Exam 2 | Musculoskeletal & Renal

Question 1

Tx and Management of Acute Fx

Answer 1

• Immobilization: casts and not moving it
• Reduction: realigning the bone structure back to normal
• Surgery: usually for comminuted breaks

Question 2

OA vs. RA | Type

Answer 2

• OA:
  
  • Happens with old age
  • Degenerative bone disease (bones degenerate as we get older)
  • Influenced by age, genetics obesity (stress on bones ⇒ accelerates bone degradation), joint injury/overuse
• RA:
  
  • Autoimmune disease
  • Influenced by genetics and environmental factors

Question 3

OA vs. RA | Pathophysiology

Answer 3

• OA:
  
  • Loss of cartilage at those joints ⇒ bone rubs against each other ⇒ leads to inflammation
  • Loss of proteoglycans (responsible for structure and hydration of cartilage) ⇒ loss of cartilage
  • Releases specific enzymes that degrade cartilage and collagen ⇒ decreases proteoglycan formation
  • Bone spurs and becomes denser and harder ⇒ gives bone more pressure and increases risk of more tears on bone ⇒ body recognizes it as abnormal ⇒ helps drive inflammation to joint so IS response of redness, warmth, etc. occurs
• RA:
  
  • Inflammatory response: Inflammatory markers of cytokines, prostaglandins, monocytes, etc. → eats at joints and inflames and degrades synovial fluid
  • Antibodies: B-cell differentiation turns B-cells to plasma cells that have antibody-antigen complexes that destroys cartilage (body doesn’t recognize them as normal ⇒ keeps degrading cartilage)

Question 4

OA vs. RA | Sx

Answer 4

• OA:
  
  • Pain in morning but gets better with rest
  • Pain w/ joint use
  • Pain w/ motion bc of loss of synovial fluid
  • Decreased ROM bc of loss of synovial fluid
  • Bouchard’s nodes: small bony growths that appear on middle joint of finger
  • Crepitus: escaping air pockets in space ⇒ cracking noise ⇒ air bubbles popping into matrix spaces
• RA:
  
  • Painful joints: pain persists >30 mins and prolonged
  • Tender joints
  • Stiff joints: usually hands and feet stiff in morning
  • Caplan syndrome: rheumatoid nodules in organs

Question 5

MOA for all drug classes in treating RA

Answer 5

• NSAIDs: anti-inflammatory COX enzyme inhibition
• Glucocorticoids: tampers and blunts immune response → stunts inflammation
• Biologic Disease-Modifying Anti-Rheumatic Drugs (DMARDs):
  
  • Methotrexate: blunts rapid cell growth by blocking folate synthesis ⇒ inhibits DNA synthesis ⇒ stunts cell growth and reproduction
  • Leflunomide: acts on antibody-antigen part of disease process by limiting B-cell proliferation → reduces antibody production → reduces autoimmune attack ⇒ no inflammation
  • Tumor Necrosis Factor (TNF) Inhibitors: blocks TNF process in which cytokines are involved in inflammation ⇒ blunts inflammation process

Question 6

Pathophysiology of gout

Answer 6

• ↑ Uric acid build up ⇒ hyperuricemia → uric acid crystallization → crystals deposited in joints ⇒ IS attacks it ⇒ gout attack of degradation, damage, redness, pain, swelling in affected joint sites
  
  • Due to either overproduction of uric acid from purine metabolism or underexcretion of uric acid via kidneys (uric acid production & secretion imbalance)
    
    • Uric acid byproduct of purine metabolism
      
      • Purine found in red meats, seafood, and organ meats
  • Usually deposited in big toe bc of low pH and cool environment

Question 7

Gout Characteristics | Stages of Gout

Answer 7

• Asymptomatic gout: happens before gout attack where uric acid in blood ⇒ causes urate to form crystals
• Acute intermittent gout: gout attack begins → causes pain, swelling, stiffness, redness, fatigue, fever
• Chronic tophaceous gout (Tophi/Tophi Cysts): long term complication of gout that’s an advanced stage where urate crystals form hardened lumps → erodes bone and cartilage
  
  • May impact kidneys due to uric crystals being deposited there and forming stones
  • Can cause irregular shape of nail’s skin

Question 8

Gout Characteristics | Contributing Factors

Answer 8

• Diet: food high in purines → red meat, seafood, etc.
• ETOH: damages kidneys ⇒ harder to excrete uric acid
• Medications
• Medical conditions including genetics

Question 9

Gout Characteristics | Nursing considerations

Answer 9

• If we mitigate uric acid build up ⇒ we slow Sx onset
• Educate pts to stay away from purines
• Hydrate to help flush out uric acid

Question 10

Drug-drug interaction w/ Allopurinol

Answer 10

• Allopurinol MOA: inhibits xanthine oxidase needed for uric acid production → reduces uric acid lvls in blood (↓ hyperuricemia) → prevents uric acid crystal formation in joints
• Interacts w/ thiazide diuretics: thiazide dries out body leaving behind uric acid bc it’s a diuretic that works on kidneys by drying it out and excreting Na+, but doesn’t do anything to uric acid so it just leaves it in body
  
  • Allopurinol reduces uric acid lvls + thiazide leaves uric acid in = allopurinol works harder to try and reduce uric acid
• Interacts w/ aspirin: avoid these two bc aspirin increases uric acid formation)
  
