Final Comp InterMS SG

WK 1 - Burns, Pressure Injuries, Medications

1st Line of Defense

• Breach in skin triggers 2nd line (inflammatory response).

• If overwhelmed, triggers 3rd line (adaptive immunity).

Temperature Regulation

• Through blood flow and sweat gland activity; damage can lead to temperature instability.

Maintains Fluid and Electrolyte Balances

• Damaged tissue can cause major fluid shifts and electrolyte loss.

Associated Aging Changes

• Thinning epidermal/dermal layer.

• Decreased melanocytes: susceptible to sun.

• Flattening dermal-epidermal junction: slow skin repair.

• Loss of subcutaneous fat: increased risk of pressure injuries.

• Skin is thinner, drier, slower to heal, more vulnerable to injury, infection, and temperature extremes.

• Nursing Actions: gentle handling, hydration, sun protection, pressure relief.

Pressure Injury

• aka pressure ulcer, bedsore, decubitus ulcer.

• Caused by tissue compression between bony prominence and external surface.

• Common sites: sacrum, heels, hips, medical devices (e.g., NC, NG/ET tubes, compression stockings).

• Risk Factors: immobility, undernutrition, aging skin, excess moisture (incontinence), cognitive impairment, vascular disease, DM.

• Complications: slow healing, sepsis, kidney failure, osteomyelitis.

• Be considerate and cautious about where medical devices are placed and know how to prevent wounds.

Friction and Shear

• Friction: when skin is dragged across a surface.

• Shear: deeper tissues shift under stationary skin, disrupts circulation.

Assessment and Intervention

• Pressure Injuries are preventable if risks are recognized and interventions applied before tissue integrity is compromised.

• Implement 'Skin care bundle': frequent skin checks, nurse education and documentation, moisture management, correct surfaces, turning schedule, nutritional support.

• Common tool: Braden Scale.

Pressure Injury Stages

• Stage 1: Intact skin, nonblanchable erythema.

• Stage 2: Partial thickness, shallow open ulcer with red/pink wound bed. May present as intact/ruptured blister.

• Stage 3: Full thickness. Subcutaneous tissue seen, but bone/muscle/tendon is not exposed.

• Stage 4: Full thickness with bone/tendon/muscle exposed.

• Suspected Deep Tissue Injury (SDTI): localized purple/maroon intact skin or blood-filled blister due to underlying soft tissue damage from friction or shear. Mushy or boggy than surrounding tissue.

• Unstageable: Wound bed covered by enough slough/eschar that the stage cannot be determined.

Non-Surgical Management

• Step 1: Clean wound of debris and exudate (Normal Saline, wound cleaners).

• Step 2: Debride to remove necrotic tissue if necessary.

• Step 3: Apply appropriate dressing to support wound healing.

How to Detect Melanoma (ABCDE)

• Asymmetry

• Border (irregular)

• Color (uneven)

• Diameter ($>6$ mm - but can be smaller)

• Evolution (changed over time)

Burns Initial Management (ABCDE)

• Airway: patency and signs of inhalation injury (e.g., intubation needed, C-spine precautions until clear in smokers).

• Breathing: breathing, lung sounds, $O_2$ sat. Possible CO poisoning.

• Circulation: assess BP, HR, vascular perfusion, pulses, cap refill. Start fluid resuscitation.

• Disability: check neuro deficit and gross deformity (smoke inhalation, burns don't typically change mentation).

• Exposure: examine major injuries and maintain warm environment. Remove anything in contact with patient. NEVER use ice or cold water (restricts circulation).

Fluid Resuscitation

• Body fluid is present but not in the right place, causing low blood volume in vessels $<br>ightarrow$ low BP $<br>ightarrow$ shock.

• Lactated Ringer's is fluid of choice.

• Parkland Formula.

Phases of Burn Injury

• Emergent (Resuscitation)

  • From time of injury until restoration of capillary permeability ($48-72$ hrs).

  • Fluid shifts from interstitial spaces back into intravascular space.

  • Focus: Preventing hypovolemic shock.

• Acute (Healing)

  • Begins once capillary permeability is restored.

  • Focus: Infection control, wound care, pain management.

  • Continues until wound closure.

• Rehabilitative (Restoration)

  • Overlaps healing phase and continues after acute care setting.

  • Focus: Optimization of functional ability.

Degree of Burns

• First Degree Burn: superficial, painful, red, epidermis peels, heals $hicksim1$ week.

• Second Degree Burn:

  • Superficial: dermis, re-epithelialization, partial thickness, blister, $hicksim2$ weeks heal.

  • Deep: dermis, deeper, requires all 3 phases; partial thickness; blister rare and not painful; moderate edema; $hicksim2-5$ weeks healing.

• Third Degree Burn: all layers destroyed into fat, full thickness, no pain, severe edema, all phases of healing required. Needs grafting, weeks to months for healing.

• Fourth Degree Burn: all layers of skin destroyed into muscle, tendon, bone. Full thickness, black color, severe edema, no blister and no pain (no nerve endings), usually lethal, associated with complete loss of function.

Burn Anatomical Changes

• Vascular

  • Burn shock/hypovolemic shock = capillary leak syndrome.

  • Inflammatory response causes capillaries to leak fluid, albumin, and electrolytes into interstitial space (third spacing).

  • ADH and aldosterone are released to combat loss, but leaky capillaries lead to hyponatremia.

  • K+ released from injured cells into intravascular space $<br>ightarrow$ hyperkalemia.

  • Hemoconcentration from vascular dehydration $<br>ightarrow$ increased hematocrit, increased blood viscosity $<br>ightarrow$ decreased blood flow to organs, increased risk for blood clots.

• Cardiac

  • Fluid third spacing $<br>ightarrow$ BP decreases, HR increases (compensatory), Cardiac Output (CO) decreases ($CO = HR imes SV$).

  • Decreased preload (less blood for heart to pump).

  • Increased afterload (vasoconstriction makes it harder for heart to push blood).

  • Hyperkalemia Treatment: Insulin, calcium, dextrose (K cocktail) to pull potassium into cells. Monitor for arrhythmias.

• Respiratory

  • Respiratory failure from smoke/irritants causing airway swelling and decreased gas exchange.

  • Fluid leaks into lungs, building up in alveoli, making $O_2$ transfer difficult.

  • Carbon monoxide binds to hemoglobin better than $O_2$, impairing oxygen transport.

  • TOP PRIORITY IS CONTINUOUS AIRWAY ASSESSMENT: Assess breath sounds, sudden cessation of wheezing = EMERGENCY (obstruction).

• Gastrointestinal

  • Decreased CO $<br>ightarrow$ decreased blood flow to GI tract; SNS reduces blood flow.

  • Curling Ulcer: acute stress-induced gastroduodenal ulcer due to impaired GI blood flow.

    • PPIs (omeprazole): inhibit proton pumps, reduce stomach acid.

    • H2 blockers (famotidine): block H2 receptors, decrease acid secretion.

    • Early enteral feeding.

• Metabolic

  • Body enters hypermetabolic state, increasing need for $O_2$ and calories (double/triple normal). Occurs in two phases:

    • Ebb (first 48 hours): hypometabolism. Body in shock, prioritizing circulatory stability and organ perfusion. Focus: resuscitation.

    • Flow (after capillary permeability reestablished): hypermetabolism. Body shifts to healing. Managed with aggressive metabolic support (labs, enteral nutrition).

• Immunologic: Burn disrupts/destroys protective tissue, increasing infection risk. Activates inflammatory response and suppresses immune functions.

WK 2 - Anemia, SCD, Transfusion Therapy, Medications

Sickle Cell Disease (SCD)

• Genetic blood disorder, hemoglobin mutation on beta chain $<br>ightarrow$ sickle shapes.

• Autosomal recessive inheritance (one copy from each parent). Occurs in people of all races/ethnicities, especially 1 in 365 Black/AA.

• RBC lifespan is $hicksim10-20$ days.

• Sickle cells become rigid, clump, block blood flow $<br>ightarrow$ poor perfusion, hypoxia, furthering sickling.

Vasoocclusive Event (VOE) (Sickle Cell Crisis)

• Triggers are anything impacting oxygenation.

• Number one triggers: hypoxia and dehydration.

• Other triggers: smoking, stress, weather changes, high altitudes, blood loss, strenuous exercise.

• Repeated VOE can lead to permanent hemoglobin changes.

• Reduces person's function and lifespan.

Physical Assessment for SCD

• Neurologic: signs of stroke (weakness/drooping, facial drooping, unequal strength, impaired gait, trouble speaking, confusion).

• Cardiovascular: weak, slow capillary refill (check pulses, especially pedal).

• Respiratory: Signs of acute chest syndrome (pulmonary infiltrates, febrile, chest pain, related to SCD – a cause of death).

• Gastrointestinal: Splenomegaly/hepatomegaly (overworking with RBCs).

• Genitourinary: reduced flow to kidney, priapism (sustained penile erection due to VOE).

• Musculoskeletal: joint swelling (site of clumping, necrotic degeneration; assess for swelling, temp, color, ROM).

• Skin: pallor, ashy, jaundice.

• Psychosocial: anxiety, pain, depression.

• Many issues due to poor perfusion.

• First management priorities: OXYGEN, PAIN, and HYDRATION.

Lab Assessment: SCD

• HPLC (High Performance Liquid Chromatography): preferred diagnosis method.

• Sickle cells screen (Sickledex): % of hemoglobin S (HbS) (carrier $hicksim35-45$, disease $>90$).

• Hgb: $hicksim5-9$.

• Hct: $hicksim17-29$.

• Elevated reticulocytes (anemia of long duration), elevated bilirubin (damaged RBCs release iron and bilirubin, leading to jaundice), elevated WBC (chronic inflammation due to hypoxia/ischemia, higher infection risk).

Prioritize Hypotheses

• Pain due to poor tissue perfusion and joint destruction with low oxygen levels.

  • Managing pain: Opioids (acute), hydroxyurea (long-term, produces fetal hemoglobin), L-Glutamine (lengthens RBC life), crizanlizumab (prevents sickling/clumping). Hydration. Integrative therapies.

