immunological disorders.ppt Generic BSN unit 7

Lecture on Adult Health Nursing

1. IMMUNOLOGICAL DISORDERS MEHMOOD AHMED NURSING INSTRUCTOR BSN YEAR II SEMESTER III ADULT HEALTH NURSING UNIT VII IMMUNOLOGICAL DISORDERS KGH SCHOOL OF NURSING

2. OBJECTIVES By the end of the session learners will be able to : 1. Discuss Immunologic disorders. 2. Discuss the diagnostic, medical and surgical management of the below mentioned disorders 3. Apply nursing process including assessment, planning, implementation and evaluation of care provided to the clients with immunological disorders 4. Develop a teaching plan for a client experiencing disorders of the immunology. HIV/ AIDS Hypersensitivity and autoimmunity disorders

3. GRAVES DISEASE Auto-immune problem that cause thyroid gland to produce more thyroid hormones which is called hyperthyroidism. Basic anatomy of thyroid gland: Situated in front of trachea Butterfly shape Produce thyroid hormone

4. Negative feedback mechanism:

5. FUNCTION OF THYROID HORMONE (T3 AND T4) Burn calories and fast digestion Stimulate sympathetic nervous system Increase body temperature Replace dying cell with normal

6. CAUSES In Grave's disease, the body is producing an antibody called Thyroid-stimulating immunoglobulin (TSI) which produces the same effect on the body as Thyroid-stimulating hormone (TSH). This leads to excessive production of thyroid hormone (T3 and T4). Grave's disease is a cause of hyperthyroidism due to an autoimmune condition.

7. SIGN & SYMPTOMS Weight loss Increase temperature Heat intolerance Increase heart rate Diarrhea Unique symptoms: Ophthalmic changes (Exophthalmos) Goiter

8. EXOPHTHALMUS

9. DIAGNOSIS TSH (T3 & T4) TSH receptor antibody

10. NURSING INTERVENTION Provide cool and calm environment Improve nutritional status Monitor heart rate and temperature Emotional support

11. SYSTEMATIC LUPUS ERYTHEMATOSUS (SLE) Progressive systematic inflammatory disease, damage major organ or system. Auto-immune disease characterized by formation of auto antibodies and immune complex. Most common auto antibody is DNA. Systematic = Multiple organs Erythematosus = Reddening of skin Lupus = Disease affecting skin or major organ

12. TRIGGER FACTOR OF SLE Genetics Immunological Environmental factors (UV light, drugs, hormones like estrogen changes) These all factors does APOPTOSIS (program cell death)

13. Pathogenesis of SLE

14. Malar rash (butterfly mark) Discoid rash

15. Diagnosis of SLE Anti nuclear antibody (ANA) Anti ds-DNA C3 level

16. Treatment NSAIDs Corticosteroids Immunosuppressive drugs Wear protective clothing, sunglasses, and sunscreen when in the sun. Get preventive heart care. Stay up-to-date with immunizations. Have tests to screen for thinning of the bones (osteoporosis). Avoid tobacco.

17. RHEUMATOID ARTHRITIS An autoimmune disorder, rheumatoid arthritis occurs when your immune system mistakenly attacks your own body's tissues. It’s a chronic inflammatory disease of joints specifically “ synovium”

18. Immune system attacks the synovium. Synovitis occurs resulting in thickening of synovium and destroy cartilage and bone The tendons and ligaments that hold the joint together weaken and stretch. Gradually, the joint loses its shape and alignment.

