FINAL CHRONIC

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Last updated 2:10 AM on 5/3/26
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68 Terms

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Braden scale

Assess risk for pressure injury:

  • sensory perception

  • moisture (ex. due to incontinence)

  • activity/mobility

  • nutrition

  • friction/shear

Score: 6-23

  • <18 → at risk MUST implement preventative measures

<p><mark data-color="yellow" style="background-color: yellow; color: inherit;">Assess </mark><span style="color: red;"><mark data-color="yellow" style="background-color: yellow; color: inherit;">risk for pressure injury:</mark></span></p><ul><li><p>sensory perception</p></li><li><p>moisture (ex. due to incontinence)</p></li><li><p>activity/mobility</p></li><li><p>nutrition </p></li><li><p>friction/shear </p></li></ul><p><strong><mark data-color="blue" style="background-color: blue; color: inherit;">Score:</mark></strong> 6-23 </p><ul><li><p><span style="color: red;">&lt;18</span> → at risk <span style="color: blue;"><strong>MUST </strong></span>implement preventative measures </p></li></ul><p></p>
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Psoriasis

Immune disorder causing chronic inflamm of skin

  • skin cell produc. > shedding → epidermal thickness

Signs: occur anywhere → elbows, knees, palms, soles, scalp

  • thick, raised red patches w/ silvery flaking scales

  • painful & itchy

Lab: based on signs

  • elevated CRP & ESR (serum inflamm markers)

Tx: no cure

  • topicals/ointments (corticosteroid, retinoids), uv light therapy (kills cells), methotrexate

Care:

  • pt are better in warmer climate → uv kills cells

<p><mark data-color="yellow" style="background-color: yellow; color: inherit;">Immune disorder causing chronic inflamm of skin </mark></p><ul><li><p><span style="color: red;">skin cell produc. </span><strong>&gt; </strong><span style="color: blue;">shedding</span> → epidermal thickness </p></li></ul><p><strong><mark data-color="blue" style="background-color: blue; color: inherit;">Signs:</mark></strong> occur anywhere → elbows, knees, palms, soles, scalp</p><ul><li><p><span style="color: red;">thick, raised red patches</span> w/ silvery flaking scales</p></li><li><p>painful &amp; itchy </p></li></ul><p><strong><mark data-color="red" style="background-color: red; color: inherit;">Lab:</mark></strong> based on signs</p><ul><li><p><span style="color: blue;">elevated CRP &amp; ESR </span>(serum inflamm markers)</p></li></ul><p><strong><mark data-color="purple" style="background-color: purple; color: inherit;">Tx:</mark></strong> no cure </p><ul><li><p>topicals/ointments (corticosteroid, retinoids), uv light therapy (kills cells), methotrexate </p></li></ul><p><strong><mark data-color="green" style="background-color: green; color: inherit;">Care:</mark></strong></p><ul><li><p>pt are better in warmer climate → uv kills cells </p></li></ul><p></p>
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Skin cancer

Cause: uv radiation

Types:

  • (#1) basal cell carcinoma → usually tx b/c localized

  • melanoma → harder to tx

Labs: changes in skin (size, color, sensation)

Tx: chemo, radiation

Care:

  • limit sun exposure (spf 30, hats/long sleeve)

  • monthly self exams

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Burn injuries types

1) Superficial (sunburn)

  • affect only epidermal

  • signs: mild erythema/hypersensitivity

  • tx: resolves in 24-72 hrs (no meds necess.)

2) superficial partial thickness

  • affect epidermis & superficial

  • signs: very painful b/c exposed nerve endings, wet weeping pink blisters, cap refill normal

  • tx: heals in 1-2 wks

3) deep partial thickness

  • affect epidermis & extend into deeper portions

  • signs: appear waxy (no weepy blister), pink/cherry red, vary pain, NO cap refill

4) full thickness

  • affect epidermis, dermis, subcut tissue, maybe muscle/bone

  • destroy hair follicles, sweat gland, nerve ending → poor temp control & no pain

  • tx: skin graft

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Burn injuries

Risk: pt age & medical hx

Effects: burn shock & fluid/electrolyte imbalance secondary to massive fluid shifts

  • fluids/electro leak out of intravascular space into interstitial b/c increased cap perm.

  • initial: hyerK

  • late: hypoK & hypoN

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Burn injury stages

1) emergent

  • goal: resolve immediate life threat → baseline eval, airway, fluids, prevent hypothermia, initiate wound care

  • care: 100% humidified o2, place large bore iv cath (fluid resus), warming measures (ex. blanket)

2) immediate (after resus & stabilize 48-72hr later)

  • goal: wound healing & closure, optimal nut., prevent infection & pain

  • care: assess labs (protein, wbc, albumin), wound care, nut. (maybe feeding tube)

3) rehab (may last for years)

  • goal: rehab & pyschological support

  • care: community resources, teach pt how to apply pressure garment (prevents hypertrophic scarring)

    • pt w/ burn may lack sweat gland & skin graft is sensitive to light

    • increased metabolic rate & caloric need post burn

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HIV

Virus that attacks body’s immune system

  • targets CD4+ lymphocytes → integrate rna into host cell dna through reverse transcriptase

Cause: STI (#1), blood, breast milk

  • fluid MUST come in contact w/ mucous membrane/injected into bloodstream

Lab: annual screening

  • viral load & cd4 count to establish baseline

Tx: no cure → proper managment

  • antiretroviral therapy (ART)

  • w/o proper tx → AIDS develops

Care:

  • avoid food that irritate bowel (raw fruit/veg, carbonated)

  • may need enteral/parenteral nut.

