NURS 323 PBL 3 Study Guide

medications for MI

"The individual should be given an aspirin immediately (ticlopidine if allergic to aspirin) along with nitrates and morphine for pain"

myocardial infarction (MI)

"heart attack; death of myocardial tissue (infarction) caused by ischemia (loss of blood flow) as a result of an occlusion (plugging) of a coronary artery; usually caused by atherosclerosis"

Blood pressure normal value

120/80 mmHg

Hypertension value

140/90 mmHg or higher

Carbamazepine (Tegretol)

2nd most commonly prescribed, used for partial and tonic/clonic seizures Much better tolerated than Dilantin, often preferred drug of choice Adverse effects are leukopenia, anemia, and thrombocytopenia Must obtain a CBC at baseline before beginning medication and then periodically when on it

Epilepsy

A condition of 2 or more seizures 24 or more hours apart Everyone who has epilepsy has experienced a seizure but not everyone who has a seizure has epilepsy

Treatment of Status Epilepticus

A medical emergency Drugs Lorazepam (Ativan) IV Phenytoin (Dilantin) IV Fosphenytoin (Cerebyx), phenobarbitals

Fondaparinux (Arixtra) — LMW

A synthetic anticoagulant Selective inhibition of factor XA Enhances activity of anti-thrombin, but no direct affect on thrombin Therapeutic uses Prevention of DVT, following surgery Treatment of acute PE Treatment of acute DVT in conjunction with Coumadin Coumadin blocks absorption of Vitamin K, so the body cannot make pro-thrombin Takes 6-8 hours to work Adverse effects — bleeding, thrombocytopenia, spinal or epidural hematoma

Confirmation of emergence from coma

Ability to respond to yes/no questions about self or environment Ability to discriminate among objects in environment

Calcium Channel Blockers- Dihydropyridines. Nifedipine (Procardia) VND: Very Nice Drugs. Verapamil, Nifedipine, Diltiazem

Act on arterioles, direct on smooth muscle on arterioles themselves, end in "-ipine" Greatest impact on vessels and heart. Calcium normally increases the heart rate at the SA node and conduction velocity (AV node) and force of contraction from myocardium Dihydropyridines work on the arterioles Nifedipine also blocks calcium channels to vasodilate, increase in HR Can be used for angina pectoris, essential hypertension, migraines, and suppressing premature labor

Angiotensin II Receptor Blockers (ARBS): adverse effects and education

Adverse effects — angioedema, fetal harm, renal failure Education when starting a blood pressure medication: Tell them about how it will decrease their blood pressure, educate them on sitting and standing slowly to not have an orthostatic event because they will feel different

Beta Blockers (BB): adverse effects

Adverse effects — fluid retention, fatigue, decreased blood pressure, decreased heart rate or MI if it aggravates other arrhythmias Be careful with asthmatic patients too REMEMBER THE B's: Bradycardia and heart Blocks, Breathing problems and Bronchospasms, Banned from asthma patients, Bad for HF patients, Blood sugar masking, Blood pressure lowered

ACE inhibitors: adverse effects

Adverse effects: , intractable cough, angioedema (allergic reaction, hives, urticaria), renal failure, Hyperkalemia/increased potassium REMEMBER: ACE! Angioedema, Cough, and Elevated potassium "for example, ACE Inhibitors are known for producing hyperkalemia and an intractable cough (means a cough that does not go away). If we have a patient with this type of cough, we need to give these patients something else because there are many other drugs to lower BP; " Do not use in pregnant women, can cause fetal injury Can become hypotensive on 1st dose Also dysgeusia (altered taste), or neutropenia

HMG-CoA-Reductase Inhibitors (STATINS): adverse effects

Adverse effects: Headaches, rashes, GI disturbances, myopathy, hepatotoxicity, Complaints of lower leg muscle aches Liver function tests assessed throughout medication implementation

Nicotinic Acid (Niacin): adverse effects

Adverse effects: Skin flushing, itching, GI disturbances, hepatotoxicity, hyperglycemia, gouty arthritis "The Niacin flush" Checking liver function and glucose tests

Calcium Channel Blockers- Nifedipine (Procardia), Verapamil (Calan) and Dilitazem (Cardizem) ADVERSE EFFECTS

Adverse effects: constipation, facial flushing, vertigo, swelling in ankles / edema, gingival hyperplasia, heart block on EKG Toxicity: severe decrease in BP and HR, heart blocking at AV node, tachydysrhythmias Need to know baseline blood pressure and pulse prior to admin

data processing deficit

Agnosia: Deficit of recognition of the form and nature of objects, typically as a result of brain damage. Involves loss of recognition through one sense, but maybe other senses can still recognize Produced by dysfunction in the primary sensory area or in interpretive areas of the cerebral cortex Dysphasia: The impairment of comprehension or production of language, semantic processing. Comprehension or use of symbols is disturbed or lost Associated with stroke that involves MCA middle cerebral artery Aphasia: The loss of comprehension or production of language Acute Confusion states Dementias: Characterized by loss of >1 cognitive or intellectual function Decrease in orientation, general knowledge and information, vigilance, recent memory, remote memory, concept formation, abstraction, reasoning, or language Causes include degeneration, CVA, compression, toxins, metabolic disorders, biochemical imbalances, demyelination, and infections S/Sx are grouped according to type of memory deficit Amnestic dementia — loss of recent memory Cognitive dementia — loss of remote memory Intentional dementia — loss of vigilance and executive function Altered behavior