19. Risk factors Genetic Female to male ratio 3:1 Environmental factors

20. Fast-acting, first line drugs Non-steroidal anti-inflammatory drugs (NSAIDs) Corticosteroids Analgesic drugs Slow-acting, second line drugs (Disease-Modifying Anti-rheumatic Drugs / DMARDs) Hydroxychloroquinine (Plaquenil) Methotrexate (Rheumatrex) Azathioprine (Imuran) Human monoclonal antibody to TNF-alpha Infliximab (Remicade) Adalimumab (Humira) Etanercept (Enbrel) TREATMENT OF RHEUMATOID ARTHRITIS

21. MULTIPLE SCLEROSIS It’s an autoimmune disease that affects the  myelin sheath  of the central nervous system (CNS). This leads to inflammation and scarring of the nerve, which causes a decrease in nerve transmission.

22. Pathophysiology of Multiple Sclerosis Dendrites : receive the signal needed to create some type of action. This signal goes down to the soma. Soma : (which means body) and this structure helps pass on the signal it just received from the dendrites to the rest of the neuron. Then the signal goes down this long area known as the  axon.  For the axon to be able to deliver this signal properly to either  another neuron, muscle, or gland , it must be nicely be  insulated and protected  by the  myelin sheath , which is made up of  Schwann cells.  These cells consist of fats and proteins.

23. Multiple Sclerosis It’s an autoimmune condition, which means the immune system is actually attacking the myelin sheath found on the nerve. It affects the nerve cells in the brain and spinal cord, and this leads to many  sensory and motor type problems .

24. Signs and Symptoms Emotionally and cognitive : Fatigued Depressed Trouble articulating speech Issues swallowing Mood swings Trouble thinking (focusing, solving, keeping thoughts etc.) Motor symptoms: Weakness or paralysis of limbs, trunk or head Diplopia Spasticity of muscles

25. Sensory symptoms: Numbness and tingling Patchy blindness (scotomas) Blurred vision Vertigo Tinnitus Decrease hearing Romberg sign +ve Lhermitte’s sign: transient sensory symptoms as electric shock radiating down the spine or into the limbs with flexion of neck. Signs and Symptoms

26. Cerebellar sign: Nystagmus ( Nystagmus is an involuntary rhythmic side-to-side, up and down or circular motion of the eyes that occurs with a variety of conditions .) Ataxia ( the presence of abnormal, uncoordinated movements. This usage describes signs & symptoms without reference to specific diseases .) Cognitive problems Dysphagia Elimination   (nerves are affected that control the bladder/bowel and their sphincters) Bowel : constipation/diarrhea or incontinence Signs and Symptoms

27. It is a clinical disorder in which chronic dysfunction of exocrine glands characterized by dryness of mouth, eyes and other areas covered by mucus membranes. Immune system attacks moisturizing producing glands leads to xerostomia and keratoconjuctivitis More than 90% patients are women Average age is 50 years. SJOGREN’S SYNDROME

28. Clinical features Dry eyes Parotid gland enlargement Dryness of mouth Dysphasia

29. MYASTHENIA GRAVIS It is an autoimmune condition where the body attacks the receptors that allow for voluntary muscle control, which leads to muscle weakness. VOLUNTARY MUSCLES INVOLVED: Eyes: usually the 1 st sign Throat Face Arms and legs Respiratory (severe)

30. In Myasthenia Gravis, the nicotinic acetylcholine receptors are attacked by antibodies created by the immune system. This limits the amount of acetylcholine that can transmit to the receptor leading to muscle weakness. In addition, the thymus gland plays a role in myasthenia gravis in that it may create the antibodies that attack the nicotinic receptors.

31. SIGN & SYMPTOMS HALLMARK: Muscle weakness– it gets worse with activity (especially repetitive activity) but will improves after resting the muscles. W= weakness neck, arms, face and legs. Muscles of limb and trunk less often affected. E= eye lids drooping “ptosis” 90% patient experience eye problem A= appearance mask like, very sleepy expression K= keep choking/gagging when eating N= no energy E= intraocular muscle involvement ---- strabismus (crossed eyes) double vision S= slurred speech (hoarse voice) S= shortness of breath Sign and symptoms may be precipitated by emotional stress, pregnancy, menses, secondary illness, trauma, temperature extremes, hypokalemia, ingestion of drugs with neuromuscular blocking agents, surgery.

