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    3220 Final

    Seizure Disorders2 Major Pathways Result in Brain Damage

    Hypoxiabrain uses 20% of oxygen in body

    Uses a lot more oxygen than other organs

    Ischemialess oxygen & glucose, more wastes

    Focalstroke, collateral circulation

    Each section in brain has a specific job so depending where it is, effect function

    Brain has good collateral circulation to deal with focal damage Block off 1 arteryblood travel through different path to get to tissue

    Globalreversible to irreversible

    Entire brain effected at same time

    When cut off entire oxygen supply

    Some areas of brain are damaged faster

    Causes of brain damage:

    Ischemia from heart attack, cardiac arrest

    Head traumaconcussions, hematomas

    Infections in brain: encephalitis

    Brain tumor Stroke, Brain Attack, or Cerebrovascular Accident (CVA)

    Hypoxia from drug use, respiratory arrest

    Seizures

    Low glucose levels in brain cause brain damage

    Global Brain Injury

    Treatments: oxygen & perfusion, cooling to decrease metabolic needs, blood sugar control

    During recovery, damage from:

    excitatory amino acids & calcium cascade,

    &

    brain swellingvasogenic, & cytotoxic (toxins built up)

    nowhere for swelling to go, but babies have this ability

    Manifestations of Diffuse/ Global Brain Injury:

    Stepwise, rostral to caudal descent into coma

    First - Level of consciousness (LOC)

    Can be subtle.. talking and then sleepy

    Pupillary changes

    Tell if difference between pupils.. control of dialation is effected by reflex that occurs with brain injury

    Oculomotor response

    Motor response

    Patterns of breathing, circulation

    Your most important assessment: Level of Consciousness

    Alert

    Confusion & Disorientation

    Delirium-inability to pay attention

    Obtundationextremely sleepy but can wake up

    Stupor-barely waking up

    Coma (Glasgow)

    Pupillary changes

    Indicates the presence and level of brain stem dysfunction

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    Oculomotor Response

    Eye movement

    Nystagmusuncontrolled rapid movements from side to side and the room feels like its spinnin

    Dolls Eyes- eyes fixed in one direction and when turn head, eyes go in same direction

    Alert, awake eyes will track straight ahead even if turn head

    Motor Response

    Level of brain dysfunction Determine most severely damaged side

    Patterns of Breathing

    Rate, rhythm, pattern

    Sighing & yawning

    Cheyne-Stokes- rapid deep breathing follow by slower shallow breathing

    Gasping breath

    Hyperventilation

    Very irregular

    Increased Intracranial Pressure (ICP) causes

    -when brain swells and no where to go, compression of tissue so blood cant low easily and the heart has to force blood

    inat higher pressure to get circulation into brain

    Increased blood volume

    Increased cerebral spinal fluid

    Increased brain tissue

    High Intracranial pressure Effects

    Obstructs cerebral blood flow

    Destroys brain cells

    Herniationpart of brain normally position in certain areas due to membrane s and base of skull.. moves into

    compartments normally wouldnt be

    Cushings Triad

    High blood pressure - WHY???

    Brain tells heart to produce higher pressure

    Slow pulse

    Good perfusion but doesnt create more pressure

    Wide pulse pressure

    LATE signs of increased ICP

    Whats a brain attack?

    Do you know someone who has had a stroke?

    A. yes

    B. no

    What manifestations did they have? Dysfunction on 1 side of body, facial droop, aphasia

    Cerebrovascular Accident (CVA)

    BRAIN ATTACK!!!!

    TYPES:

    Ischemic stroke- blockage so lack of blood supply to certain part of brain

    Hemorrhagic stroke-blood vessel bursts and leaks out

    Ischemic Stroke Types:

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    Transient ischemic attack (TIA)

    Last 1 hrspasm of blood vessel or short term blockage

    Thrombotic stroke (large vessel)

    Clot forms at specific location (atherosclerosis)

    Lacunar infarct (small vessel stroke)

    Embolic stroke (moving clot)

    Clot moving around body

    Temporary Ischemic Attack (TIA)-may need treatment to prevent major stroke

    Focal ischemic cerebral neurological deficits

    Usually last less than 1-2 hours

    Temporary disturbance in cerebral blood flowreverses before infarction occurs

    Where would embolus be most likely to occur from?

    A. Left side of heart

    B. Lower extremities

    C. Right side of heart

    D. Lungs

    Most frequent sites of arterial and cardiac abnormalities causing ischemic stroke

    Clinical Manifestations

    Sudden in onset, not LOC

    Usually one-sided

    Most commonweakness of face and arm

    Otherunilateral numbness, vision loss, aphasia, dysarthria, and sudden, unexplained imbalance or ataxia

    Treat based on damage: embolic and thrombi

    Location of brain damage

    RIGHT Brain Damage

    Paralysed LEFT side

    Behavior: quick, impulsive

    Spacial & perceptual deficits

    LEFT Brain Damage

    Paralysed RIGHT side

    Behavior: slow, cautious

    Speech & language deficits

    Depression

    3 hours attack! Treatment of the Brain

    Must be immediateuse of early identification, special medical teams

    Differentiate type of strokeWHY?

    Treatment with new medications and procedures

    Better recovery if area surrounding ischemic area (penumbra) has circulation restored fast

    What medication is used to treat ischemic stroke first?

    A. Anticoagulantsheparin, warfarin

    Too latealready coagulating

    B. Anti platelet aggregationaspirin, Plavix

    C. ThrombolyticstPA, tissue plasminogen activator

    D. Vitamin K, coagulation factors

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    Which should not use tPA?

    A. Ischemic stroke

    B. Myocardial infarction

    C. Pulmonary embolism

    D. Hemorrhagic stroke

    Seizure disorders

    -not a disease but symptom of several types of disorders Seizure = Sudden, disorderly discharge of a group of cerebral neurons (focus)

    Convulsionmotorseizure: moving of arm and legs.. cause convulsion(rhythmic changes in muscle length)

    Not a disease but symptom

    Common in children, elders

    Epilepsyseizure disorder without identifiable cause

    Idiopathic- dont know cause

    Seizure Treshold affected by:

    Congenital defects

    Tumors

    Vascular lesions

    Metabolic abnormalities

    Head injury

    Fever

    Drug and alcohol use/withdrawal

    Infections

    Medications

    Manifestations of seizuresdepends on how far of neuron movement spreads

    +/- Bizarre muscle movements-smacking of eyes, licking of lips

    +/- Unusual sensations, perceptions

    (Tactile, odors, sounds, visual)

    +/- Loss of consciousness: when middle centers of brain are effectedEXACT MANIFESTATIONS DEPEND ON LOCATION OF FOCUS AND SPREAD IN THE BRAIN

    Seizure Terms

    Aura-change in sensation person notices shortly before going to have seizure

    Earliest part of the seizure, can protect self so dont get hurt

    Prodroma

    Hours-days leading up

    Postictal state-wake up from deep sleep can become combativeness

    Post seizure, global change

    Have you been with someone having a seizure?