Cholinesterase Inhibitors : adverse effectss

All come with adverse side effects Cholinergic — decreased HR and BP GI upset, headache, liver injury, bronchoconstriction

Memantine

Alzheimer's treatment — modulates effects of glutamate at NMDA receptors (memory and learning) 1st drug in new NMDA drug class Indicated for moderate and severe AD Better tolerated than cholinesterase inhibitors Adverse effects of dizziness, headache, confusion, constipation

Rivaroxaban (Xarelto)

Another oral anticoagulant, more favorable, newer Selective inhibition of factor XA, inhibiting production of thrombin Rapid onset, fixed dose, decreased bleeding risk no INR testing needed No antidote, because it is safer and poses less risk for serious bleeds Prevention of DVTs, PEs following total hip and knee replacement S/P surgery, strokes in patients with afib Adverse effect is bleeding Both coumadin and xarelto are unsafe for pregnancy, can cause pregnancy-related hemorrhage

Aspirin (ASA)

Antiplatelet Drugs Suppress Platelet Aggregation most common — suppresses thrombus formation in arteries Inhibits cyclooxygenase Used for prophylaxis for ischemic CVA, TIAs, chronic stable angina, unstable angina, coronary stenting to prevent re-occlusion, primary prevention of MI Adverse effects — increased risk of bleeding Textbook: "Aspirin suppresses platelet aggregation by causing irreversible inhibition of COX-1, the enzyme that makes TXA2. Because platelets lack the machinery to synthesize new COX-1, the effects of a single dose persist for the life of the platelet (about 8 days)."

HMG-CoA-Reductase Inhibitors (STATINS): specific names

Atorvastatin (Lipitor) and Simvastatin (Zocor)

Potassium-Sparing Diuretics: general information

Blocks aldosterone (this promotes sodium and water excretion, but not potassium) Avoid eating foods high in potassium, risk of hyperkalemia, avoid salt substitutes

left sided heart failure

Blood backs up into the lungs and congests the pulmonary circulatory system

How the RAAS increases blood pressure

Blood pressure drops. The sympathetic nervous system is stimulated (fight or flight). Kidney cells called juxtaglomerular cells are stimulated to release Renin. Renin enters circulation and activates substance in liver called angiotensinogen. Angiotensinogen turns into Angiotensin I. ACE (Angiotensin-Converting-Enzyme) is found on the surface of lungs and kidney endothelium and converts Angiotensin I into Angiotensin II. Angiotensin II acts on smooth muscle vessels and constricts them. The kidneys are stimulated to conserve sodium and water — increase in blood volume. Adrenal cortex produces aldosterone, which also stimulates kidneys and lowers calcium / potassium level — increase in blood volume. Pituitary gland releases ADH (antidiuretic hormone) so the kidneys keep water — increase in blood volume. Blood vessels constricting and blood volume increasing results in increased blood pressure.

Traumatic Brain Injury (TBI)

Blunt trauma: "closed" trauma, head strikes a hard surface or rapidly moving object strikes the head Dura remains intact, brain tissue is not exposed to the environment, May result in both focal brain injuries and diffuse axonal injuries Open trauma: a break in the dura exposes cranial contents to environment results in focal brain injuries

Cerebrovascular accident (CVA) = stroke

Brain experiences loss of oxygen Categorized as hemorrhagic (blood vessel rupture, blood in brain) and Ischemic (blockage) TIAs are not true CVAs, more like warning stroke Transient ischemic attack is a temporary blockage of blood vessels disrupting blood flow, clot will dissolve within artery

Valproic Acid (Depakote)

Broad spectrum for generalized seizures, myoclonic, tonic, and clonic, and absence, and atonic Toxic effects — hepatotoxicity and pancreatitis, watch liver function tests

Cardiac Glycoside (Digoxin): Adverse effects

Can cause severe arrhythmias, very narrow therapeutic window Have to monitor apical heart rate, drug levels in blood. Diagnostic lab tests taken every day to determine drug level and electrolyte levels Non-cardiac adverse effects: anorexia, decreased appetite, nausea and vomiting, fatigue

diagnostic testing for alzheimer's

Cannot be confirmed until death with autopsy Can test to rule out other disorders: PET Scan: confirm an early diagnosis, CT scan shows more brain atrophy than occurs with normal aging, MRI evaluates condition of brain and r/o intracranial lesions, EEG evaluates the brain's electrical activity, CSF analysis rules out CSF infection, Cerebral blood flow studies

Angiotensin-Converting Enzyme Inhibitors - ACE Inhibitors: specific names

Capotopril (Capoten), Enalapril (Vasotec), Lisinopril (Zestril) "Prils"

Beta Blockers (BB): specific names

Carvedilol (Coreg), Bisoprolol (Zebeta), Metoprolol (Toprol) End in "olol"

Detection, Evaluation, and Treatment of High Cholesterol

Cholesterol screenings: Every 5 years for adults over age 20, including a total cholesterol (<199), HDL cholesterol (>60 mg/dL desirable), LDL cholesterol (<100 mg/dL desirable), triglycerides (<150 mg/dL desirable) Treatment of elevated LDL cholesterol: Therapeutic lifestyle changes: Weight control with a low-fat diet, encouraging eating plenty of raw vegetables, fruits, bran, drinking 2000 mL of fluid to prevent constipation, exercising, smoking cessation

