Path0 Exam II.txt

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  1. Influenza
    • —Most common Upper respiratory Infection(URI)
    • —Transmission is by aerosol by droplet nuclei
    • —Three types of Infection:
    • —-Upper respiratory infection (rhinotracheitis)—
    • -—Viral pneumonia (orthomyxoviridae family) —
    • -Respiratory viral infection followed by a bacterial infection —
  2. Influenza Three types of Infection:
    • —-Upper respiratory infection (rhinotracheitis)—
    • -—Viral pneumonia (orthomyxoviridae family) 
    • —-Respiratory viral infection followed by a bacterial infection —
  3. —Influenza Incubation:
    1-4 days
  4. —Influenza —CM:(8)
    • similar other upper resp. viruses,
    • chills,
    • malaise,
    • fever,
    • headache (HA),
    • muscle aches,
    • non-productive cough(NPC),
    • sore throat(ST),
    • profuse nasal drainage—
  5. —Influenza Complications:
    • Viral pneumonia,
    • sinusitis,
    • Otitis media,
    • bronchitis,
    • bacterial pneumonia—
  6. —Influenza DX: (3)
    • Usually by s/s,
    • labs,
    • xray for pneumonia—
  7. —Influenza TX:
    • No absolute treatment- no antibiotics,
    • Early Tx to manage side effects and minimize spread (keep to UR tract),
    • Anti-viral drugs
    • ***FLU Vaccine****— —
  8. Pneumonia
    Acute inflammation of lung caused by microbial organism
  9. Leading cause of death in the United States from infectious disease
    Pneumonia
  10. —Discovery of____ ____ and ____ decreased morbidity and mortality rates from Pneumonia
    sulfa drugs and penicillin
  11. —Typical Pneumonia
    bacteria in the alveoli
  12. —Typical Pneumonia Lobar:
    affect an entire lobe of the lung
  13. Typical Pneumonia —Bronchopneumonia:
    patchy distribution over more than one lobe
  14. Pneumonia- Atypical
    Viral and mycoplasmainfections of alveolar septum or interstitium
  15. Pneumonia —Etiology (4)
    • —Likely to result when defense mechanisms become incompetent or overwhelmed
    • —↓ Cough and epiglottal reflexes may allow aspiration—
    • Mucociliary mechanism impaired —
    • —Alteration of leukocytes from malnutrition— Increased frequency of gram-negative bacilli from leukemia, alcoholism, and diabetes mellitus—
  16. Pneumonia —Etiology:Mucociliary mechanism impaired by (5)
    • —Pollution
    • —Cigarette smoking
    • —Upper respiratory infections—
    • Tracheal intubation 
    • —Aging
  17. Pneumonia —Etiology:
    Three ways organisms reach lungs—
    • Aspiration from nasopharynx or oropharynx
    • Inhalation of microbes such as Mycoplasma pneumoniae —
    • Hematogenous spread from primary infection elsewhere in body— —
  18. Pathophysiologic Course of Pneumococcal Pneumonia
    (PIC)
  19. Types of Pneumonia: —Community-acquired pneumonia (CAP) (5)
    • —Lower respiratory infection of lung 
    • —Onset in community or during first 2 days of hospitalization—
    • 4 million U.S. adults diagnosed yearly
    • —Highest incidence in midwinter—
    • Smoking important risk factor— —
  20. CAP Pneumonia:Organisms implicated (4)
    • **Streptococcus pneumoniae,most common
    • —Haemophilus influenzae
    • Legionella—
    • Mycoplasma
    • —Chlamydia —
    • Can be viral:
  21. CAP Pneumonia viral causes:
    • influenza
    • RSV
    • adenovirus
    • parainfluenza virus
  22. CAP Pneumonia —Three-step approach to treatment (ppt)
    • Assess ability to treat at home
    • Calculate PORT (Pneumonia Patient Outcomes Research Team)
    • Clinician decision for inpatient or outpatient
  23. CAP Pneumonia (book): (2)
    • Antibiotics- empiric antibiotic therapy (home)
    • Hospitalization for more severe cases
  24. Hospital-acquired pneumonia 
     (2)
    —Occurring 48 hours or longer after admission and not incubating at time of hospitalization— Second most common nosocomial infection
  25. Risk factors for HAP
    • —Immunosuppressive therapy—
    • General debility —
    • Endotracheal intubation
  26. resp. disorders involving inflammation of the lung structures, such as the alveoli and bronchioles
    Pneumonia
  27. Causes of opportunistic pneumonia: (4)
    • Bacterial and viral causative agents—
    • Pneumocystis jiroveci pneumonia (PCP)—
    • Cytomegalovirus—
    • Fungi
  28. —Opportunistic pneumonia: —Patients at risk :— (4)
    • Severe protein-calorie malnutrition—
    • Immune deficiencies—
    • Chemotherapy/radiation recipients—
    • Transplant recipients
  29. Pneumonia:—Clinical manifestations of (opportunistic) PCP: —
    • Fever—
    • Tachypnea —
    • Tachycardia—
    • Dyspnea—Nonproductive cough
    • —Hypoxemia —
  30. —Pneumonia Pathophysiology —4 Stages
    • Stage 1: Congestion from outpouring of fluid to alveoli—
    • —Stage 2: Red hepatization
    • Stage 3: Gray hepatization
    • Resolution—
  31. —Pneumonia Pathophysiology ——Stage 1: Congestion from outpouring of fluid to alveoli (3) (what happens)
    • Organisms multiply —
    • Infection spreads
    • —Interferes with lung function
  32. —Pneumonia Pathophysiology Stage 2: Red hepatization (3)
    • Massive dilation of capillaries —
    • Alveoli fill with organisms, neutrophils, RBCs, and fibrin—
    • - Causes lungs to appear red and granular, similar toliver
  33. —Pneumonia Pathophysiology 
    (Stage3) Gray hepatization (2)
    • —↓ Bloodflow 
    • —Leukocyte and fibrin consolidate in affected part of lung
  34. —Pneumonia Pathophysiology: —Resolution (3)
    • —Resolution and healing if no complications
    • —Exudate lysed and processed by macrophages—
    • Tissue restored
  35. Tuberculosis (3)
    • —World’s foremost cause of death from asingle infectious agent — 
    • —Drug-resistant forms 
    • —Mycobacterium tuberculosis hominis —Aerobic—Protective waxy capsule—Can stay alive in “suspended animation” for years—
  36. Mycobacterium tuberculosis hominis (3)
    • —Aerobic—
    • Protective waxy capsule
    • —Can stay alive in “suspended animation” for years—
  37. TB: Etiology and Pathophysiology (5)
    • Spread via airborne droplets 
    • Inhaled bacilli pass down bronchial system and implant themselves on bronchioles or alveoli
    • Multiply with no initial resistance
    • —Replicates slowly and spreads via the lymphatic system
    • If cellular immune system is activated-Tissue granuloma forms
  38. TB —Brief exposure ___ causes infection—
    rarely