    A. Yes

    B. No

    What do you do?

    Protect their head, lower them to the floor, turn them on their side

    Local (Partial) or Widespread (generalized)

    Partialstart in one lobe, so no loss of consciousness if simple, or, if complex, spreads to both lobes, leading to

    impaired consciousness

    Simple stays in location, complex spread to both lobe lead to impaired consciousness

    Generalizedspread widely and fast to both lobes, so loss of consciousness

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    Absence Seizures

    Often confused with simple partial

    NOT just a blank stare

    Motion (automatisms, eyelid movement)

    Lasts a few seconds

    Cease in adulthood or evolve into motor seizures

    PHENOBARBITOL, PHENYTOIN WORSEN!!!

    Attonic or akinetic seizures

    Drop attacks - sudden loss muscle

    tone for a few minutes

    Familial

    Rule out syncope

    Generalized motor seizures (Tonic-clonicgrand mal)

    Tonic phase

    - simple partial seizure is prodrome

    - loss of consciousness

    - sharp tonic muscle contractions

    - incontinence

    Clonic phase

    - brain fights back, alternating contraction and relaxation, slowing

    - postictal: altered LOC, sleepy

    Drugs wont help up to 40%

    Other treatments:

    Brain surgery

    Ketogenic diet

    Vagal nerve stimulator

    Anti Epileptic Drugs (AEDs)Lack of adherence (compliance) is the major reason for poor control!!

    Balance of seizure control and adverse effects of the AEDs

    Important to diagnose type of seizure, as it affects choice of AEDs

    May need to adjust doses and add meds

    Adjust dosages using plasma drug levels

    Why use plasma drug levels?

    A. Seizures may be infrequent, making it hard to monitor effectiveness

    B. Non-compliance may be an issue

    C. With multiple drugs, hard to know which is causing effects

    D. All of the above

    4 mechanisms of AEDs:

    Block sodium channels, neurons repolarize more slowly, stops rapid firing

    Block calcium channels, same

    Block glutamate (excitatory neurotransmitter) receptors

    Block excitiatory response

    Increase GABA (inhibatory neurotransmitter)

    Common problems with AEDs

    Rapid withdrawal can lead to severe seizuresmust do so gradually

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    Most AEDs cause CNS depression, ESPECIALLY with other CNS depressants like alcohol

    Many AEDs are metabolized by the liver, induce liver enzymes, and change metabolism of other meds, including other

    AEDs

    Enzyme induction leads to inactivation of normal dose oral contraceptives, and warfarin

    -unanticipated pregnancytoxic to the fetus

    Most AEDs can have negative effects on the fetus, but seizures have worse effects on the fetus

    Two major types of AEDs

    Traditional, including: phenytoin (Dilantin)

    carbamazepinemore tolerated by people

    valproic acid

    phenobarbitolcheap , many adverse effects

    ethosuximide

    Well known, cheaper, more adverse effects

    Newer, including:

    gabapentin, lamotrigine, topiramate dont need to know

    Not as tested, more expensive, but fewer adverse effects

    Phenytoin (Dilantin)

    Normalizes sodium flux in neurondoesnt fire as often

    Raises seizure threshold

    For partial and tonic clonic seizures, but NOT absence seizures

    Phenytoin adverse effects

    CNS: dizziness, sluggishness, confusion

    (Avoid alcohol, other CNS depressants)

    GI: nausea, constipation

    Rashesstop! Dangerous to immune system

    Gingival hyperplasialoss of teeth

    (use folate rinse)

    Drug Nutrient interactions of phenytoin

    INDUCES hepatic metabolism of vitamin

    B12, folate, vitamin D, vitamin K

    DISPLACES folate from plasma proteins

    Phenytoin metabolism USES UP folate

    Adverse effects of phenytoin

    Teratogenic (palate, lip, heart)

    Folate supplementation REDUCES RISK

    Monitor Phenytoin serum levels!Highly bound to plasma proteins

    Note FREE, UNBOUND phenytoin levels

    NARROW THERAPEUTIC INDEX! Of what is therapeutic and what is actually toxic

    Liver has limited ability to metabolizekeep 10-20 mcg/mL therapeutic range

    Phenytoin Toxicity

    Sedation

    Nystagmus

    Ataxialose balance

    Diplopiadouble vision

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    Cognitive impairment

    Phenytoin has many drug interactions

    Many drug incompatibilities

    (Do NOT mix C/ other parenteral Rxs)

    INDUCES hepatic p-450 enzymes

    DISPLACES other drugs, nutrients from plasma proteins

    BINDS to proteins in enteral feedings

    Carbamazepine

    Similar to phenytoin, but fewer side effects

    Can cause leukopenia, anemia, thrombocytopenia, even fatal aplastic anemia (bone marrow shut down) - rarely

    Phenobarbital

    Can be used for simple partial

    Also used (infrequently) for complex-partial, tonic-clonic and febrile seizures

    Similar adverse effects as phenytoin but NO EFFECT ON FOLATE, NO GINGIVAL HYPERPLASIA

    Long time to stabilize blood levels

    Valpoic acid (Depakote)

    Gamma aminobutyric acid (GABA), an inhibitory neurotransmitterincreasing GABA

    For ALL generalized seizures

    75% of partial seizures controlled also

    Also used for bipolar disorder

    Valproic Acid Adverse Effects

    Teratogenic (neural tube defects) - avoid in pregnancy

    Hepatotoxicity, pancreatitis (avoid infants, elderly)

    CNS depression (avoid alcohol, etc.)