Bile Acid-Binding Resins

Cholestyramine (Questran) and Colestipol (Colestid) Not a first line Decrease in LDL and Increase in VLDL in some pts Method of action: Increases LDL receptors AND Prevents absorption of bile acids Therapeutic use: Reduction of LDL cholesterol alongside a low cholesterol diet (requires diet education) Adverse effects: Constipation (education to drink 2 L water a day), also decreases uptake of fat-soluble vitamins Fibric Acid Derivatives (Fibrates)

Seizure classes

Classes Generalized — engages a bilateral network of neurons Focal — involves a localized network of neurons Seizure can begin in any lobe, can become bilateral 30 seconds to 2 minutes ,Alert and conscious, Sensory, cognitive, emotional Tonic, atonic, clonic, myoclonic, myoclonic-atonic, clonic-tonic-clonic Photosensitivity = reflex seizures Absence - Daydreaming, blank and unresponsive, eyelid flutter, atypical absence Myoclonic -Muscle-jerk Tonic/Atonic -Tonic, muscle stiffening, falls with injury atonic, muscle relax, floppy Tonic/Clonic - jerking, shaking, breathing difficulty, epileptic

Levels of consciousness (LOC)

Confused — disoriented to surroundings, impaired judgment, may need cues to respond to commands Lethargic — drowsy, need gentle verbal or touch stimulation to initiate a response Obtunded — responds slowly to external stimulation, needs repeated stimulation to maintain attention and response Stuporous — responds only minimally with vigorous stimulation, may only moan as a verbal response Comatose — no observable response to any external stimuli

Vasodilators: Sodium Nitroprusside (Nitropress)

Dilator, profound decrease in blood pressure Fast acting antihypertensive, used in HTN emergencies, given IV and immediate, causing low BP very fast Can give cyanide poisoning, be careful

Drugs for Multiple Sclerosis

Disease-modifying therapy — Decrease frequency and severity of relapses, decrease development of brain lesions, decrease future disability, help maintain quality of life Immunomodulators — interferon beta, glatiramer acetate, natalizumab, fingolimod Immunosuppressants — Mitoxantrone — 1st developed to treat cancer, then found to treat MS Poses risk for toxicity — toxicity to bone marrow, cardiotoxicity, and fetal harm​

Patient education and nursing interventions for antihypertensives

Do not stop taking abruptly Take medication as prescribed, do not miss or double up doses Avoid smoking and eating foods high in sodium (soups) Encourage exercising Monitor blood pressure drug therapy, logging daily BP Encourage small changes in diet, exercise, alcohol intake, stress level, weight monitoring May lead to depression, could also be predisposed Sexual dysfunction can occur, impacted by BP Stand up slowly — hypotension side effect and monitoring PO forms should be given with food Administer IV med slowly and use IV pump

multiple sclerosis supportive measures

During acute exacerbations Bed rest massages prevention of fatigue and pressure ulcers, turning bowel and bladder training, going only on the clock treatment of bladder infections with antibiotics physical therapy to help with gait issues counseling

Education for hypertension

Eat healthy, reduce salt intake, take medication regularly, increase exercise, manage stress, smoking cessation, alcohol cessation

High ceiling Loop Diuretics: Indications

Edema associated with heart failure, Hepatic or renal disease, Hypertension, hypercalcemia

Gemfibrozil (Lopid)

Effects on plasma lipoproteins Decreases plasma triglyceride content Decreases VLDL levels Increases HDL Method of action is UNKNOWN Reduces high levels of plasma triglycerides (VLDLs) Adverse effects: rashes, gallstones, GI disturbances, myopathy, and hepatotoxicity

Hematomas

Extradural hematomas, AKA epidural hematomas Arteries are the source of bleeding, higher velocity than regular vein Results in herniation through the foramen magnum S/Sx: loss of consciousness at time of injury (lucid periods may follow) as mass accumulates, increasing severity headache, vomiting, drowsiness, confusion, seizure, hemiparesis Clinical manifestations of temporal lobe herniation begins with ipsilateral pupillary dilation and then contralateral hemiparesis Subdural hematoma Tearing of bridging veins is what causes the rapidly and subacutely developing subdurals Other sources include torn cortical veins or venous sinuses and contused tissue Subdural space fills with blood and herniation can result Acute subdural hematoma Classic beginning of headache, drowsiness, restlessness, agitation, slowed cognition and confusion Sx worsen over time and process, loss of consciousness, respiration pattern changes, pupillary dilation Intracerebral Hematomas Intraparenchymal hemorrhages Small blood vessels traumatized by shearing forces Intracerebral hematoma expands, increases ICP, and compresses brain tissues As ICP rises, clinical manifestations of temporal lobe herniation may appear

Thiazide Diuretics: general information

First choice / first line to give for hypertension because side effects are not as intense Still risk of hypokalemia, still monitor potassium Works in the nephron and not the loop, which is why they are not as strong

High ceiling Loop Diuretics: Specific name

Furosemide (Lasix)

High ceiling Loop Diuretics: Nursing interventions

Give potassium, know normal potassium levels and watch for hypokalemia They are going to start urinating a lot! Be aware of that as their nurse. Take in the morning, not at night. Make sure they are safe to ambulate, it can cause hypotension Patient education: Maintaining proper nutrition, intake, and fluid volume Pay attention to potassium rich foods like bananas, oranges, dates, raisins, plums, fresh vegetables, potatoes, fish, whole grain cereal, legumes, avocado Frequent lab testing may be required with treatment K+ potassium supplementation if K level is lower than 3 mEq/L (hypokalemic) (should be 3.5 to 5.5 for normal)