  39. TB Transmission requires ____, ____ or ____ exposure —
    close, frequent, or prolonged
  40. Tb spread by: (5)
    • —via airborne droplets when infected person:
    • Coughs—,
    • Speaks—,
    • Sneezes—,
    • Sings—,
    • Spread
  41. TB not spread by
    Not by hands or objects
  42. TB —Favorable environments for growth:
    • —Upper lobes of lungs 
    • —Kidneys 
    • —Epiphyses of bone
    • —Cerebral cortex
    • —Adrenal glands
  43. TB ________ and _______ patients are at higher risk for disease
    —Immunosuppressed and diabetic
  44. TB- Classes 0-4

    —
    • 0 = No TB exposure—
    • 1 = Exposure, noinfection—
    • 2 = Latent TB, nodisease—
    • 3 = TB, not clinically active
    • —4 = TB suspected
  45. TB Clinical Manifestations: Early stages are
    usually free of symptoms
  46. TB —Clinical Manifestations:
    • —Fatigue—
    • Malaise—
    • Anorexia— —
    • Weight loss—
    • Low-grade fevers—
    • Night sweats— —
    • —Cough becomes frequent-—Produces white, frothy sputum
    • Cough-—Hemoptysis is not common and is usually associated with advanced disease—
  47. TB Clinical Manifestations Acute symptoms
    • (generalized flu symptoms)—
    • High fever—
    • Chills
    • —Pleuritic pain—
    • Productive cough—
  48. Initial TB Infection
    • —Macrophages begin a cell-mediated immune response —
    • Takes 3–6 weeks to develop positive TB test—
    • Results in a granulomatous lesion or Ghon complex
  49. Ghon complex
    • —Nodules in lung tissue and lymph nodes—
    • Caseous necrosis inside nodules
    • —Calcium may deposit in the fatty area of necrosis
    • —Visible on x-rays—
  50. Primary TB
  51. Miliary TB
    • —Miliary TB lesions look like grains of millet in the tissues—
    • Meat inspection was introduced to keep them out of the food supply—
    • Pasteurization of milk was introduced to keep TB out of the milk supply—
  52. Secondary TB
    • —Reinfection from inhaled droplet nuclei
    • Reactivation of a previously healed primary lesion —
    • Immediate cell-mediated response walls off infection inairways
    • —Bacteria damage tissues in the airways, creating cavities—
    • Signs of chronic pneumonia: gradual destruction of lungtissue—
    • “Consumption”: eventually fatal ifuntreated—
  53. Atelectasis:
    • incomplete expansion of the lung, or a portion of the lung 
    • obstruction, lung compression (tumor,pneumothorax/pleural effusion, increased recoil due to loss of surfactant, from
    • fluid, mucous, congestion, *anesthesia & surgery)
  54. Atelectasis:CM:
    • Tachypnea,
    • tachycardia,
    • dypsnea,
    • cyanosis,
    • hypoxemia,
    • diminished chest expansion & breath sounds, intercostal retractions,
    • s/s depend on area involved: large=tracheal shift
  55. Atelectasis:Tx:
    • depends on size & area involved,
    • reduce airway obstruction,
    • cough & deep breathing,
    • ambulation,
    • positioning,
    • O2
  56. Bronchial Asthma:
    • –Chronic,episodes of airway obstruction due to hyper-responsiveness & airway inflammation that are usually reversible
    • –22.2 million Americans, 3.8 are children under 18, prevalence is up, morbidity &mortality down
  57. Lower Respiratory: Asthma
    • Exaggerated hypersensitivity & response to a variety of stimuli
    • Increased presence of inflammatory cells: eosinophil's, lymphocytes & mastcells=damage to bronchial epithelium
    • T1 &B cell immune response, antibody production to antigens & parasites
    • Cytokine& TNF contribute to chronic inflammation 
    • Extrinsic or Intrinsic
  58. Lower Respiratory: Asthma Extrinsic
    Atopic, Type I hypersensitivity rxn to allergen or antigen
  59. Lower Respiratory: Asthma Intrinsic
    Non-atopic, due to URI, exercise, hyperventilation, cold air, drugs, & chemical, pollutants, hormones, emotional upsets….
  60. Asthma: Extrinsic: Phases:
    • Acute Phase,
    • Late Phase
  61. Asthma: Extrinsic: 3 major characteristics:
    • Bronchospasm, (bronchoconstriction)
    • Increased mucous production,
    • & Edema,
  62. Asthma: Extrinsic: prolonged attack:
    air trapping & hyperinflation of lungs
  63. Asthma: Extrinsic: Severe form:
    (refractory) childhood form
  64. Asthma: Extrinsic:CM:
    • Wheezes,
    • chest tightness,
    • tachypnea,
    • dypsnea,
    • prolonged expiration,
    • acute bronchoconstriction (narrowed airways) /attack,
    • attacks vary person to person,
    • may be s/s free
  65. Asthma: Extrinsic:DX:
    • Pulmonary Function Studies (PFTS)
    • Spirometry measures:
    • * Forced vital capacity -FVC,
    • Forced expiratory volume -FEV,
    • * Peak expiratory flow PEF,
    • Tidal volume,
    • Expiratory & *Inspiratory reserve capacity,
    • H & P
  66. Asthma Tx:
    • Medications:
    • Prevention & education,
    • Relaxation and breathing techniques
    • Allergy testing and desensitization=allergan immunotherapy
  67. Asthma Tx:Medications:
    • Bronchodialtors,
    • Leukotriene modifiers,
    • Antihistamines,
    • Anti-inflammatorty drugs
  68. Asthma Tx: Prevention &education,
    to decrease exposure to triggers (irritants & factors) that precipitate asthma attacks
  69. Pulmonary Embolism (PE)Develops when
    a blood-borne substance lodges in a branch of the pulmonary artery & obstructs blood flow
  70. Almost all PE develops from
    thrombi that broke loose from a DVT of extremities

    (venous stasis,venous endothelial injury, hypercoagulability states,p.500-1)
  71. PE: Mechanical obstruction, neuro-humoral reflexes which cause:
    • vasoconstriction,
    • reduced blood flow causes reflex bronchoconstriction in area,
    • impaired gas exchange, &
    • loss of alveolar surfactant
  72. PE: ____ & ____ can develop from massive vasoconstriction & Large clot
    Pulmonary HTN & Right Heart Failure
  73. PE: CM:
    • Depends on size & location of the PE:
    • Chest pain,
    • dypsnea,
    • tachypnea
    • –if pulmonary infarction: pain becomes pleuritic and severe with inspiration
    • –Impaired gas exchange: Moderate hypoxemia w/o CO2 retention
    • – small emboli in peripheral branches may be asymptomatic, if repetitive can reduce the size of the pulmonary-capillary bed+ Resulting in Pulmonary Hypertension
    • –Large (see next slide)= pleuritic pain & breathlessness, RR rapid & shallow, apprehension, slight fever, cough withblood streaked sputum, Tachycardia=Why?