• Potential for infection, sepsis, multiple organ dysfunction syndrome (MODS), and death.

  • Prevention and early detection: Hydration, Oxygen, Transfusion (apheresis to remove sickles while giving normal cells).

Care for Patients in Sickle Cell Crisis

• Remove constrictive clothing (promote blood flow).

• Extend extremities (promote venous return).

• Don't raise knee position of bed; elevate bed no more than 30 degrees.

• Administer $O_2$ and pain meds.

• Infuse NS IV.

• Be prepared to administer transfusion therapy.

• Keep room temperature comfortable.

• Check circulation in extremities hourly: pulse ox, peripheral pulses, cap refill.

Prevention of Sickle Cell Crisis

• Drink $hicksim3-4$ L liquids daily.

• Practice deep breathing.

• Stay warm in cold weather.

• Avoid alcohol and illicit drugs.

• Avoid smoking, nicotine, tobacco.

• Avoid strenuous exercise.

• Avoid hot/cold extremes, overheating, overexposure to sun.

• Avoid unpressurized airplane cabins and high altitudes.

• Mild, low-impact exercise 3x/week when not in crisis.

• Regular PCP visits.

• Yearly flu/COVID vaccines, ask about pneumonia vaccine.

• Contact PCP for signs of illness/infection.

• Notify all HCPs about SCD, especially anesthesia.

Anemia

• Reduction in RBCs, hgb, or hct. Clinical indicator, not a disease.

• Primary labs: M-Hb $<14$ g/dL, F-Hb $<12$ g/dL.

• Each type has distinct signs/treatment, but common s/s: pallor, fatigue.

• Causes: Decreased RBC production (iron, B12, folic acid deficiencies, aplastic), blood loss (acute/chronic), increased RBC destruction (G6PD deficiency, autoimmune).

Iron Deficiency Anemia

• S/S: fatigue, pallor, SOB.

• Tx: oral ferrous sulfate, parenteral iron (venofer, iron dextran, ferumoxytol).

• Nursing: assess for bleeding, fatigue's impact on ADLs.

• Patient Edu: PO on empty stomach (1 hr before/2 hrs after meals) for best absorption. Avoid dairy, antacids, coffee, tea (limits absorption). Best absorbed with Vit C. IV can cause anaphylaxis (BLACK BOX), monitor 30-60 min post dose (most common issues in first 15 min). SE: GI upset, black/dark stools.

Vitamin B12 Deficiency (Cobalamin)

• S/S: fatigue, pallor, SOB, anorexia, glossitis. Neurological symptoms (numbness/tingling in extremities, lack of coordination).

• Tx: oral/sublingual B12. IM injections for pernicious anemia.

• Nursing: safety regarding neurological symptoms.

• Patient Edu: dietary modifications (vegans need nutritional yeast/fortified grains). Pernicious anemia (lack of intrinsic factor for B12 absorption) requires lifelong tx adherence.

Folate Deficiency Anemia

• S/S: fatigue, pallor, SOB, anorexia, glossitis.

• Tx: folic acid oral or parenteral (based on severity).

• Nursing: rule out Vit B12 deficiency, assess alcohol use. If alcoholism-related, need B1 (thiamine) too.

• Patient Edu: oral/parenteral based on severity, can be with or without food.

Aplastic Anemia

• RBC deficiency due to impaired cell regulation of bone marrow, failing to produce cells.

• Can be caused by infections, radiation, toxic chemical/drug exposure.

• S/S: often pancytopenia (reduced RBC, WBC, platelets): fatigue, pallor, SOB, frequent infections, bruising.

• Tx: ID and remove underlying cause. Blood transfusion (RBC, platelets). Immunosuppressive therapy (if autoimmune). Bone marrow stimulants (filgrastim-neupogen for WBCs/neutrophils). Stem cell transplant.

• Nursing: bleeding precautions, possible neutropenic precautions.

• Patient Edu: recognize bleeding/infection signs, when to seek help.

Anemia of Chronic Disease/Inflammation

• S/S: usually overlapped by chronic condition; fatigue, pallor, SOB.

• Tx: Erythropoiesis stimulating agents (epoetin alfa, darbepoetin alfa).

• Nursing: monitor hgb regularly for response to ESAs.

• Patient Edu: manage chronic disease to control anemia.

G6PD Deficiency

• Genetic disorder (mainly men), deficiency of G6PD.

• S/S: appear only during/after hemolytic episode: sudden fatigue, weakness, jaundice, dark tea-colored urine, splenomegaly.

• Tx: remove or avoid trigger. Blood transfusion, hydration, possible oxygen.

• Nursing: encourage hydration, monitor urine output.

• Patient Edu: be aware of triggers (Fava beans), hereditary.

Leukemia

• Cancer affecting blood due to loss of cellular regulation $<br>ightarrow$ uncontrolled production of immature WBCs.

• Classified by: speed of progression (Acute/Chronic) and cell type (lymphoblastic/myeloid).

  • Acute: rapid progression (ALL, AML).

  • Chronic: asymptomatic for years (CLL, CML).

• Risk Factors: exact cause unknown; genetic/environmental; ionizing radiation (chemo), chemical/drug exposure.

• S/S: fatigue, unexplained weight loss, frequent infections, prone to bruising/bleeding.

• Labs: decreased hgb, hct. WBC low, normal, or high (due to blast cells).

• Diagnosis: Bone marrow biopsy is definitive test. Increased blast cells. Determines type/severity.

• Tx: Chemotherapy (main). Bone marrow/stem cell transplant. Targeted therapy (tyrosine kinase inhibitors for CML). Immunotherapy. Radiation.

• May require neutropenic precautions (immunocompromised by useless immature cells).

• Without intervention, can cause death from infection or hemorrhage.

• Nursing Interventions: Protection against infection (main focus).

  • Neutropenic precautions: strict hand hygiene, private room, limit visitors, avoid fresh flowers/plants, avoid undercooked/unpasteurized foods; limit invasive procedures. Frequent vitals (fever is first infection sign).

• Risk for bleeding (reduced clotting).

WK 3 - Osteoporosis, Rheumatoid Arthritis, Osteoarthritis, Osteomyelitis, Medications

Lab Assessment

• Serum Calcium: $9-10.5$ mg/dL. Hypercalcemia: metastatic bone cancers, Paget disease, healing fractures. Hypocalcemia: osteoporosis, osteomalacia.

• Serum Phosphorus: $3-4.5$ mg/dL. Hyperphosphatemia: bone fractures, bone tumors. Hypophosphatemia: osteomalacia.

• Alkaline Phosphatase (ALP): $30-120$ units/L. Elevations: metastatic bone/liver cancer, Paget disease, osteomalacia.

• Serum Muscle Enzymes CK-MM: $55-170$ units/L (men), $30-135$ units/L (women). Elevations: muscle trauma, muscle dystrophy, effects of electromyography.

• Calcium and phosphorus stored in bone. In fractures, these are main labs.

Osteoporosis

• Silent disease (diagnosed upon first fracture).

• Chronic disease of cellular regulation where bone loss causes significant decreased density, increasing fracture risk.

• Bone Mineral Density (BMD): reflects bone strength, assesses fracture risk, diagnoses osteopenia/osteoporosis.

• BMD T-score:

  • $-1.0$ or greater: Normal Bone Density.

  • $-1.0$ to $-2.5$: Osteopenia (low bone mass, precursor to osteoporosis).

  • $\le -2.5$: Osteoporosis.

  • Lower score = less bone density.

• Excess carbonation and lack of Vit D can contribute.

• Health promotion strategies are crucial in osteopenia.

Risk Factors for Primary Osteoporosis

• Non-modifiable: Older age ($>50$), menopause/oopherectomy (low estrogen), family history, white/Asian ethnicity, history of fracture after 50.

• Modifiable: Low body weight (LBW) and thin build, chronic low calcium/Vit D, androgen/estrogen deficit, current smoking (disrupts absorption), high alcohol intake ($2+$/day), chronic steroid therapy (inhibits bone reabsorption), poor nutrition, lack of exercise/prolonged decreased mobility (promote mobility and strength training to help osteoblast activity).

Health Promotion

• Teach healthy lifestyle practices.

• Nutrition: Calcium and Vit D intake (e.g., dairy, fortified grains). Osteomalacia = softening of bone due to vitamin/mineral lack.

• Avoid alcohol and stop smoking (affect nutrient absorption, reduce blood flow, interfere with osteoblast activity).

• Limit carbonated beverages (high phosphorus levels disrupt nutrient processing, osteoblast-osteoclast balance).

• Exercise and weight-bearing exercises.

Diagnostics for Osteoporosis/Osteopenia

• Lab Assessment: Serum calcium and Vit $D_3$ yearly.

• Imaging: X-ray of spine and long bones (helpful for very bad density/current fracture) AND DXA scan (Bone Mineral Density test - follow-up recommended).

Pharmacologic Management

• Recommended for postmenopausal women and men $>50$ when: $<-2.5$ with no risk factors OR $<-1.5$ with risk factors/previous fracture.

• Inhibits Osteoclast Activity (Reduces Bone Resorption/Breakdown):

  • Bisphosphonates: e.g., alendronate/Fosamax (most common).

    • Nursing Considerations: full glass of water, empty stomach, stay upright for at least 30 min (prevent GI effects). Maintain good oral health (prevent osteonecrosis of jaw).

  • RANKL Inhibitors: e.g., denosumab/Prolia.

• Stimulates Osteoblast Activity (Builds Bone):

  • Estrogen Agonist/Antagonists (SERM): e.g., Tamoxifen, Raloxifene/Evista (estrogen is good for bones).

  • Parathyroid Hormone Analogs: e.g., Teriparatide/Forteo (not long-term, promotes osteoblast activity).

  • Sclerostin Inhibitor: Romosozamab/Evenity.

• Bisphosphonates and RANKLs reduce bone breakdown; SERMs, Parathyroid Hormone Analogs, and Sclerostin Inhibitors build bone.

• RANKL and Sclerostin inhibitors are often for autoimmune conditions, targeting proteins in bone remodeling.

Osteoarthritis (OA)

• Most common form of arthritis. Progressive deterioration and loss of articular cartilage and bone in one or more joints.