Vasodilators: Nitroglycerin

Given for angina, can cause severe drop in blood pressure (which activates increased HR from resultant reflex) Powerful, dramatic decrease in venous pressure quickly Can come in many forms, gel, patch, sublingual, IV Adverse effects — hypotension, resultant reflex tachycardia

Focal brain injuries

Grossly observable brain lesions in cortical contusions (bruising) Force of impact typically produces contusions or bruises on the brain Contusion causes tears in blood vessels May be coup (direct impact area) or contrecoup (area opposite of where the force occurred / the line of force) Clinical manifestations of contusion May include immediate loss of consciousness, Loss of reflexes, Transient cessation of respiration, Brief period of decreased HR and BP (VS may stabilize within a few seconds), Reflexes return next, Regain of consciousness, Return to full alertness takes variable periods of time (minutes to days)

good cholesterol

HDL (high density lipoprotein) (>60 mg/dL desirable)

Altering the RAAS for a patient with HTN

HTN is impacted by overactivation of the RAAS. By administering medications like ACE-inhibitors and ARBs, the activity of the RAAS is opposed and blood pressure will decrease.

right sided heart failure

Hepatic veins become very congested with blood, leading to hepatomegaly and venous congestion (JVD, edema, ascites / abdomen). Can be caused by left sided heart failure.

Thiazide Diuretics: Specific name

Hydrochlorothiazide (Hydrodiuril)

Pupillary Changes — Changes in pupillary size give insight to level of brain stem dysfunction

Hypothermia may cause fixed pupils Hypoxia and severe ischemia cause large and fixed pupils. Occasionally, pupils remain small even in severe hypoxia

Primary hypertension

Idiopathic, no identifiable cause, develops over time

Other Drugs that alter plasma lipid levels

If cholesterol levels have not changed from other drugs... Try Drug combinations if just one has been tried Niacin and Lovastatin Simvastatin and Ezetimibe Pravastatin and Aspirin Atorvastatin and amlodipine Also try alternatives Fish oil ,Plant stenol, and sterol esters ,Estrogen ,Cholestin

The purpose of the RAAS

Increase in blood pressure

High ceiling Loop Diuretics: Contraindications

Known allergy, or an allergy to sulfonamide antibiotics, Hepatic coma, Severe electrolyte losses

bad cholesterol

LDL (low density lipoprotein) highest contributor to CHD (<100 mg/dL desirable)

Beta 2 receptors

Located in airway smooth muscles, bronchodilation and vasodilation relaxes smooth muscle

Responsibility of a Nurse with Thrombolytics

Look at lab levels: PT, aPTT, INR depending on medication (if on heparin or coumadin) Know what lab result goes with what medication Lab needs to match to the scales or the orders Heparin within perimeters, if falling out then decrease or increase No signs of bleeding in mouth, urine, rectum, skin sites, or any tubes Must have accurate calculations Second RN to check prior to administration Education on noticing bleeding, oozing, blood in bowel movement

Diuretics that cause hypokalemia

Loop and thiazide diuretics

Angiotensin II Receptor Blockers (ARBS): Specific names

Losartan (Cozaar), Valsartan (Diovan), Candesartan (Atacand) All end in "sartan"

Angiotensin II Receptor Blockers (ARBS): general information

Mechanism of action Blocks access of angiotensin II to dilate arterioles and veins decrease excretion of potassium, decrease aldosterone release increase renal excretion of sodium and water Used for hypertension, HF, diabetic nephropathy, MI, CVA prevention, or for migraine headaches Do not increase levels of bradykinin or kinase II, If a patient can't take ACE inhibitor because of cough, ARBs may be a substitute

Ezetimibe (Zetia)

Mechanism of action and impact on plasma lipids Inhibits cholesterol absorption Therapeutic use — decreases total cholesterol, LDL cholesterol, and apolipoprotein B Adverse effects: Myopathy, hepatitis, rhabdomyolysis, thrombocytopenia, pancreatitis

multiple sclerosis medications

Medication Corticotropin, prednisone, or dexamethasone Used to reduce edema of myelin sheath during exacerbation Do not prevent future exacerbations Acute attack — short course of methylprednisolone, with or without a short prednisone taper Interferon beta-1a or interferon beta-1b to reduce relapses Other useful medications to treat MS Chlordiazepoxide / Librium to mitigate mood swings Baclofen or dantrolene to relieve spasticity Bethanechol to relieve urinary retention and urgency

Cholinesterase Inhibitors

Medications for Alzheimer's — prevent breakdown of acetylcholine by acetylcholinesterase (AchE), front line drug Indicated for mild to moderate AD, helps slow progression but there is no cure Drugs recommended by FDA for AD, shown to improve cognition, behavior, and function, decreasing disease progression Donepezil (Aricept) for mild to moderate AD Rivastigmine (Exelon) for mild to severe AD Galantamine (Razadyne) for mild to moderate AD

HMG-CoA-Reductase Inhibitors (STATINS): general information

Most effective drugs for lowering LDL, 1st line in drug therapy for hypercholesterolemia Decrease of LDL cholesterol by 30 to 40% Increase of HDL cholesterol Non-lipid beneficial CV actions — Decreases risk of CV events AND Increases bone formation Therapeutic uses: Hypercholesterolemia Primary and secondary prevention of CV events Diabetes

High Ceiling Loop Diuretics: general information

Most potent diuretics, used when they need rapid diuresis because of rapid onset Typically last for several hours, even if there is renal impairment, diuretic action still continues Decreased fluid volume leads to a decrease return of blood to the heart — low BP, low pulmonary and systemic vascular resistance, low central venous pressure, low LVEDP