  • Allopurinol reduces uric acid lvls + aspirin increases uric acid lvls = increases uric acid lvls together and makes it harder for allopurinol to work

Question 11

Renin-angiotensin-aldosterone complex system and it’s related hormone involvement

Answer 11

• Low BP / Low Fluid Volume triggers system bc it means body isn’t perfusing
• Kidneys senses this → secretes renin
• Renin converts angiotensinogen from liver → angiotensin I
• Angiotensin-converting enzyme (ACE) from lungs converts angiotensin I → angiotensin II
• Angiotensin II stimulates…
  
  • Vasoconstriction ⇒ increases BP
  • Adrenal cortex to make aldosterone that stimulates K+/Potassium excretion + Na+/Sodium reabsorption which results in water reabsorption bc water follows Na+

Question 12

Vasopressin

Answer 12

• Is an antidiuretic hormone only for pts that’s fluid down or hypotensive bc it causes peripheral vasoconstriction
• Pts fluid down or hypotensive → body secretes antidiuretic hormone called vasopressin
• Vasopressin acts on kidney by telling it to hold onto sodium which also retain water to keep fluid volume up
  
  • Ie. during overwhelming infection, IS causes capillaries and blood vessels to be leaky → give vasopressin which is a vascular presser to combat the pt’s vasodilation → retains fluid
• Systemic vascular resistance (SVR): narrowness/tightness of blood vessels that heart has to pump blood thru to supply organs and tissues
  
  • Hypotensive pts → have dilated blood vessels ⇒ low SVR bc blood can move through dilated blood vessels easy ⇒ heart doesn’t have to pump hard
  • Hypertensive pts → have constricted blood vessels ⇒ high SVR bc blood has harder time moving thru narrow blood vessels ⇒ heart pumps harder
    
    • High SVR in hypertensive patients ⇒ stiffer, less responsive blood vessels ⇒ harder for meds to dilate them and lower BP

Question 13

Acute Cystitis | What & Cause

Answer 13

• What: bladder infection that can later cause → Pyelonephritis
• Cause: E. coli

Question 14

Pyelonephritis | What & Causes

Answer 14

• What: Kidney inflammation where bacteria left bladder and traveled to become kidney infection
• Causes:
  
  • Frequent UTIs like acute cystitis can cause pts to develop pyelonephritis
    
    • So technically, most common cause is E. coli bacteria traveling to become kidney infection
  • If pt continuously have bladder infections or obstructions (stones)

Question 15

Source of creatinine breakdown

Answer 15

• Muscles
• Older you get ⇒ muscles break down ⇒ kidneys excrete it
• Pts w/ kidney failure ⇒ can’t excrete creatinine

Question 16

Causes of proteinuria in glomerulonephritis

Answer 16

• Glomerulonephritis: inflammation glomerulus where blood is filtered and where proteins are usually retained in blood ⇒ unable to filter properly bc vessels are infected ⇒ proteins stays in filtrate
  
  • Infection
  • Immune response (2 things happen):
    
    • Antigen-antibodies form bacterial infections makes capillary system leaky bc it’s trying to get it eaten by phages ⇒ proteins stays in urine ⇒ makes urine frothy
    • Permeability ⇒ proteins goes to urine
  • Glomerular damage: antigen-antibody complex damages cells bc it’s marking it to be eaten ⇒ causes cell leakage
  • Proteinuria and Hematuria if severe

Question 17

Nursing considerations for loop diuretic (ie. furosemide (Lasix), torsemide, bumetanide (Bumex))

Answer 17

• Monitor electrolytes, esp K+/potassium and Na+/sodium: med acts on ascending nephron loop and blocks reabsorption of sodium, chloride, water + increases excretion of potassium ⇒ potassium lvls need more monitoring
  
  • Norm K+ lvls: 3.5 – 5
  • Norm Na+ lvls: 135 – 145
  • Examples:
• Monitor vitals, hold for BP < 90/60 and call provider bc low BP means low fluid volume
• Monitor daily weight and strictly record all of pt’s intake and output fluids
• Give med earlier in day to minimize nocturia
• Common doses: 20 – 80 mg QD (once/day) or BID (twice/day)

Question 18

MOA of spironolactone

Answer 18

• Blocks aldosterone from binding to its receptors in distal nephron → decreases reabsorption of sodium and chloride so water excretion increases + potassium excretion decreases bc aldosterone stimulates its excretion → makes this med “potassium-sparing”
  
  • Remember that aldosterone regularly stimulates K+/Potassium excretion + Na+/Sodium reabsorption which results in water reabsorption bc water follows Na+

Question 19

Phenazopyridine (Pyridium) Side Effects

Answer 19

• Urine red-orange-brown discoloration
• Mild-headache, dizziness, stomach cramping
• Not antibiotic, just calms bladder spasms and other symptoms

Question 20

Nursing considerations for antibiotic therapy treatment of UTIs

Answer 20

• If ordered, get C&S before starting any UTI antibiotic therapy
• Tell pt to take full course of antibiotics even if they’re feeling better bc of antibiotic resistance
• Caution female pts UTI antibiotics decreases oral contraceptive effectiveness
• Hydrate
• Wipe front → back
• Before beginning therapy, assess drug allergies, renal functions (BUNs), liver functions (LFTs), cardiac function, other labs, potential drug interactions