• Mainly in weight-bearing joints.

• Primary OA: Aging, genetic factors.

• Secondary OA: joint injury, obesity, repetitive stress to joints.

• Bone spurs form, causing inflammation and pain.

• S/S: Joint pain and stiffness (worse with activity), crepitus ('Rice Krispies'), decreased ROM, joint effusions, Heberden's and Bouchard's nodes (enlarged metatarsals of hands).

• Diagnosis: Joint changes on X-ray.

• Treatments: Tylenol or NSAIDs (Celecoxib preferred - first line). Steroid injections for inflammation.

• Non-pharm Tx: RICE, capsaicin, glucosamine.

• Surgical: THA (Total Hip Arthroplasty) or TKA (Total Knee Arthroplasty) if pharm/non-pharm fail.

Rheumatoid Arthritis (RA)

• Chronic, progressive, systemic inflammatory autoimmune process affecting synovial joints (can affect all organ systems).

• Characterized by remissions and exacerbations.

• More common in Euro-American women ($2-3 imes$ more likely than men).

• S/S: morning stiffness $>30$ min (most common complaint), swollen, tender joints, fatigue, fever, weight loss, decreased ROM.

• Affects Entire System (Extra-Articular Complications):

  • Pulmonary: interstitial lung disease, pleural effusion.

  • Cardiac: pericarditis, increased risk of CVD.

  • Ocular: scleritis, dry eyes (Sjögren's syndrome in $10-30$ of RA patients).

  • Vasculitis: inflammation of small blood vessels.

  • Neurologic: peripheral neuropathy, cervical spine instability.

• Labs: increased ESR, CRP, +ANA, Anti-CCP (sensitive for early RA).

• Tx:

  • Disease Modifying Antirheumatic Drugs (DMARDs): e.g., methotrexate (teratogenic – strict birth control needed).

  • Biological Response Modifiers (BRMs): e.g., etanercept/Enbrel (also teratogenic).

  • NSAIDs (mainly for inflammation control).

  • Corticosteroids (for med SE like immunosuppression, GI upset; long-term affects bone health).

• Non-pharm Management: Encourage gentle ROM exercises, joint protection. Apply warm packs for stiffness, cold for inflammation.

WK 4 - Fractures, Gout, Medications

Gout

• Type of inflammatory arthritis caused by hyperuricemia (high uric acid in blood).

• Uric acid crystals deposit in synovial fluid of joints, causing pain/inflammation $<br>ightarrow$ seen as big toe flare-up.

• Risk Factors: men, $>50$ yo, obesity, family history, chronic alcohol use, medications (thiazides, aspirin, immunosuppressants e.g., cyclosporine, levodopa).

• Triggers: red meat, organ meat, shellfish, alcohol (especially beer).

• Phases:

  • Phase 1: Asymptomatic hyperuricemia.

  • Phase 2: Acute gouty arthritis (often in great metatarsal joint of big toe).

  • Phase 3: Tophaceous arthritis (with inadequate management – crystallization under skin, kidney stones, kidney disease).

• Drug Therapy: Goal = maintain serum uric acid level $<6$ mg/dL.

  • Acute attacks: NSAIDs (indomethacin), colchicine (GI upset), Corticosteroids (oral/injection) – these help with inflammation, not uric acid levels.

  • Uric acid reduction: probenecid (promotes uric acid excretion).

  • Chronic management: allopurinol or febuxostat (lowers uric acid); lifestyle modifications (eliminate red meat, shellfish, alcohol).

Complications of Fractures

• VTE (DVT, PE): most common and fatal (patients often anticoagulated due to decreased mobility).

• Bone or soft tissue infection: from superficial skin infection to osteomyelitis.

• Complex Regional Pain Syndrome (CRPS): pain receptors remain active even after healing.

• Rare but potententially limb or life-threatening:

  • Acute Compartment Syndrome: pressure builds up inside closed muscle compartment, cutting off blood supply.

    • Tx: fasciotomy (surgical incision to relieve pressure), possible amputation.

  • Fat Embolism Syndrome (FES): fat globules released from yellow bone marrow, similar to PE, clotting small blood vessels. Occurs within $12-24$ hours after injury.

    • Tx: supportive treatment, including high Fowler's and non-rebreather mask.

Priority Interventions of Fractures

• Acute pain: relieve pain, improve comfort, support healing, allow participation in care.

• Decreased mobility: promote safe mobility as early as possible to prevent complications.

• Potential for neurovascular compromise: swelling or misalignment can cut off blood flow or compress nerves. Considered emergency.

Non-surgical Management of Fractures

• If bone is misaligned, closed reduction may be needed before immobilization.

• Immobilization Devices:

  • Casts: plaster or fiberglass (check tightness, allow one finger between cast/skin; re-cast if too loose after swelling subsides).

  • Splints/Braces: allow for swelling and adjustability.

  • Slings: support limb, reduce strain.

  • Traction: uses pulling force to maintain alignment (Buck's, skeletal).

    • Buck's: boot/strap connected to weight system; used pre or post-hip surgery to relieve muscle spasms.

    • Skeletal: less frequent, pins/wires inserted directly into bone connected to external frame (high infection risk).

    • Never manually lift weights without MD order or allow weights to rest on floor.

Surgical Management

• ORIF (Open Reduction and Internal Fixation): anesthesia required. Surgeon makes incision to realign bone ends directly, held in place with internal hardware (plates, screws, rods). Most common, allows early mobility.

• External Fixation: pins/screws inserted through skin into bone, connected to external frame (e.g., halo). 'Bridges' fracture, holds it in place.

WK 5 - Alzheimer's, Parkinson's, Seizures, Meningitis, Medications

CNS Structure and Function

• CNS = brain/spinal cord. Command center for data processing, decision-making, motor response.

• Brain covered by meninges: Dura, Arachnoid, Pia.

  • Cerebrum: 4 main lobes. Frontal (thinks, plans, short-term memory, speech). Parietal (touch, spatial). Temporal (hearing, memory). Occipital (vision).

    • Frontal Lobe Affected: Broca's area $<br>ightarrow$ expressive aphasia (knows what to say, can't express it, frustrated).

    • Temporal Lobe Affected: Wernicke's area $<br>ightarrow$ receptive aphasia (can talk, but speech is gibberish, often unaware).

  • Cerebral Cortex: higher-level thinking.

  • Cerebellum: coordination and balance.

  • Brainstem: life-sustaining functions (BP, HR, RR).

• Spinal Cord: pathway for messages between brain and body.

• Symptoms based on area of blood flow lack.

Cranial Nerves (Selected)

• I: Smell

• II: Visual Acuity

• III, IV, VI: Extraocular Movements (EOMs). Pupillary function tests CN III.

• V: Facial sensation

• VII: Facial Movement

• VIII: Hearing and balance

• IX: Gag reflex, swallowing

• X: Gag reflex, say 'Ah'

• XI: Shoulder/neck movement

• XII: Tongue movement

Diagnostics

• CT Scan: FIRST LINE for acute neuro changes (detects hemorrhage, hydrocephalus).

Alzheimer's Disease (AD) Prevention

• No proven prevention. Chronic health problems can contribute.

• Promote healthy lifestyle: regular physical exercise, balanced diet, avoid smoking/excess alcohol, social engagement, regular check-ups (manage RF), safety measures (wear helmets).

AD Assessment - Stages

• Early (Mild): mild cognitive impairment.

• Moderate: severe cognitive decline, personality changes (irritation), wandering, disorientation.

• Late (Severe): severe impairment, unable to communicate, cannot perform ADLs, cannot recognize loved ones.

• Stages are not always linear; patients can shift between characteristics.

• Cognitive changes: short-term memory, communication impairment.

  • Apraxia: sequence of actions out of order.

  • Aphasia: trouble producing language.

  • Anomia: difficulty naming things.

  • Agnosia: difficulty recognizing faces/objects.

• Behavior changes: aggressiveness (physical/verbal), mood swings.

• Self-management changes: decreased interest and ability to perform ADLs.

AD Diagnosis

• Health history and physical assessment: mainly with family to determine symptomology.

• Cognitive testing: Mini Mental State Exam (MMSE) and MoCA (assess memory, attention, language, problem-solving).

• Labs: rule out other reversible causes of confusion (thyroid, B12, electrolytes, infection).

• MRI/CT: rule out tumor/stroke. PET scan can see proteins/plaques in severe AD.

• Genetic testing for early-onset family history (APOE gene) does not guarantee AD.

AD Pharmacologic Management

• Cholinesterase Inhibitors: delay destruction of ACh (slow cognitive decline).

  • Donepezil (Aricept), Rivastigmine (Exelon).

  • Monitor HR (can cause bradycardia and dizziness).

• NMDA Receptor Antagonist: blocks excess glutamate that can damage nerve cells (for memory/cognition).

  • Memantine (Namenda) - used for advanced AD.

• Monoclonal Antibodies: reduce amyloid plaques.

  • Aducanumab (very expensive, new, limited data).

AD Planning

• Managing memory/cognitive dysfunction: routines, memory aids, short sentences, simple words.

• Preventing injuries/falls: no rugs/clutter, good lighting, assistive devices.

• Prevent elder abuse: assess for injuries inconsistent with story, encourage respite care for caregivers.

• Managing s/s at end of life: focus shifts to palliative care. Late stages: issues breathing, swallowing, aspiration pneumonia.

Parkinson's Disease (PD)

• Progressive neurodegenerative disorder affecting mobility. Certain neurons die, leading to decreased dopamine. ACh becomes more active, affecting muscle control, leading to contractions.

• 4 Cardinal S/S:

  • Tremor (resting tremor - 'pill rolling').

  • Muscle rigidity.

  • Bradykinesia or akinesia (slow or no movement).

  • Postural instability (difficulty maintaining upright posture).

• Cognitive changes can occur in late-stage PD.

PD Etiology and Incidence

• Idiopathic, but genetic mutations can cause some cases.

• Environmental factors: pesticides, toxins.

• Age ($>40$ yo) and family history increase risk.

• Affects men more than women.

PD Assessment and Diagnosis

• Affects both autonomic and somatic systems (initially somatic, progresses to autonomic).