  • avoid high risk (use condom, reduce partners, no share needles)

  • hygiene → hand wash, avoid crowds

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Stages of HIV

Stage 1: acute

  • develop 2-4 post exposure → very contagious

  • hiv rapidly spread → increase viral load → body can still control the virus → CD4 return to normal levels (500 cells/mm3)

  • signs: temporary flu like symp (fever, chills)

Stage 2: chronic

  • prolonged → last several decades w/ tx or a decade w/o

  • low CD4 → 200-499

  • sign: asymp but STILL contagious

    • nonspecific sign → resp. tract infection, enlarged lymph

Stage 3: aids

  • CD4: <200 = aids

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HIV tx

Antiretroviral therapy (ART)

  • interfere w/ ability of hiv to reproduc. & suppress virus

  • use: confirmed case, pre/post exposure prophylaxis

  • uses multiple agents & adherence is required

    • atleast 95% adherence for tx to be effective

    • eval renal & hepatic

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Pneumonia

Inflamm of lung parenchyma from infection

Signs: pleuritic chest pain, cough, fever

Lab: chest x-ray

  • elevated wbc, crp, positive sputum

  • starts as resp. alka → later: resp. acid

Tx:

  • bronchodilator: albuterol or combivent → open airway

  • antibiotic → broad then specific

Care:

  • SaO2 >92%

  • position: good lung down, hob 30

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TB

Resp. infection caused by mycobacterium tuberculosis

  • spread via aerosolized droplet (NOT direct contact) → airborne precaut.

Types:

  • latent → asymp. & NOT contagious

  • active → abnormal chest x-ray/sputum

Signs: hemoptysis (coughing blood), weight loss, night sweat

Lab: tuberculin skin test (mantoux test) → assess induration (size/firm)

Tx: 3-9 months

  • 2 phases: intensive → continuation

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Asthma

Intermittent, reversible airway obstruction from inflamm → increase mucus, bronchospasm

Signs: wheezing, dyspnea, coughing, increased sputum/RR, tachy

Lab: spirometry, chest x-ray, abg

Tx: anti-inflamm (inhaled corticosteroid), bronchodilator

Care:

  • maintain o2 >90%

  • teach action plan, pursed lip, peak flow meter

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Laryngeal cancer

Originate from squamous cells that line larynx/hypopharynx/ esophagus entry → slow develop

Risk: (#1) tabacco & alcohol

Signs: change in voice (lower, raspy, >2 wks), persistent sore throat, ear pain

Lab: laryngoscopy, barium swallow

Tx: radiation, chemo, surgery

Care: post op

  • trach care/suction, pulmonary hygiene (deep breath), nut., emergency equip at bedside

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Hypertension

BP that is above normal “silent killer”

Types:

  • primary (#1) → multifactorial, chronic

  • secondary → caused by underlying, acute

Signs: increase bp

  • late → headache, chest pain, sob, vision change

Lab: >2 bp reading at SEPARATE times

Tx: slowly & cautious

  • start w/ 1-2 med (LOW doses) → diuretic, beta block, ½ dose for older

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HTN complications

Hypertensive crisis

  • hypertensive urgency → bp very high but no sign of organ damage

  • hypertensive emergency → bp >180/120 + possible damage

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Coronary artery disease (CAD)

Obstruct/dysfunc of blood vessels that deliver o2 rich blood to heart muscles → ↓ perfusion of myocardial tissue

Cause: atherosclerosis (harden/narrow of arteries b/c plaque)

Risk: elevated serum lipids

  • cholesterol >200, trig. >150

Sign: asymp until 40% block → angina

Lab: lipid profile

Tx: surgery (ex. stent)

  • aspirin (stop aggregate)

  • nitroglyercin (relief) → every 5 min x3

Care: bleeding precaut.

  • diet: decrease saturated fat (meat, whole milk), increase complex carb (whole grain)

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Peripheral artery disease (PAD)

Narrow/block of vessels that carry blood from heart to upper/lower extremities → deprive o2 → ischemia, necrosis

Cause: atherosclerosis

Signs: intermittent claudication (#1) → muscle pain b/c lactic acid buildup, foot pain worse w/ elevation, coolness, thin shiny skin

Lab: vascular assessment (palp, auscul, inspect), ABI

Tx: meds, angioplasty

Complications: nonhealing ulcers + gangrene → may need amputation

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Venous thrombus

Blood clot in vein → potential to break off (thromboembolism)

Signs: Virchow’s triad

  • stasis, endothelial injury, hyercoag.

Sign: swell, tender, redness, warmth

Lab: duplex ultrasound (confirm), D-dimer (+ test)

Tx: heparin or enoxa. (for active clot only) → transition to long term oral anticoag (warfarin (INR 2-3))

Care: watch out for bleed (bruise, petechiae, hematuria)

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Venous insufficiency

Occurs when leg veins do not allow blood flow back to heart → blood flow backward & pools in leg

Sign: “heavy pain”, skin change (brown), varicose vein, venous stasis ulcer (ankles/calves)

  • twisted, enlarged vein

Tx: surgery

  • sclerotherapy, vein ligation & stripping

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HF

Progressive disease characterized by myocardial cell dyfunc. & muscle weakening

Sign: fatigue, weight gain, tachy

  • left side: sob, crackles, fatigue, cool/weak

  • right: JVD, hepatomegaly, ascites, edema

Types:

  • HFrEF → inability to pump forward “weak pump

    • EF <45%

  • HFpEF → unable to relax & fill “stiff, improper fill

    • EF >45% but low CO

Lab: ecg

  • troponin, BNP/NT-proBNP (released in response to high bp/fluid)

