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1 Click on the arrow to proceed to the next slide.

2  Click on the to proceed to the next slide  Click on the to go back to the previous slide  Click on the to go to the “sections” slide  You will be given opportunities throughout to test your knowledge

3  Identify keys components to the pathophysiology of alcohol withdrawal and neurological involvement  Identify the body’s responses to stress and how the HPA axis relates to aging  Identify the signs, symptoms, and behaviors of alcohol withdrawal  Apply learned concepts to a case study involving the care of the patient in alcohol withdrawal  Identify how genetics and metabolism are related in alcohol abuse  Identify inflammation and it’s role in comorbidities associated with alcohol abuse

4  Case Study (1) Case Study (1)  Neurological Pathophysiology(2) Neurological Pathophysiology(2)  Hypothalamic-pituitary-adrenal Axis(HPA Axis), “fight or flight”, & Generalized Stress Response(3) Hypothalamic-pituitary-adrenal Axis(HPA Axis), “fight or flight”, & Generalized Stress Response(3)  Signs & Symptoms of alcohol withdrawal(4) Signs & Symptoms of alcohol withdrawal(4)  Symptom Management(5) Symptom Management(5)  Nursing Interventions(6) Nursing Interventions(6)  Genetics & Metabolism (7) Genetics & Metabolism (7)  Alcoholic Liver Disease & Inflammation (8) Alcoholic Liver Disease & Inflammation (8

5 31 year old male, admitted to your unit for alcohol detox, states he had his last drink over 24 hours ago, and exhibits the following signs and symptoms-  Complains of nausea but no vomiting  Tremulousness  States he has a tight “rubber band” feeling around his head  Profuse sweating Click here to return to datahere

6  Feels intense anxiety  Denies hallucinations  Denies agitation  Knows the current place and time We will come back to this case study later in the tutorial ClickClick here to return to datahere

7  Neurons- nerve cells that communicate to each other using electrical and chemical signals (neurotransmitters)  Synapse- giving and receiving ends where neurotransmitters are transported from one neuron to the next  Presynaptic neurons release neurotransmitters to receptors on the postsynaptic neuron Lovinger, 2008

8 gamma -Aminobutyric acid (GABA) Glutamate GABA Glutamate Microsoft, 2007

9  Main inhibitory neurotransmitter in the human body  Found in all areas of the brain  Regulates neuronal excitability throughout the body  Binds to GABA receptors in the presynaptic and postsynaptic phases of transmission  Alcohol enhances GABA by increasing the inhibitory effects (sedative effect)  Current drugs in the benzodiazepine and barbiturate families can replace alcohol in the brain for successful and non life threatening alcohol withdrawal treatment Lovinger, 2008

10 NIAAA, 2009 Benzodiazepines bind here

11  Exhibits excitatory effects on the brain  Like GABA, is found all over the brain  Binds to NMDA receptors in the brain  Acute alcohol exposure inhibits glutamate transmission, causing neuronal excitability (leading to seizures)  Chronic alcohol exposure increases the number of NMDA receptors  Increased numbers of NMDA receptors leads to withdrawal hyper excitability and alcohol induced neuronal damage when GABA cannot produce inhibitory effects  Involved in cognitive functions such as learning and memory  Drugs that act to reduce receptors involved with glutamate such as memantine and topiramate are either being studied or used for treatment Lovinger, 2008

12  GABA is an inhibitory neurotransmitter  GABA and alcohol bind to the same receptors  In alcohol withdrawal treatment, benzodiazepines bind to those same receptors, preventing neurological withdrawal symptoms  Glutamate in an excitatory neurotransmitter  Alcohol binds to certain receptors to produce sedating effects and long term use causes increased NMDA receptors  In the absence of alcohol, NMDA and glutamate create excitability since GABA is not present to inhibit this (seizures)

13  Neuroendocrine response to stress (Brain)(Hormones)  Contributes to psychological and physiological responses to alcohol  Ultimately stimulates glucocorticoid secretion  Three way relationship exists between alcohol use, glucocorticoid secretion, and aging Hutchison & Spencer, 1999