  74. PE: CM: Large
    • pleuritic pain & breathlessness,
    • RR rapid & shallow,
    • apprehension,
    • slight fever,
    • cough with blood streaked sputum,
    • Tachycardia
  75. Pts with massive PE :
    • sudden collapse,
    • crushing sub-sternal chest pain,
    • possible loss of consciousness,
    • shock:
    • - rapid & weak pulse,
    • - hypotension,
    • - cyanosis,
    • - diaphoresis &
    • - distended neck vein (JVD)
  76. PE:Dx:
    • Blood gases,
    • H & P,
    • D-Dimer,
    • Venous ultrasound (Doppler) &
    • contrast venogram of extremities,
    • lung scans,
    • CT of chest,
    • possible pulmonary angiogram,
    • Ventilation/Perfusion scan,
    • ECG
  77. PE: Tx:
    • Prevent DVT/emboli,
    • Oxygenation &monitoring,
    • pharmacologic preventative & therapeutic use of anticoagulants,
    • surgery into vena cava if life threatening,
    • preventative surgery:
  78. PE TX preventative surgery:
    • venous ligation
    • & vena cave plication:clip or filter/sieve to catch clot (Greenfield filter)
  79. Pulmonary Arterial HTN:
    • A disorder characterized byan elevation of pressure w/in the pulmonary circuit,
    • is rare & debilitating;
  80. Pulmonary Arterial HTN: results in:
    • abnormal proliferation & contraction of vascular smooth muscle,
    • coagulation abnormalities,
    • & marked intimal fibrosis  obliteration or obstruction of pulmonary arteries & arterioles,
  81. Pulmonary Arterial HTN:leads to
    • Right heart failure,
    • low CO & death if untreated 
    • –Pulmonary circuit is low pressure, thin walled
  82. Pulmonary Artery HTN:Types:
    • Primary
    • Seconday
  83. Pulmonary Artery HTN:Primary
    • idiopathic & familial: mutation in gene
    • -Inherited autosomal dominant, low penetrance
  84. Pulmonary Artery HTN: Secondary to another disease:
    as with COPD & CHF
  85. Pulmonary Arterial HTN: CM:
    • Persistent high pressures in PA, with nl Leftventricle pressures differentiating it from LHF,
    • SOB,
    • decreasing exercise tolerance, RHF,
    • Peripheral edema
  86. Pulmonary Arterial HTN: Dx:
    • Pulmonary Wedge Pressure measurement,
    • H & P &
    • R/O other causes
  87. Pulmonary Artery HTN:Tx:
    • Improve R heart function,
    • O2,
    • BP & Cardiac meds,
    • Viagra
    • Lung transplant
  88. Chronic Obstructive Pulmonary Disease
    • Diseases of airflow obstruction:
    • Chronic Bronchitis, Emphysema, Chronic Asthma 
    • Progressive,may be partially reversible
    • 4th leading cause of death in US
  89. COPD Risk Factors
    • Cigarette smoking 
    • Infection Heredity(Emphysema)
    • Aging
  90. Emphysema:Pathophysiology: Structural changes
    • Hyper inflation of alveoli
    • Destruction of alveolar walls
    • Destruction of alveolar capillary walls
    • Narrowed, tortuous, small airways
    • Loss of lung elasticity
    • Small bronchioles become obstructed with mucus
  91. Emphysema Clinical Manifestations
    • Dypsnea on exertion 
    • Minimal cough, little or no sputum
    • Tachypnea, use of intercostal muscles
    • Over-distended alveoli, air trapping
    • Hypoxemia, Hypoxia with hypercapnia 
    • Weight loss
  92. Emphysema Clinical Manifestations Over distension Presents with :
    • Flattened diaphragm 
    • Increased A/P chest diameter (barrel chest)
    • Diminished Breath sounds 
    • Prolonged expiratory phase
  93. Chronic Bronchitis Pathophysiology:
    • Excessive production of mucus in the bronchi
    • Recurrent persistent cough 
    • Structural changes
  94. Chronic Bronchitis Pathophysiology: Structura changes
    • Hyperplasia of mucus-secreting glands
    • Increase in goblet cells
    • Disappearance of cilia
    • Chronic inflammatory changes &narrowing of small airways
    • Altered function of alveolar macrophages
  95. Chronic Bronchitis Manifestations
    • Frequent,productive cough 
    • Copious muco-purulent sputum
    • Frequent respiratory infections
    • Increased AP diameter chest; scattered crackles, rhonchi, wheezing
    • Dyspnea on exertion 
    • Normal weight 
    • Hypoxemia (low O2) & hypercapnia (^CO2)
    • Right sided heart failure
    • Ruddyappearance
  96. COPD Complications
    • (Cor Pulmonale)Hypertrophy of right side of heart (s/s) 
    • Acute Exacerbation of Chronic Bronchitis:
    • Acute Respiratory Failure
    • Peptic Ulcer & Gastroesophageal Reflux Disease
    • Pneumonia
  97. COPD Complications: Acute Exacerbation of Chronic Bronchitis:
    • Worsened cough,
    • hemoptysis,
    • wheezing,
    • increased Dyspnea,
    • changes in color, amount, consistency of sputum
  98. COPD Diagnostic Studies
    • Chestx-ray (early may be normal)
    • H & H- Hemoglobin and hematocrit.(elevated)
    • Pulmonary function studies
    • Serum alpha1 Antitrypsin
    • ABG’s(later sign - low PaO2, high PaCO2)
    • ECG(later sign – right ventricular strain)
  99. COPD Collaborative Care Goals:
    • –Improve ventilation
    • –Promote secretion removal
    • –Prevent complications & progression of symptoms
    • –Improve quality of life
    • –Prevent exacerbations and hospitalizations
    • –Prevent complications (pneumonia, CHF, respiratory failure)
  100. COPD Medical Management
    • Pharmacological Therapy–Bronchodilators, Anti-inflammatory drugs etc
    • Respiratory Therapy
    • Nutritional Therapy
    • Pulmonary Rehabilitation
    • Lung transplant/lung reduction 
    • OxygenTherapy –Low-flow
  101. COPD Nursing Implications: Ineffective Airway Clearance
    • elevate HOB/sit
    • adequate hydration (2-3 liters) teach effective cough technique
    • Chest physiotherapy
    • bronchodilator with C & DB exercises
  102. COPD Nursing Implications: Impaired Gas Exchange
    • elevate HOB/sit & support upper arms
    • Monitor O2 & O2 saturation,
    • ABG’s
    • Teach: pursed lip breathing, flutter valve, use of MDI’s 
    • S/S of hypercapnia
    • avoidance of CNS depressants, 
    • administer O2 as ordered,
    • frequent rest periods
  103. COPD Nursing Implications: Imbalanced
    Nutrition: less than body requirements: Teach:
    • Caloric intake,
    • high-protein,
    • high-calorie
    • Rest periods after food intake
    • Six small meals throughout day
  104. COPD Nursing Implications: Risk for Infection:
    Assess :
    • changes in sputum
    • increased cough,
    • dypsnea and respiratory rate 
    • abnormal breath sounds 
    • fever,
    • chills
  105. COPD Nursing Implications: Risk for Infection: Teach:
    • S/S infection/exacerbation, 
    • hand hygiene, 
    • avoid URI exposure, 
    • Pneumococcal vaccination, 
    • medical attention early, 
    • Remain indoors during significant air pollution
  106. žPhysiology of Blood Pressure 
    BP =
    • SVR (PVR) X CO
    • Vascular resistance
  107. žPhysiology of Blood Pressure:
    Neural Mechanisms Rapid & Short Control:
    • —ANS & Cardiovascular ctrin brain,
    • PNS nerve impulses to heart & BV through periph nerves,
    • Vaga lstimulation= slowing of HR,
    • Sympathetic stimulation= increase HR & Contractility—
    • Baroreceptors & Chemoreceptors: Intrinsic receptorsthat sense pressure and chemical changes to regulate BP—
    • Extrinsic reflexes to alter BP, (BP response to pain,cold temp)ž
  108. žPhysiology of Blood Pressure:
    Adrenergic receptors —
    • Alpha 1,
    • alpha 2—
    • Beta 1,
    • beta 2
  109. žPhysiology of Blood Pressure: žHumoral Mechanisms:
    • *Renin/Angiotensin/Aldosterone system,
    • *Vasopressin (Antidiuretic Hormone, ADH)
    • Sympathetic neurotransmitter: Epinephrine, short & long term regulationž
  110. žPhysiology of Blood Pressure: žSystolic BP:
    • measures the pressure in the arteries when the heart beats (when the heart muscle contracts).
    • height of pressure pulse,
    • —Blood & Pressure during systole
  111. žPhysiology of Blood Pressure: Diastolic BP:
    • measures the pressure in the arteries between heartbeats (when the heart muscle is resting between beats and refilling with blood).