32. COMPLICATION Myasthenia Crisis (acute exacerbation) includes: Severe muscles weakness Respiratory failure Aspiration Respiratory infections

33. DIAGNOSTIC STUDIES Assessment: Have pt look up for 2-3 minutes; if Myasthenia Gravis, patient will have increased droop of eyelids. EMG may show muscle fatigue Tensilon test- in MG reveal improved muscle contractility after IV anticholinesterase agent edrophonium chloride (tensilon) Also diagnosis cholinergic crisis- muscle weakness gets worse Keep atropine on hand to counteract effects of tensilon

34. Anticholinesterase inhibitors- prevents anticholinestersase from breaking down ACh; helps neurotransmission. Monitor dose! Mestinon, Prostigmine Corticosteroids- decrease immune response Prednisone Plasmapheresis - removes ACh antibodies and short-term improvement. THERAPEUTIC MANAGEMENT

35. Continued assessment of CNS Medications are to be given in timely manner, teach as needed about disease. Assess person’s knowledge of disease and planned medical treatment, Signs and symptoms of crisis. Medication knowledge . Nursing interventions

36. PARKINSON’S DISEASE Parkinson's disease (PD) is a neurodegenerative disorder that affects predominately dopamine-producing (“dopaminergic”) neurons in a specific area of the brain called substantia nigra. Substantia nigra is part of the basal ganglia which is part of the midbrain that controls movements.

37.  ROLE OF DOPAMINERGIC NEURONS They release the neurotransmitter  dopamine, which allows us to have accuracy with movement . Normally in the nervous system there is a balance between acetylcholine (an excitatory neurotransmitter) and dopamine (an inhibitory neurotransmitter ). Therefore, the loss of dopamine leads to more acetylcholine being able to produce more excitatory affects to the neurons in the basal ganglia and this leads to  overstimulation …..tremors, rigidity (increased cholinergic activity) etc.

38. SIGN & SYMPTOMS The primary symptoms of Parkinson's disease are all related to voluntary and involuntary motor function and usually start on one side of the body. 1) Tremors :  Trembling in fingers, hands, arms, feet, legs, jaw, or head. Tremors most often occur while the individual is resting. Tremors may worsen when an individual is excited, tired, or stressed. Pill-rolling :  tremors of the hands and fingers looks like the patient is rolling a pill between fingers and hands. 2) Rigidity :  Stiffness of the limbs and trunk, which may increase during movement. Loss of fine hand movements can lead to cramped handwriting ( micrographia ) and may make eating difficult. Cogwheel rigidity : when moving the patient’s arms passively toward the body they jerk or push back slightly

39. 3) Bradykinesia :  Slowness of voluntary movement. Bradykinesia together with stiffness can also affect the facial muscles and result in an expressionless, "mask-like" appearance. Automatic movements are involuntary and subconsciously like blinking of eyelids, swinging of arms while walking, swallowing of saliva,

40. Enhance dopamine transmission by increasing amount of dopamine available and reducing cholinergic activity Anticholinergic agents such as congentin and artane Bromocriptine is given to stimulate dopamine receptors directly Treatment

41. Supervision of and teaching about medication administration. Information about the side effects that might occur and how to handle these. Patient needs adequate physical therapy. Maintain maximum joint function and range of motion. Improve posture and gait. Nursing interventions

42. Nursing Interventions for Parkinson’s Disease Safety Issues: Patient needs to wear low heel shoes and avoid rubber soles (they tend to stick to the floor and can cause tripping). The soles should be smooth (not slick). For balance: move slowly when changing positions…rubber tip cane that is single point can help. Education on how to deal with freezing episodes  Try to change direction of movement….rather then continue going to the side go forward. Consciously lift the legs (as in marching) with each step or pretend they are walking over an object.