Tx: diuretic, ACE inhibitor (#1), beta block

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Cancer

Uncontrolled growth of malignant cells that compromise normal cells

Risk: exposure to carcinogen → cellular mutation

Types:

  • solid tumor → arise from specific organ (ex. lung)

  • hematological → from cells (ex. leukemia)

Staging: TNM (tumor size, spread to lymph, metastasis)

Sign: CAUTION

Lab: biopsy

Tx: radiation, chemo, bone marrow transplant

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End of life

Pt goals guide treatment

Signs: dyspnea, anorexia, delirium, depression

  • late → gurgling, terminal bubbling

Care:

  • suctioning, position (lateral w/ elevated head), antimuscinaric/anticholinergic to dry up secretions

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Anemia

Reduction in o2 carrying capacity b/c less rbc or reduction in hemoglobin

Causes: blood loss, inadequate rbc produc, increased rbc destruct., deficiency

Types:

  • iron defic. (#1) → insuff. hemoglobin to carry o2

    • sign: hypoxia, pallor, fatigue

    • lab: low serum ferritin, low H&H

    • tx: red meat, dark leafy, dried beans, fortified cereal/bread (take w/ vit C)

  • vit b12 → need for func. of CNS, formation of rbc, dna reg.

    • sign: cns changes → spinal cord degen, altered mental

    • lab: b12 assay

    • tx: animal protein → meat, seafood, egg, dairy

  • folic acid → need for formation of heme for rbc mature

    • sign: pallor, tachy, dizzy

    • lab: cbc

    • tx: fortification of cereal/grains → supplements for preg.

  • sickle cell → cause hemoglobin to be sticky → block blood flow → hypoxic

    • sign: vassooclusion → pain swell

    • tx: o2 therapy, avoid cold

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Polycythemia vera

Disorder of bone marrow → makes blood more viscous (thick) → slow circulation & o2 exchange

  • increase in volume of rbc BUT still hypoxic

Cause: JAK2 gene

Sign: takes years for symp → sob, headache, risk for clot

Lab: routine blood test

Tx: therapeutic phlebotomy (remove blood)

Care:

  • hydration (3L/day), elevate legs

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Diabetes Insipidus (DI)

Deficiency of ADH (helps regulate h2o)

  • reduce ability of kidney to collect/concentrate urine → excessive dilute urine → “DRY INSIDE

Signs:

  • polyuria, polydipsia, hemoconcentration (elevated serum sodium & hematocrit), skin tenting, dry mucous mem., weak pulse

Med:

  • desmopressin or vassopressin

    • cause water reabsorption in kidneys

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DI Management

Diagnostic:

  • low →urine electrolytes, urine osmo. (<200), USG (<1.005)

  • high → serum

  • when serum osmo increases but no increase in urine osmo

Care:

  • maintain adequate fluid status PO or IV

    • at risk for circulatory collapse

  • mouth care → for dry mucous membranes

  • watch for dehydration, hypovolemia, hypernatremia

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SIADH

Excessive release of ADH

  • renal reabsorption of water → water intoxic. → cellular edema → dilutional hyponatremia “SOAKED INSIDE

Signs: volume overload + hyponatremia

  • weight gain, tachy, crackles, distended neck vein, headache, personality change, hostility

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SIADH Management + Tx

Diagnostic:

  • low → serum

  • high → urine electro., urine osmo, USG

Care:

  • PO fluid restriction & increased salt intake

    • comfort measure for thirst → ice chips

Tx:

  • diuretics, hypertonic sodium chloride IV

    • SLOW correction of hyponatremia (risk brain damage)

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SIADH vs DI

knowt flashcard image
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Hypothyroidism

function of thyroid → metabolism

  • associated w/ iodine deficiency (needed for thyroid synth.)

Signs:

  • ↓ energy, fatigue, increased sleep, weight gain, susceptible to cold temp, dry skin, thin hair, CO

Diagnostic: Low T3 & T4, high TSH

Tx: levothyroxine

  • taken FIRST thing in morning (1hr b/f meal or 3 hr after)

  • start at low dose and increase gradual → lifelong

  • side effects: weight loss, nervous, tremor, insomnia

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Myxedema coma (hypothyroidsm complication)

Emergencyhypoxia and co2 retention, fluid/electro. imbalance, hypothermia

Signs:

  • increased sensitivity to sedatives, analgesics, anesthetic

  • CO → bradycardia, hypotension

Tx:

  • IV thyroid hormone

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Hyperthyroidism

Accelerated metabolism and overstim. of SNS

  • usually caused by Grave’s

Signs: everything is increased

  • elevated HR, heat intolerance, gastric activity (BM/D), increased app, weight loss, exophthalmos & goiter

Diagnostic: high T3 & T4, low TSH

<p><mark data-color="yellow" style="background-color: yellow; color: inherit;">Accelerated metabolism and overstim. of SNS</mark></p><ul><li><p>usually caused by <span style="color: red;">Grave’s</span></p></li></ul><p><strong><mark data-color="blue" style="background-color: blue; color: inherit;">Signs: </mark></strong>everything is increased</p><ul><li><p>elevated HR, heat intolerance, gastric activity (BM/D), increased app, weight loss, <span style="color: red;">exophthalmos &amp; goiter</span></p></li></ul><p><strong><mark data-color="red" style="background-color: red; color: inherit;">Diagnostic:</mark></strong> <span style="color: blue;">high T3 &amp; T4, low TSH</span></p><p></p>
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Hyperthyroidism Tx

Meds:

  • long term → antithyroid

  • short term → iodine prep. (decrease blood flow through thyroid)

  • beta block (slow HR, decrease palpitations)

Surgery: thyroidectomy

  • for pt w/ hypersecreting tumor or tracheal compress. unresponsive to med

  • establish “normal” thyroid function before surgery

  • complications:

    • removal of all parathyroid tissue → hypoparathyroidism

    • laryngeal nerve damage → affect swallow/voice

<p><strong><mark data-color="yellow" style="background-color: yellow; color: inherit;">Meds:</mark></strong></p><ul><li><p>long term → antithyroid</p></li><li><p>short term → iodine prep. (decrease blood flow through thyroid)</p></li><li><p>beta block (slow HR, decrease palpitations)</p></li></ul><p><strong><mark data-color="blue" style="background-color: blue; color: inherit;">Surgery:</mark></strong> thyroidectomy</p><ul><li><p>for pt w/ hypersecreting tumor or tracheal compress. unresponsive to med</p></li><li><p>establish “normal” thyroid function before surgery</p></li><li><p><u>complications:</u></p><ul><li><p>removal of all parathyroid tissue → hypoparathyroidism</p></li><li><p>laryngeal nerve damage → affect swallow/voice </p></li></ul></li></ul><p></p>
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Thyroid storm/thyrotoxicosis (hyperthyroidism complication)

Signs:

  • tachycardia, fever, systolic hypertension, abd pain, tremors, change in LOC

Care:

  • Airway + fluid resuscitation

  • cooling blankets

  • meds: glucocorticoids

    • ↓ conversion of T4 to more active T3

    • ↓ release of TSH

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Hypoparathyroidism

Lack of parathyroid hormone → calcium not mobilized from bones/conserved in kidney/absorb in small intest. → hypocalcemia

  • Cause: (#1) removal of parathyroid

Signs: ↓ Ca (Ca plays major role in membrane potential, neuronal excit., muscle contract.)

  • numbness/tingling around mouth/hand/ft, tetany (severe muscle spasm → can cause laryngospasm & airway compromise), skeletal deformity, positive Chvostek sign & Trosseau

Diagnostic:

  • low serum calcium, serum PTH

  • high serum phosphate

<p><mark data-color="yellow" style="background-color: yellow; color: inherit;">Lack of parathyroid hormone → calcium not mobilized from bones/conserved in kidney/absorb in small intest. → </mark><span style="color: red;"><strong><mark data-color="yellow" style="background-color: yellow; color: inherit;">hypocalcemia</mark></strong></span></p><ul><li><p><strong>Cause: </strong>(#1) removal of parathyroid</p></li></ul><p><strong><mark data-color="blue" style="background-color: blue; color: inherit;">Signs:</mark></strong> <span style="color: blue;">↓ Ca</span> (Ca plays major role in membrane potential, neuronal excit., muscle contract.)</p><ul><li><p>numbness/tingling around mouth/hand/ft, <span style="color: red;">tetany</span> (severe muscle spasm → can cause laryngospasm &amp; airway compromise), skeletal deformity, <span style="color: red;">positive Chvostek sign &amp; Trosseau</span></p></li></ul><p><mark data-color="red" style="background-color: red; color: inherit;">Diagnostic:</mark></p><ul><li><p>low serum calcium, serum PTH</p></li><li><p>high serum phosphate</p></li></ul><p></p>
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Hypoparathyroidism Management + Tx

Meds: focus on raising serum calcium

  • Acute: IV calcium → followed w/ oral calcium + vit D (enhance absorp.)

  • Chronic: oral calcium + vit D

Care:

  • adhere to med → lifelong Ca supplementation

  • eat foods high in calcium BUT low in phosphorus (can bind to Ca → ↓ lvls more)

    • eat: dairy, milk, cheese, OJ, yogurt

    • avoid: beans, lentils, nuts

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Hyperparathyroidism

Hypersecretion of parathyroid hormone → hypercalcemia → leads to bone breakdown & increased renal/bowel reabsorp of Ca

Signs:

  • kidney stones, polyuria, abd pain, muscle weakness

  • cardiac change → prolonged PR, short QT, vent. dsyrhythmis

Diagnostic:

  • ↑  serum/ionized Ca, serum PTH

  • ↓ serum phosphorus

Tx:

  • furosemide → increase renal excretion of Ca

    • avoid thiazide diuretic (increase reabsorp)

Care:

  • prevent bone injury (use lift sheets)

  • if unresponsive to med → subtotal parathyroidectomy

  • increase fluid to minimize renal injury

  • decrease consump. of calcium containign antacid + vit D

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Addison’s disease

Destruction of adrenal glands → low hormones (cortisol + aldosterone)

  • mostly females

Signs: asymp until 90% of adrenal cortex destroyed

  • hypoglycemia, weight loss, depression, darken bronze hyperpigment., hyponatremia (salt craving), water loss, hyerK,

Diagnostic: test hypothalamic pituitary axis & adrenal cortex, serum electro

Care:

  • replacement of cortisol, fix electrolyte imbalance, maintain fluids

  • take hormone replace daily

<p><mark data-color="yellow" style="background-color: yellow; color: inherit;">Destruction of adrenal glands → </mark><span style="color: red;"><mark data-color="yellow" style="background-color: yellow; color: inherit;">low hormones (cortisol + aldosterone)</mark></span></p><ul><li><p>mostly females </p></li></ul><p><strong><mark data-color="blue" style="background-color: blue; color: inherit;">Signs:</mark></strong> asymp until <span style="color: green;">90%</span> of adrenal cortex destroyed </p><ul><li><p>hypoglycemia, weight loss, depression, <span style="color: red;">darken bronze hyperpigment.</span>, hyponatremia (salt craving), water loss, hyerK,</p></li></ul><p><strong><mark data-color="red" style="background-color: red; color: inherit;">Diagnostic: </mark></strong>test hypothalamic pituitary axis &amp; adrenal cortex, serum electro</p><p><strong><mark data-color="purple" style="background-color: purple; color: inherit;">Care:</mark></strong></p><ul><li><p>replacement of cortisol, fix electrolyte imbalance, maintain fluids</p></li><li><p>take hormone replace daily </p></li></ul><p></p>
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Adrenal crisis (addison’s comp.)