Cardiac Glycoside (Digoxin): general information

Naturally occurring compound Profound effect on mechanical and electrical properties of the heart — increases contractility, giving a very strong contraction, increasing cardiac output Hemodynamic benefits: Increased CO, decreased sympathetic tone, increased urine production, decreased renin release Electrical effects: alters electrical properties, increasing firing rate of vagal fibers and response to SA node to acetylcholine Neurohormonal effects: modulates activity in neurohormonal system, suppresses renin release in kidney, decreases sympathetic outflow from CNS, increases sensitivity of cardiac baroreceptors Positive inotropic action in the heart that increases force of contraction and contractility Pharmacokinetics: distributed across the placenta, eliminated through renal excretion, half-life is 1.5-2 days but can be prolonged with renal dysfunction

Seizure assessment

Neural assessment — mental status, PERRLA, sensory — breaking cotton swab in half to differentiate sharp-dull and ataxia for visual confirmation, reflexes of muscles, gait or pattern of walking and balance, cranial nerve testing (I, II, IV, V, VI, VII, XI)

medication for angina

Nitroglycerin to open up coronary arteries. Pill or spray for "safe" / stable angina, taken before strenuous activity Patch for unstable or chronic angina , taken daily, not PRN, rotating location daily

Nicotinic Acid (Niacin): general information

Not a first line Reduces LDL and TG levels Increases HDL levels better than any other drug Decreased production of VLDLs Therapeutic uses: Decreasing TG levels and increasing HDL levels

Warfarin (Coumadin) Oral Anticoagulant

PO Anticoagulant inhibits the synthesis of clotting factors, includes factor XA and thrombin, oldest oral anticoagulant Blocks biosynthesis of factors VII, IX, X and prothrombin (Vitamin K dependent clotting factors) Therapeutic uses — long term prophylaxis of thrombosis Prevention of venous thrombosis and associated PE Prevention of thromboembolism, especially in pts with prosthetic heart valves Prevention of thrombosis during atrial fibrillation Carries a significant risk of hemorrhage Half life is 1.5-2 days, pretty long! Must check INR or PT (prothrombin time) which should be 2-3 times the target for most patients and if it is too high, the dosage should be decreased

Isosorbide dinitrate or mononitrate

PO form of nitrate Relief of acute angina, long term prophylaxis of angina

angina

Pain in the heart region caused by lack of oxygen

Heparin: general information

Parenteral Anticoagulants Rapid acting anticoagulant enhances the activity of antithrombin, a protein that inactivates thrombin and factor XA (clotting factors), and without those the production of fibrin is reduced and clotting is suppressed IV or subcutaneous Uses — pulmonary embolism, evolving stroke CVA, DVT (deep vein thrombosis), pregnancy (doesn't cross placenta), open heart surgery, renal dialysis

Direct Thrombin Inhibitors

Parenteral Anticoagulants II Bivalirudin (Angiomax) is given IV Inhibits thrombin directly. Works independently of anti-thrombin, inhibits clot-bound thrombin as well as free thrombin. Causes less bleeding and fewer ischemic events. Can be "turned off" easily Therapeutic use — preventing clot formation, combined with aspirin Method of action Facilitates action of anti-thrombin, prevents conversion of fibrinogen to fibrin, and prevents activation of factor XIIIA Adverse effects — headache, nausea, back pain, ridiculously expensive compared to heparin (one vial is about 1K)

Low Molecular Weight Heparin: general information

Parenteral Anticoagulants, only given SubQ and it is easy to use preparations composed of molecules that are shorter than those found in unfractionated heparin First line therapy for prevention of DBTs 3 Types available: Enoxaparin (Lovenox) is most common, Dalteparin (Fragmin), and Tinzaparin (Innohep) Enoxaparin is dosed by weight preferentially inactivates factor XA Therapeutic use:Prevention of DVT after surgery, treatment of established DVT with or without a pulmonary embolism, prevention of ischemic complications (unstable angina, arrhythmias especially atrial fibrillation with highest clot risk), multiple trauma and acute spinal injuries

Good to know about Medications for Seizures

Phenytoin (Dilantin), Carbamazepine (Tegretol), and Phenobarbital induce the synthesis of hepatic drug-metabolizing enzymes and can accelerate inactivation of other drugs - Oral contraceptives — hormonal, sometimes you can't take birth control if you have hormonal seizures - Warfarin (Coumadin) For all antiepileptic drugs (AEDs), you need to be able to monitor plasma drug levels, monitoring adherence, determining the cause of last seizure, and identifying the cause of toxicity Withdrawal of AEDs must be done very gradually, can trigger status epilepticus if abrupt All AEDs may pose a risk of suicidal thoughts and behavior Most AEDs cause CNS depression

Nursing Interventions for neuro / hematoma

Physical examination, cannot be overlooked Pupillary checks Report changes in LOC immediately Prepare for diagnostic testing and or surgical intervention

Coma

Produced by bilateral hemisphere damage or suppression by medications, hypoglycemia, toxins, or a brain stem lesion that suppresses RAS In coma, there is no verbal response to environmental stimuli Light coma — purposeful movement Deep coma — no response to any stimuli at all

