricles at a rate greater than 100 bpm. The QRS complex is wide, bizarre and >0.12 seconds. As the heart rate increases, the ventricles do not have the opportunity to completely empty and refill. Therefore, cardiac output is decreased and adequate amounts of blood are not circulated to vital organs. Once the heart rate exceeds 160 impulses per minute, there is usually no effective pumping action of the heart and the patient presents with PULSELESS V-Tach. This patient requires immediate defibrillation. It is possible to have a pulse with V-Tach, however this will degrade into a life threatening dysrhythmia if left untreated.
 
Ventricular Fibrillation (V-Fib) 
With V-Fib there are many impulses initiated from many locations within the ventricles. As a result the cardiac output is nonexistent and the patient will not have a pulse. The fibrillation may be fine or course waves. As the amplitude of fibrillation waves decreases so does the chance of successful defibrillation and reorganization of a viable perfusing rhythm.

dieselotherapy:

Ventricular Tachycardia (V-Tach)

Ventricular Tachycardia is a dysrhythmia that usually originates from a single site within the ventricles at a rate greater than 100 bpm. The QRS complex is wide, bizarre and >0.12 seconds. As the heart rate increases, the ventricles do not have the opportunity to completely empty and refill. Therefore, cardiac output is decreased and adequate amounts of blood are not circulated to vital organs. Once the heart rate exceeds 160 impulses per minute, there is usually no effective pumping action of the heart and the patient presents with PULSELESS V-Tach. This patient requires immediate defibrillation. It is possible to have a pulse with V-Tach, however this will degrade into a life threatening dysrhythmia if left untreated.

 

Ventricular Fibrillation (V-Fib)

With V-Fib there are many impulses initiated from many locations within the ventricles. As a result the cardiac output is nonexistent and the patient will not have a pulse. The fibrillation may be fine or course waves. As the amplitude of fibrillation waves decreases so does the chance of successful defibrillation and reorganization of a viable perfusing rhythm.

(via nclexstudyguide)

nurse-blog:

Medication SUFFIXES

  • "Caine" - Local Anesthetics
  • "Done" - Opioid analgesics
  • "Mycin" - Antibiotics
  • "Micin" - Antibiotics
  • "Oxacin" - Broad Spectrum Anti-biotics
  • "Vir" - Anti-virals
  • "Dine" - anti-ulcer agents (H2 Histamine Blockers)
  • "Lam" - anti-anxiety agents
  • "Pam" - anti-anxiety agents
  • "Nuim" - neuromuscular blockers

(via nclexstudyguide)

dieselotherapy:

Skill: assessing pupil response.
Lets look a little closer at this particular skill.
First up, the pupil isn’t actually anything at all. A hole at the centre of the iris that controls the amount of light entering the eye. The size of this hole is controlled by 2 muscles within the iris. The pupilloconstrictor (controlled by the parasympathetic nervous system) and the pupillodilator (controlled by the sympathetic nervous system). So I guess what we are really assessing here is the iris response.
Pupil contraction (parasympathetic response):
When a light intensity increases across the rods and cones of the retina, impulses travel via the optic nerve to the pretectal nucleus of the upper midbrain.
From here impulses travel to the Edinger-Westphal nucleus, and onwards via the III cranial nerve (occulomotor) to the pupilloconstrictor muscle of the iris… causing contraction (miosis).
Pupil dilation (sympathetic response):
When light intensity decreases, impulses travel from the retina via the optic nerve to neurones on the hypothalamus where it takes a convoluted neuronal journey through the lateral brainstem to the spinal cord, down across the apex of the lung, back up alongside the internal carotid into the skull, through the inferior orbital fissure. Finally, it travels along the V cranial nerve (trigeminal) that innervates the pupillodilator muscle of iris… causing dilation (mydriasis).
How to assess pupillary reflexes.
Ideally, pupillary reflexes should be examined in a dim environment. If the patient is conscious, ask them to fix their gaze on a target some distance behind you ( If they re-focus on you or your torch, there may be pupil constriction as a result of accomodation).
Use a neurotorch or cheap penlight torch. This is for 2 reasons:
Using a superbright concentrated light will not be appreciated by a conscious patient.
Doctors do not (as a rule) carry neuro torches. They borrow the nurses. They forget to give them back.
Size and Equality.
The pupil size is documented as the diameter in millimetres. Tools to help you estimate this size include pupil gauges located on most Glasgow Coma Scale records and many neuro torches.
You may also find it useful in your written documentation to include descriptors such as: pinpoint, small, midposition, large, dilated.
Aniscoria: Up to 20% of the population have a slight difference in pupil size and is considered a normal variant. This difference should not be greater than 1mm and pupil reactivity should be normal.
Shape:
The pupil shape can be documented as round, irregular, oval or keyhole. Causes of irregular pupils include cataract surgery or the implantation of intra-occular lenses.
Oval pupils may be a result of compression of the III cranial nerve as a result of raised intracranial pressure (ICP). As ICP increases, the pupil will continue to dilate and eventually become non-reactive to light.
Keyhole pupils are seen in patients post iridectomy (a common part of cataract surgery). They may still react to light but usually the reactivity is sluggish.
Reactivity:
The pupil response to light is assessed by shining a neuro torch (or low powered penlight torch) separately into each eye. Tip: shining the torch onto the pupil from directly above may make assessment difficult due to ‘glare’ reflected off the cornea. Instead, position yourself in front of the eye and shine the beam from slightly off to one side.
Document pupil reactivity to light separately.Reactivity may be:
Brisk
Sluggish
Non-reactive.
At the same time look for the normal pupillary constriction response in the opposite eye. This is called the consensual pupillary response.
Accommodation:
This is the normal constriction of the pupil that occurs when a conscious patient is asked to shift their focus from a distant object, to a close one.
Causes of abnormal pupils:
Unequal pupils:
Mydriasis: One pupil is dilated and non-reactive whilst the other is normal. May be caused by compression of the III cranial nerve, compression of the posterior communicating artery or by direct damage to the nerve endings in the iris sphincter muscle.
Following a traumatic brain injury an increase in intracranial pressure can lead to the uncus (part of the temporal lobe) squeezing against the tentorium and pressing against the III cranial nerve resulting in a dilated pupil (mydriasis) on the affected (ipsilateral) side.If pressure continues to increase, contralateral dilation will also occur.
Horner’s Syndrome: One pupil is smaller than the other and has a decreased response to light and accommodation. There is ptosis of the eyelid on the affected side. Caused by loss of sympathetic intervention to the pupil due to a lesion in the brainstem of spinal cord, or damage to the hypothalamus. There is also decreased sweating (Anhidrosis) of some or all of the face. Causes of Horner’s syndrome include carotid artery dissection, nasopharyngeal tumours, brachial plexus injury.
Dilated pupils:
Drug induced mydriasis: bilateral dilation as a result of drugs including antihistamines, hallucinogens, amphetamines, anticholinergics, dopamine or barbiturates. May be caused by medication used for ophthalmic examination such as atropine, scopolamine, or by anoxia or brain death.
Mental or emotional stimulation: Dilation may also be caused by sexual arousal or increased mental effort.
Constricted pupils
Miosis: Bilateral pinpoint pupils (usually too small to figure out if they are responding to light or not). May be caused by disruption to the sympathetic pathway due to intraocular inflammation or direct trauma, a pontine haemorrhage, or due to the effect of drugs such as opiates, pilocarpine or acetylcholine.
Equal pupils:
Hippus: Initially react to light but then alternate between dilated and constricted. May indicate early compression of III cranial nerve. May indicate injury to the midbrain or barbiturate toxicity.
Relative Afferent Pupillary Defect (RAPD): When light is shone into the effected eye there is a sluggish reaction. There is a normal consensual reaction when light is shone into the opposite eye, but when the light is quickly shone back to the effected eye it will dilate. This is known as the swinging flashlight test (see video below) and may indicate optic neuritis, retinal detachment or infection or direct optic nerve damage.
In conclusion, a pupil assessment is a quick but important skill that can give a great deal of information. The eyes may indeed be the windows to the soul. But the pupils are the manholes to the ongoing neurological status of your patient.
(x)
 

dieselotherapy:

Skill: assessing pupil response.

Lets look a little closer at this particular skill.

First up, the pupil isn’t actually anything at all.
A hole at the centre of the iris that controls the amount of light entering the eye.
The size of this hole is controlled by 2 muscles within the iris.
The pupilloconstrictor (controlled by the parasympathetic nervous system) and the pupillodilator (controlled by the sympathetic nervous system).
So I guess what we are really assessing here is the iris response.

Pupil contraction (parasympathetic response):

When a light intensity increases across the rods and cones of the retina, impulses travel via the optic nerve to the pretectal nucleus of the upper midbrain.