• Motor Symptoms: Resting tremor, bradykinesia, muscle rigidity, postural instability/balance problems.

• Non-motor Symptoms (later stages): Depression, anxiety, cognitive impairment, sleep disturbances, autonomic dysfunction (constipation, orthostatic hypotension, excess perspiration).

• Diagnosis based on clinical findings after ruling out other neuro diseases.

• New tool: Dopamine Transporter (DaT) scan.

• Meds can help with non-motor symptoms.

PD Planning

• Promote mobility.

• Non-surgical Management:

  • Medication Therapy: levodopa/carbidopa (Sinemet) - most common. Levodopa converts to dopamine in brain, carbidopa helps it get there.

  • Dopamine Agonists: pramipexole (Mirapex), ropinirole (Requip). Mimic dopamine action. SE: dyskinesia, orthostatic hypotension, hallucinations.

  • MAO-B Inhibitors: rasagiline mesylate (Azilect). Block MAO-B from breaking down dopamine. Avoid tyramine-containing foods (smoked cheese, fermented/cured foods) - can cause severe hypertension/headache.

• Surgical Management:

  • Deep Brain Stimulation (DBS): electrodes implanted in brain to stop involuntary movements (used when drug effects wane).

Seizures - Pharmacologic Management (Antiepileptic Drugs - AEDs)

• Certain drugs work better for specific seizure types.

• Hydantoins: tonic-clonic seizures. Frequent drug level monitoring. Gingival hyperplasia. e.g., Phenytoin (Dilantin), Fosphenytoin (Cerebyx). Phenobarbital (teratogenic).

• Carboxamides: partial seizures. e.g., Carbamazepine (Tegretol), Oxcarbazepine (Trileptal).

• Valproates: broad-spectrum, teratogenic. e.g., Valproic acid (Depakene), Divalproex sodium (Depakote).

• Succinimides: absence seizures only. Gingival hyperplasia. e.g., Ethosuximide (Zarontin).

• Pyrrolidines: broad-spectrum. e.g., Levetiracetam (Keppra).

• Phenyltriazines: broad-spectrum. Watch for RASH (Stevens-Johnson Syndrome - SJS). e.g., Lamotrigine (Lamictal).

Meningitis

• Infection of the meninges (pia mater and arachnoid) of the brain and spinal cord.

• Types: viral (more common, less severe), bacterial (more severe).

• Spread: from nearby areas (ear infection, dental abscess).

• Risk Factors: Head/spine injury/procedures (skull fracture, brain/spinal surgery, lumbar puncture) causing CNS opening. Immunocompromised (HIV/AIDS, cancer, splenectomy). Incomplete/no meningococcal vaccination.

• Key S/S (Classic Triad):

  • Fever

  • Nuchal rigidity (stiff neck)

  • Altered mental status

• Other s/s: headache, photophobia, n/v, seizures, positive Kernig's/Brudzinski's signs.

• Brudzinski Sign: Bending neck causes hips and knees to flex.

• Kernig Sign: Knees cannot extend due to pain when hip is flexed $90$ degrees.

Meningitis Nursing Interventions

• Isolate if bacterial suspected (droplet precautions) - FIRST ACTION.

• Collect blood cultures, prepare for lumbar puncture (confirms viral/bacterial).

• Administer antibiotics ASAP after cultures.

• Monitor for increased ICP, seizures, neuro changes (support for HA/pain if ICP is high).

• Frequent vital signs and neuro checks.

• Prognosis: Good with prompt treatment ($hicksim90$ survival).

• Complications of delayed treatment (bacterial): brain damage, seizures, stroke, hearing loss.

• Untreated, increased ICP can lead to brain herniation and death (pressure on brainstem).

• Prevention: Encourage vaccination (primary prevention), practice good hygiene.

WK 6 - SCI, TBI, Stroke, MS, Meds

Multiple Sclerosis (MS)

• Chronic, progressive, autoimmune disease. Characterized by remissions and exacerbations (flares).

• Autoimmune response $<br>ightarrow$ inflammation $<br>ightarrow$ demyelination $<br>ightarrow$ plaque (lesions) formation in CNS $<br>ightarrow$ interrupted nerve transmission (symptoms).

• Affects myelin and nerve fibers of brain and spinal cord (CNS).

• Leading cause of neurologic disability in young and middle-aged adults.

• Symptoms are varied; each patient experiences differently.

Types of MS

• Clinically Isolated Syndrome (CIS): Isolated neurologic symptoms ($>24$ hrs) attributed to MS. May be a warning sign. MRI may or may not show MS evidence.

• Relapsing-Remitting (RRMS): Majority of cases at diagnosis. Relapses and remission periods, partial or complete recovery after relapse.

• Secondary Progressive (SPMS): Begins as RRMS, then transitions to steady neurological decline, with or without relapses.

• Primary Progressive (PPMS): Slow, steady worsening of neurological function from the beginning, without early relapses or remissions.

MS Etiology and Genetic Risk

• Genetic predisposition: higher risk with 1st-degree relatives.

• Environmental factors: low Vit D levels, smoking, viral infections (e.g., EBV).

• Geographic prevalence: more common in northern latitudes.

• Demographic: more common in women ($2-3 imes$ more than men).

• Usually occurs in people $20-50$ yo.

MS Symptoms

• Fatigue (most common), vision problems (e.g., vision loss - common early s/s), numbness/tingling, muscle weakness and spasticity (heavy, stiff extremities), gait disturbance, bladder/bowel dysfunction (frequency, retention, diarrhea, constipation), cognitive changes (memory, ADLs).

• Symptoms vary, can be vague, non-specific, intermittent. Patients should keep a 'symptom diary'.

MS Diagnosis

• Usually diagnosed by ruling out other conditions.

• MRI of brain detects plaques in brain/spinal cord (from demyelination). Must have plaques in at least 2 areas for diagnosis. Frequent MRIs to check medication effectiveness.

• Lumbar puncture: positive oligoclonal bands (an indicator, not definitive diagnosis).

• Evoked potential testing: measures speed of nerve response to stimuli (non-invasive).

MS Pharmacology

• Disease Modifying Therapies (DMTs): slow disease progression.

  • Injectables: interferon beta-1a (Avonex, Rebif), glatiramer acetate (Copaxone).

  • Oral Meds: fingolimod (Gilenya - causes bradycardia), dimethyl fumarate (Tecfidera), teriflunomide (Aubagio). Common SE: facial flushing, GI disturbances.

  • Infusions (IV): natalizumab (Tysabri), ocrelizumab (Ocrevus). High incidence of reactions during first doses, given in infusion centers.

• Acute Attack: High-dose corticosteroids (methylprednisolone IV or oral prednisone) to reduce inflammation.

• Symptom Control: Damage to neurons causes symptoms; meds address these.

  • Fatigue: amantadine, modafinil.

  • Spasticity: baclofen, tizanidine.

  • Pain/Neuropathy: gabapentin, pregabalin.

  • Bladder dysfunction: oxybutynin (for overactive bladder).

  • Depression: SSRIs/SNRIs.

  • Bowel issues: stool softeners, laxatives.

MS Actual/Potential Problems

• Impaired immunity due to disease and drug therapy.

• Decreased/impaired mobility due to muscle spasticity, intention tremors, and/or fatigue (PT/OT important).

• Decreased visual acuity and cognition due to brain neuron dysfunction (regular eye exams, symptom diary, cognitive therapy, memory aids).

Spinal Cord Injury (SCI)

• Damage to spinal cord resulting in loss of motor function, sensation, or autonomic control.

• Classification:

  • Complete: no motor or sensory function below injury.

  • Incomplete: some function or movement below level of injury.

• Plegia = paralysis; Paresis = weakness.

SCI Etiology and Incidence

• Trauma is leading cause ($>1/3$ from vehicle crashes).

• Others: falls, GSW/violence, sports/recreation accidents.

• Health Promotion: avoid risks, use protective measures, wear seat belts, avoid substances, deep pools ($>9$ ft for diving).

SCI Assessment

• Emergency Management: Immobilize spine IMMEDIATELY (C-collar and backboard).

• Follow ABCs:

  • Airway with C-spine precautions.

  • Breathing: assess respiratory effort.

  • Circulation: control bleeding, monitor perfusion.

• Sensory Perception and Mobility Assessment:

  • Cervical: quadriplegia (tetraplegia), all 4 extremities. Respiratory complications (C1-C5).

  • Thoracic/Lumbar: paraplegia, only lower extremities. Varying bladder/bowel control.

  • Sacral: loss of bowel/bladder and sexual function.

• Priority in SCI is ABCs (respiratory is likely compromised).

SCI Immediate Complications

• Spinal Shock: temporary loss of motor, sensory, reflex function below injury (lasts days-weeks, function returns).

• Neurogenic Shock (above T6): hemodynamic instability (cannot perfuse tissues). Caused by loss of sympathetic tone.

  • Hypotension, bradycardia, warm/dry skin.

  • Provide BP support via fluids or vasopressors.

• Respiratory Compromise: airway and breathing issues. Most notable in cervical injuries (C1-C4).

• Hemodynamic Instability: risk of shock, multisystem organ failure (from trauma/hemorrhage, distinct from neurogenic shock).

SCI Chronic Complications

• Autonomic Dysreflexia (above T6): EMERGENCY. Sudden hypertension due to noxious stimuli below injury level (bladder/bowel related).

  • S/S: sudden headache, sweating above injury, bradycardia, hypertension.

  • Interventions: sit patient upright, dangle legs (lowers BP), give anti-HTN (IV labetalol), remove tight clothing/noxious stimuli.

• Pressure injuries.

• Infection and sepsis (especially with skin breaks and poor pulmonary hygiene).

• Muscle spasticity and contractures.

• DVT/PE (due to immobility and altered circulation).

• Depression and psychosocial issues.

• Bowel and bladder dysfunction.

SCI Actual/Potential Problems

• Potential for respiratory distress/failure due to aspiration, decreased diaphragmatic innervation, or decreased mobility (shallow breathing).

• Potential for cardiovascular instability (shock/autonomic dysreflexia) due to loss/interruption of sympathetic innervation or hemorrhage.