    • lowest pressure pulse,
    • Closure of aortic valve,
    • recoil of aorta and artery pressure,
    • when heart is not pumpingž
  112. žPhysiology of Blood Pressure: Mean Arterial Pressure:
    the product of cardiac output (SV x HR) X Peripheral Vascular resistancež
  113. HTN is Most common risk factor for:
    • myocardial infarction 
    • —Stroke
    • ESRD and dialysis (along with *diabetes)
  114. Primary or Essential HTN:
    • Chronic elevation in BP that is not caused by another disease/disorder,
    • cause unknown; 
    • it tends to be familial and is likely to be the consequence of an interaction between environmental and genetic factors
  115. Secondary HTN:
    elevation in BP caused by another disorder such as kidney disease
  116. žMalignant HTN:
    • Can develop from HTN,
    • potentially fatal ,
    • sudden,
    • marked hypertension:
    • emergency
  117. HTN In Pregnancy:
    • Gestational HTN,
    • Pre-Eclampsia,
    • Eclampsia
  118. HTN Risk factors: Constitutional:
    • Family history,
    • race,
    • age changes,
    • insulin resistance
  119. HTN Risk factors: Lifestyle:
    •  * Smoking,
    • Sodium intake,
    • saturated fat intake,
    • Obesity & sedentary lifestyle,
    • Alcohol consumption,
    • electrolyte intake (low K+)
  120. Target organ damage form HTN:
    • —Heart:
    • —Brain:
    • Kidney:
    • Peripheral vascular disease (PVD) —
    • Eyes: Retinopathy
  121. Target organ damage form HTN:Heart:
    • Left ventricular hypertrophy LVH,
    • MI,
    • Angina,
    • heart failure,
    • coronary arteries—
  122. Target organ damage form HTN:Brain:
    • Stroke,
    • TIA (Transient Ischemic Attack, "mini-stroke") 
    • increased dementia,
    • narrowing &vessel sclerosis—
  123. Target organ damage form HTN:Kidney:
    • nephrosclerosis & Chronic renal disease,
    • Hypertensive kidney disease,
    • accelerates other forms, i.e. diabetic KD
  124. Range for Normal BP
    • Sys.< 120
    • Dia < 80
  125. Range for PreHTN
    • Sys: 120-139
    • Dia: 80-89
  126. BP range for Stage 1 HTN
    • sys.140-159
    • Dia: 90-99
  127. BP range for Stage 2 HTN
    • Sys. >or = 160
    • Dia > or = 100
  128. BP range for HTN Crisis
    • Sys. > 210
    • Dia > 120
  129. žStepped Treatment Approach:
     žNormal – 119/79 or less
    —No treatment needed
  130. žStepped Treatment Approach: Pre-hypertension – 120-139/ 80-89
    —Behavioral modificationsž
  131. žStepped Treatment Approach:
    Stage 1 hypertension – 140-159/ 90-99—
    Thiazide diuretic (for most patients)ž
  132. žStepped Treatment Approach:
    Stage 2 hypertension – > 160/ >100—2
    drug combinationž
  133. The Renin/Angiotensin/Aldosterone system
  134. Renal HTN :žA Secondary HTN
    • žLargest single secondary cause of HTN is renal diseasež
    • Acute kidney diseases cause retention of NA, H2O,decreased UOP
    •  Also chronic pyleonepritis, ESRD, diabeticnephropathy, others…
  135. Renal HTN :žA Secondary HTN: žMain problem:
    Renovascular HTN that results from decreases renal blood flow through artery ->this Increases activation of the Renin/AngioT/Aldost system=increasedPVR, NA & H2O retention,
  136. Renal HTN :žA Secondary HTN: Types:
    • atherosclerosis  (proximalrenal artery)
    • fibromuscular dysplasia (noninflammatory, affects renalarteries & branch vessels) ž
  137. žRenal Artery stenosis: Manifestations
    • Older than 50, previously normotensive (normal bp)-Athero
    • žYounger than 30 previously normotensive (fibromuscular)ž
    • Hypokalemia results from increased aldosterone levelsž
    • Abnormal bruit, lack of family Hx HTN
    • žHTN less than 1 year (distinguish from primary/essential)
    • ž
  138. žRenal Artery stenosis:Dx
    • Assess renal function & renin system (labs),
    • renal perfusion studies (bloodflow & for stenosis),
    • Renal Arteriography,
    • Duplex Ultrasonic scans,
    • CT with contrast,
    • MRAž
  139. žRenal Artery stenosis: Tx:
    • Goal stabilize Renal fxn.,
    • control BP,
    • Angioplasty or revascularization to restore blood flow, 
    • drugs (often ACE inhibitors with caution)
    • Lifestyle: Diet, exercise, regular follow up for BP checks & any lab testing
    • Pharmacological Therapies:
  140. Renal Artery stenosis: Tx:Pharmacological Therapies:
    • —Diuretics-1stline of drugs to treat HBP
    • Effective
    • Few side effects
    • Other medications
  141. Orthostatic (Postural) Hypotension
    • Abnormal dropin BP, with change to upright position pooling of blood in lower body
    • Decrease incerebral perfussion= dizzyness, faint, lightheaded, * Falls
  142. Orthostatic (Postural) Hypotension Causes:
    • Wide variety:
    • diseases that decrease vascular volume (dehydration),
    • impaired muscle pump (bedrest, SCI) of cardiovascular reflexes,(aging, medications, ANS disorders,
  143. Orthostatic (Postural) Hypotension Causes: Dx
    • Postural BP testing,
    • Pulse rate: increase 10 or less bpm = aging baroreceptors,
    • greater than 100bpm=Tachycardia sugestive of dehydration/volume depletion
  144. Orthostatic (Postural) Hypotension Causes:TX
    slow position changes & safety precautions, pharmacologic treatment   O
  145. žLipid Structure and Function:Major Lipids –
    • cholesterol, triglycerides—
    • -encapsulated by lipoproteins
  146. žLipid Structure and Function:
    Five major lipoproteins:
    • chylomicrons,
    • VLDL- Very-low-density lipoprotein,
    • IDL- Intermediate-density lipoproteins,
    • LDL- Low-density lipoprotein (bad), and
    • HDL—- High-density lipoprotein(good=happy)
  147. žLipid Structure and Function:
    _____ control interactions & metabolic fate of
    lipoproteins
    žApoproteins

    – lipid + proteins “apoproteins”
  148. Sžites of lipoprotein synthesis
    • —Small intestine: chylomicron synthesis 
    • —Liver: synthesis and release of VLDL and LDL; synthesis of HDL
  149. ____ primary transport pathway for triglycerides
    _____ primary carrier of cholesterol
    žVLDL;žLDL
  150. High-density lipoproteins :
    • (“goodcholesterol”)
    • made in the liverž ž
    • go out to the peripheral tissues and pick up lipidž - carry it back to the liver
  151. Hypercholesterolemia: žTypes
    • Primary – develops independent of other causes-genetic—
    • Secondary – associated with other health problems and behaviors-Obesity,DM ž
  152. Total Cholesterol Level: Less than 200 mg/dL
    Desirable level that puts you at lower risk for coronary heart disease. A cholesterol level of 200 mg/dL or higher raises your risk.
  153. Total Cholesterol Level:200 to 239 mg/dL
    Borderline high
  154. Total Cholesterol Level:240 mg/dL and above
    • High blood cholesterol.
    • A person with this level has more than twice the risk of coronary heart disease as someone whose cholesterol is below 200 mg/dL.
  155. HDL Cholesterol Level: 
    Less than 40 mg/dL (for men)
    Less than 50 mg/dL (for women)
    • Low HDL cholesterol.
    • A major risk factor for heart disease.
  156. HDL Cholesterol Level: 60 mg/dL and above
    • High HDL cholesterol.
    • An HDL of 60 mg/dL and above is considered protective against heart disease.