Severe hypovolemia & hypotension

Cause: pt who have underlying adrenal hypofunction who undergo stressful event

  • Na & fluid loss, hyperK, hypogycemia

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Cushing’s disease

Excessive circulating glucocorticoid (cortisol) or ACTH → excess hormones

Signs:

  • hyperglycemia, thin/friable skin, moon face, male sexual characteristic develop in female (breast atrophy, voice deepen)

Diagnostic: assess cortisol, suppression test, serum electrolytes

Care:

  • prevent fluid overload

  • turn pt frequently/protect skin

Tx: meds that interfere w/ ACTH & glucocorticoid produc.

  • monitor adrenal supress → hypoglycemia & hypona

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Diabetes Mellitus

Group of disorders characterized by ↑ blood glucose lvls

Cause: insulin deficiency, resistance, both

  • glucose cannot cross cell membrane to enter cell so it remains in bloodstream - insulin is the “key

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T1DM

Insulin producing beta cells of pancreas are destroyed → NO insulin

Signs: polyuria, polydipsia (increased thirst), polyphagia (increased app)

  • primary cause of diabetes in children

Tx: insulin

  • subcutaneously

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T2DM

Defect in cell membrane → even though insulin is present, the cell “resists” it

  • leads to ↑ insulin demand & beta cell failure

Signs: polyuria, polydipsia, polyphagia, poor wound heal, visual disturbance

  • more common in adult

Tx: oral meds

  • sulfonylureas → stim pancreas to produce insulin

  • biguanides → decrease hepatic glucose output

  • alpha glucosidase inhibitor → delay intestional absorp of glucose

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Diagnosis for DM

Hemoglobin: 6.5% or higher

  • measures amount of glucose that binds to rbc

Fasting blood glucose: >126 mg/dL

  • no caloric intake for at least 8 hrs

Two-hour postprandial test: >200 mg/dL

  • blood sample taken prior to consump then after at 1 hr & 2hr post

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DKA (DM comp.)

Inadequate insulin for cells to obtain adequate glucose for normal metabolism

  • rapid breakdown of fat stores → release fatty acids → converts to ketone → lead to metabolic acid.

  • increased release of hormones (glucagon & cortisol) → severe hypergylcemia

Diagnostic:

  • blood glucose >250

  • blood pH <7.3

  • serum bicarb <16

Signs: polyuria, kussmual, fruity acetone breath

Tx:

  • administer o2

  • correct electrolyte PRIOR to insulin (will make hypoK worse)

  • priority: fluid → potassium → insulin

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Hyperosmolar hyperglycemic syndrome (HHS)(DM comp.)

Occurs when there is enough insulin to prevent rapid fat/ketones but NOT enough to prevent hyerglycemia (>600)

  • leads to osmotic diuresis → electro imbalance, neurological defect

  • EXTREME dehydration

Tx: IV insulin, NaCl infusion

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Seizures

Sudden burst of uncontrolled electrical activity in brain → temp disrup of normal func.

Causes: trauma, surgery, tumors, strokes, electrol.

  • Chronic = epilepsy

    • Diagnosis: 2 unprovoked seizures that occur at least 24 hrs apart

Signs: *document when seizure starts, presentation, how long it last

  • 4 phases

    • prodromal → precedes seizure (confusion, anxiety mood, anger)

    • aural → sensory warning leading up to seizure (flashing light, visual disturbance, smells, voices)

    • ictal → seizure itself

    • postictal → rest & recovery (5-30min until baseline)

  • Other: episodes of daydreaming, unilateral muscle move., repetitive unconscious moves (lip smack, chew, swallow)

Diagnostic: CT/MRI, ECG (may need to repeat)

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Tonic clonic (seizures)

Formerly “grand mal” → (#1) generalized seizure

  • involves both hemispheres

2 phases

  • Tonic → body stiffens, last for 10-20 sec

  • Clonic → jerking of extremities, last 30-40 sec

    • cyanosis, excess saliva, tongue/cheek biting

  • postictal: soreness & fatigue → pt may sleep for hours & not feel normal for hrs-days

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Status epilepticus (seizure comp.)