• Potential for secondary SCI due to hypoperfusion, edema, or delayed spinal column stabilization.

• Decreased mobility and sensory perception due to spinal cord damage and edema.

Transient Ischemic Attack (TIA)

• 'Mini stroke' - a warning sign of future stroke.

• Temporary blockage of blood flow to brain.

• Symptoms resolve within 24 hours (usually $<1$ hour).

• No permanent brain damage.

• Common Signs: sudden weakness, numbness, vision changes, slurred speech, confusion.

• Same RF as stroke: HTN, DM, smoking, Afib.

• Urgent evaluation is critical; 1 in 3 will have a stroke later.

Stroke (Cerebrovascular Accident - CVA)

• Interruption of perfusion (blood flow) to any part of the brain resulting in infarction (cell death).

• Medical emergency. Permanent brain damage can occur within minutes to hours; longer delay = more damage.

• Signs of stroke (BE FAST):

  • B: Balance - loss of balance or coordination.

  • E: Eyes - changes in vision.

  • F: Face - drooping features on one side.

  • A: Arms (and legs) - weakness in a limb.

  • S: Speech - difficulty speaking or understanding others.

  • T: Time - call 911/emergency services ASAP.

Stroke Types

• Acute Ischemic Stroke (AIS): blockage of cerebral or carotid artery, reduced blood flow/$O_2$ to brain tissue (more common).

  • Thrombotic Stroke: clot forms within cerebral artery due to atherosclerosis/plaque rupture (develops slowly).

  • Embolic Stroke: clot/debris from elsewhere (e.g., heart) travels to brain (acute, sudden, no warning).

• Hemorrhagic Stroke: blood vessel rupture, bleeding into brain tissue/spaces around brain (more deadly).

  • Intracerebral Hemorrhage (ICH): bleeding directly into brain tissue.

  • Subarachnoid Hemorrhage (SAH): bleeding into space between brain and skull. Usually due to:

    • Aneurysm: weakened artery wall bulges and bursts.

    • Arteriovenous Malformation (AVM): abnormal tangle of vessels that can rupture.

Stroke Etiology and Genetic Risk

• Combination of genetic and environmental factors.

• Leading Causes: HTN (***), smoking, DM, hyperlipidemia, obesity, sedentary lifestyle, stress, family history of early heart disease.

• OCPs also increase clot formation risk.

• 1 in 3 US adults has at least one of these conditions/habits.

Stroke Incidence and Prevalence

• 5th leading cause of death in US.

• Women have higher incidence than men (longer life expectancy, hormones, atypical symptoms leading to delayed treatment).

• Stroke belt (Mississippi, Alabama, Georgia) has higher incidence.

• Survivor rate increasing, death rate decreasing.

Stroke Health Promotion/Disease Prevention

• CDC recommends ABCs of heart health under medical supervision:

  • Aspirin use when appropriate.

  • Blood pressure control.

  • Cholesterol management.

  • Smoking cessation.

Stroke Management - Initial Contact

• ABCs and Symptom/Health History

  • Airway: ensure patency.

  • Breathing: assess respiratory rate and $O_2$ sat.

  • Circulation: HTN common and may be protective; treat cautiously (lower BP steadily).

• Symptoms: Onset time is critical ('last known well') for tPA eligibility.

• Health History: Current meds (anticoagulants - apixaban, warfarin) are important for hemorrhagic stroke risk and thrombolytic contraindications. History of previous stroke/TIA, bleeding disorders, HTN, DM, Afib, recent surgery.

Stroke Diagnostics

• Lab Assessment: elevated H&H, WBC, blood glucose, HgbA1c, PT/INR, aPTT (also troponin to rule out MI).

• Imaging: CTP/CTA, MRA, US. Immediate brain imaging (CT NO CONTRAST - first test).

• Upon ED Presentation: CODE STROKE protocol: rapid coordination (ED RN/MD, Stroke team/neurologist, radiology, lab), NIHSS to quantify severity.

• Goal: Identify candidates for thrombolysis (tPA) or thrombectomy.

Treatment of Acute Ischemic Stroke (AIS)

• Goal: restore cerebral perfusion.

• Two main treatments:

  • IV Fibrinolytic Therapy (Alteplase - tPA): Only FDA-approved drug for ischemic stroke.

    • Must be given within $3-4.5$ hours of symptom onset ('last known well' time).

    • Door-to-needle time $\le 45$ min.

    • BP must be $<185/110$ mmHg before and during treatment (may require rapid anti-HTN).

  • Endovascular Interventions (Thrombectomy): Surgical removal of clot with stent placement. Can be done up to 24 hours post-onset.

Treatment of Acute Hemorrhagic Stroke (AHS)

• Goal: stop bleeding, reduce brain damage.

• Stop bleeding; reverse anticoagulants (e.g., Vit K).

• Lower BP: SBP goal $<140-160$ mmHg.

• Control ICP: Change in LOC is earliest sign of increased ICP. Elevate HOB to $30$ degrees, maintain head/neck alignment. Avoid coughing, straining, suctioning.

• Seizure prevention: prophylactic AEDs (e.g., Keppra).

• Surgical Options: Craniotomy to remove clot or stop bleeding. External Ventricular Drain (EVD) if hydrocephalus develops (relieves ICP).

Stroke Care Coordination

• Ongoing drug therapy:

  • Antiplatelets: aspirin, clopidogrel (prevents clots).

  • Anticoagulants: warfarin, apixaban (for Afib/clotting risks).

  • Statins: lower cholesterol, stabilize plaques.

  • Anti-HTN: control BP, reduce stroke risk.

  • DM meds: control blood sugar.

• Eight Core Measures (for better outcomes):

  • VTE prophylaxis.

  • Discharge on antithrombotic therapy.

  • Discharge on anticoagulant therapy for Afib/flutter.

  • Antithrombotic therapy started.

  • Discharge on statin meds (if indicated).

  • Stroke education for patient/caregiver.

  • Smoking cessation counseling.

Traumatic Brain Injury (TBI)

• Damage to brain from external mechanical force (disrupts brain function).

• Severity varies.

• Diagnosis: CT/MRI (CT first for life-threatening emergencies, MRI for soft tissue damage).

• Causes: Falls (most common), MVAs, sports injuries, assaults/violence (GSW, blast injuries).

TBI Assessment

• AIRWAY (***).

• Spinal precautions.

• History (amnesia, LOC, seizure).

• Monitor s/s of increasing ICP: headache, vomiting, altered consciousness, pupil changes.

• Frequent neurological assessments.

TBI Types

• Two main classifications:

  • Closed (blunt): most common. Skull intact, brain bruised (falls, MVA).

  • Open (penetrating): object breaks through bone, hits brain tissue (more severe).

• Primary Brain Injury: happens at time of injury.

  • Focal (specific area) or Diffuse (widespread damage).

  • Mild, moderate, severe (determined by GCS).

• Secondary Brain Injury: Occurs after initial injury, worsens outcomes (further damage not from initial impact).

  • Increased intracranial pressure (ICP).

  • Hypotension (systemic hypotension decreases brain perfusion).

  • Infections.

  • Seizures (disrupted electrical activity).

TBI Brain Hemorrhage Types

• Intracerebral hemorrhage: bleeding inside brain tissue.

• Subarachnoid hemorrhage: bleeding into space between brain and arachnoid membrane.

• Epidural hematoma: bleeding between skull and dura mater (most linked to trauma).

• Subdural hematoma: bleeding between dura mater and arachnoid mater (most linked to trauma).

TBI Treatment

• Medical Management:

  • Monitor and manage ICP.

  • Osmotic (mannitol), hypertonic saline ($3\%$ hypertonic saline) as needed.

  • Maintain adequate oxygenation and BP.

  • Prevent/treat seizures.

  • Control pain and provide sedation proactively to decrease ICP.

• Surgical Intervention:

  • Evacuate hematoma (burr hole, craniotomy).

  • Decompressive craniectomy (for brain swelling).

  • Repair skull fractures if needed.

• Cushing's Triad (for increased ICP):

  • Widened pulse pressure.

  • Bradycardia.

  • Irregular respirations.

WK 7 - Otitis Media, Hearing Loss, Glaucoma, Cataracts, Medications

Cataracts

• Lens opacity distorts image (cloudiness).

• S/S: blurred/cloudy vision, glare and halos around lights, poor night vision, faded color perception, frequent prescription changes (early signs). No pain, just cloudy vision.

• Etiology/Prevalence: Can be present at birth or develop later. Often age-related (most common), trauma (radiation, chemo), toxin exposure. Can occur with other diseases. Lens thickens, becomes less flexible with age. Most Americans develop by 75 yo.

• Treatment: CATARACT SURGERY IS THE ONLY TREATMENT; no intervention means progression.

  • Phacoemulsification (most common): topical/local anesthetic. Probe inserts into lens, uses sound waves to break up lens, then removed.

  • Extracapsular Cataract Extraction (ECCE): removes lens whole. More invasive, more stitches. For more severe cataracts.

• Surgery Care:

  • Preop: procedure is short ($15-30$ min), eye drops may be prescribed.

  • Postop: eye drops prescribed (hand hygiene essential, don't touch tip to eye). Wear eye patch at night.

  • Symptoms to report: severe pain (not typical), vision loss, increasing redness/swelling, green/yellow thick discharge, eyelid swelling, flashes of light or floaters.

  • Activity Restrictions: avoid rubbing/touching eye; avoid activities increasing IOP (heavy lifting, bending over, straining).

Glaucoma

• Group of eye disorders resulting in increased IOP. Increased IOP decreases blood flow to eyes. Aqueous humor helps maintain IOP.

• Usually asymptomatic in early stages.

• Tissue damage starts in periphery and moves inward, causing 'tunnel vision'.

• Can lead to permanent vision loss if untreated.

• Early S/S: possible headache, eye ache.

• Late S/S: seeing halos around lights, losing peripheral vision, irreversible optic nerve damage.

• Glaucoma Types:

  • Primary Open Angle Glaucoma (POAG): most common. Slow, painless loss of peripheral vision (like a clogged drain, slowly occluding).

  • Angle Closure (Closed Angle) Glaucoma: Sudden onset. MEDICAL EMERGENCY. Drainage angle closes, rapid IOP increase (sink suddenly obstructed).