43. ACQUIRED IMMUNODEFICIENCY SYNDROME AIDS

44. HIV Human immunodeficiency virus A specific type of virus (a retrovirus) HIV invades the helper T cells to replicate itself.

45. AIDS Acquired Immunodeficiency Syndrome HIV is the virus that causes AIDS Disease limits the body’s ability to fight infection A person with AIDS has a very weak immune system

46. HIV in Body Fluids Semen 11,000 Vaginal Fluid 7,000 Blood 18,000 Amniotic Fluid 4,000 Saliva 1 Average number of HIV particles in 1 ml of these body fluids

47. HIV Life cycle The seven stages of the HIV life cycle are: 1) binding 2) fusion 3) reverse transcription 4) integration 5) replication 6) assembly 7) budding

48. HIV LIFE CYCLE Binding (also called attachment): HIV binds (attaches itself) to receptors on the surface of CD4 cells. Fusion: The HIV envelops & CD4 cell membrane fuse(join together)which allows HIV to enter the CD4 cell. Reverse Transcription: Inside the CD4 cell, HIV releases and use s reverse transcriptase (an HIV enzyme) to convert its genetic material----- HIV RNA into HIV DNA. The conversion of HIV RNA to HIV DNA allows HIV to enter the CD4 cell nucleus and combines with cell genetic material--- cell DNA

49. 4. Integration: Inside the CD4 cell nucleus, HIV releases integrase (an HIV enzyme). HIV uses integrase to insert (integrates) its viral DNA into the DNA of CD4 cell. 5. Replication: once integrated into CD4 cell DNA, HIV begins to use the machinery of CD4 cell to make long chain of HIV proteins. The protein chain are the building blocks of more HIV. 6. Assembly : New HIV proteins and HIV RNA move to the surface of the cell and assemble into immature (non-infectious HIV). 7. Budding : Newly formed immature (non-infectious HIV) pushes itself to outside of the host cell CD4. the new HIV releases protease (an HIV enzyme). The protease acts to break up the long protein chains. The smaller HIV proteins combine to form mature infectious HIV

50. Four Stages of HIV

51. Stage 1 - Primary Characterized by acute infection Short, flu-like illness Fever Sore throat Headache Fatigue Nausea and vomiting Rash lymphadenopathy –

52. This symptoms generally occurs within 2-4 weeks after HIV exposure and last 2-10 weeks Virus replicate rapidly Increase ----Serum HIV RNA copies Decrease----CD4 cell numbers Increase ---- HIV-specific CD8 cell numbers

53. Stage 2 - Asymptomatic Lasts for an average of ten years This stage is free from symptoms The level of HIV in the blood drops to very low levels HIV antibodies are detectable in the blood HIV replication continue and they remain infectious

54. Stage 3 - Symptomatic The symptoms are mild The immune system deteriorates Emergence of opportunistic infections and cancers

55. Stage 4 - HIV  AIDS The immune system weakens When viral load and immunodeficiency remain significant levels, serious opportunistic infections occurs= AIDS End stage of HIV infection Without treatment death occurs within 3 to 5 years The illnesses become more severe leading to an AIDS diagnosis

56. Opportunistic Infections associated with AIDS Bacterial Tuberculosis (TB) Strep pneumonia Viral Kaposi Sarcoma Herpes Influenza (flu)

57. Kaposi’ Lesions

58. Opportunistic Infections associated with AIDS Parasitic Pneumocystis carinii Fungal Candida Cryptococcus

59. Routes of Transmission of HIV Sexual Contact: Blood Exposure: - Injecting drug use/needle sharing -Occupational exposure -Transfusion of blood products Perinatal: - Transmission from mother to baby -Breastfeeding

60. Through Bodily Fluids Blood products Semen Vaginal fluids Breast Milk

61. How HIV attacks the body 1. The virus enters the body through the mucous membranes or through a break in the skin. HIV invades a host cell (T-cell: a key part of the immune system) The virus uses the cell’s resources to reproduce Eventually the host cell is destroyed 2. The virus multiplies within the body 3. More and More t-cells are destroyed

62. As the number of t-cells drops, the immune system gets weaker -The body loses its ability to resist infections and diseases that a healthy immune system could fight off.