    Inhibits platelet aggregation

    NO BEHAVIORAL EFFECTS

    Every time have seizure compromise oxygen and can injure fetus

    Benzodiazepinesstop seizures rapidly

    Diazepine receptors potentiate GABA

    Used for rapid cessation of seizures

    MONITOR for respiratory depression

    Clonazepam (klonopin)

    A benzodiazepine for maintenance therapy of absence, akinetic seizures

    2

    nd

    generation AEDS

    oxcarbazepine (Trileptal)

    lamotrigine (Lamictal)

    gabapentin (Neurontin)

    pregabalin (Lyrica)

    topiramate (Topamax)

    Magnesium Sulfate

    For seizures caused by hypomagnesemia (eclampsia, hypothyroidism, alcohol withdrawal)

    Side effects from hypocalcemia (CNS depression, hypotension, hypothermia, circulatory collapse)

    Monitor serum magnesium levels

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    Preload- volume; too much or too little

    Afterload; hypertension or CAD inc afterload ventricle will have a lot of ressitance and will have to work

    harder

    Myocardial Contractilityforce of contraction

    Heart Rate CO= sv x hr

    Invasive: lines into neck floating into pulmonary artery

    Other ways: are you making urine (indicated good blood flow to kidneys)

    Heart Failure: Primary Cause**biggest one is MI

    Coronary artery disease

    Hypertension

    Rheumatic heart disease- comes from rheumatic fever

    Developed from streptococcus infectionif not treated with antibiotics or on time

    Fever cause damage to heart valves

    Congenital heart defects

    Pulmonary hypertension- right side

    Cardiomyopathy-

    Hyperthyroidism- overactive; increased oxygen demand

    Valvular heart disease

    Heart Failure: Precipitating Causes (at risk for HF, may not have it, stable HF without symptoms that cause acute

    exacerbation of HF)

    Anemia

    Infection- fever, tachycardia

    Thyrotoxicosis

    Hypothyroidism

    Bacterial endocarditisIV drug users, poor mouth care, bacteria stick to valve effect blood flow

    Pulmonary disease- COPD

    Hypervolemiatoo much preload

    Left Heart Failure

    Categorized as systolic or diastolic

    Do not always exist independent of one another: Patients with systolic dysfunction may also have diastolic dysfunction.

    Left hear failure: systolic failuremore common

    CO will be low because not difusing vital organs

    Systolic failure

    Inability of heart to pump blood effectively and perfuse vital organs

    Most common causes are coronary heart disease, dilated cardiomyopathy, htn, and valvular disease

    End result: left ventricle dilated & hypertrophied

    Huge/floppy and not contracting well

    Hallmark decreased ejection fraction

    Ejection Fraction- calculate using echocardiogram

    Systolic failure: may be 5-10%, not pumping enough blood, cause left over blood sit in left ventricle back up to left

    atrium and into lungs causing shortness of breath

    Amount of blood ejected per beat

    Estimated by doing an echocardiogram

    Normal is 60-75%

    Decrease is hallmark of ventricular failure

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    Left heart failure: Systolic Failure

    Systolic heart failure

    Increased workload enlarges left ventricle leading to decreased function

    Prevents forward flow of blood

    Blood backs up into the left atrium & pulmonary veins

    Can lead to pulmonary edema

    Can lead to stress on right ventricle

    Symptoms

    Pulmonary vascular congestion Dyspnea

    Orthopnea

    Cough/frothy sputum

    Fatigue

    Decreased urine output

    Edema

    Exam Systolic Failure

    Cyanosis- seen in finger tips

    Ralessimilar to crackles

    Pleural effusions

    Hypotension/hypertension- low cardiac output

    S3 gallop- heart in heart failure ; sounds like when you say Kentucky

    Extra blood slashing around ventricle

    Evidence of underyling CAD or hypertension

    Compensatory Mechanisms

    -in low cardiac output state; want to inc cardiac output and overtime leading to worsening heart failure

    Sympathetic Nervous System Activity

    Triggered by low CO state

    Increased catecholamine release

    Increased heart rate

    Increased myocardial contractility

    Peripheral vasoconstriction

    Neurohormonal Response

    Decreased CO causes decreased blood flow to kidneys

    Kidneys release renin, which converts to angiotensinogen to angiotensin I

    Angiotensin I, converted by angiotensin converting enzyme in lungs, to angiotensin II

    Adrenal cortex releases aldosterone

    Retain Na and H20

    Peripheral vasoconstriction

    Neurohormonal response continued

    Decrease in cerebral perfusion pressure

    Posterior pituitary secretes antidiuretic hormone (ADH)

    Water reabsorption in renal tubules

    Proinflammatory cytokines also released

    Endothelin released

    Dilation

    Enlargement of the chambers of the heart

    Muscle fibers of the heart stretch

    Increased contraction initially leads to increased CO

    Eventually mechanism fails

    Hypertrophy

    Increase in muscle mass & cardiac wall thickness

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    Will lead to an increase CO but poor contractility and increased 02 consumption

    Myocardial Hypertrophy

    Myocyte growth

    Up to 6x increase left ventricle

    Ventricular stiffness

    Left heart failure: diastolic failure

    Heart failure with preserved systolic function or ejection fraction Can occur alone or with systolic heart failure

    More common in women

    Results from decreased compliance of left ventricle

    Symptoms:

    Dyspnea on exertion

    Fatigue

    Crackles

    Diagnosis

    Based on 3 factors:

    Signs/symptoms of heart failure

    Normal ejection fraction

    Evidence of diastolic dysfunction

    Pulmonary Edema or Acute Decompensated Heart Failure

    Symptoms:

    -dyspnea

    -increased work of breathing

    -pink, frothy sputum

    Exam:

    -VQ mismatch-crackles up to neck, feel like they are drowning (given ativan and lasix) may need to be put on ventilator

    Right Heart Failure (can be caused by pulmonary hypertension)

    -Inability of the right ventricle to provide adequate blood flow into the pulmonary circulation

    can result from left heart failure, copd, cystic fibrosis

    pressure rises in the systemic circulation, causing edema and hepatosplenomegaly (large liver and spleen)

    -blood back up to right ventricle, to atrium and to the rest of body.. will see edema, fluid build up in systemic

    circulation

    Right Failure

    FatigueDependent edema

    Distention jugular veins

    Liver engorgement

    Ascitesresult of liver disease

    Anorexia, GI distress

    Cyanosis

    Inc. peripheral venouspressure

    Diagnostic Tests

    CBC: elevated WBC cause infection increase work load on heart

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    Low HandH is anemia

    Chemistries

    LFTs

    TFTs-hypo/hyperthyroidism

    BNP levelelevated sign of heart failure

    ABGlooking at pO2may show hypoxia

    Echo- measure ejection fracture, look at valves itself

    EKG-changes may be indicative of left ventricular hypertrophy

    CXR- xray fluid in lungs, heart enlarged Angiogram- look at coronary arteries, invasive, risks involved, determine if any calcification

    BNP levels

    Brain Natriuretic Peptide

    Secreted from the left ventricle in response to stretch

    -comes from left ventricle in response to stretch

    -normal in pneumonia but elevated in heart level

    -false high in kidney failure because secreted in kidney

    Can be elevated in patients with:

    Renal dysfunction

    Large pulmonary embolism (due to atrial stretch)

    Severe sepsis

    Heart Failure

    Severity of heart failure graded on the New York Heart Associations functional classification scale