  • Secondary Glaucoma: arises from another health condition or trauma.

Glaucoma Etiology/Prevalence

• Anyone can develop glaucoma.

• Common in people with DM or HTN; African Americans $>40$ yo; anyone over $60$ (especially Hispanic/Latinos); family history.

• Most common cause of blindness in North America.

Glaucoma Management

• Pharmacologic (mainly for open-angle glaucoma):

  • Prostaglandin Analogs: e.g., latanoprost (Xalatan). Increases outflow of aqueous humor.

  • Beta-blockers: e.g., timolol (Timoptic). Reduce aqueous humor production. Non-specific (can block $B<em>1$ or $B</em>2$), avoid in asthma/heart blocks. Monitor BP and pulse.

  • Alpha Agonists: e.g., brimonidine (Alphagan). Decreases fluid production and increases drainage.

  • Carbonic Anhydrase Inhibitors (CAIs): e.g., dorzolamide (Trusopt). Decreases aqueous humor production. Do not administer in patients with sulfa allergies.

  • Cholinergic (Miotic) Agents: e.g., pilocarpine. Increases outflow by contracting ciliary muscle and opening drainage angle.

• Surgical (Closed-angle glaucoma often requires acute intervention/surgery):

  • Laser Trabeculoplasty: for open-angle; laser opens drainage, drain placed to decrease IOP.

  • Tube Shunt Surgery: tube bypasses trabecular mesh; drains aqueous humor.

  • Cyclophotocoagulation: for open/closed-angle; focuses on ciliary body, decreases aqueous humor.

  • Laser Peripheral Iridotomy (LPI): for angle closure only. Hole made in iris to drain aqueous humor, reducing IOP.

• Main Goal: Reduce IOP.

How to Use Eyedrops

• Instill as prescribed (only affected eye).

• If $>1$ eyedrop med, wait $5-10$ min between instillations.

• Wash hands before drops.

• Keep tip clean, don't touch eye.

• Punctal Occlusion: apply pressure to punctal duct for $hicksim1$ min to prevent systemic absorption.

• Follow up every $1-3$ months or as directed.

WK 8 - Heart Failure, Acute Coronary Syndrome, Valvular Heart Disease, Medications

Cardiac Physiology

• Cardiac Output (CO): amount of blood heart pumps in one minute ($CO = HR imes SV$).

• Heart Rate (HR): number of heartbeats in one minute.

• Stroke Volume (SV): amount of blood ejected from left ventricle with each beat ($60-100$ mL/beat).

• Preload: amount of blood returning to heart and stretching ventricles before contraction (volume).

• Afterload: pressure heart has to pump against to eject blood (resistance).

Cardiovascular Changes Associated with Aging

• Cardiac valves become thicker and stiffer (especially aortic and mitral) $<br>ightarrow$ murmurs.

• Conduction system: fewer pacemaker cells in SA node $<br>ightarrow$ higher risk for dysrhythmias.

• Left Ventricle wall may thicken (hypertrophy).

• Aorta and large arteries stiffen, lose elasticity (compliance).

• Baroreceptors become less sensitive to BP changes $<br>ightarrow$ greater risk for orthostatic hypotension (OH).

Diagnostic Labs

• Serum Cardiac Enzymes: Troponin = most specific marker of myocardial injury. Elevated for $10-14$ days.

• Serum Lipids (desirable levels):

  • Total cholesterol: $<200$ mg/dL.

  • Triglycerides: $<150$ mg/dL.

  • HDL: $>60$ mg/dL (good, cardioprotective).

  • LDL: $<100$ mg/dL (bad).

  • Off levels contribute to plaque buildup (atherosclerosis).

• Other tests:

  • C-reactive protein (non-specific inflammatory marker).

  • BNP (B-type natriuretic peptide) = high levels associated with heart failure (released when heart stretched/under pressure).

Diagnostic Tests

• Angiography (Arteriography): visualizes blood flow through arteries with contrast (iodine). Checks for blocks.

• Cardiac Catheterization: invasive, assesses coronary arteries, heart chambers. Can include angioplasty (PCI: balloon $ightarrow$ stent).

  • Confirm iodine allergy.

  • Can be radial, femoral, brachial; left or right sided.

• EKG: records electrical activity of heart.

• Electrophysiological Study (EPS): invasive, maps electrical conduction (for complex arrhythmias).

• Exercise Electrocardiography (Stress Test): assesses heart response to physical stress (chemical or treadmill) to detect ischemia not at rest.

• Echocardiography: US of heart showing structure and motion.

• Transesophageal Echocardiography (TEE): US probe into esophagus for clearer images of posterior heart.

• Myocardial Nuclear Perfusion Imaging (MNPI): radioactive tracers to assess blood flow and tissue damage (more invasive).

Heart Failure (CHF)

• 'Pump failure' - chronic, life-threatening if untreated.

• Main Etiologies: MI (ischemic heart disease), HTN, Heart muscle disease (cardiomyopathy), Valvular disorders, Arrhythmias (e.g., Afib), Congenital heart defects.

• Other Contributing Conditions (Comorbidities): Diabetes, Kidney disease, Thyroid issues, COPD, alcohol/drug use, Infections, Anemia.

• Incidence/Prevalence: Most common reason for hospital admission in $>65$ yo. African Americans at increased risk.

Left-Sided Heart Failure

• Two types: Systolic (heart can't pump), Diastolic (heart can't fill).

• Blood backs up into the lungs, causing pulmonary congestion (LEFT = LUNGS).

• S/S: Dyspnea (SOB, especially with exertion), orthopnea (SOB when lying down), paroxysmal nocturnal dyspnea (sudden awakening with shortness of breath), fatigue, cough/pink frothy sputum (hallmark sign), crackles/rales, cool/pale skin (poor perfusion/output).

• Can lead to Right-Sided Heart Failure.

Systolic vs. Diastolic HF

• Systolic HF (Heart Failure with reduced Ejection Fraction [HFrEF] $<40\%$): Heart wall is weak and stretched out. Impaired contractility.

• Diastolic HF (Heart Failure with preserved Ejection Fraction [HFpEF] $>50\%$, normal $50-70\%$): Heart wall stiff and thick. Impaired filling ability.

Right-Sided Heart Failure

• Often results from Left-sided failure (right ventricle works harder to push blood into congested lungs).

• Blood backs up into body (RIGHT = REST of the body) $<br>ightarrow$ peripheral edema.

• S/S: peripheral edema, JVD, ascites, splenomegaly, hepatomegaly, n/v/loss of appetite (congestion from fluid buildup).

Classification and Staging of HF

• Describes how much HF limits ADLs.

• Class I: high risk for developing HF.

• Class 1: cardiac structural abnormalities/remodeling, no HF symptoms.

• Class II or III: current or prior HF symptoms.

• Class IV: refractory end-stage HF.

Compensatory Mechanisms (When CO is insufficient)

• Sympathetic Nervous System (SNS) stimulation: increases HR, vasoconstricts.

• Renin-Angiotensin System (RAS) activation: decreased flow to kidneys stimulates renin release, causing vasoconstriction and raising BP through $Na^+$/$H_2O$ retention.

• Myocardial Hypertrophy: heart muscles enlarge over time to improve pumping efficiency.

Heart Failure Assessment

• Lab Assessment: BNP, Serum electrolytes, ABGs (compensation due to less $O_2$).

• Imaging:

  • ECHO: best tool to diagnose HF.

  • Chest X-ray: can show cardiomegaly.

HF Pharmacologic Management

• Drugs that REDUCE AFTERLOAD (dilate arteries):

  • ACE Inhibitors: e.g., lisinopril, enalapril.

  • ARBs: e.g., losartan, valsartan (dilate arteries, reduce afterload, suppress fluid retention).

  • Angiotensin Receptor Neprilysin Inhibitors (ARNIs): e.g., sacubitril/valsartan (Entresto).

  • Monitor electrolytes (especially potassium). Do not give with history of angioedema.

• Drugs that REDUCE PRELOAD (dilate veins):

  • Diuretics: e.g., furosemide, bumetanide, torsemide.

  • Nitrates: e.g., nitroglycerin, isosorbide dinitrate (dilate veins). DO NOT TAKE WITH ED MEDS (sildenafil) - severe hypotension risk.

  • ACE inhibitors/ARBs (can somewhat reduce preload).

• Drugs that ENHANCE CONTRACTILITY/POSITIVE INOTROPES (increase heart contraction):

  • Digoxin: Assess apical pulse 1 full min before (hold if HR $<60$ bpm). Watch for digoxin toxicity (nausea, vision changes - halos, irregular heartbeat). Low potassium increases toxicity risk. Taken 2 hours apart from antacids (decreases absorption).

  • IV Infusions: dobutamine, dopamine, milrinone (Primacor). For severe decompensated HF; increase arrhythmia likelihood (continuous EKG monitoring). Used for end-stage HF patients awaiting transplant.

HF Surgical Management

• Heart Transplantation: Definitive option for refractory end-stage HF (limited donors, comorbidities complicate candidacy).

• Left Ventricular Assist Device (LVAD): Mechanical pump helps left ventricle pump blood.

• Biventricular Pacemaker (Cardiac Resynchronization Therapy - CRT): helps both sides of heart beat in sync.

• Implantable Cardioverter-Defibrillator (ICD): implanted device to detect and correct life-threatening arrhythmias (shocks for high-risk patients).

Heart Disease Intervention Medications (General)

• ACE inhibitors/ARBs: relax vessels, reduce workload.

• Beta-blockers: slow HR, lower BP, decrease $O_2$ demand.

• Diuretics: reduce fluid overload, swelling.

• Nitrates: relieve chest pain (angina).

• Antiplatelets/Anticoags: prevent clots (aspirin, warfarin).

• Statins: lower cholesterol, reduce plaque buildup.

Angina Pectoris

• Chest pain caused by temporary imbalance between coronary artery $O<em>2$ supply and cardiac muscle $O</em>2$ demand.

• Types:

  • Chronic Stable Angina (CSA): discomfort with moderate to prolonged exertion in familiar pattern. Responsive to nitroglycerin.