From here impulses travel to the Edinger-Westphal nucleus, and onwards via the III cranial nerve (occulomotor) to the pupilloconstrictor muscle of the iris… causing contraction (miosis).

Pupil dilation (sympathetic response):

When light intensity decreases, impulses travel from the retina via the optic nerve to neurones on the hypothalamus where it takes a convoluted neuronal journey through the lateral brainstem to the spinal cord, down across the apex of the lung, back up alongside the internal carotid into the skull, through the inferior orbital fissure. Finally, it travels along the V cranial nerve (trigeminal) that innervates the pupillodilator muscle of iris… causing dilation (mydriasis).

How to assess pupillary reflexes.

Ideally, pupillary reflexes should be examined in a dim environment.
If the patient is conscious, ask them to fix their gaze on a target some distance behind you ( If they re-focus on you or your torch, there may be pupil constriction as a result of accomodation).

Use a neurotorch or cheap penlight torch. This is for 2 reasons:

Using a superbright concentrated light will not be appreciated by a conscious patient.

Doctors do not (as a rule) carry neuro torches.
They borrow the nurses.
They forget to give them back.

Size and Equality.

The pupil size is documented as the diameter in millimetres. Tools to help you estimate this size include pupil gauges located on most Glasgow Coma Scale records and many neuro torches.

You may also find it useful in your written documentation to include descriptors such as: pinpoint, small, midposition, large, dilated.

Aniscoria:
Up to 20% of the population have a slight difference in pupil size and is considered a normal variant. This difference should not be greater than 1mm and pupil reactivity should be normal.

Shape:

The pupil shape can be documented as round, irregular, oval or keyhole.
Causes of irregular pupils include cataract surgery or the implantation of intra-occular lenses.

Oval pupils may be a result of compression of the III cranial nerve as a result of raised intracranial pressure (ICP).
As ICP increases, the pupil will continue to dilate and eventually become non-reactive to light.

Keyhole pupils are seen in patients post iridectomy (a common part of cataract surgery). They may still react to light but usually the reactivity is sluggish.

Reactivity:

The pupil response to light is assessed by shining a neuro torch (or low powered penlight torch) separately into each eye.
Tip: shining the torch onto the pupil from directly above may make assessment difficult due to ‘glare’ reflected off the cornea. Instead, position yourself in front of the eye and shine the beam from slightly off to one side.

Document pupil reactivity to light separately.
Reactivity may be:

Brisk

Sluggish

Non-reactive.

At the same time look for the normal pupillary constriction response in the opposite eye. This is called the consensual pupillary response.

Accommodation:

This is the normal constriction of the pupil that occurs when a conscious patient is asked to shift their focus from a distant object, to a close one.

Causes of abnormal pupils:

Unequal pupils:

Mydriasis: One pupil is dilated and non-reactive whilst the other is normal.
May be caused by compression of the III cranial nerve, compression of the posterior communicating artery or by direct damage to the nerve endings in the iris sphincter muscle.

Following a traumatic brain injury an increase in intracranial pressure can lead to the uncus (part of the temporal lobe) squeezing against the tentorium and pressing against the III cranial nerve resulting in a dilated pupil (mydriasis) on the affected (ipsilateral) side.
If pressure continues to increase, contralateral dilation will also occur.

Horner’s Syndrome: One pupil is smaller than the other and has a decreased response to light and accommodation. There is ptosis of the eyelid on the affected side.
Caused by loss of sympathetic intervention to the pupil due to a lesion in the brainstem of spinal cord, or damage to the hypothalamus. There is also decreased sweating (Anhidrosis) of some or all of the face.
Causes of Horner’s syndrome include carotid artery dissection, nasopharyngeal tumours, brachial plexus injury.

Dilated pupils:

Drug induced mydriasis: bilateral dilation as a result of drugs including antihistamines, hallucinogens, amphetamines, anticholinergics, dopamine or barbiturates.
May be caused by medication used for ophthalmic examination such as atropine, scopolamine, or by anoxia or brain death.

Mental or emotional stimulation: Dilation may also be caused by sexual arousal or increased mental effort.

Constricted pupils

Miosis: Bilateral pinpoint pupils (usually too small to figure out if they are responding to light or not).
May be caused by disruption to the sympathetic pathway due to intraocular inflammation or direct trauma, a pontine haemorrhage, or due to the effect of drugs such as opiates, pilocarpine or acetylcholine.

Equal pupils:

Hippus: Initially react to light but then alternate between dilated and constricted.
May indicate early compression of III cranial nerve.
May indicate injury to the midbrain or barbiturate toxicity.