    Scale indicates how little or much activity it takes to make patient symptomatic

    Class I: No symptoms with activity

    Class II: Symptoms with ordinary exertion-walking to mailbox

    Class III: Symptoms with minimal exertion-getting up to bathroom

    Class IV: Symptoms at restmay be on transplant list

    Stages of Heart Failure

    A. at risk for HF but without structural heart disease or symptoms

    B. Structural heart disease but without signs or symptoms of HF

    C. Structural heart disease with prior or current symptoms of HF

    D. refractory HF requiring specialized interventions-not responding to intervention

    Disorders of the myocardium: cardiomyopathies

    Diverse group of diseases that primarily affects myocardium

    Most result of remodeling caused by MI/neurohormonal response to ischemic heart disease and hypertension

    Can be secondary to toxic exposure, connective tissue disorders, infiltrative & proliferative disorders, nutritional

    deficiencies

    Many cases are idiopathic

    Many different forms of cardiomyopathy: dilated, hypertrophic, or restrictive

    Disorders of the myocardium: cardiomyopathies

    1. Dilated

    Most common form

    Left ventricle becomes enlarged & dilated. cant pump as efficientlydecreases CO

    Contractility decreased in left ventricle

    Sinus tachycardia, atrial & ventricular dysrhythmiasv tach- lethal

    Systemic or pulmonary thromboembolism

    Eventually leads to left heart failure

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    Associated conditions: ischemic heart disease, alcoholism, pregnancy, infection, nutritional deficiencies,

    exposure to toxins

    2.Hypertrophic cardiomyopathy

    Chamber volume decreased (left ventricle)

    Compliance decreased, particularly left ventricle

    Heart wall thickens, less space for blood

    Less blood fills from chamber & is pumped out

    Can develop atrial & ventricular dysrhythmias Associated conditions: hypertension, aortic stenosis, inherited defect of muscle growth

    Young athletes drop dead without symptosm

    Inherited

    Need inc preload to give blood a push out .. need more volume

    3. Restrictive cardiomyopathy

    Portions of heart wall become rigid & lose flexibility- decrease contractility

    Compliance decreased

    Eventually leads to right heart failure

    Conditions associated with: amyloidosis, sarcoidosis, hemochromatosisprotein build up in heart

    Takotsubo cardiomyopathy

    -broken heart syndrome

    -stress inducedintense sudden stress release of catecholamine; inc workload on heart might feel like have heart attack

    -sudden weakening of heart

    -octopus pot in japaneese

    -can cause lethal heart rhythms

    Parkinsons DiseaseWhat is happening to the brain?

    -Extra pyramidal system controls movement

    Deliver dopamine through striatum to the globus pallidus which converts nerve impulses and coordinates our

    movements

    -not enough dopamine because neurons that produce dopamine are being killed and dying off so balance of GABA is

    thrown off (too much ACH) causing disturbed movement

    -takes a lot of damage and long period of time in order to see symptoms

    A disorder of balance

    1. Not enough dopamine(dopamine producers are dying) and

    2. Relatively too much acetylcholine, in the striatum

    3. Not enough GABAinhibition of the control center for movement coordination, the Globus Pallidus

    4. Uncontrolled neuron firing leading to DYSKINESIA, other symptoms of PD

    Why do people develop Parkinsons or its symptoms?

    Parkinsons Diseasecaused by:

    Geneticproblems with the destruction of alpha synuclein, a toxin that kills dopaminergic neurons.

    Alpha synuclein forms fibrils called Lewy bodies seen on autopsy, diagnostic for PD

    Environmentaltoxins, like cocaine, pesticides

    Brain damage due to vascular diseases (diabetes, etc.), tumors, viruses, encephalitis

    Parkinsonism (symptoms of Parkinsons) caused by anti-psychotic medications (reversible)meds

    block dopamine receptors in the extrapyramidal system

    Not disease itself, not cause by killing off neurons

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    Progressive death of dopaminergic neurons

    Early symptoms:

    Tremors at rest, especial a hand, on one side

    Pill rolling

    Head bobbing

    Late symptoms:

    Rigidity, cogwheel movement

    Inability to initiate movement, bradykinesia, akinesia

    Gait problems, hunched, forward leaning Balance problems, cantstop

    Bradykinesia

    Slowness in initiatingmovements

    Cannot stop easily

    Shufflinggait

    Micrographia (very small handwriting)

    Cannot move slowly (fall risk)

    Fenestration- big to tiny movements and cant stop

    Top part of body continute to propel forward and feet get caught up

    POSTURAL INSTABILITY IS VERY CONCERNINGmore and more steps to compensate

    Problems beside movement, gait

    Facial expressionstiff, appears unemotional, less blinking so looks like staring

    Eatingdifficult swallowing, drooling, prone to choking, difficult to feed self

    Speechsoft voice, poor articulation

    Cant distinguish words

    Emotionslabile, depression

    Increase tear formation

    Weight lossloose clothing

    Dementia20-40%

    Off balance, too much ACHDiaphoresissweating

    Salivation - drooling

    Lacrimationcrying

    Sebaceous secretionoily skin

    Constipation

    Urinary incontinence

    Prolonged urination

    How does this person look socially?

    What is the initial reaction to this person?

    Need for support, vs. appearance

    Difficulties with ADLs, quality of lifeHUGE role for nursing care!

    http://www.youtube.com/watch?v=IYbFFevRW_Q&feature=share&list=PL54C9B18894D14360

    How can this condition be treated?

    Symptomcontrol, vs. cure

    Medicationsmore dopamine, less acetylcholine

    Nutritionproteins inhibit absorption, Vitamin B 6 needed to convert meds to dopamine

    Activitymay respond to focused activities

    Continuous motion stop shaking

    Surgerymedication delivery, stem cell/transplants, brain stimulation, destruction of pallidus

    http://www.youtube.com/watch?v=IYbFFevRW_Q&feature=share&list=PL54C9B18894D14360http://www.youtube.com/watch?v=IYbFFevRW_Q&feature=share&list=PL54C9B18894D14360http://www.youtube.com/watch?v=IYbFFevRW_Q&feature=share&list=PL54C9B18894D14360
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    Pump deliver medication directly into blood streaminstead of GI tract where protein can iinterfere

    with absorption

    Electrode into brain and stimulateadjust stimulation until symptoms go away

    Destrcructive surgery to globus pallidus and this reduces over stimulation

    Strategies with medication

    Goal: more stimulation of dopamine receptors in the striatum

    1. Make moredopamine

    2. Recycledopamine (reuptake inhibitor) 3. Stimulate dopamine receptorswithout dopamine

    4. Stop dopamine breakdown by stopping COMT and MAO-B

    Goal: less acetylcholine stimulation (anti-cholinergics)

    Most effective: treatment of levodopa

    Levodopa CAN cross blood brain barrier

    Levodopa gets converted to dopamine in a reaction using dopa decarboxylase enzyme and Vitamin B6

    PERFECT, right?