  157. LDL Cholesterol Level: Less than 100 mg/dL
    Optimal
  158. LDL Cholesterol Level: 100 to 129 mg/dL
    Near or above optimal
  159. LDL Cholesterol Level:130 to 159 mg/dL
    Borderline high
  160. LDL Cholesterol Level: 160 to 189 mg/dL
    High
  161. LDL Cholesterol Level:190 mg/dL and above
    Very high
  162. Arteriosclerosis:
    • hardening of the arteries ž 
    • the formation of fibro-fatty lesions in the intimal lining of medium to large arteries ž
  163. Arteriosclerosis: Causes
    • No confirmed cause:
    • Epidemiology has identified predisposing Risk Factors
  164. Arteriosclerosis: Risk factors (non-changeable)—
    • # 1 Hypercholesterolemia: Hyperlipidemia, *LDL & Inflammation—
    • —Increased age
    • —Family history CHD
    • —Male
    • —Genetic alterations in lipoprotein levels—
    • Postmenopausal women, decreased estrogen levels the to protect heartž
  165. MI 7th-8th decades of life are _____ men & women
    equal
  166. Atherosclerosis: Changeable Risk Factors:
    • —Smoking (CHD & Sudden death)
    • —Obesity
    • —HTN
    • —High blood cholesterol levels—
    • Diabetes
  167. Atherosclerotic Lesions:
    Types:
    • Fatty streak
    • —Fibrous atheromatous plaque
    • —Complicated lesion
  168. Atherosclerosis: CM
    • žInsidious onset, no CM for between 20-40 years
    • Fibrous plaquesž CM depend on vessels involved & extent of obstructionž
    • Narrowed arteries=
    • -ischemia,
    • -possible infarction,
    • -sudden obstruction,
    • -hemorrhage,
    • -rupture,
    • -thrombosis & emboli,
    • - endothelial damage,&
    • - aneruysym due to weakening of BV wall
    • žAny organ tissue, most common heart, brain, kidneys,lower extremities, & small intestine ž
  169. Atherosclerosis Dx:
    • Angiogram  ž
    • Coronary artery Ultrasoundž
    • Perfusion studiesž
    • Cholesterol levelsž
  170. Atherosclerosis TX
    • Eliminate or reduce as many changeable risk factors as possible ->education
    •  žPharmacologic to reduce cholesterol levels
    • žAntiplatelet therapy (Aspirin) ž
    • Surgeries: Coronary Artery stents, Bypass Graft, Thrombectomy/ Embolectomy, ž ž ž
  171. Atherosclerosis:žTeaching, Assessment & Evaluations
    • Patient and family education
    • Early preventative screening—
    • low-cholesterol and low-saturated-fat diet
    • —STOP smoking
    • Regular follow-up appointments/& cholesterol testing 
    • —LDL less than 100—
    • Teach S/S MI, cardiacor other tissue ischemia (pain, pallor, possible occlusion: decreased pulse & cool (extremity) paresthesias
    • Medication education—
    • Proper HTN Management & followup
  172. Vasculitis
    Group of disorders that cause inflammatory injury and necrosis of the blood vessel wall
  173. Vasculitis Can result from:
    • direct injury,
    • infectious agents,
    • immuneprocess, or
    • secondary to a disease such as SLE (lupus). cold (frostbite),
    • irradiation (sunburn)
    • mechanical injury,
    • toxins may cuse secondary vessel damage=necrosis
  174. Vasculitis žCM:
    • Fever,
    • myalgia,
    • arthralgia,
    • malaise,
    • Anti-Neutrophil
    • Cytoplasmic Antibodies (ANCA) are seen in small vessel disease which are auto-antibodies which are directed against proteins in the cytoplasm of neutophils
  175. Vasculitis žTypes:
    Small, Medium & Large vessel
  176. Vasculitis —Tx:
    High dose corticosteroids
  177. Hypercoagulability:
    hemostasis in an exaggeratedform; predisposes to thrombosis
  178. Hypercoagulability: Types
    • —Increased platelet function
    • —Increased clotting activityž
  179. Hypercoagulability: Clot characteristrics
    • —Arterial
    • —Venous
  180. Hypercoagulability: 
    Increased platelet function:
    General causes
    • Increased number of platelets & disturbances in blood flow—
    • Damage to vascular endothelium—
    • Increased platelet sensitivity to factors causing adhesion & aggregationž
  181. Hypercoagulability: increased platelet function: Disease states associated with —
    • Atherosclerosis—
    • DM
    • —Smoking—
    • HTN —
    • Thrombocytosis
    • —Increased lipid or cholestrol ž
  182. Hypercoagulability:ž
    Increased clotting activity: 
    General causes:
    • —Activation of coagulation system from primary (genetic) or secondary (acquired) disorders affecting coagulation components of blood
    • ž
  183. Hypercoagulability:
    increased clotting activity—: 
    Disease states associated with
    • Pregnancy/puerperium 
    • —Oral contraceptives—
    • Postoperative state
    • —Immobility—
    • CHF—
    • Malignancies— ž
  184. Acute Coronary Syndromes:
    Diagnostic changes :—
    ECG changes
    • T-wave inversion
    • ST-segment depression or elevation
    • Abnormal Q wave—
  185. Acute Coronary Syndromes:
    Serum cardiac markers
    • Proteins released from necrotic heart cells
    • Myoglobin,
    • creatine kinase,
    • troponin ž
  186. Chronic Ischemic Heart Disease
    • žImbalance in blood supply and the heart’s demands for oxygen
    • —Less blood
    • -Atherosclerosis
    • -Vasospasm
    • -Thrombosis —
    • Higher oxygen demand
    • -Stress
    • -Exercise
    • -Coldž
  187. ž3 Types of Angina
    • Stable angina—
    • Variant angina—
    • Silent myocardial ischemia—
  188. Stable angina—
    Pain when heart’s oxygen demand increasesž
  189. Variant angina
    —Pain when coronary arteries spasmž
  190. Silent myocardial ischemia—
    Myocardial ischemia without pain
  191. Pathophysiology of Angina
    • žžChest pain that resultsfrom ischemia is termed anginaž
    • When O2 requirements of the heart are greater than the supply of O2 it is getting, heart muscle becomes ischemic ( a restriction in blood supply to tissues)ž 
    • žOxygen imbalance may be from a reduced coronary blood flow or from a need for increased oxygen ž  ž
  192. The four major risk factors associated with coronary heart disease and angina are:— ž
    • cigarette smoking—
    • diabetes 
    • —elevated blood lipid levels
    • —hypertension
  193. Complications of A MI
    • žHeart failurež
    • Cardiogenic shockž
    • Pericarditis
    • žThrombo-emboli ž
    • Rupture of the heart
    • žVentricular aneurysms ž
  194. Pericarditis is
    an inflammation of the pericardium (the fibrous sac surrounding the heart)
  195. Malfunctioning Heart Muscle:
    Cardiomyopathy:
    Malfunctioning heart muscle can cause heart failure if:
    • —Ventricles are unusually thick so there is not a normal amount of room for blood inside them(hypertrophic cardiomyopathy)— 
    • —Ventricles are too stiff to stretch (restrictive cardiomyopathy)— 
    • —Ventricles are too weak to pump out the blood that is in them (MI, myocarditis, dilated cardiomyopathy)ž
  196. Nursing Diagnoses and Outcomes:
    Acute Pain, Chest, related to cardiac disease —Desired outcome:
    acute chest pain will be resolved with the use of drug therapy without injury to the heart occurring.—
  197. Nursing Diagnoses and Outcomes:
    Decreased Cardiac Output related to therapeutic effects of drug —Desired outcome:
    patient’s blood pressure will decrease to therapeutic levels but will not decrease to the level of hypotension.— ž
  198. Nursing Diagnoses and Outcomes:
    Riskfor Injury related to orthostatic hypotension and dizziness secondary to adverse effects of drug therapy —Desired outcome:
    patient will not sustain injury because of orthostatic hypotension and dizziness.ž ž
  199. ____ _____ are endogenous cardiac hormones which are ____ in Heart failure;
    Natriuretic peptides; elevated
  200. Pathophysiology of Heart Failure (HF) :
    Cardiac output ____ when the ___ ventricle is unable to eject its normal volume of blood during ____
    decreases; left; systole
  201. Pathophysiology of Heart Failure (HF):
    ____ ____ decreases space for blood filling, decreased contractility due to ____ ____
    decreased EF,
    increased ____ as a compensatory M., &
    afterload,
    decreased ____ ____,
    pump ____ and ____ ____
    • Enlarged muscle;