Relative Afferent Pupillary Defect (RAPD): When light is shone into the effected eye there is a sluggish reaction. There is a normal consensual reaction when light is shone into the opposite eye, but when the light is quickly shone back to the effected eye it will dilate.
This is known as the swinging flashlight test (see video below) and may indicate optic neuritis, retinal detachment or infection or direct optic nerve damage.

In conclusion, a pupil assessment is a quick but important skill that can give a great deal of information.
The eyes may indeed be the windows to the soul. But the pupils are the manholes to the ongoing neurological status of your patient.

(x)

 

(via nclexstudyguide)

I am reblogging this because someone reblogged this and said this is not true. She said she’s an ICU Nurse. Let me tell you Maam (12 reasons so far …that’s her tumblr name) am glad for the comment but didn’t you notice the word “usually”? It is very different from the word “always”. So please do not brag your being an ICU Nurse my dear.

All of the photos I am posting here is from Mosby Elsevier to help out students and nclex takers tackle nursing exams and such. I have been practicing as a Registered Nurse since 1998 in our country. By the time I got here in the US I needed to pass the NCLEX for me to be able to work as a Nurse here. I am just sharing my study material here hoping to encourage other nursing students especially those who will take the nclex.

NCLEX exam is a textbook exam, it is not always based on the real world of clinical practice.

Cadiovascular Disease in Pregnancy (Rheumatic heart disease, congenital heart defects and mitral valve prolapse account for the greatest incidence of cardiac disease in pregnancy)
Clinical manifestations indicative of cardiac decompensation are those of impending CHF:
- frequent cough, progressive dyspnea
- progressive general edema, jugular vein distention (JVD)
- syncope with exertion
- excessive fatigue for level of activity
- dysrhythmia
- congested breath sounds
- cardiac decompensation increases with length of gestation; highest incidence of CHF is observed at 28 to 32 weeks’ gestation

TREATMENT
Management of the pregnant client
- good nutritional intake; iron supplement; may require decrease in calories to avoid excessive weight gain
- limited physical activity
- sodium and fluids may be limited but not severely restricted
- diuretics and digitalis may be given
- may be hospitalized at 28 to 32 weeks’ gestation because of impending CHF
- if coagulation problems occur, heparin is used because it does not cross the placenta
- prophylactic antibiotics (penicillin) to prevent infection (endocarditis) Cadiovascular Disease in Pregnancy (Rheumatic heart disease, congenital heart defects and mitral valve prolapse account for the greatest incidence of cardiac disease in pregnancy)
Clinical manifestations indicative of cardiac decompensation are those of impending CHF:
- frequent cough, progressive dyspnea
- progressive general edema, jugular vein distention (JVD)
- syncope with exertion
- excessive fatigue for level of activity
- dysrhythmia
- congested breath sounds
- cardiac decompensation increases with length of gestation; highest incidence of CHF is observed at 28 to 32 weeks’ gestation

TREATMENT
Management of the pregnant client
- good nutritional intake; iron supplement; may require decrease in calories to avoid excessive weight gain
- limited physical activity
- sodium and fluids may be limited but not severely restricted
- diuretics and digitalis may be given
- may be hospitalized at 28 to 32 weeks’ gestation because of impending CHF
- if coagulation problems occur, heparin is used because it does not cross the placenta
- prophylactic antibiotics (penicillin) to prevent infection (endocarditis)

Cadiovascular Disease in Pregnancy (Rheumatic heart disease, congenital heart defects and mitral valve prolapse account for the greatest incidence of cardiac disease in pregnancy)

Clinical manifestations indicative of cardiac decompensation are those of impending CHF:
- frequent cough, progressive dyspnea
- progressive general edema, jugular vein distention (JVD)
- syncope with exertion
- excessive fatigue for level of activity
- dysrhythmia
- congested breath sounds
- cardiac decompensation increases with length of gestation; highest incidence of CHF is observed at 28 to 32 weeks’ gestation

TREATMENT
Management of the pregnant client
- good nutritional intake; iron supplement; may require decrease in calories to avoid excessive weight gain
- limited physical activity
- sodium and fluids may be limited but not severely restricted
- diuretics and digitalis may be given
- may be hospitalized at 28 to 32 weeks’ gestation because of impending CHF
- if coagulation problems occur, heparin is used because it does not cross the placenta
- prophylactic antibiotics (penicillin) to prevent infection (endocarditis)