    Problems with levodopa treatment

    Destruction of neurons continues, so dose has to increase, and meds stop working in a few years

    Absorption problems: gradual and On-Off phenomenon

    Levodopa is broken down peripherally (outside of brain) too, so only 2%actually reaches the brain

    Need for Vitamin B6 to change levodopa to dopamine, but higher B6 levels cause more peripheral breakdown

    Side effects of excessdopamine itself are severedyskinesias, and psychosis

    Amino acid compete, poor absorption, blood levels drops (good controlbad control) and patients will

    drop

    Need b6 to be converted, b6 that changes rest of body cant pass the brain (accumulate b6 peripherally

    causing breakdown)

    On-Off phenomenon

    Dyskinesia suddenly turns to bradykinesia

    Large neutral amino acids in proteins in foodscompete with levodopa for absorption

    Remedies:

    Nutritional - redistribute protein in evening meal

    More protein in evening meal and not morning when they are taking medication

    Use implanted pump to deliver constant dose of levodopa

    Levodopa side effects

    Alldirectly related to dosage

    Nausea and vomitingeffect on chemoreceptor trigger zone in brain

    Dyskinesias like head bobbing, grimacing, ballismus, choreoathetosis

    Postural hypotension

    Dysrhythmias

    Psychosis with hallucinations, night terrors, paranoia (use clozapine)

    Cant treat with antipsychosis

    BEST THING TO DO IS TO REDUCE TOTAL DOSE OF LEVADOPA

    Darkening of urine, sweat

    What do you do for each?

    Drug holidaysin hospital, dangerous

    Take off levadopa, then put back on and patient will do better

    When stop levadopa can go into freezing mode where cant intiate movement at all

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    Adding carbidopa to levadopa decreases these problems

    Reduces total peripheral levodopa, and all side effects

    Less need for Vitamin B6

    Delivers 10%of levodopa dose to brain, not 2%

    Drug of FIRST choice: dopamine agonist

    -more likely to cause psychosis as reaction than dysknesia

    5 drugs, main one is pramipexole(Mirapex)

    Stimulate dopamine receptor even though not dopamine, cross of BBB, and causes same effect asdopamine itself

    Less dyskinesia, but more chance of psychosis

    Side effects: sleep attacks, hallucinations, and postural hypotension

    First drug used in younger patients

    Not good for older patients or those with advanced disease

    Other PD meds

    COMT inhibitorsEntacaponestop breakdown of levodopa

    Increase levodopa avail to make into dopamine

    SeligilineMAO-B inhibitor, stops breakdown of dopamine, may stop destruction of dopamine neurons,

    stopping PD progression!!!

    Stop neuron from dying and prevent progression of Parkinson disease

    Amantadinemany actions, inhibit dopamine uptake and increase release

    Central Anticholinergicsblock cholinergic (acetylcholine) receptors, side effects like dry mouth, blurred vision,

    tachycardia, constipation

    Non medication treatments

    Transplanted cells:

    Stem cells

    Fetal brain cells

    Pallidotomy - unilateral

    Deep brain stimulation - reversible

    Nutritional Activity

    Heart Failure TreatmentMedical Nutritional Therapy in Heart Failure

    Should promote a diet to control sodium and fluid retention, maintaining a healthy body weight, and providing a

    diet adequate in vitamins, minerals, and proteins

    May have other comorbidities such as diabetes, hypertension, obesity, or kidney failure

    Heart failure may need low sodium but id diabetic teach about carbohydrate too

    Kidney failure need low protein

    Nutrition

    Sodium should be restricted

    If preserved or depressed EF, restrict to 2-3 gm/day

    Moderate to severe,

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    Potatoes, tomatoes, oranges and banana

    Weight Monitoring

    Weigh yourself at the same time everyday, wearing the same thing

    Keep a record

    If gain 2 pounds in one day or 5 pounds in a week, call provider

    Cardiac Cachexia

    Weight loss of more than 6% of the previous normal weight over 6 months associated with heart failure

    Need more calories because greater work of breathing

    Occurs in 10-15% of clients with heart failure

    Seen in advanced disease

    Undernutrition due to one or a combination of:

    Increased nutrient losses

    Unmet increased nutritional requirements

    Decreased nutritional intake

    malabsorption

    Medical treatment

    Diuretics

    Inhibitors of RAAS systemBeta blockers

    Digoxin

    Effect preload, afterload, contractility, RAAS system

    Diuretics

    First line drugs for patients with signs of volume overload

    Lose too much volume-dehydration case dry mucus membrane, low BP, high heart rate

    Reduce blood volume and therefore decrease preload and afterload, edema, and cardiac dilation.

    Must watch blood pressure

    Diuretics: Thiazides Ex. Hydrochlorothiazide (Hydrodiuril): oral agent

    Produce moderate diuresis

    Used for long term therapy

    Ineffective when GFR is low

    If CO is low, not good filtration of blood to kidneys so GFR is low

    Should be above 60

    Adverse effect: hypokalemia, hyponatremia

    Diuretics: Loop Diuretics

    Ex. Furosemide (Lasix)

    Produce profound dieresis

    Patient may take water pill for CHF but if come in with acute exacerbation (pilm edema) will treat with

    IV lasix

    Also called high ceiling agents

    Promotes fluid loss even with low GFR

    Will still have effect of dieresis

    Used for severe heart failure

    Oral or IV

    Adverse Effects: hypokalemia, dehydration, ototoxicity

    Hypokalemia can cause digoxin otoxicity

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    Loop Diuretics: drug interactions

    Digoxin

    Ototoxic drugs : aminoglycoside antibiotics

    Potassium sparing diuretics

    Lasix with potassium sparing diuretics to keep potassium normal

    Aldosterone

    Promotes ventricular remodeling

    Promotes myocardial fibrosis Activation of SNS (causes tachycardia)and suppression of norepinephrine uptake in the heart

    Promotion of vascular fibrosis

    Acts to promote sodium uptake in exchange for potassium excretion

    Diuretics: Potassium Sparing Diuretics

    Ex. spironolactone (Aldoactone) - nonselective

    eplerenone (Inspra)- selective

    Promote small amount of diuresis

    Used to counteract K loss caused by thiazide and loop diuretics

    Adverse Effect: Hyperkalemia, gynecomastia

    Be cautious if combined with an ACE I or ARB

    Pregnancy category C

    Can give with loop thiazide diuretics

    Give with foods high in potassium

    Spironolactone

    Prolongs survival in patients with HF primarily by blocking receptors for aldosterone

    Guidelines recommend adding to standard therapy in patients with moderately severe or severe therapy