Seizure activity lasting >5 min OR >2 seizures w/o full recovery of conciousness

Cause: head trauma, hydrocephalus, drug/alc withdrawal (anticonvulsive)

  • >30 min can cause resp failure, brain damage, death

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Seizure management + tx

Med:

  • antiepileptic/anticonvulsants → ex. gabapentin, levetiracetam, lamotrigine, topiramate

    • do not stop abruptly → can precipate seizure

    • side effects: diplopia (blur vision), ataxia, drowsiness

Care:

  • bed in lowest position, suction at bedside, do not force object in mouth, turn pt to side to prevent aspiration, do NOT restrain

  • driving restrictions

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Parkinson’s

Progressive neurological disorder affecting movement, balance, coordination → loss of dopamine producing brain cells

Signs:

  • resting tremor, muscle rigidity, slow/loss move (bradykinesia/akinesia), postural instability (falls), shuffle & wide gait

Diagnostic: ≥2 cardinal symptoms are observed

Tx: focus on controlling symp

  • (#1) dopamine receptor agonist → mimic dopamine

    • side effect: disorder of impulse control (gambling), LE edema, urinary freq

  • anticholinergics → reduce tremor/drool (not used in older due to side effect)

  • dopamine pre-cursor (cardidopa-levodioa) → for advanced stage

Care:

  • fall risk (short, deliberate steps), psychosocial (depression)

<p><mark data-color="yellow" style="background-color: yellow; color: inherit;">Progressive neurological disorder affecting movement, balance, coordination →</mark><span style="color: red;"><mark data-color="yellow" style="background-color: yellow; color: inherit;"> loss of dopamine</mark></span><mark data-color="yellow" style="background-color: yellow; color: inherit;"> producing brain cells</mark></p><p><strong><mark data-color="blue" style="background-color: blue; color: inherit;">Signs:</mark></strong></p><ul><li><p><span style="color: red;">resting tremor</span><span style="color: rgb(10, 9, 9);">, </span><span style="color: red;">muscle rigidity</span><span style="color: rgb(23, 21, 21);">,</span><span style="color: red;"> slow/loss move </span>(bradykinesia/akinesia), <span style="color: red;">postural instability</span> (falls), <span style="color: red;">shuffle &amp; wide gait</span></p></li></ul><p><strong><mark data-color="red" style="background-color: red; color: inherit;">Diagnostic: </mark></strong><span style="color: blue;">≥2 </span>cardinal symptoms are observed</p><p><strong><mark data-color="purple" style="background-color: purple; color: inherit;">Tx: </mark></strong>focus on controlling symp</p><ul><li><p><strong>(</strong><span style="color: red;"><strong>#1</strong></span><strong>) dopamine receptor agonist </strong>→ mimic dopamine</p><ul><li><p><u>side effect:</u> disorder of impulse control (gambling), LE edema, urinary freq</p></li></ul></li><li><p><strong>anticholinergics </strong>→ reduce tremor/drool (not used in older due to side effect)</p></li><li><p><strong>dopamine pre-cursor</strong> (cardidopa-levodioa) → for advanced stage</p></li></ul><p><strong><mark data-color="green" style="background-color: green; color: inherit;">Care:</mark></strong></p><ul><li><p>fall risk (short, deliberate steps), psychosocial (depression)</p></li></ul><p></p>
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Multiple Sclerosis

Chronic progressive neurological disorder → nerves of CNS degenerate → demyelination of nerve fiber + buildup of scar tissue/plaque

Signs: slow nerve conduction → impaired sensation, move, think

  • numbness in limb, unsteady, muscle spasm, memory, vision, bladder dysfunc, speech impair

Diagnostic: no specific → ruling out other conditions (takes month-yrs)

Tx: no cure

  • beta interferon, immunosuppressive → slow progession

  • corticosteroid - tx attacks, inflamm

Care: collab with pt to improve ROM, increase venous return/prevent stiff

  • rest period to prevent fatigue/overheat

  • bowel/bladder control → self cath may be needed, increase fluid/fiber

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Stroke

Occurs when there is an interruption of blood supply to the brain from ischemia or hemorrhage

  • also known as “brain attack” or “cva”

Risk factors: htn, smoking, hypocholesterolemia

Signs:

  • left sided strokes lead to right side deficit (& vice versa)

  • swallowing, speech, receptive aphasia (loss of comprehension), excessive aphasia (loss of produc of language), global aphasia (no communication)

Diagnostic: CT/MRI

  • STAT head CT → initial - looks for bleed and determine tx

Care: understand pt baseline, supportive, preventative

  • monitor serum electrolytes (esp. Na)

  • bedside swallow screen (NPO until cleared), tuck chin when swallow, thicken liquids, oral care, elevate paralyzed/weak limbs to prevent edema

<p><mark data-color="yellow" style="background-color: yellow; color: inherit;">Occurs when there is an </mark><span style="color: red;"><mark data-color="yellow" style="background-color: yellow; color: inherit;">interruption of blood supply to the brain </mark></span><mark data-color="yellow" style="background-color: yellow; color: inherit;">from ischemia or hemorrhage</mark></p><ul><li><p>also known as “brain attack” or “cva”</p></li></ul><p><strong><mark data-color="blue" style="background-color: blue; color: inherit;">Risk factors:</mark></strong> htn, smoking, <span style="color: blue;">hypocholesterolemia</span></p><p><strong><mark data-color="red" style="background-color: red; color: inherit;">Signs:</mark></strong></p><ul><li><p>left sided strokes lead to right side deficit (&amp; vice versa)</p></li><li><p>swallowing, speech, receptive aphasia (loss of comprehension), excessive aphasia (loss of produc of language), global aphasia (no communication)</p></li></ul><p><strong><mark data-color="purple" style="background-color: purple; color: inherit;">Diagnostic:</mark></strong> CT/MRI</p><ul><li><p><span style="color: red;">STAT head CT </span>→ initial - looks for bleed and determine tx</p></li></ul><p><strong><mark data-color="green" style="background-color: green; color: inherit;">Care: </mark></strong><span style="color: blue;">understand pt baseline</span>, supportive, preventative</p><ul><li><p>monitor serum electrolytes (esp. <span style="color: blue;">Na</span>)</p></li><li><p><span style="color: purple;">bedside swallow screen </span>(NPO until cleared), tuck chin when swallow, thicken liquids, oral care, elevate paralyzed/weak limbs to prevent edema</p></li></ul><p></p>
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Transient ischemic attack (TIA)