    • ventricle dilation;
    • preload;
    • stroke volume
    • weak & less effective
  202. Pathophysiology of Heart Failure (HF) The heart muscle ____ (____) to provide more contractile force to try to____ cardiac output
    • enlarges (cardiomyopathy)
    •  improve
  203. Pathophysiology of Heart Failure (HF) :
    *Electrical conduction impairment:
    atrial & ventricle arrhythmias (Atrial Fibrillation most common)
  204. Pathophysiology of Heart Failure (HF) :
    *Ejection Fraction:  ž ž
    Amount of blood pumped out of ventricles with each contraction, decreases significantly ž
  205. Pathophysiology of Heart Failure (HF) :ž*In HF, ____-sided failure occurs first, then ___-sided failure
    left; right
  206. NY Classification of Chronic HF:
    Class I
    Pt are asymptomatic; no limitation on activity
  207. NY Classification of Chronic HF:
    Class II
    • Pts are short of breath or fatigued by moderate activity- 2 flights of stairs
    • comfortable at rest or mild activity
    • slight limits on activity
  208. NY Classification of Chronic HF:
    Class III
    • its are short of breath or fatigued with very mild activity- 1/2 flight of stairs
    • comfortable only at rest
    • marked limitations of activity
  209. NY Classification of Chronic HF:
    Class IV
    • Pts are exhausted, sob, fatigued @ rest
    • any activity brings on discomfort and symptoms
    • severe limitations- only bed or chair
  210. žTreatment: HF
    • Drugs, No cure ž
    • Several cardiac drug classes are used to treat 
    • **Polypharmacy is considered the standard and most effective treatmentž
    • Drug therapy has been effective in increasing survival of individuals with CHF, but do not decrease overall mortality 
    • ž**Goal is to maintain clinical stability, improve symptoms, quality of life, and exercise tolerance in patients with all phases of CHF
    • žMay decrease fluid volume, stimulation of the autonomic nervous system &have direct action on both the cardiac muscle and the specialized electrical conduction system of the heartž
  211. HF: Clinical Manifestations (CM) Depend on:
    • —extent of the disease &
    • type of cardiac dysfunction, 
    • rapid or slow onset, 
    • right or left, 
    • systolic or diastolic
    • (overall r/t impaired pumping of heart:—
  212. HF: Clinical Manifestations:
    • May be relatively asymptomatic
    • Decrease renal blood flow & GFR, compensatory mechanisms,
    • NA + H2O retention (Renin/AngioT Aldost. Sys.) —S.O.B & other Resp
    • —Fatigue & limited exercise tolerance—
    • Fluid retention & edema—
    • Cachexia & malnutrition—
    • Cyanosis—
    • Diaphoresis—
    • Tachycardia—
    • Mental confusion—
    • Pulmonary Edema &
    • Pulmonary Hypertension,
    • & Bronchospasm
    • Dypsnea,
    • cyanosis,
    • Orthopnea,
    • paroxymal nocturnal dypsnea — ž
  213. HF: Systolic Failure/ Dysfunction
    • Impaired/decreased myocardial contractility
    • Decreases EF & CO
    • Compensatory M. able to maintain adequate cardiac fxn resting
    • EF less than 40% (norm:65%+)
    • žIncreased preload, ventricle dilation, Ventricle wall tension= can lead to accumulation of blood in atrial & venous system=Pulmonary or peripheral edema
    • From conditions that impair contractile fxn: ischemic HD,
    • cardiomyopathy,
    • & conditions of Volume or pressure overload
  214. Diastolic Failure/ Dysfunction
    • Normal EF
    • **Impaired diastolic ventricular relaxation=decreased filling=decreased preload, stroke volume & CO*exercise
    • Compensatory Mech. able to maintain adequate cardiac fxn resting
    • Ventricle pressures elevated=Pulmonary & venous congestion
    • žPrevalence increases with age, women, obesity, HTN, DM
    • Conditions that impede expansion of ventricle
    • (pericardial effusion, pericarditis), those that increase wall thickness & chamber size (Myoc. Hypertrophy), &delay diastolic relaxation (ischemic HD)
    • žBlood unable to move freely into L ventricle,
    • Increased pressure moves backward into L atrium, to pulmonary/venous system= decreased lung compliance, increased work breathe
  215. HF žDiagnosis
    • **Ejection fraction (40% or less)ž ž ž 
    • Risk factor assessmentž
    • Echocardiogram: measurement of heart & size &perfusion: Ejection fractionž
    • H & P (edema, wt,vitals, s/s)ž
    • Labs: multiple: BNP, anemia, liver congestion, electrolytes
    • žChest xray žEKGžCentral Venous Pressure monitoringž
    • CMRI, CT scans:
  216. HF: Nursing Intervention
    • žDepends on level of disease & settingž
    • Vitals Q4 hrs,
    • daily weights,
    • strict I & O
    • žSodium restrictions,
    • dietary educationž
    • Pharmacological educationž
    • Teach to keep BP, pulse & weight diaryž
    • Teach & Monitor for peripheral edema (increases)
    • žPrompt Appt. for weight gain, increased edema or any pulmonary s/s
    • žElevate legs if peripheral edema
    • žHF support information, American Heart Assoc.ž ž
  217. The ____, with hormones from the ____,
    regulates energy production
    liver;pancreas
  218. Insulin: Actions on glucose
    • —Increases glucose transport into skeletal muscle and adipose tissue—
    • Increases glycogen synthesis—
    • Decreases gluconeogenesis—
  219. Insulin:Actions on glucose fats & proteins
    • Anabolic in nature—
    • Promotes glucose uptake by target cells and provides for glucose storage as glycogen
    • —Prevents fat and glycogen breakdown—
    • Inhibits gluconeogenesis and increases protein synthesis — —
  220. Glucagon: Actions on glucose
    • Promotes glycogen breakdown—
    • Increases gluconeogenesis—
  221. Insulin is
    a peptide hormone, produced by beta cells in the pancreas, and is central to regulating carbohydrate and fatmetabolism in the body. It causes cells in the liver, skeletal muscles, and fat tissue to absorb glucose from the blood.
  222. Glucagon is
    a peptide hormone, produced by alpha cells of the pancreas, that raises blood glucose levels. Its effect is opposite that of insulin, which lowers blood glucose levels.[1] The pancreas releases glucagon when blood sugar (glucose) levels fall too low. Glucagon causes the liver to convert stored glycogen into glucose, which is released into the bloodstream.
  223. Glucagon: Actions on glucose, fats & proteins—
    • Catabolic in nature
    • —Increases transport of amino acids into hepatic cells—
    • Increases breakdown of proteins into amino acids for use in gluconeogenesis
    • —Increases conversion of amino acids into glucose precursors— — —
  224. Counter Regulatory Hormones 
    Catecholamines
    • Epinephrine and norepinephrine—
    • Help to maintain blood glucose levels during periods of stress
  225. Counter Regulatory Hormones
    ——Growth hormone—
    • Increases protein synthesis in all cells of the body,
    • mobilizes fatty acids from adipose tissue, and
    • antagonizes the effects of insulin
    • —
  226. Counter Regulatory Hormones
    Glucocorticoids
    • —Critical to survival during periods of fasting and starvation—
    • Stimulate gluconeogenesis by the liver—
  227. Tissue Types and Functions of the Pancreas:
    Acini
    —Secrete digestive juices into the duodenum
  228. Tissue Types and Functions of the Pancreas:
    —Islets of Langerhans
    • —Secrete hormones into the blood—
    • Composed of beta cells that secrete insulin, alpha cells that secrete glucagon, and delta cells that secrete somatostatin —
  229. Pre-diabetes:
    impaired fasting plasma glucose and impaired glucose tolerance
  230. Pre-diabetes:Fasting plasma glucose of
    110-125 impaired glucose tolerance test OGTT
  231. Diabetes Type 1:results from
    • Loss of beta cell function—
    • An absolute insulin deficiency
  232. Diabetes Type 2 results from:
    • —Impaired ability of the tissues to use insulin—
    • A relative lack of insulin or impaired release of insulin in relation to blood glucose levels—
  233. —Type 1 Diabetes Mellitus
    • —Lack of insulin production or