    Drugs that inhibit RAAS

    RAAS plays important role in hemodynamic changes that occur when cardiac output is low

    4 groups:

    ACE inhibitors ARBs

    Direct renin inhibitors

    Aldosterone agonists

    Ace Inhibitors

    Ex. Captopril, enalapril

    Block production of angiotensin II, decrease release of aldosterone, and suppress breakdown of bradykinins

    Results in dilation of arterioles and veins

    Can prolong life

    Usually combined with beta blocker and diuretic

    Preload and afterload will decrease if dialation in vessels because dont have to pump hard against increasesresistance

    Start on LOW DOSE due to dialation can become hypotensive

    Benefits

    Improved blood flow to kidneys

    Reduces preload and afterload

    Excretion of sodium and water

    stops progression of cardiac remodeling

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    Adverse Effects

    Hypotension

    Hyperkalemia

    Intractable cough

    Angioedemalips and tongue swell up (most severe reaction)

    Renal failure in patients with bilateral renal artery stenosisno blood flow to kidneys

    Pregnancy category X

    ARBs Effects are similar to ACE

    Reserved for those who cannot tolerate an Ace

    Improve ejection fraction, reduce heart failure symptoms, increase exercise tolerance, decrease hospitalization,

    enhance quality of life, and reduce mortality

    Direct Renin Inhibitor

    Only 1 availablealiskiren(Tekturna)

    Effects similar to ACE I and ARBs

    Acts on renin to inhibit conversion of angiotensin into angiotensin I

    Causes less angioedema and cough than ACE I

    Beta Blockers

    Ex. carvedilol (Coreg), bisoprolol (Zebeta), sustained release metoprolol (Toprol XL)

    Can improve LV ejection fraction , increase exercise tolerance, slow progression of heart failure, reduce the need

    for hospitalization, and prolong survival

    Protects the heart from excessive stimulation and dysrhythmias

    Doses initiated at low dose and gradually increased

    May take 1 -3 months to see benefits

    **AFFECT HR MORE THAN BP

    Adverse Effects

    Fluid retention and worsening heart failure

    Fatigue

    Hypotension

    Bradycardia or heart block

    SLOW HEART RHYTHYMS CAN BE DANGEROUS

    Inotropic AgentsCONTRACTILITY: FORCE OF CONTRACTION

    Chronotropy: rate of contraction

    Digoxin

    Sympathomimetics

    Increase cardiac output by increasing contractility and reducing neurohormonal activation

    Used for systolic heart failure (bc systolic is the PUMPING diastolic is the FILLING)

    DigoxinTreat symptoms at the time; not used for acute episode of heart failure

    Cardiac glycoside

    Can be given po or IV

    Positive inotropic agent

    Increases cardiac output

    Can alter the electrical activity of the heart

    Second line agent

    Cannot prolong life

    Digoxin and Potassium (inverse: when dig is low, potassium is high)

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    K ions compete with digoxin on the Na/K ion pump

    When K is low, binding of digoxin is increased, causing toxicity

    When K is high, digoxin is reduced

    Digoxin: Adverse Effects

    Narrow therapeutic window- -want to keep levels normal

    On high level of window, will see side effects of toxicity

    Normal level 0.5-1.5

    Must be monitored closely Decreased dose if renal impairment

    Nausea, vomiting (usually happens first)

    fatigue

    visual disturbancesyellow tinge

    Dysrhythmias

    IV dose = digloading

    Drug Interactions

    Diuretics

    ACE inhibitors and ARBs

    Sympathomimetics

    Quinide- increase dig level by decrease renal excretion of dig

    verapamilcalcium channel blocker

    Pharmokinetics

    Absorption is variable

    decreased by foods high in bran

    Eliminated by renal excretion

    Can take 6 days to reach plateau

    Treatment of Digitals Intoxication

    Stop drug

    Gastric lavageActivated charcoal

    Hemodialysis

    Digibind

    antidysrhythmics

    Sympathomimetics: Dopamine

    Must be given IV in hospital

    Weight based

    Catecholamine, activates:

    beta adrenergic receptors in the heartincrease HR

    Dopamine receptors in the kidneyinc blood flow to kidney so inc urine output

    Alpha adrenergic receptors in blood vessels (at high doses)down side bc when activate alpha

    andrenergic will inc vascular resistance leading to constriction

    Short term rescue measure for severe acute heart failure

    Dobutamine

    Given IV in the hospital

    Preferred over dopamine

    Synthetic catecholamine, causes:

    Selective activation of beta adrenergic receptors

    Does not activate alpha receptors

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    Phosphodiesterase Inhibitors

    Ex. Milrinone

    Continuous IV infusion

    increased contractility and promotes vasodilation

    dec preload/afterload

    results from an increase in cAMP secondary to inhibition of PDE3

    cAMP should allow heart to pump more effic and inc contractility.. and phos tries to ibhibit this from

    happening soooo inhibitor prevents phos from inhibiting

    Used for patients in acute heart failure, not responding to traditional treatment

    Vasodialator

    Isosorbide and hydralizine are usually combined

    Can be used as an alternative to ACE or ARB

    Isosorbide casues dilation of veins, can improving congestive symptoms

    Can cause hypotension, tachycardia

    Hydralizone causes dilation of arterioles, improving cardiac output and renal blood flow

    Can cause hypotension, tachycardia

    Intravenous Vasodialators

    Nitroglycerin

    Venodilator, decreases venous pressure-dec preload/afterloadused for chest pain

    Used for acute pulmonary edema

    Sodium nitroprusside (Nitropress)

    Dilates arterioles and veins, reduces afterload and increases cardiac output

    Used for short term therapy

    Nesiritide (Natrecor)

    Synthetic human BNP

    Meds to avoid in heart failure

    NSAIDS

    Calcium channel blockers

    TZDstheophylline

    Surgical treatment heart failure

    Cardiac transplantation is ultimate treatment for end stage heart failure

    Coronary revascularization

    Mitral valve repair

    LV reconstruction

    Device Therapyabnormal/fast heart rhytyms

    Implanted cardioverter defibrillator-zap into normal heart rhythms

    Cardiac resynchronization

    Ventricular assist device (VAD)usually on left side

    Mechanical devices that can assist and support the circulation

    Used for:

    Bridge to transplant

    Bridge to decision

    Destination therapy

    Exercise training

    In past, bed rest was recommended

    Now we know that inactivity is detrimental

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    Exercise can improve clinical status, increase exercise capacity, and improve quality of life

    No blood pressure

    Judge CO by pink, warm, making urine, not lethargic

    INR kept at 2.5/3high so dont have clotting but this may cause a hemmorhagic stroke

    If CO is lowinc RPM to improve it

    Monitoring

    Watch for reduction in symptoms

    JVD, edema, rales Increased capacity for physical activity

    Lower BNP

    Improved quality of life

    Thyroid Problems and Treatment

    A negative Feedback System

    Endocrine System

    Glands

    Hormones-attach to cells that are receptive and hormones turn activity of cell of or on?