Alzheimer's Disease

Progressive degenerative disorder of the cerebral cortex Cortical degeneration mostly in frontal lobes (ability to make decisions), but atrophy occurs in all areas of the cortex Familial Alzheimer's — The affected person has an inherited abnormal mutation in 1 of 3 genes: PS1, PS2, or APOE Sporadic Alzheimer's — APOE is gene responsible for the production of a protein that transports cholesterol and other fats throughout the body Protein involved in the structure and function of outer wall of a brain cell How does AD happen? Exact cause is unknown, 4 factors contribute Neurochemical factors, maybe a deficiency in acetylcholine, submetastatin, substance p, norepinephrine, etc Anti-brain antibodies — Autoimmune etiology Once plaques form, complement proteins attach to plaques and attract microglia which release toxins to destroy the plaques Aging and injury decrease oxygen and glucose transport, impair the blood brain barrier, and cause mitochondrial defects that alter cell metabolism Viral factors in CNS Trauma Brain tissue of AD pts have 3 distinguishing features: Neurofibrillary tangles formed out of proteins in the neurons Beta amyloid plaques Granulovacuolar degeneration of neurons — Causes enlargement in ventricles, Early cerebral changes include formation of microscopic plaques, Later atrophy of cerebral cortex itself Plaques: The more beta-amyloid plaques present, the more severe the dementia. Amyloid in the plaques are hypothesized to exert neurotoxic effects Absence of acetylcholine Problems with neurotransmitters and enzymes associated with metabolism may play a role in the disease The severity of dementia is equal to the decreased amount of neurotransmitter acetylcholine

Nitrates nursing implications

Proper technique: Do not chew or swallow sublingual form, educate patient on keeping it under the tongue and letting it dissolve completely to work fastest because it gets to blood stream fast, they may feel a burning sensation Do not put over any wounds, skin needs to be intact Remove old dermal patch of it before adding new dose To decrease tolerance, remove topical forms at night and reapply in morning for a nitrate-free period in the body Only take as needed when experiencing first anginal pain Monitor VS during acute exacerbations Instruct patients about potential of severe headache (blood maybe not being in head from vasodilation) and then about burning Educate about lying down when taking it, to decrease dizziness or fainting from hypotension If pain occurs: Stop activity and sit down. Take sublingual. Wait 5 min. If no relief, take 2nd SL. Wait 5 min. If no relief, take 3rd SL. If no relief after 3rd SL/15 min, call 911. Do not try to drive. Educate about taking blood pressure at home, they want to switch arms, uncross legs, don't move arms around

What is the left side of the heart connected to?

Pulmonary circulation (Goal is to pump oxygenated blood)

s/sx of left sided heart failure

Pulmonary edema DROWNING: Difficulty breathing, Rales/crackles, Orthopnea, Weakness, Nocturnal paroxysmal dyspnea, Increased heart rate (Sinus tachycardia), Nagging cough, Gaining weight

multiple sclerosis

Results from progressive demyelination of white matter of brain in spinal cord, leading to widespread neurologic dysfunction S/Sx — unpredictable or difficult to describe Transient or may last weeks Patient reveals 2 initial symptoms Vision problems — blurred vision or diplopia Sensory impairment 50% have weakness or numbness in 1 or more limbs, spinal Symmetric cerebellar problems with ataxia and nystagmus Emotional lability (judgment impaired), dysphagia, poorly articulated speech, muscle weakness and spasm, hyperreflexia, urinary problems, intention tremor, gait ataxia,

S/Sx of right sided heart failure

SWELLING: Swelling in legs/feet/abdomen, Weight gain, Edema (pitting), Large neck veins (JVD), Lethargic, Irregular heart beat, Nausea, Girth of abdomen abscess from swelling liver

Phenobarbital

Seizures Suppresses seizures without causing generalized CNS depression Controls tonic-clonic seizures, Partial seizures, and Status epilepticus Adverse effect — sedation but can develop tolerance Pediatrics — irritability, hyperactivity, depression, sleep disorders, cognitive abnormalities

Potassium-Sparing Diuretics: Specific names

Spironolactone (Aldactone) Aldosterone Antagonists Eplerenone (Inspra), Nonaldosterone Antagonists (Triamterene)

Inotropic Agents: Dopamine, Dobutamine

Sympathomimetics — noradrenergic drugs Mimics the sympathetic nervous system Dopamine — natural occurring catecholamine neurotransmitter in the SNS Activates beta-1 adrenergic in the heart, kidney, and blood vessels I ncreases heart rate, dilates renal blood vessels, activates alpha-1 receptors Typically seen in ICU, low dose for "renal perfusion" or "renal dose", In order to increase and activate beta 1 for heart, this increases HR Dobutamine increases HR, this is synthetic, and selective in activating beta 1 receptors

ACE Inhibitors: general information

These drugs inhibit the enzyme that converts angiotensin I to angiotensin II because angiotensin II constricts blood vessels. Arterial dilation, lowers BP, venous dilation, suppression of aldosterone Therapeutic uses: hypertension, HF, myocardial ischemia, diabetic and nondiabetic nephropathy, and prevention of MI, CVA/stroke, or death for CV high risk patients Most given orally, except for Enalaprilat (given IV)

TPA — tissue plasminogen activator

Thrombolytic binds with plasminogen to form an active complex, catalyzes conversion of other plasminogen molecules into plasmin to digest to fibrin of clots Therapeutic uses — MI, acute ischemic strokes only, and acute massive PE, NOT hemorrhagic stroke

Streptokinase (Streptase)

Thrombolytic was the oldest and 1st blood clot dissolving agent, no other medications dissolve clots Binds plasminogen Uses — acute coronary thrombosis, used for MI, ischemic CVA, DVT, massive PE Adverse effects — bleeding, intracranial hemorrhage greatest risk, antibody production, lower blood pressure, fever

Non-aspirin Antiplatelet Drugs that Suppress Platelet Aggregation

Ticlopidine (Ticlid) — to prevent CVA Inhibits ADP-mediated aggregation to prevent stroke Adverse hematologic effects Clopidogrel (Plavix) — well tolerated, prevents stenosis of coronary stents from cath lab, 2ndary prevention for MI, ischemic stroke, ADP receptor antagonist like aspirin Glycoprotein receptor antagonist — super aspirin, administered IV with low dose aspirin and heparin Most effective antiplatelet drugs, most common is eptifibatide (integrilin) Used for ACS, short term to prevent ischemic events from occurring

What is the right side of the heart connected to?