Temp episode of neurologic dysfunc caused by brief interruption of blood supply to brain

  • “mini stroke”

  • no cell death or perm damage, symp resolve in 24 hrs, typically not detected in brain scans

Tx:

  • meds: antiplatelet & statin

  • surgery: carotid endarterectomy, stent

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Ischemic stroke

Inadequate blood flow to the brain from partial or complete occlusion of an artery

  • (#1) stroke

Tx: TPA - reestablish blood flow through blocked artery to prevent cell death

  • pt must be appropriate “candidate” and screened carefully

  • must be administered within 3.4.5 hrs of symp onset

  • no recent gi bleed, stroke, head trauma, no major surgery within 14 days

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Hemorrhagic stroke

Bleeding within the brain caused by rupture of vessel

Cause: htn

Comp: aneurysm rebleeding, cerebral vasospasm

Tx: control bp, aneurysm clipping or coiling

  • poor prognosis

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Cataracts

Alteration in lens protein/chemical change → gradual clouding of lens

Risk: exposure to UV

Signs: worse w/ progression

  • vision → clouded, blurred, dim, halo around light source, double vision in single eye

Diagnostic: visual acuity test & direct ophthalmoscope exam (checks opaqueness)

Tx: (#1) surgical removal of lens (replace w/ artificial)

Care:

  • administer mydriatic (dilating) & cycloplegic (paralyzing) eye drops pre-op, drainage & prevent increase in IOP post-op (fluids, fiber, hob)

  • maintain eye patch

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Glaucoma

Characterized by increased 1) increased IOP, 2) optic nerve atrophy & damage, 3) peripheral vision loss

  • Normal IOP = 11-21

Types:

  • primary open angle (gradual): asymp → gradual loss of peripheral vision (both eyes) and tunnel vision (advanced)

    • IOP 22-32

  • angle closure (acute): medical emerg → IOP rises very quick & signs include severe eye pain, visual disturbance, reddening

    • IOP >50

Tx: eye drops (decrease aqueous humor, drain fluids → ↓ IOP)

  • surgery:

    • laser trabeculoplasty → open clogged drainage canals

    • filtering surgery → meshwork to allow aqueous humor to exit

    • drainage implants

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Macular degeneration

Responsible for sharp, central vision → driving, reading, recog. faces

Types:

  • Dry (#1)(can progress to wet): presence of drusen bodies (yellow deposits under retina)

  • Wet: when abnormal blood vessels grow under macula → fragile & leak blood & fluid → macula raises from usual position

Signs: distorted central vision → straight lines appear disorted/wavy, difficulty recognizing faces

Diagnostic: Amsler grid, fluorescein angiogram

Tx: no cure

  • supplements (vit C, E, leutin, zeaxanthin), laser surgery

<p><mark data-color="yellow" style="background-color: yellow; color: inherit;">Responsible for sharp, </mark><span style="color: red;"><mark data-color="yellow" style="background-color: yellow; color: inherit;">central vision </mark></span><mark data-color="yellow" style="background-color: yellow; color: inherit;">→ driving, reading, recog. faces</mark></p><p><strong><mark data-color="blue" style="background-color: blue; color: inherit;">Types:</mark></strong></p><ul><li><p><strong>Dry </strong>(#1)(can progress to wet): presence of <span style="color: rgb(243, 172, 12);">drusen</span> bodies (yellow deposits under retina)</p></li><li><p><strong>Wet: </strong>when abnormal <span style="color: red;">blood vessels </span>grow under macula → fragile &amp; leak blood &amp; fluid → macula raises from usual position</p></li></ul><p><strong><mark data-color="red" style="background-color: red; color: inherit;">Signs</mark></strong>: distorted central vision → <span style="color: blue;">straight lines appear disorted/wavy, difficulty recognizing faces</span></p><p><strong><mark data-color="purple" style="background-color: purple; color: inherit;">Diagnostic:</mark></strong> Amsler grid, fluorescein angiogram</p><p><strong><mark data-color="green" style="background-color: green; color: inherit;">Tx:</mark></strong> no cure</p><ul><li><p>supplements (vit C, E, leutin, zeaxanthin), laser surgery</p></li></ul><p></p>
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Meniere’s disease

Disorder of inner ear → leads to vertigo, tinnitus, hearing loss

Cause: unknown → infection, high stress, trauma, excess endolymphatic fluid

  • mainly affect females 40-60

Signs: varies → n/v/d, abd pain, uncontrollable eye move

Diagnostic: based on presentation/ruling out

Tx: no cure → goal is decrease body fluid & CNS stim.

  • meds (diuretics, antiemetics, antivertigos)

  • surgery for severe: vestibular nerve transection, labrynthectomy (removal) → result in total hearing loss

Care:

  • avoid sudden move, bright lights, caffeine/alcohol, at least 8hr sleep, acupuncture

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Osteoporosis

Chronic condition results in deterioration of bone tissue & density → risk for fracture

  • #1 bone disease

  • rate of bone resorption (osteoclast) > bone rebuilding (osteoblast)

Risk: aging, calcitonin, estrogen, ↑ parathyroid hormone

Diagnostic: “silent disease” not diagnosed until fracture/fall/strain

Signs: kyphosis of dorsal spine, loss of height, back pain

Tx + care: prevention & early screening are KEY → prevent/slow progression

  • ↑ calcium & vit D (help w/ collagen synth & bone form.)