14 So now what? Cortisol released from the adrenal glands of the kidneys prevent further release of CRH and ACTH. Is this a negative or positive feedback loop? Think about it and save it for the end of the section. Stressful situation (alcohol intoxication) HypothalamusPituitary Gland Adrenal GlandsHint: Roll mouse over body parts to reveal what they release. Hutchison & Spencer, 1999 & Microsoft 2007 Adrenal Gland

15  Alcohol use stimulates the HPA Axis  Length of stimulation depends on amounts of alcohol consumed or blood alcohol level (BAC) Hutchison & Spencer, 1999 & Microsoft 2007

16  Blood alcohol levels (BAC) and HPA Axis activation have a strong genetic component  Strong evidence exists of a defective gene, not allowing the correct metabolism of alcohol  People with this gene have significant high cortisol levels Hutchison & Spencer, 1999

17 Aging people are more at risk for HPA Axis overstimulation Why?  Recovery is slower  The feedback loop takes longer to get the message back  Getting rid of catecholamines takes longer  Cortisol levels eventually will cause neuronal death Hutchison & Spencer, 1999

18 Norepinephrine/ Noradrenaline Released Alpha 1 Alpha 2 Beta 1 Beta 2 Diaphoretic Increased Blood Pressure Dilated Pupils GI Tract off Lowers Insulin Increased HR Increased Respirations

19 A patient in acute alcohol withdrawal is experiencing sweats (diaphoresis) and an increase in heart rate (tachycardia). What is causing this? Click on the correct answer Sympathetic Nervous System System HPA AxisDelirium

20  Accurate nursing assessment of patients with alcohol dependence can help to eliminate or minimize negative patient outcomes  Recognizing/identifying signs/symptoms/behaviors of those at risk for alcohol withdrawal syndrome McKinley, 2005

21  Tremors  Sweating  Nausea  Vomiting  Agitation  Anxiety  Auditory disturbances  Clouding of sensorium  Visual/Tactile disturbances Autonomic Hyperactivity Neuropsychiatric Alterations McKinley, 2005

22  Signs/symptoms can appear within 24 hours of last drink  Peak of s/s happen as early as 24 hours and stop around 48 hours  Delirium tremens typically occur between hours after last drink  Delirium tremens is considered an emergency and can end in death McKinley, 2005

23  Excessive activation of NMDA increases the chance of seizures  Long term exposure to alcohol depresses GABA, making brain more vulnerable to seizures  For nurses, the implication would be to assess patient history of withdrawal/detox and treat more aggressively those who are most at risk  48% of inpatient alcoholics who suffered seizures had gone through several detoxifications in their pasts  In the same study, 12% of alcoholics who had seizures during detoxification had little to no history of detoxification Becker, 1998

24  Clinical Institute Withdrawal Assessment (CIWA)  Selective Severity Assessment (SSA)  CAGE questions  Alcohol Withdrawal Syndrome Type Indicator  Alcohol Use Disorders Identification Test

25 CIWA is a 10 item rating scale that discriminates symptoms of gastric distress, perceptual distortions, cognitive impairment, anxiety, agitation, and headache Ragasis,2004

26 Nausea/Vomiting Paroxysmal Sweats  0 No Nausea/Vomiting  1-3 Mild nausea  4-6 Intermittent Nausea with Dry Heaves  7-Constant Nausea, Dry Heaves, Vomiting  0-No sweat visible  1-3 Barely Sweating  4-6 Beads of Sweat Obvious on Forehead  7- Drenching Sweats Click here to return to data

27 Tremors Anxiety  0-No tremors  1-3 Not visible, but can be felt fingertip to fingertip  4- Moderate with arms extended  7-severe, even without arms extended “Do you feel nervous?”  0-No anxiety/at ease  1-3 Mildly anxious  4-6 Moderately anxious  7-Acute panic, anxiety Click here to return to data

28 Agitation Headache/Fullness  0-Normal activity  1-3 Somewhat more than usual  4-6 Moderately fidgety/restless  7-Paces back and forth, thrashing about  None  1-Very mild  2-Mild  3-Moderate  4-Moderately sever  5-Severe  6-Very severe  7 - Extremely severe Click here to return to data

