Exam 2 | Musculoskeletal & Renal Flashcards
1
Q
Tx and Management of Acute Fx
A
- Immobilization: casts and not moving it
- Reduction: realigning the bone structure back to normal
- Surgery: usually for comminuted breaks
2
Q
OA vs. RA | Type
A
- 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
3
Q
OA vs. RA | Pathophysiology
A
- 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)
4
Q
OA vs. RA | Sx
A
- 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
5
Q
MOA for all drug classes in treating RA
A
- 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
6
Q
Pathophysiology of gout
A
- ↑ 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
- Uric acid byproduct of purine metabolism
- Usually deposited in big toe bc of low pH and cool environment
- Due to either overproduction of uric acid from purine metabolism or underexcretion of uric acid via kidneys (uric acid production & secretion imbalance)
7
Q
Gout Characteristics | Stages of Gout
A
- 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
8
Q
Gout Characteristics | Contributing Factors
A
- Diet: food high in purines → red meat, seafood, etc.
- ETOH: damages kidneys ⇒ harder to excrete uric acid
- Medications
- Medical conditions including genetics
9
Q
Gout Characteristics | Nursing considerations
A
- 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
10
Q
Drug-drug interaction w/ Allopurinol
A
- 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
11
Q
Renin-angiotensin-aldosterone complex system and it’s related hormone involvement
A
- 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+
12
Q
Vasopressin
A
- 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
13
Q
Acute Cystitis | What & Cause
A
- What: bladder infection that can later cause → Pyelonephritis
- Cause: E. coli
14
Q
Pyelonephritis | What & Causes
A
- 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)
- Frequent UTIs like acute cystitis can cause pts to develop pyelonephritis
15
Q
Source of creatinine breakdown
A
- Muscles
- Older you get ⇒ muscles break down ⇒ kidneys excrete it
- Pts w/ kidney failure ⇒ can’t excrete creatinine