    • calcium: 1200 mg/day

    • vit D: 15 min/day or 800-1000 units

  • meds: bisphosphonates - inhibit osteoclast, calcitonin, estrogen

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Osteomyelitis

Infection of bone from direct bone contamination (open frac, trauma), extension of soft tissue infection, bloodborne spread

Signs: pain not relieved by rest, swelling/warmth/tender on site

Diagnostic: bone biopsy (#1)

Tx: antibiotic therapy (IV x4-6 weeks → then transition to PO (long term))

  • surgery/debridement of infected tissue/bone, amputation for severe

Care:

  • ↑ protein, vit for wound heal

  • thermal therapy (hot + cold)

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Fractures

Disruption or break in continuity of a bone (emergency)

  • usually occur in young/old (b/c bones are porous/weak)

Diagnostic: radiography or CT

Care:

  • assess neurovascular, immbolize w/ splinting, cover open frac w/ sterile dressing (do NOT attempt to reduce)

  • diet: protein, calcium, vit

  • pulmonary hygiene: deep breath/cough

Tx:

  • nonsurgical: closed reduction (fractures are manually manipulated & realigned)

  • surgical: open reduction w/ internal or external fixation (hardware)

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Fracture tx

Casts: very rigid → made from fiberglass → may take 24-72 hrs to dry (handle with palms of hands)

  • assess “CMS” → circulation, movement, sensation

  • 5 Ps → pain, pallor, pulselessness, paresthesia, paralysis

    • notify provider if noticed

External fixation device: manage open fractures w/ soft tissue damage OR support for complicated/comminuted (crush, splintered)

  • discomfort minimal → early ambulation, elevate limb, pin care

Traction: short term → pulling force to injury

  • must be continuous → weights NEVER removed unless order

  • ropes must be unobstructed & weight hanging freely

Amputation: removal of part of body

  • DO NOT put pillow under → flat or prone instead

  • wrap limb to prevent edema + better fit for prosthetic

  • phantom pain common

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Fracture complications

Neurovascular compromise:

  • any source of ↓ blood flow and o2 to tissues

Compartment syndrome:

  • pressure in compartment causing compression of nerves/blood vessels

Venous thromboembolism/fat embolism:

  • clots can hinder circulation and travel to lungs

Traumatic rhabdomyolysis:

  • damaged muscle tissue releases proteins and electrolytes into blood → damage heart & kidneys

Hemorrhage, hypovolemia:

  • severe loss of blood

Malunion and nonunion:

  • fractures fail to heal in correct alignment

Disuse syndrome:

  • muscle atrophy with loss of strength

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Osteoarthritis

Slow progressive disorder involving breakdown of cartilage within joint & underlying bone change “wear and tear

  • usually involve weight bearing joints → knees, hips, feet, lumbar spine

Risk: older, female (estrogen)

  • regular moderate exercise shown to likelihood/progress.

Signs: joints impacted ASYMMETRICALLY

  • pain worse w/ activity → relieved by rest, crepitus

Diagnostic: based on signs, x-ray (may only show in advanced)

Tx: no cure

  • meds: acetaminophen (not exceed 4 g daily)

    • nsaids: risk of bleed

  • joint replacement: for severe

    • assess for orthostatic hypotension & dizziness

    • hip precautions (for 6-12 wks) → no flex >90 degrees, raised toilet, no crossing leg

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RA

Chronic, systemic, autoimmune inflammatory disease characterized by inflamm that affect daithrodial (freely moving) joints

  • commonly affect hands, wrist, knees symmetrically

Signs: SYMMETRICAL joint pain, morning stiffness >30 min

Diagnostic: combination (labs (ESR, CRP), radiograph/ultrasound, signs)

Tx:

  • initial: analgesic (acetam., narcotic), nsaid, glucocorticoids

  • if ineffective → methotrexate

  • surgery

Care:

  • keep up w/ vax (NO live vaccines)

<p><mark data-color="yellow" style="background-color: yellow; color: inherit;">Chronic, systemic, autoimmune inflammatory disease characterized by</mark><span style="color: red;"><mark data-color="yellow" style="background-color: yellow; color: inherit;"> inflamm that affect daithrodial (freely moving) joints </mark></span></p><ul><li><p>commonly affect <span style="color: blue;">hands, wrist, knees </span>symmetrically </p></li></ul><p><strong><mark data-color="blue" style="background-color: blue; color: inherit;">Signs:</mark></strong><span style="color: red;"> SYMMETRICAL </span>joint pain, morning stiffness &gt;30 min</p><p><strong><mark data-color="red" style="background-color: red; color: inherit;">Diagnostic: </mark></strong>combination (labs (ESR, CRP), radiograph/ultrasound, signs) </p><p><strong><mark data-color="purple" style="background-color: purple; color: inherit;">Tx: </mark></strong></p><ul><li><p><strong>initial: </strong>analgesic (acetam., narcotic), nsaid, glucocorticoids</p></li><li><p>if ineffective → methotrexate </p></li><li><p>surgery</p></li></ul><p><strong><mark data-color="green" style="background-color: green; color: inherit;">Care:</mark></strong></p><ul><li><p>keep up w/ vax (<span style="color: red;">NO</span> live vaccines)</p></li></ul><p></p>
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Gout

Accumulation of uric acid crystals in joints → body attempt to get rid of them resulting in inflamm

Risk: red meat/seafood/alcohol, use of thiazide diuretic

Sign: starts w/ inflamm of great toe

Diagnostic: observing crystal in synovial fluid

Tx: avoid high purine foods

  • meds:

    • acute: pain relief & inflamm (nsaid)

    • chronic: allopurinol (lower uric acid)