    • —Production of defective insulin—
    • Affected patients need exogenous insulin—
  234. —Type 1 Diabetes Mellitus Complications
    • —Diabetic ketoacidosis(DKA)—
    • Hyperosmolar non-ketotic syndrome—
  235. —Type 2 Diabetes Mellitus
    • —Most common type
    • —Caused by insulin deficiency and insulin resistance
    • —Many tissues are resistant to insulin—
    • Reduced number insulin receptors—
    • Insulin receptors less responsive— —
  236. —Type 2 Diabetes Mellitus :
    comorbid conditions
    • —Obesity
    • —Coronary artery disease
    • —Dyslipidemia
    • —Hypertension
    • —Microalbuminemia (protein in the urine)—
    • Enhanced conditions for embolic events (blood clots)— 
    • These comorbidities are collectively referred to as metabolic syndrome or insulin-resistance syndrome or syndrome X— —
  237. Treatment for DM: Type 1
    Insulin therapy
  238. Treatment for DM Type 2—
    • Lifestyle changes—
    • Oral drug therapy—
    • Insulin when the above no longer provide glycemic control—
  239. Clinical Manifestations of Diabetes
    • —Polyuria—
    • Polydipsia—
    • Polyphagia—
    • Glycosuria—
    • Unexplained weightloss—
    • Fatigue
    • —Hyperglycemia—
  240. —Other Symptoms of Hyperglycemia
    • —Recurrent blurred vision—
    • Paresthesias —
    • Skin infections—
  241. —Criteria for Diagnosis of DM
    —Hemoglobin A1C (Glycosylated hemoglobin)
    > 6.5%
  242. —Criteria for Diagnosis of DM:
    —Fasting Blood Glucose (FBG) —
    > 126 mg/dl
  243. —Criteria for Diagnosis of DM:
    2 hr plasma glucose
    > 200 mg/dl during OGTT
  244. —Criteria for Diagnosis of DM: Patient with
    classic  symptoms of hyperglycemia or hyperglycemic crisis w/ a random plasma glucose > 200 mg/dl
  245. DM: —Blood Tests  (4)
    • —Fasting blood glucose test 
    • —Casual or Random blood glucose test (not diagnostic in & of itself)—
    • Capillary blood tests and self-monitoring of capillary blood glucose levels —
    • Glycosylated hemoglobintesting – A1C (gold standard for diagnosis and DM management) —
  246. Acute Complications of Diabetes:
    • —Diabetic ketoacidosis
    • —Hyperglycemia
    • —Ketosis
    • —Metabolic acidosis—
    • Hyperosmolar hyperglycemic state—
    • Hypoglycemia— —
  247. Definitive Diagnosis of Diabetic Ketoacidosis
    • Hyperglycemia (bloodglucose levels >250 mg/dL)—
    • Metabolic acidosis— =
    • -Low bicarbonate (<15 mEq/L)
    • -—Low pH (<7.3)—
    • Ketosis: Ketonemia, &moderate Ketonuria (positive at 1:2 dilution) produces from the from break down of fats such as trigylcerides into glycerol and fatty acids
    • —Fluid/Electrolyte imbalance: intracellular to extracellular fluid shifts, possible Hypokalemia and Hyponatremia —
    • CNS depression, decreased sensorium—
    • CM: a day in advance may have: polydypsia, plyuria, n/v,marked fatigue, fruity breath, abdominal pain—
    • Can progress to stupor, coma —
  248. Characteristics of Hyperosmolar Hyperglycemic State (HHS)
    • —Hyperglycemia (blood glucose >600 mg/dL)—
    • Hyperosmolarity (plasma osmolarity >310 mOsm/L) pulls H20 out of cells, including brain
    • Dehydration,electrolyte imbalance (Hypokalemia)
    • The absence of ketoacidosis—
    • Depression of the sensorium(CNS s/s that can lead to coma)—
  249. Characteristics of Hyperosmolar Hyperglycemic State (HHS) CM:
    • polyuria,
    • weakness,
    • dehydration,
    • thirst,
    • many neurologic as progresses
  250. Major Long-Term Complications of DM
    (Both Types)
    • —Macrovascular (atherosclerotic plaque)—
    • Microvascular (capillary damage) (—Retinopathy— Neuropathy— Nephropathy—)
  251. Pathologic Changes With Diabetic Peripheral Neuropathies
    • —Thickening of the walls of the nutrient vessels that supply the nerve
    • —Leading to the assumption that vessel ischemia plays a major role in the development of neural changes—
    • Segmental demyelinization process that affects the Schwann cell—
    • Accompanied by a slowing of nerve conduction— —
  252. Classification of Diabetic Peripheral Neuropathies
    • Somatic
    • —Autonomic—
  253. Classification of Diabetic Peripheral Neuropathies —Autonomic
    • —Impaired vasomotor function
    • —Impaired gastrointestinal function—
    • Impaired genitourinary function—
    • Cranial nerve involvement
  254. Classification of Diabetic Peripheral Neuropathies: Somatic
    • —Polyneuropathy(bilateral sensory)—
    • Mononeuropathy —
    • Amyotrophy
  255. Metabolic Syndrome Characteristics
    • —High plasma triglycerides —
    • Low HDL 
    • —Hypertension—
    • Systemic inflammation (CRP) —
    • Abnormal fibrinolysis —
    • Abnormal function of the vascular endothelium—
    • Macrovascular disease —
  256. —Contributing Factors to Metabolic Syndrome + Diabetes Mellitus
    • —Obesity and insulin resistance—
    • Increased resistance to the action of insulin
    • Impaired suppression of glucose production by the liver
    • —Hyperglycemia and hyperinsulinemia — —
  257. Hypoglycemia
    • —Abnormally low blood glucose level-usually due to excess insulin in blood,
    • but can result from oral hypoglycemic agents (also called insulin reaction)— —
    • Mild cases can be treated with diet—higher intake of protein and lower intake of carbs—to prevent a rebound postprandial hypoglycemia — —
  258. Hypoglycemia: blood glucose level
    below 50 mg/dL
  259. Hypoglycemia Precipitating factors: Type 1
    • —Error in insulin dose—
    • Failure to eat, particularly if took insulin
    • —Increased exercise—
    • Decreased insulin need after removal of stress situation—
    • Insulin changes
    • —Change in injection site—
    • Alcohol consumption decreases gluconeogenesis, caution ingestion in large quantities or on empty stomach— —
  260. Hypoglycemia Symptoms 2 Types:
    • *Altered Cerebral function &
    • Activation of the ANS (PNS)
  261. Hypoglycemia Symptoms Early—
    • *Headache,
    • *Confusion,
    • *difficulty thinking & problem solving,
    • PNS first: hunger, then
    • SNS: irritability,
    • tremor,
    • sweating,
    • tachycardia,
    • diaphoresis,
    • constriction of vessels in skin=cool & clammy —
  262. Hypoglycemia Symptoms Later—
    • Hypothermia,
    • *seizures, 
    • —*Coma and death will occur if not treated
    • S/S variable among different individuals, (age, disease level, other medications that affect ANS
    • Always check a Blood Sugar Level prior to giving any medication to alter blood sugar level (raise or lower) —
  263. Glucose-Elevating Drugs
    • —Oral forms of concentrated glucose
    • -—Buccal tablets, semisolid gel
    • —I.V. 50% dextrose in water (D50W)—
    • Glucagon (glycogenolysis, glycogen stores have to be available: approx. 75 grams if glycogen stored)
    • —Oral Diazoxide (Proglycem) —
  264. Nursing Implications:
    —Overall concerns for any diabetic patient increase when the patient:
    • —Is under stress—
    • Has an infection
    • —Has an illness or trauma
    • Is pregnant or lactating—
  265. Nursing Implications:
    Thorough patient education is essential regarding:—
    • Disease process
    • —Diet and exercise recommendations—
    • Self-administration of insulin or oral drugs
    • —Potential complications— —
  266. Nursing Implications:Assess for signs of hypoglycemia- If hypoglycemia occurs:
    • —Give glucagonor
    • —Have the patient eat glucose tablets or gel, corn syrup, honey, fruit juice, or non-diet soft drink
    • Then Have the patient eat a small snack such as crackers or half a sandwich (protein)
    • Monitor blood glucose levels frequently until stable
  267. Nursing Implications:—Monitor for therapeutic response of pharmacologic therapy & Lifestyle changes
    • —Decrease in blood glucose levels to the level prescribedby physician—
    • Measure hemoglobin A1c to monitor long-term compliance to diet and drug therapy—
    • Watch for hypoglycemia and hyperglycemia—
  268. —Categories of Endocrine Disorders:
    • —Primary disorders —
    • Secondary disorders—
    • —Tertiary disorders —