    Feedback Mechanisms

    Altered Endocrine Function: 2 types

    Hyposecretion of hormone

    Hypersecretion of hormone

    Pituitary hormones, target tissues, and feedback mechanisms

    `

    Anterior pituitary gland produce specific hormones and determine if turn on or off

    -when it becomes aware the metabolism is too low, produces TSH

    -stimulates thyroid gland and will produce 2 hormones (t3 and t4) and provides feedback to pituitary gland to

    shut off tshif messed up producing too much or too little hormone

    Thyroid Hormone production

    Thyroid takes up iodide (50 x other tissue), joins to glycoproteins using enzyme

    Released as T3 and T4, over 99% protein bound in blood

    Only free amount (1%) act on tissues

    In peripheral tissues all converted to bioactive form, T3

    T4 is precursor, T3 is active and change production in nucleus to change degree of energy use in cell

    speeds it up to create heat and change way cell is acting will cause heart to beat harder and faster

    T3 goes into cell nucleus, changes DNA to increase energy use

    What happens if not enough iodine intake?

    To T3 and T4 levels? Decrease To TSH levels? Increase

    To the thyroid gland itself? Inc in size, press on trachea so person cough, hoarse voice, difficult to swallow, hard

    to flex the neck

    3 effects of increased cellular energy use due to T3

    1. Increased metabolic rate

    2. Increased heart rate and strength

    3. Growth and development, esp. brain, nervous system, and skeletal muscle

    Hypothyroidismlow and slow

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    Congenital or acquired

    Decreased production of thyroid hormones (T3, T4)

    Causes symptoms & Myxedematype of edema develops for mucoid fluid (diff texture)

    Primarytype from the thyroid glanddue to damage, surgically removed, exposed to radiation

    Secondarytype from the anterior pituitaryisnt working in negative feedback so not creating TSH the way it

    shouldmore trouble than hypothyroidism

    Primary Hypothyroidism

    Thyroid gland cannot produce thyroid hormones (T3, T4), so these are low Because low T3 and T4, anterior pituitary produces more TSH to stimulate the thyroid, and serum TSH is high

    tSH much more sensitive indicator.. t3/t4 will go down but TSH will be increased

    t3/t4 not as sensitive because protein bound.. tsh will detect much earlier

    Secondary Hypothyroidism

    Anterior pituitary doesnt produce TSH to stimulate thyroid, so

    Thyroid doesnt make T3 and T4

    Serum levels of BOTH TSH and T3 & T4 are low

    When T3 is low

    First, subtle changes like cold intolerance, low temp, slow reflexes, slower mentation

    Then dry skin, facial edema, hair loss/brittle hair, eyebrows thin, constipation, lethargy, decreased facial

    expression, mental slowness

    Finally, MIXEDEMAmucoid edema, and coma

    Hypothyroidism treatments

    Replace missing T3as early as possible in newborn

    Needed in newborn, for brain development

    Treat underlying cause, if secondary

    Monitor treatment with TSH & decreasing symptoms

    Exemplar: Levothyroxine - synthetic, identical, brands NOT interchangable

    Some brands more active than others

    Overdose = hyperthyroid symptoms

    Hyperthyroidism manifestationstoo much t3

    -Excess thyroid hormone secretion

    -Causes sympathetic NS symptoms: inc HR, temp, BP, resp rate, go through calories quickly, eat a lot and lose weight,

    tremor, nervous

    -Thyrotoxicosisthyroid is toxic

    -Thyroid storm crisis, hyperthermia, tachycardia, delerium, due to stressor

    Clinical Manifestations

    Increase in metabolism

    Increase in oxygen consumption

    Increase in sensitivity to stimulation of SNS

    Hyperthyroidism labs:

    High serum T3, T4

    High metabolic rate, O2 consumption

    LOW TSH (feedback to anterior pituitary!), can be normal or sl. high

    Radioactive iodine uptakehow fast concentrate into thyroid gland determine if uptake is too fast and if it is

    hyperactive

    Graves Diseasemost common cause of hyperthyroidism

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    Autoimmune disordercreates antibodies that take place of TSH on thyroid gland and stimulate thyroid gland

    causing overgrowth of thyroid gland from overstimulation

    Thyroid Stimulating Antibodies

    Goiter

    Exophthalmoseyeballs bulging out

    Hyperthyroid to hypo

    Hyperthyroidism treatments

    Deal with dangerous symptoms! Medications to decrease thyroid function

    Radioactive iodine to kill thyroid cells, then replace thyroid hormones if needed (131 I)

    Surgical removal of gland tissue

    Treat autoimmune disease

    2 main anti-thyrotoxic medications

    Propylthiouriacil (PTU)good in pregnancy, less crosses placenta, less peripheral conversion to T3

    Methimazole (Tapazole)longer half life, so only once a day

    Same main mechanism: inhibits enzyme (peroxidase) needed to make T3 & T4

    Same problem effects: rare agranulocytosis, rashes

    Giving non-radioactive iodine

    Immediately suppresses T3, T4

    Cant use long term

    Lugols

    Managing severe symptoms

    Beta blockers- slow HR so dont go into heart failure

    Coolinguse a cooling blanket

    Sedation

    Exopthalamos: eye drops, surgery, steroids

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    Polypharmacy Administration of many drugs together

    Administration of more medication than are clinically indicated

    Precise number is variable, but generally 5 to 10

    Includes prescribed medications, over the counter medications, herbal supplements

    Balance is required between over and underprescribing

    Multiple medications usually needed to manage clinically complex older adults

    Ex. 76 y/0 female patient with COPD, T2DM, osteoporosis, htn, and osteoarthritis would probably

    require 12 medications

    Factor Contributing to Polypharmacy

    Multiple providers- doctor shop to get medications they want

    Non adherence-

    Underreporting symptoms-not getting right medications

    Taking others medications-daughter has metformin so take her medications for own diabetes

    Diastolic and lopressorboth beta blockers; low heart rate

    Expense

    Confusion between brand name and generic name

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    Example

    Doctor changes from one med to another within the same therapeutic class; but the patient doesnt stop

    taking the first med. (two drugs doing the same thing, maybe not educated to stop the first drug)

    For example: You are taking Protonix 40mg and Dr. gives you a prescription for Prevacid 30mg. Both of these drugs are

    in the same therapeutic class Proton Pump Inhibitors and work the same way. No one should be on both these meds.