29 Does the light appear to be too bright? Is the color different? Does it hurt your eyes? Are you seeing anything that is disturbing to you? Are you seeing things you know aren’t there?  0-None  4-Mild sensitivity to light to occasionally seeing things you can’t  7-Constant visual hallucinations

30 Are you aware of sounds around you? Are they harsh? Do they frighten you? Are you hearing anything disturbing? Are you hearing things you know aren’t there?  0-None  2-Very mild harshness of ability to frighten  3-Moderate  4-Moderately severe hallucinations  5-Severe hallucinations  6-Extremely severe hallucinations  7-Continuous hallucinations

31 Do you feel any itching, or pins and needles? Any numbness or burning? Do you feel bugs crawling on or under your skin?  0-None  1-Very mild itching  2-Mild itching  3- Moderate itching  4-Moderate hallucinations  5-Severe hallucinations  6-Extremely severe hallucinations  7-Continuous hallucinations

32 “ What day is it? Where are you? Who am I?”  0-oriented  1-Cannot do serial additions or uncertain of dates  2-Disoriented to date but not by more than 2 days  3-Disoriented for date by more than 2 days  4-Disoriented to time/place

33 Prepare to use your critical thinking skills and assess your patient in alcohol withdrawal!

34  Patient is sweating profusely Patient is sweating profusely  Exhibits moderate tremors when asked to extend arms Exhibits moderate tremors when asked to extend arms  Appears to be restless and jittery during assessment Appears to be restless and jittery during assessment  Patient complains of intense headache, a “rubber band” is tight around his head Patient complains of intense headache, a “rubber band” is tight around his head  Patient complains of intense anxiety Patient complains of intense anxiety  Patient denies audio/visual/tactile hallucinations Patient denies audio/visual/tactile hallucinations  Patient is alert and oriented to self, place and time Patient is alert and oriented to self, place and time  Patient complains of moderate nausea, no vomiting Patient complains of moderate nausea, no vomiting Objective DataSubjective Data Click here to review the case study! Click here to return to case study

35  Profuse sweating 4-7 Profuse sweating  Moderate tremors 4 Moderate tremors  Moderate agitation 4-6 Moderate agitation  Moderate headache 4-6 Moderate headache  Intense anxiety 4-6 Intense anxiety  No hallucinations 0  Oriented 0  Mild nausea 1-3 Mild nausea Score range is Now what? Objective Data Subjective Data Click on individual signs/symptoms to take you to the scores

36  Benzodiazepines are given, to meet receptors in the brain alcohol is no longer binding to, to prevent hyperexcitibility and seizures  Intravenous fluids  Anti inflammatory medications for the headache  Thiamine (patients often malnourished)  Multivitamin (patients often malnourished)  Folic Acid (patients often malnourished)  Therapeutic relations with patient (support) Always remember to continue to use the nursing process for outcomes and continued care!

37 The processing of alcohol involves…. 1. Gastrointestinal tract absorption 2. Alcohol distribution in the body 3. Liver metabolism Genetics and Environmental factors influence these processes NIAAA, 2007

38  GI Surgeries  Concentration of alcohol in beverage  Rate of consumption  Presence of food in the stomach

39 Liver Enzymes (Needed for alcohol breakdown) Cytosolic alcohol dehydrogenase (ADH) Mitochondrial aldehyde dehydrogenase (ALDH2) NIAAA, 2007

40 The amount of alcohol metabolized in the body relies on: Liver Size & Body Mass Genetics have influences on ADH & ALDH and affect how people metabolize alcohol This can help to explain why certain groups of people have variances in levels of alcohol abuse NIAAA, 2007

41  Alcoholic Liver Disease (ALD)  Alcoholic Cardiomyopathy  Alcohol Related Dementia  Peripheral Neuropathy  Gastritis  Pancreatitis