  • Unstable Angina (UA): chest pain at rest, with exertion, severely limits activity. Not responsive to nitro. Medical emergency, can progress to MI. No troponin elevation, no permanent damage.

  • Vasospastic Angina (Variant or Prinzmetal Angina): chest pain/discomfort from coronary artery spasm, typically at rest (early morning/late PM). Triggered by extreme cold, stimulants (cocaine, amphetamines), emotional stress.

NSTEMI vs. STEMI

• NSTEMI (Non-ST Elevation MI):

  • Partial block of coronary artery.

  • Troponin normal then elevates, or already elevated.

  • Tx: medications and percutaneous intervention (PCI - assessment and intervention in cath lab).

• STEMI (ST Elevation MI):

  • ST elevation in $2+$ leads on ECG (extensive damage).

  • Complete block of coronary artery.

  • Troponin is elevated (more heart muscle damage).

  • EMERGENCY.

  • Tx: immediate reperfusion (PCI preferred; fibrinolytics if PCI not possible).

Acute Coronary Syndrome (ACS) - Etiology + Genetic Risk

• Atherosclerosis is main factor.

• Modifiable RF: uncontrolled HTN, smoking, DM, hyperlipidemia, obesity, sedentary lifestyle, stress.

• Non-modifiable RF: family history of early heart disease.

ACS Incidence and Health Promotion

• Average age of first MI: $65$ yo (M), $72$ yo (F).

• AEDs available in public spaces.

• Controlling modifiable RF is critical.

ACS S/S

• Chest pain/pressure (can radiate to arm, jaw, back; intermittent or sustained).

• SOB.

• N/V.

• Diaphoresis.

• Lightheadedness/anxiety.

• Atypical s/s in women/DM: indigestion, pressure between shoulder blades, jaw pain, non-cardiac symptoms.

ACS Assessment

• Lab Assessment: Troponin T and I (specific for MI/cardiac necrosis).

• Imaging Assessment: Chest X-ray (rule out aortic dissection).

• Other Diagnostic Tests: 12-lead EKG WITHIN 10 MIN OF INITIAL PRESENTATION (18-lead EKG for right/posterior heart). Cardiac catheterization for assessment/intervention.

ACS Management

• NITROGLYCERIN ('Nitro'):

  • Relieves chest pain/angina by improving blood flow to heart (decreases preload and afterload).

  • Routes: Sublingual tab/spray ($0.3-0.6$ mg q5min, up to 3 doses), Transdermal (ointment/patch).

  • Transdermal application: clean, dry, hairless area. Rotate sites. Remove patch before defibrillation. Remove patch after $12-14$ hours daily (prevent tolerance).

  • Considerations: Check BP before each dose (hold if SBP $<90$ mmHg). Monitor for headache (give Tylenol), dizziness, hypotension. DO NOT give with PDE-5 inhibitors (sildenafil) - severe hypotension risk.

• MONA (for MI):

  • Morphine: pain relief, reduces preload and anxiety (if nitro ineffective).

  • Oxygen: if SpO2 $<90\%$ or in distress.

  • Nitroglycerin: vasodilation to relieve chest pain.

  • Aspirin: antiplatelet to prevent further clotting.

• If new onset angina at home, chew aspirin $325$ mg (four $81$ mg baby aspirins) immediately and call 911.

ACS Reperfusion (mainly for STEMI)

• Goal: open blocked artery for acute MI.

• Two strategies:

  • Thrombolytic Therapy.

  • Percutaneous Coronary Intervention (PCI): non-surgical, opens narrowed/blocked coronary arteries to restore blood flow. Treatment of choice.

    • Pre-procedure: consent, labs (CBC, coag), NPO, allergies (iodine).

    • Post-procedure: monitor for bleeding, chest pain (if PCI failed), arrhythmias, neurovascular checks (5 P's). Diminished/absent pulse is perfusion problem.

Coronary Artery Bypass Graft Surgery (CABG)

• Bypasses blocked coronary arteries by grafting vessels from other body parts to restore blood flow (for severe disease/damage).

• Procedure: Median sternotomy, cardiopulmonary bypass machine, grafts from saphenous vein, internal mammary artery, radial artery. Grafts sewn beyond blockage.

• Post-op: Monitor hemodynamics (BP, HR, CO), manage pain/sedation, watch for bleeding/infection, respiratory care (deep breathing), assess neurovascular status of graft extremities, early mobilization.

• Complications: hypotension, hypothermia, hypertension, bleeding, cardiac tamponade, change in LOC (often anesthesia-related).

Home Care Coordination

• Management: wound care, activity limitations.

• RF Modification: smoking cessation, heart-healthy diet, activity.

• Sexual activity: when able to walk 2 flights of stairs without symptoms.

• Drug Therapy: ASA (may need dual therapy - aspirin + Plavix), Beta-blockers, ACE/ARBs, statins, nitrates (patient may be on most/all).

• Healthcare Resources: AHA, Mended Hearts.

WK 9 - NSR, SB, ST, A.Fib, PVC, V.Fib, Asystole, Medications

Electrophysiologic Properties of the Heart

• Automaticity: ability to generate an electrical impulse.

• Excitability: ability to respond to stimulus.

• Conductivity: ability to pass signal to neighboring cells.

• Contractility: ability to contract (squeeze) after stimulation.

Reading EKG Strips

• Vertical axis: voltage. Horizontal axis: time.

• Standard strip = 6 seconds (30 large boxes).

• Each large box = $0.20$ sec (5 small boxes).

• Each small box = $0.04$ sec.

Normal EKG

• P wave: atrial depolarization (contraction). Normal: $<0.12$ seconds (3 small boxes).

• PR interval: time for impulse from SA node through AV node to ventricles. Normal: $0.12-0.20$ sec (3-5 small boxes).

• QRS complex: ventricular depolarization (contraction). Normal: $0.06-0.10$ sec (1.5-2.5 small boxes).

• T wave: ventricular repolarization (relaxation).

• QT interval: total time for ventricle to depolarize and repolarize.

• ST Segment: time between ventricular depolarization and repolarization (resting phase).

• ST elevation in 2 or more different leads = STEMI.

Sinus Rhythms

• Upright, consistent P-waves (identical).

• PRI constant ($0.12-0.20$ sec).

• $1:1$ ratio of P wave to each QRS.

• R-R is regular.

Normal Sinus Rhythm (NSR)

• Rate: $60-100$ bpm.

• Regular rhythm.

• P waves present, one P wave before each QRS complex.

• PR interval: $0.12-0.20$ second and constant.

• QRS duration: $0.06-0.10$ second and constant.

Sinus Tachycardia (ST)

• Rate: $>100$ bpm.

• Sympathetic nervous system stimulation or vagal (parasympathetic) inhibition increases SA node discharge rate.

• Causes: anxiety, hypovolemia, exercise, fever, sepsis, hypoxemia; drugs causing sympathetic stimulation.

• Tx: Treat underlying cause.

Sinus Bradycardia (SB)

• Rate: $<60$ bpm. Excessive vagal (parasympathetic) stimulation.

• S/S: syncope (blackouts, fainting), dizziness, weakness, confusion, hypotension, diaphoresis, SOB, chest pain.

• Causes: meds like beta-blockers, calcium channel blockers, digoxin.

• Treatment:

  • Stable (not symptomatic): treat underlying cause. If beta-blocker overdose suspected, give GLUCAGON (IM injection).

  • Unstable (symptomatic): first line is usually EKG. Atropine $0.5$ mg IV push. Transcutaneous Pacing (TCP) - external, painful, emergency from defibrillator. Transvenous pacing - internal, catheter with pacing wire into vein. Permanent pacemaker.

Pacemakers

• Small devices placed under skin to control abnormal heart rhythms. Avg lifespan: $10$ years.

• Combo pacemaker/defibrillator devices also available (ICD).

• Avoid strong electromagnetic fields (magnets, telecom transmitters).

• Shouldn't lift arm, lift more than $10$ lbs after implantation.

• NOT ALL PACEMAKERS ARE MRI SAFE.

• Carry pacemaker ID card, wear medical alert bracelet.

• Single chamber and dual chamber (A-pace and V-pace).

Atrial Rhythms

• Originate within atria, NOT SA node. Not 'classic' P-waves.

• Typically fast (controlled $<100$ bpm or uncontrolled $>100$ bpm).

• QRS complexes can be narrow or wide.

Atrial Fibrillation (AFib)

• Supraventricular arrhythmia. Atrium is fibrillating (quivering, erratic electrical firing).

• Completely irregular. No distinct P waves. Variable R-R intervals. Narrow QRS complexes.

• High stroke risk.

• Etiology/Incidence: most common dysrhythmia in developed world. Affects $12.1$ million in US.

• Risk Factors: HTN, CAD, HF, valvular disease, hyperthyroidism, post-cardiac surgery, $>65$ yo. More women affected.

• Chaotic rhythm decreases ventricular filling, decreasing CO ($hicksim20\%$ reduction). Allows blood to pool, increasing clotting risk.

• Associated with atrial fibrosis and loss of muscle mass (overworking).

• Treatment: Goal is to convert to NSR, but not always possible for older adults.

• Medications:

  • Rate Control: slow ventricular response (metoprolol, atenolol - beta-blockers; diltiazem, verapamil - CCBs; digoxin).

  • Rhythm Control: restore/maintain NSR (amiodarone, sotalol - potassium channel blockers; flecainide, propafenone - sodium channel blockers).

  • Anticoagulation: prevent clot formation due to blood stasis in atria (apixiban, dabigatran - DOACs; warfarin - Vit K antagonist).

• Procedural Intervention:

  • Electrical Cardioversion: converts AFib to NSR using synchronized electric shocks.

  • Catheter Ablation: destroys small areas of heart tissue triggering AFib.

  • MAZE procedure: creates scar tissue in atria to block abnormal impulses.

  • Left Atrial Appendage Occlusion 'Watchman Device': closes off left atrial appendage (where most AFib clots form).

Ventricular Rhythms

• Potentially more life-threatening than atrial dysrhythmias (left ventricle pumps $O_2$ blood for vital organ perfusion).