  269. —Categories of Endocrine Disorders:
    —Primary disorders —
    Originate in the target gland responsible for producing the hormone—
  270. —Categories of Endocrine Disorders:
    Secondary disorders—
    The target gland is essentially normal,but its function is altered by defective levels of stimulating hormones or releasing factors from the pituitary system.—
  271. —Categories of Endocrine Disorders:
    Tertiary disorders
    • —Result from hypothalamic dysfunction 
    • —Both the pituitary and target organ are understimulated — —
  272. —Manifestations of Hypopituitarism
    • —(Usually occur gradually—
    • Can present as an acute and life-threatening condition—)
    • —Being chronically unfit—
    • Weakness and fatigue
    • —Loss ofappetite—
    • Impairment of sexual function
    • —Cold intolerance—
  273. Secondary  Adrenal Insufficiency resulting from Hypopituitarism leads to
    decreased ACTH is the most serious, including nausea,weakness, anorexia, fever and orthostatic hypotension (usually the last to manifest). —
  274. Measurement of Hypothalamic-Pituitary-Target Cell Hormones
    • —Serum cortisol—
    • Serum prolactin—
    • Serum thyroxine and TSH—
    • Serum testosterone (male)/serum estrogen (female) and
    • serum LH/FSH—
    • Serum GH/insulin-like growth factor-1—
    • Plasma osmolality and urine osmolality—
    • MRI of Hypothalamus—
    • Hormone stimulation/or suppression tests (ACTH) —
  275. Hormones Essential for Normal Body Growth and Maturation
    • —Growth hormone (GH) or Somatotrophin from anterior pituitary somatotropes, 191 amino acid peptide —
    • Insulin beta cells pancreas, carbohydrate metabolism —
    • Thyroid hormone, metabolic rate, serum calcium 
    • —Androgens, sex hormones —
  276. Growth Hormone
    • —Produced by somatotropes in the anterior pituitary—
    • Necessary for linear bone growth in children
    • —Stimulates cells to increase in size and divide more rapidly—
    • Enhances amino acid transport across cell membranes—
    • Increases the rate at which cells use fatty acids
    • —Decreases the rate at which cells use carbohydrates—
  277. —Effects of Growth Hormone Excess in Adults
    • —Over growth of the cartilaginous parts of the skeleton—
    • Enlargement of the heart and other organs of the body—
    • Metabolic disturbances resulting in altered fat metabolism and impaired glucose tolerance
    • —When occurs in adults after epiphyses of long bones fuse/close  —
  278. Thyroid Gland-Secretes three hormones essential for proper regulation of metabolism
    • —Thyroxine (T4)
    • —Triiodothyronine (T3)—
    • Calcitonin (lowers/helps remove calcium levels in ECF)—
  279. —Major Functions of Thyroid Hormone
    • —Thyroid Follicular cells: Increase metabolism and protein synthesis throughout body—
    • Thyroid C cells lower calcium & phosphate through hormone calcitonin 
    • —Influences growth and development in children
    • —Mental development and attainment of sexual maturity —
  280. Hypothyroidism:  
    Deficiency in Thyroid Hormones
    *Primary:
    abnormality in the thyroid gland itself
  281. Hypothyroidism:  
    Deficiency in Thyroid Hormones:
    —*Secondary:
    results when the pituitary gland is dysfunctional and does not secrete TSH—
  282. Hypothyroidism:  
    Deficiency in Thyroid Hormones:
    *Tertiary:
    results when the hypothalamus gland does not secrete TRH, which stimulates the release of TSH—
  283. *Cretinism
    • —Hyposecretion of thyroid hormone during youth
    • —low metabolic rate,
    • retarded growth and sexual development,
    • possible mental retardation
  284. —*Myxedema
    • —Hyposecretion of thyroid hormone during adulthood
    • Decreased metabolic rate,
    • loss of mental and physical stamina,
    • weight gain,
    • loss of hair,
    • firm edema,
    • yellow dullness of the skin
  285. —Manifestations of Hypothyroidism
    • —Low circulating thyroid hormone—
    • Mental and physical sluggishness
    • —Myxedema —
    • Somnolence, Lethargy —
    • Decreased cardiac output, bradycardia
    • —Constipation—
    • Decreased appetite (Anorexia)
    • Hypoventilation—
    • Cold intolerance—
    • Coarse, dry skin and hair, thick skin —
    • Weight gain—
  286. Myxedematous coma: Emergency: Tx:
    • Correct hypothermia,
    • cardio-resp failure,
    • correct Fluid & Electrolyte/metabolic
    • Imbalances: hyponatremia, hypoglycemia,lactic acidosis (CO2 retention & hypoxia) —
  287. Manifestations of Hyperthyroidism
    • —High circulating thyroid hormone—
    • Graves disease—
    • Thyroid storm 
    • —Restlessness,
    • irritability,
    • anxiety,
    • nervousness —
    • Wakefulness—
    • Increased cardiac output—
    • Tachycardia and palpitations
    • —Diarrhea, increased appetite—
    • Dyspnea
    • —Heat intolerance,i
    • ncreased sweating—
    • Flushing—
    • Muscle weakness—
    • Difficulty sleeping,results in fatigue —
    • Thin and silky skin and hair
    • —Weight loss—
    • Altered menstrualcycle —
  288. —Measures Used to Diagnose Thyroid Disorders—:
    • Measures of T3, T4, and TSH—
    • Resin uptake test 
    • —Assessment of thyroid auto antibodies
    • Radio iodine(123I) uptake test 
    • —Thyroid scans (i.e., 123I, 99mTc-pertechnetate)
    • Ultrasonography—
    • CT and MRI scans 
    • —Fine-needle aspiration (FNA) biopsy of a thyroid nodule —
  289. Hyperthyroidism:  
    Excessive Thyroid Hormones —Caused by several diseases
    • —Graves’ disease—
    • Plummer’s disease (toxic nodular disease)
    • —Multinodular disease
    • —Thyroid storm (induced by stress or infection, exacerbation or emergency state of hyperthyroidism)— —
  290. Graves Disease
    —State of hyperthyroidism, goiter and ophthalmopathy
  291. Addison’s Disease
    • —Primary Adrenal Insufficiency: destruction of Adrenal Cortex—
    • Deficient Adrenal Cortical Hormones, & ACTH
    • Lack of feedback inhibition—
    • Chronic metabolic disorder like DM type 1, lifetime hormone replacement, may not become apparent until 90% of gland is affected—
  292. Addison’s Disease Causes:
    • #1 cause Auto-Immune disorder,
    • also caused by TB,
    • rare:
    • metastatic carcinoma,
    • fungal infection,
    • cytomegalovirus…others, adrenal hemorrage —
  293. —Glucocorticoid Hormone Excess: Cushing syndrome (hypercortisolism)
    • —ACTH or other glucocorticoids 
    • -—Pituitary form results from excessive production of ACTH by a tumor of the pituitary gland —
    • -Adrenal form caused by a benign or malignant adrenal tumor 
    • - —Ectopicform, non-pituitary ACTH-secreting tumor— —
  294. —Glucocorticoid Hormone Excess: Cushing syndrome (hypercortisolism)
    CM:
    • —Altered fat metabolism
    •  —Muscle weakness—
    • Muscle wasting—
    • Purple striae 
    • —Osteoporosis —
    • Derangements in glucose metabolism —Hypokalemia —Gastric acid secretion
    • —Hirsutism, mild acne, and menstrual irregularities
    • —Increased facial & Body hair—
    • Hypertension from sodium retention—
  295. Cushing's Syndrome (Hormone Excess) —Original DX:
    was from a tumor of pituitary gland with excessive production of ACTH only
  296. —Without treatment Cushing's syndrome can lead to:
    death—
  297. Cushing's syndrome DX
    • cortisol hypersecretion: 24 hr urine,
    • loss of diurnal pattern of cortisol secretion (elevated inappropriatelylate at night),
    • plasma ACTH,
    • Cortisol suppression or stimulation tests,
    • MRI,
    • CT scans—
  298. Cushing’s Syndrome TX:
    • Correct or remove the cause of hypercortisolism without permanent damage to adrenal or pituitary gland.
    • Surgery,
    • irradiation,
    • pharmacotherapy (type and amount depends on cause of hypercortisolism)
    • —Transsphenoidal removal of pituitary adenoma, hemi-hypophysectomy, cortisol replacement therapy—
    • Unilateral or Bilateral Adrenalectomy, ectopic ACTH tumors removed when possible, Drugs:block steroid synthesis  — —

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