Venous circulation (it receives deoxygenated blood)

Calcium Channel Blockers- Verapamil (Calan) and Dilitazem (Cardizem) VND: Very Nice Drugs. Verapamil, Nifedipine, Diltiazem

Verapamil and Diltiazem act on arterioles AND the heart Agents act on vascular smooth muscle, hemodynamic effects are vasodilation, decreased arterial pressure, increased coronary perfusion, and decreased contraction Can be used for angina pectoris, essential hypertension, migraines, and mainly cardiac dysrhythmias Diltiazem blocks calcium channels in heart and blood vessels

Cardiac Glycoside (Digoxin): Has a close relationship with ...

Very close relationship with potassium for inotropic actions Requires adequate amounts of potassium; relationship of K+ to inotropic action Drug binds to potassium site of sodium-potassium ATPA pump Low level increases risk of toxicity, High potassium level diminishes effectiveness

Additional Alzheimer's treatments

Vitamin E NSAIDs Estrogen Ginkgo biloba Drugs for neuropsychiatric symptoms

Warfarin (Coumadin): the antidote

Vitamin K Diet is really important. Either need to eat leafy greens regularly or not eat any at all to keep Vitamin K levels constant

Fosphenytoin (Cerebyx)

Water soluble, does not burn vein like Dilantin Developed to not have as many side effects as Dilantin

assessment of alzheimer's

What to look for? Insidious onset, barely perceptible at first, very slow History is obtained from a family member or a caregiver Early changes include: Forgetfulness, Subtle memory loss without loss of social skills or behavior patterns, Difficulty learning and retaining new information, Inability to concentrate, Deterioration in personal hygiene and appearance As disease progresses, s/sx indicate a degenerative disorder of the frontal lobe: Difficulty with abstract thinking and activities requiring judgment, Progressive difficulty communicating, Severe deterioration of memory, language, and motor function progressing to coordination loss and an inability to speak or write, Repetitive actions, Restlessness, nocturnal awakenings, irritability, depression, mood swings, paranoia, hostility, & combativeness Clinical Findings in Each Stage Stage I: Duration of 1 to 3 years. Memory — new learning defective, impaired declarative memory. Language — poor word list generation. Personality — apathy, irritability, depression. Motor system, EEG, and CT are normal Stage II: Duration of 2 to 10 years. Memory — more severely impaired declarative memory. Visual-spatial skills — poor construction, spatial disorientation. Language — fluent aphasia (receptive/Wernicke's aphasia). Personality — indifference and apathy. EEG — slowing. CT — normal or ventricular dilation and sulcal enlargement Stage III: Duration of 8 to 12 years. Intellectual functions severely deteriorated. Motor — limb rigidity and flexion posture. Sphincter control — urinary and fecal incontinence. EEG — Diffusely slow. CT — Ventricular dilation and sulcal enlargement Neurological exam Confirms many problems revealed during history In addition, reveals impaired sense of smell, inability to recognize and understand the form and nature of objects by touching them; gait disorders; tremors, positive snout reflex Final stages show urinary or fecal incontinence, twitching, seizures

Beta Blockers (BB): general information

Work by protecting from excessive sympathetic stimulation, preventing dysrhythmias (can slow down atrial fibrillation, or tachycardias), and improving HF Require careful control of dosage because it slows the heart and decreases BP Can be in eye drop form beta-1 receptors stimulation leads to increased heart rate; blocking it will decrease the heart rate

Preload

amount of stretch of the muscle fibers. pressure generated in LV at the end of diastole (LVEDP) determined by end-diastolic volume (which stretches the muscle fibers), or the amount of blood that fills ventricle at the end of diastole VEDV Stress causes backup of fluid, pressing plasma out of vessel walls, fluid accumulates in lung tissues Decreased preload = empty pump with too little stretch Hypovolemia decreases Starling's law — the greater the stretch, the greater the cardiac output

Vasodilators: Isosorbide (Isordil)

antianginal and gives selective dilation of veins Seen frequently in acute care, given PO

meningitis

bacterial, viral, toxins, fungal, parasites pathophysiology: CNS entry is through choroid plexus or break in blood brain barrier. the bacteria or irritants induce an inflammatory reaction by the meninges, CNS fluid, and ventricles. blood cells migrate into subarachnoid space, producing an exudate to thicken and interfere with CNS fluid increased intracranial pressure clinical manifestations: fever, chills, tachycardia, throbbing headache, photophobia, nuchal rigidity in neck, decrease in consciousness, seizures diagnosis — physical examination, CSF cultures like a spinal tap treatment — bacterial or fungal meningitis are treated with antibiotics