• Regular or irregular. P-waves absent. Fast or slow depending on impulse location.

• Main characteristic: wide QRS complexes ($>0.12$ sec).

Premature Ventricular Complexes (PVCs)

• Result of increased irritability of ventricular cells. Early ventricular complexes followed by a pause.

• Common, frequency increases with age. Not problematic if occasional.

• Concern if frequent, especially post-MI (warning sign of life-threatening rhythm like Vfib).

Ventricular Fibrillation (Vfib)

• Ventricles are quivering (NOT CONTRACTING); electrical chaos. LIFE-THREATENING! No refilling, no perfusion.

• Immediate Action: Call a CODE, start CPR until defibrillator available.

Asystole

• No electrical impulses in ventricles. No ventricular depolarization, no QRS complex, no contraction, no CO. NO PERFUSION to rest of body.

• Requires ACLS/CPR.

• DO NOT SHOCK ASYSTOLE.

CPR (Cardiopulmonary Resuscitation)

• When patient unresponsive, not breathing normally, no pulse felt within 10 seconds:

  • Rate: $100-120$ compressions/min.

  • Depth: $2-2.4$ in ($5-6$ cm).

  • Ratio: $30:2$ (compressions:breaths).

• Cardiac arrest rhythms needing CPR:

  • Ventricular Fibrillation (VF) - shockable.

  • Pulseless Ventricular Tachycardia (VT) - shockable.

  • Asystole - not shockable.

  • Pulseless Electrical Activity (PEA) - not shockable.

• ACLS (Advanced Cardiac Life Support) includes epinephrine, amiodarone, dopamine.

Cardiopulmonary Defibrillation

• Asynchronous countershock that depolarizes myocardium to stop re-entry circuit, allowing sinus node to regain control.

• Indications for shockable rhythms with CPR:

  • Ventricular Fibrillation (VF).

  • Pulseless Ventricular Tachycardia (VT).

Implantable Cardioverter/Defibrillator (ICD)

• Indicated for patients with spontaneous sustained VT or VF not caused by MI.

• Types: Transvenous (most common), Subcutaneous (younger/congenital heart defects).

• External vest-like device: worn 24/7 (except showering) as a bridge (e.g., post-MI before permanent ICD, or awaiting heart transplant).

WK 10 - Acute vs. Chronic Pancreatitis, Cholecystitis, BMI, Medications

Cholecystitis

• Inflammation of gallbladder, usually caused by gallstones (cholelithiasis) blocking cystic duct.

• Blocked duct impairs bile outflow, irritating gallbladder wall $<br>ightarrow$ ischemia, infection, possible perforation.

• Stones mainly from abnormal breakdown of cholesterol or bile salts (biliary stasis and stone formation).

• Types: Acute (most common) vs. Chronic (recurrent gallstones).

Cholecystitis Etiology/Genetic Risk

• Family/genetics.

• Patients at risk (FOUR F's): Female, Forty, Fat, Fertile.

  • Estrogen increases cholesterol in bile and slows motility.

  • Bile is more static with age.

• Other risks: T2DM, Gastric bypass surgery, rapid weight loss (increase cholesterol), Crohn's disease, SCD (pigment stones).

Cholecystitis Incidence and Prevalence

• Common in wealthy countries (high-fat, high-cholesterol diets; low fiber; sedentary lifestyle; access to birth control).

• More common in women.

Cholecystitis Assessment

• History: food intake (fatty, greasy, fried), diet changes (high fat, rapid weight loss), previous gallstones/biliary issues, birth control/estrogen use, RF (obesity, DM, family history).

• Physical assessment and S/S:

  • Abdominal pain: RUQ, epigastric region. Triggered by high fat/volume meals.

  • Positive Murphy's Sign: pain and sudden stop in inhalation when pressing under right rib cage.

  • N/V, fever.

• Signs of bile duct occlusion (late signs): jaundice, dark tea-colored urine, pale/clay colored stools (lack of bile), pruritus (bile salt accumulation).

Cholecystitis Diagnostics

• Labs: WBC, LFT (ALT, AST), bilirubin (direct/conjugated).

• Imaging:

  • US IS BEST INITIAL DX TEST.

  • X-ray, Hepatobiliary Iminodiacetic Acid (HIDA) scan.

  • Endoscopic Retrograde Cholangiopancreatography (ERCP), Magnetic Resonance Cholangiopancreatography (MRCP).

Cholecystitis Management

• Medications: ursodiol and chenodiol (long-term to dissolve/stabilize gallstones - patient must meet criteria).

• Drain: percutaneous transhepatic biliary catheter (opens blocked duct - reserved for non-surgical candidates).

• Surgical: CHOLECYSTECTOMY = GOLD STANDARD (laparoscopic). Open cholecystectomy if laparoscopic is not possible.

Acute Pancreatitis

• Acute inflammation of pancreas caused by premature activation of pancreatic enzymes that digest the organ itself (autodigestion).

• Pancreas functions:

  • Exocrine: digestion (Amylase - carbs, Lipase - fats, Protease - proteins).

  • Endocrine: blood sugar control.

• Complications: pancreatic necrosis, sepsis, ARDS (pulmonary failure accounts for >1/2 of deaths in first week), hypovolemic shock (3rd spacing), altered coagulation (DIC - rare, bleeding), multi-organ failure.

Acute Pancreatitis Etiology/Incidence

• Gallstones (40%).

• Alcohol (30%).

• Other causes: trauma, medications, autoimmune, idiopathic.

• Prognosis: good for biliary tract disease-associated pancreatitis with early treatment. Poor when alcohol-related.

• Incidence increasing; attacks common during holidays/vacations with high alcohol intake.

Acute Pancreatitis Assessment

• History: collect after pain controlled; ask about alcohol use, medical problems.

• Physical assessment and S/S:

  • Severe abdominal pain (usually mid-epigastric or LUQ).

  • Jaundice (bile duct occlusion - late sign).

  • Grey Turner's sign: flank area (purple/dark blue discoloration, indicates retroperitoneal bleeding).

  • Cullen's sign: periumbilical area (indicates intra-abdominal bleeding).

• Psychosocial assessment.

Acute Pancreatitis Diagnostics

• Labs: amylase/lipase (important!), serum bilirubin and ALT (indicate biliary cause), CBC with differential, ESR.

• Imaging:

  • Abdominal US, X-ray.

  • CT with Contrast (GOLD STANDARD DIAGNOSIS).

Acute Pancreatitis Management

• Non-surgical (1st line):

  • NPO.

  • IV fluids (for hypovolemia and 3rd spacing).

  • Pain control.

  • Electrolyte replacement (fluid shifts contribute to imbalances).

  • NG tube (for severe vomiting or biliary obstruction/gastric decompression).

  • Treat underlying cause.

  • Nutritional support (clear liquids $<br>ightarrow$ low-fat oral diet as tolerated).

• Surgical: ERCP for gallstone removal.

• Focus for Acute: underlying cause, pain management, supportive care.

Chronic Pancreatitis

• Progressive destructive disease of pancreas with remissions and exacerbations.

• Inflammation and fibrosis lead to pancreatic insufficiency.

• Causes permanent damage to both exocrine and endocrine function.

• Types:

  • Chronic calcifying pancreatitis (CCP) - most common, caused by alcoholism.

  • Chronic obstructive pancreatitis - from cholelithiasis (gallstones).

  • Autoimmune pancreatitis.

  • Idiopathic/hereditary.

Chronic Pancreatitis Assessment

• Abdominal pain, ascites (scarring of splenic vein tissue, fluid backup).

• Steatorrhea (fatty stools - lipase not breaking down fat).

• Weight loss (loss of nutrient absorption).

• Jaundice, dark urine (bilirubin overspills).

• Polyuria, polydipsia, polyphagia (3 P's related to DM, as endocrine function is lost).

• Respiratory compromise.

• Can cause DM.

Chronic Pancreatitis Management

• Non-surgical: pain control (Tylenol, NSAIDs, opioids).

  • Pancreatic Enzyme Replacement Therapy (PERT) = STANDARD OF CARE (pancreas not functioning).

  • Insulin for DM management.

  • Nutritional support (high cal, low fat, fat-soluble vitamins ADEK).

  • No alcohol or tobacco.

• Surgical:

  • Distal pancreatectomy: remove part of pancreas if localized damage/scarring.

  • Total pancreatectomy with islet cell autotransplantation (TPIAT): entire pancreas removed (patient relies on insulin, extensive supplementation).

• Focus for Chronic: managing the disease.

Anthropometric Measurements

• Non-invasive method for evaluating nutrition status.

  • Height & Weight (for weight-based meds).

  • BMI (based on height and weight).

  • BSA (used in medication dosing and burn degree).

Total Enteral Nutrition (TEN)

• Nasoenteric Tube (NET) - Short-term:

  • NG tube (most common), nasoduodenal (NDT), nasojejunal tube.

  • Initial placement must be confirmed by X-ray prior to use.

• Enterostomal Feeding Tubes - Long-term:

  • Percutaneous endoscopic gastrostomy (PEG).

  • Dual access gastrostomy-jejunostomy (PEG/J).

  • Direct percutaneous endoscopic jejunostomy (DPEJ).

• Feeding can be bolus, continuous, or cyclical.

• Complications (Safety is Priority):

  • Obstructed tube (most common) - use liquid meds, bolus before/after crushing meds.

  • Tube misplacement, dislodgement.

  • Abdominal distention, N/V.

  • Fluid and electrolyte imbalance.

  • Refeeding syndrome.

Parenteral Nutrition

• When patient cannot use GI tract for nutrition. IV nutrition with all nutrients.

• Peripheral Parenteral Nutrition (PPN):

  • Administered through peripheral IV (lower osmolarity).

  • Short-term support.

  • Can cause phlebitis, fluid overload. Not for total nutritional support.

• Total Parenteral Nutrition (TPN):

  • Administered via central line (PICC, subclavian). NOT peripheral.

  • Long-term support, 100% nutritional status.

  • Worried about REBOUND HYPOGLYCEMIA - DO NOT SUDDENLY STOP TPN (body compensates, hypoglycemia can result).

  • Monitor for technique, hyperglycemia, electrolyte imbalances.