    Doctors also may have a patient on a brand name drug and write the next prescription for a generic drug.

    For Example: A patient is taking Coumadin 5mg daily; the Doctor gives patient a prescription for Warfarin 5mg, anothertrade name for Coumadin. The patient continues to take both not realizing they are the same medication. This could

    have devastating consequences.

    Prescription drugs switching to over-the-counter (OTC) status

    For Example: A patient may take Prilosec (OTC) and get a script for Protonix, Prevacid,, etc. This is why it is so important

    that you take all the meds you take on a regular basis with you when you go to the doctor.

    Risks

    Side effects-how do you know which medication is causing a side effect

    Allergic reactions

    Interactions-how they are metabolized

    Metabolism

    Compliance secondary to complexity

    Cost

    Elderly at risk

    12% of US population but 31% of nations prescribed drugs

    Increased severity of illness, multiple pathologies, excessive prescribing

    More sensitive to drugs

    Wider individual variation

    Experience more drug reactions and drug-drug interactions

    Why elderly at risk

    Altered pharmacokinetics

    Multiple and severe illnesses

    Multidrug therapy

    Poor adherence

    May be taking a drug that they found in medicine cabinet

    To ensure safe medication practicemainly REDUCE SYMPTOMS

    Individualization of treatment

    Monitored closely for desired and adverse responses

    Regimen adjusted carefully

    Pharmokinetic changes in elderly

    Gradual progressive decline on organ function, altering the absorption, distribution, metabolism and excretion

    of drugs

    Effect drug sensitivity

    Extent of change varies among patients

    Absorption

    Rate of absorption may be delayed because of delayed gastric emptying and reduced blood flow to the gut

    Drug responses may be delayed

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    Distribution

    4 major factors can effect:

    1. increased percent body fat

    2. decreased percent lean body mass

    3. decreased total body water

    4. reduced concentration of serum albumin

    Metabolism

    Rates of hepatic drug metabolism decline with age because of reduced hepatic blood flow, reduced liver mass,and decreased activity of some hepatic enzymes

    Half lives of certain drugs may be increased, prolonging response

    Stick around longer than it is supposed to

    Excretion

    Renal drug excretion undergoes progressive decline beginning in early adulthood

    ** drug accumulation secondary to reduced renal excretion is the most important cause of adverse drug

    reactions in the elderly

    Decline in renal function is result of reductions in renal blood flow, GFR, and number of nephrons

    Should monitor creatinine clearance

    **Less lean muscle mass (creatinine is measure of kindey function but also reflects muscle mass) you must look

    at GFR or creatinine clearance, will give adequate estimeate of kidney functionjust bc low muscle mass, creatinine will

    be low but doesnt mean kindey is functioning properly

    Pharmodynamic changes

    Alteration in receptor properties

    Ex. Beta blockers less effective in elderly

    A reduction in beta receptors

    Reduction in affinity of beta receptors for beta receptor blocking agents

    Warfarin produce effects that are more intense in the elderly possibly due to an increase in receptor

    affinity

    Adverse drug reactions (ADR) and drug interactions

    ADRs are 7 times more common in the elderly

    Usually dose related

    Symptoms nonspecific

    Multiple factors predispose older adults:

    Drug accumulation secondary to reduced renal function

    Polypharmacy

    Greater severity of illness

    greater use of drugs with a low therapeutic index

    Poor adherence

    Measures to reduce ADR

    Taking a thorough drug history , including OTC

    Accounting for pharmacokinetic and pharmacodynamic changes that occur with aging

    Initiating therapy with low doses

    Monitoring responses and drug levels in order to adjust doses

    Employing simplest regimen possible

    Monitoring for reactions

    Periodically reviewing the need for medications, and discontinuing if appropriate

    Encouraging the patient to dispose of old medications

    Avoiding drugs on the Beers list

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    Nonadherance

    Between 26% and 59% of elderly dont take their meds as prescribed

    Never fill or refill prescriptions

    Account for 10% of all hospital admissions because of therapeutic failure

    Factors for nonadherance

    Unintentional:

    Forgetfulness

    Failure to understand instructions Inability to pay

    Use of complex medications

    Factors for nonadherance

    Intentional: (about 75%)

    Patient thinks that drug not needed

    Unpleasant side effects

    expense

    promoting adherence

    Simplify regimen

    Explain the treatment regimen in a clear, concise way

    Choose appropriate dosage form

    Labeling drug containers clearly

    Suggest recording drug administration

    Asking patient if they have access to pharmacy and can afford the medication

    Enlisting friend or relative to help

    Prescribing cascade

    Develops when an adverse drug event is mistaken as a new medical condition and additional medication is

    added

    Patient is at risk for developing additional adverse drug events

    Beers criteria

    Most widely used criteria to assess inappropriate drug prescribing

    List of 53 meds considered inappropriate for prescribing to older adults because of adverse reactions or

    ineffectiveness

    3 categories: meds that should be avoided, meds considered inappropriate, and those that should be used with

    caution

    High risk medications

    First generation antihistamines

    Analgesics

    Antidepressants

    Antihypertensive

    Sedative hypnotics

    Drugs for urge incontinence

    Muscle relaxants

    Anticholinergic activity

    Associated with multiple adverse drug effects:

    Memory impairment, confusion, hallucinations, dry mouth, blurred vision, constipation, nausea, urinary

    retention, impaired sweating, tachycardia

    glaucoma

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    closed angle glaucoma can go blind this is an emergency

    Atypical antipsychotics

    Increased risk for falls

    Limited evidence to support use of these meds in elderly

    Herbal supplements

    Common in elderly

    Dont always tell provider Dont consider them medications

    Most commonly usedserotonin syndrome = tachycardia

    Three Gs:

    Ginko Biloba, ginseng, garlic

    Have antiplatelet effect, problematic with prescription antiplatelet medication

    Ex. Warfarin and ginko biloba

    Most commonly used

    St johns wort

    Potential for serotonin syndrome when taken with SSRI

    Valerian root

    Not to be used with benzos , alcohol, sedatives

    Med reconciliation

    Average hospitalized patient is subject to one medication error per day

    Formal process for creating the most accurate and complete list possible of the patients medications and

    comparing those to the patients records

    Attempt to avoid duplications, omissions, errors, or potential for interactions

    Should be done at every transition of care

    Should include all medications, herbals, vitamins, otc drugs

    Brown bag medication review

    Patients are asked to bring all their medications including OTC, herbal supplements, and vitamins

    Answer questions about medications, verify what is being taken and how much, identify possible errors

    Nursing Responsibilities

    Preparing, administering, and evaluating client responses to medications

    Developing an up to date knowledge base of medications, including uses, mechanism of action, safe dosage, side

    effects, and contraindications