Low Molecular Weight Heparin: adverse effects

bleeding, immune-mediated thrombocytopenia, increased cost upfront $$$ Can be used at home and do not require aPTT monitoring so that cost is lower

Heparin: lab tests

check activated partial thromboplastin (aPTT) Normal is 25-35 seconds at therapeutic levels Increases level by 1.5-2x factor, making 60-80 aPTT If over 80 seconds, need to decrease dosage Serial labs every 4-6 hrs

Prinzmetal angina

chest pain attributed to transient ischemia of myocardium More unpredictable, exclusively at rest, often at night Pain is secondary to vasospasms of major coronary arteries, may be associated with atherosclerosis Increase in sympathetic nervous system activity leads to increase in calcium reflux, impairing production and release of prostaglandin or thromboxane Infarct possible if spasm persists for prolonged period

Arteriosclerosis

chronic disease of arterial system can occur in any artery an abnormal thickening and hardening of the vessel's walls decreases the artery's ability to change the lumen size Process gradually narrows lumen smooth muscle cells and collagen fibers migrate into the intima No elasticity = can have aneurysms, ruptures, increased blood pressure

myocardial ischemia

deficiency of blood supply to the myocardium

Secondary hypertension

due to underlying medical condition or medications

Heparin: adverse effects

fatality, hemorrhage, increased bleeding (low blood pressure, high heart rate, easily bruising, hematomas, red or black stool, hematuria, cloudy urine, pelvic pain), heparin-induced thrombocytopenia (risk for hemorrhage if platelets are too low), hypersensitivity reactions Double check with 2 RNs because there is a high rate of error. Prescribed in units and not milligrams Incorrect dosage can be fatal

Atherosclerosis

fibrous plaque calcifies and protrudes into vessel to obstruct flow of blood to distal tissue, built off fatty deposits within arteries Injury to the endothelial cells, leading to an inflammatory reaction. these inflamed cells express adhesion molecules so neutrophils and lymphocytes attach to them Oxidized LDLs are engulfed by macrophages which become foam cells that accumulate to form a lesion called a fatty streak Macrophages release growth factor and invite smooth muscle cells to produce collagen and form a fibrous plaque over the fatty plaque Complicated plaques rupture and expose underlying tissue to platelet adhesion and a rapid thrombus formation Risk factors: elevated C-reactive protein (CRP), increased serum fibrinogen, insulin resistance, oxidative stress, infection, periodontal disease Most common cause of aneurysm

unstable angina

form of acute coronary syndrome that results in reversible ischemia Signals that plaque has become complicated and an infarct may follow Transient episodes of vessel occlusion and vasoconstriction at site of plaque damage Thrombi are labile May experience anxiety, SOB, diaphoresis, Most dangerous, 20% progress to an acute MI or heart attack with/without death

Vasodilators: Hydralazine (Apresoline)

gives selective dilation of arterioles Typically IV

diastolic heart failure

left sided heart failure with PRESERVED ejection fraction. Left ventricular diastolic dysfunction. Diastole is the filling or "resting" phase. Ventricle is too stiff for normal filling of blood, so ejection fraction is normal because not enough blood fills up

systolic heart failure

left sided heart failure with reduced ejection fraction. Systolic is the contraction / squeezing phase. Left ventricle cannot eject blood properly

Beta 1 receptors

located in the heart increase in heart rate and contractility

Silent ischemia

may not know it's occurring, but mental stress, increased blood pressure, chronic stress Occurs with presence of abnormal global or regional symptomatic afferent innervation of the left ventricle Patients with diabetes with vascular changes and nerve damage, surgical denervation, nerve injured by CABG or transplant, local injury Mental stress from increase in blood pressure more than exercise, accounts for more oxygen demand Chronic stress = Hypercoagulable state

Phenytoin (Dilantin)

most common antiepileptic drug Tonic-clonic seizures and Partial seizures Not for absence seizures Therapeutic range 10-20 mcg/ml P otential for liver to detox the drug, very taxing, pay attention to drug levels very carefully Adverse effects — nystagmus, mental confusion, gingival hyperplasia, osteoporosis, toxic to veins, ataxia, sedation

Diuretics that cause hyperkalemia

potassium sparing diuretics

Heparin: antidote

protamine sulfate Given IV or SubQ, it is positively charged and neutralizes the negatively charged heparin chain

Nitroglycerin

prototypical nitrate. Large first pass effect with oral form. Sympathetic treatment of angina: Relieves chest pain, blood pressure control especially in heart attacks. IV form used for control in perioperative hypertension, HF, ischemic pain, pulmonary edema from MI, and hypertensive emergencies.

Stable angina

recurrent and predictable Transient, lasting 3 to 5 minutes Angina pectoris, may range from "heaviness" and pressure to severe pain, may radiate Caused by arterio/atherosclerosis, pain from myocardial nerve fiber irritation or lactic acid buildup Relieved by rest and nitrates

Afterload

related to the speed and extent of the shortening of myocardial fibers. The resistance or impedance to ejection of blood from LV the lighter the afterload, the faster the contraction; the heavier the afterload, the slower the contraction the pressure the ventricle overcomes to eject its contents out to the body Systemic ventricular resistance (SVR) reflects left ventricular afterload

RAAS

renin-angiotensin-aldosterone system

Cardiac output =

stroke volume x heart rate

Seizure

sudden, transient disturbances in brain function resulting from an abnormal firing of nerve impulses; may or may not be associated with convulsion Risk factors. — head trauma, genetics, smoking, hormonal changes, older age, sleep disorders, depression