42 Alcoholic Liver Disease (ALD) Fatty Liver Alcoholic Hepatitis Cirrhosis Long term alcohol abuse is leading cause of liver disease in the U.S. Alcohol, Research, & Health, 2000

43  What do you think? Click on a box to find out? NoYes

44 Repeated Alcohol Abuse Cytokines Cytokines Released Endotoxins Endotoxins Produced Promote Scar Formation Stimulate More Cytokines Activate Immune System Roll mouse over underlined words for more information. Chronic inflammation from chronic alcohol exposure can cause hepatocyte apoptosis Neuman, 2001

45  Increased numbers of cytokines continue to be activated  Increased scarring occurs  Cell injury increases  Increase in cell death  Compromised organ function  Organ failure

46 Alcoholic Liver Disease (ALD) Fatty Liver Alcoholic Hepatitis Cirrhosis Depending on what is happening to the liver, interventions lie in decreasing the inflammation, resting the organ, preventing hepatic encephalopathy, preventing ascites, and abstaining from the stressor (alcohol)

47 One role of the nurse is to provide safe patient care that contributes to ideal patient outcomes. In caring for the patient in alcohol withdrawal these include:  Keeping safety in mind (seizure pads)  Eliminate extraneous stimuli (keep it quiet)  Prevent falls (bed/chair alarms, rounding)  Watching for s/s of bleeding (since the liver might be compromised)  Critical thinking for s/s of other disease processes that might mimic AWS, as to avoid mistreating (medicating for AWS when patient might have a low blood sugar)  Monitor all values related to liver function (coagulation, enzymes, etc.)

48  Promote healing through nursing/medical interventions  Be familiar with the pathophysiology of what is going on with the patient  Look at the “whole” picture  Advocate for the patient

49 Animated images not otherwise specified, Microsoft Clip Art, (2009), obtained at Axen, D., Koranda, A., & McKay, A., (2004). Using a Symptom-Triggered Approach to Manage Patients in Acute Alcohol Withdrawal. Medsurg Nursing, February 2004, (13)1. Author unknown., Medical Consequences of Alcohol Abuse. (2000). Alcohol Research & Health., Vol. 24, No. 1. Becker, H.C., Kindling in Alcohol Withdrawal. (1998). Alcohol Health & Research World. Vol. 22, No. 1. Hutchison, K.E. & Spencer, R.L., Alcohol, Aging, and the Stress Response. (1999). Alcohol Research & Health. Vol. 23, No. 4. Lovinger, D.M., Communication Networks in the Brain: Neurons, Receptors, Neurotransmitters, and Alcohol.(2008). Alcohol Research & Health. Vol. 31 No. 3. Retrieved on the world wide web on March 31 st, 2009 at 214.htm.http://pubs.niaaa.nih.gov/publications/arh313/ htm

50 McKinley, M.G., (2005). Alcohol Withdrawal Syndrome: Overlooked and Mismanaged? Critical Care Nurse. Vol. 25, No. 3. National Institute on Alcohol Abuse and Alcoholism., (2007). Alcohol Metabolism: An Update. Retrieved on the world wide web on April 16 th, 2009 at National Institute on Alcohol Abuse and Alcoholism, 2009, Permission obtained for use of pictures/graphics. Neuman, M. G., (2001). Cytokines-Central Factors in Alcohol Liver Disease. Retrieved on the world wide web on May 2 nd, 2010 at 4/ htm. Ragaisis K.M., (2004). Alcohol Screening in the Acute Care Hospital. Journal of Addictions Nursing, 15: Saitz, R., (1998). Introduction to Alcohol Withdrawal. Alcohol Health & Research World. Vol. 22, No. 1.

51  As you have seen in previous slides, the sympathetic nervous (SNS) system, part of the GSR, is responsible for many signs and symptoms of alcohol withdrawal Click here to return to the tutorial

52 Without inflammation, injuries would not be localized and the immune system would not be able to do its job, preventing healing and further infections. Click here to return to inflammation slide

53 When the body has an “injury”, inflammation occurs, attempts to localize the injury, and calls the immune system to work as a team to heal the injury and prevent further spread or damage. Click here to return to inflammation slide


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