63. HIV Infection and Antibody Response Infection Occurs AIDS Symptoms ---Initial Stage---- ---------------Intermediate or Latent Stage-------------- ---Illness Stage--- Flu-like Symptoms Symptom-free < ---- ----

64. 70 Evolution of HIV Disease 1 12 1 2 3 4 5 6 7 8 9 10 11 12 weeks Years Window Viraemia Antibody CD4 Seroconversion illness Clin. latency Clin. AIDS

65. Blood Detection Tests Enzyme-Linked Immunosorbent Assay/Enzyme Immunoassay (ELISA/EIA) Radio Immunoprecipitation Assay/Indirect Fluorescent Antibody Assay (RIP/IFA) Polymerase Chain Reaction (PCR) Western Blot Confirmatory test

66. Urine Testing Urine Western Blot As sensitive as testing blood Safe way to screen for HIV

67. Counseling

68. Pre-test Counseling Transmission Prevention Risk Factors Voluntary & Confidential Reportability of Positive Test Results

69. Post-test Counseling Clarifies test results Need for additional testing Promotion of safe behavior Release of results

70. ANTI-RETROVIRAL Drugs Nucleoside Reverse Transcriptase inhibitors AZT (Zidovudine) Non-Nucleoside Transcriptase inhibitors Viramune ( Nevirapine ) Protease inhibitors Norvir (Ritonavir)

71. Four ways to protect yourself from HIV Abstinence Monogamous Relationship Protected Sex Sterile needles

72. 1) Abstinence It is the only 100 % effective method of not acquiring HIV/AIDS. Refraining from sexual contact Refraining from intravenous drug use 2) Monogamous relationship A mutually monogamous (only one sex partner) relationship with a person who is not infected with HIV HIV testing before marriage is necessary to prove your spouse is not infected 3) Protected Sex: Using condoms 4) Sterile Needles

73. HIV NOT TRANSMITTED BY FOLLOWING WAYS Through the air by coughing or sneezing By casual contact with an HIV-infected person (shaking hands and hugging) By using the same sports equipment, clothing, towel, brush, or furniture as an infected person. By using the same telephone, shower, bathtub, or toilet as an infected person By sharing eating utensils or dishes with an infected person Through bites of mosquitos, ticks, or other insects

74. PEOPLE INFECTED WITH HIV Since the beginning of the epidemic, 79.3 million [55.9–110 million] people have been infected with the HIV virus and 36.3 million [27.2–47.8 million] people have died of HIV. Globally, 37.7 million [30.2–45.1 million] people were living with HIV at the end of 2020 . HIV patient can live long productive lives when their HIV infection is managed. HIV patient can infect people when they engage in high-risk behavior. HIV patient can be unaware of their infection. HIV patient can be look healthy.

75. REFERENCE Brunner, L. S., & Suddarth , D. S. (2005). Text Book of Medical- Surgical Nursing (10th Edition). Philadelphia: Lippincott (Page 315-365) 10th Edition). Philadelphia: Lippincott (Page 315-365) Kathleen Talaro , Aurthur Talaro , Foudations in microbiology 2 nd edition G1-G11 www.ivcc.edu/.../ microbiology_powerpoint_presentan Vivien A.stuke ,microbiology for nurses ,7 th edition pp 58-91 Ross and Wilson ,anatomy and physiology in health and illness 8 th edition, pp 64-67 Lewis, S.L., Dirksen, S.R., Heitkemper , M.M., & Bucher, L. (2014).  Medical-Surgical Nursing: Assessment and Management of Clinical Problems  (8th ed.). St. Louis: Elsevier.