Unit 3 - Chapter 39 Alterations of renal and urinary tract system

Question 1

Obstruction

Answer 1

• anywhere in urinary tract
• kidney stones, tumors, enlarged prostate, strictures of the ureter or urethra

can cause:
1) hydronephrosis - swelling of a kidney (renal pelvis and calyces) due to a build-up of urine. It happens when urine cannot drain out from the kidney to the bladder from a blockage or obstruction. Hydronephrosis can occur in one or both kidneys.

sx
* pain either in side or back (flank pain), abdomen or groin
* pain during urination
* frequency, incomplete urination, incontinence
* nause/fever

tx
* antibiotics
* kidney stone (may pass or surgery)
* catheter to drain or nephrostomy (drains from kidney)
* worse case - dialysis or kidney transplant

2) Hydroureter is when the ureter gets bigger than normal due to a backup of urine (pee). Ureters carry urine from each kidney, to the bladder. Hydroureter can happen with other problems of the urinary tract, but it can also be the only condition present.

3) Ureterohydronephrosis (dilation of both the ureter and the pelvicaliceal system)

4) infection caused by urine accumulation d/t obstruction

Question 2

Tubulointerstitial fibrosis

Answer 2

• the accumulation of collagen and related molecules in the interstitium. Interstitial collagen is normally present in the kidney, particularly type I and III, which serve as structural scaffolding
• an imbalance between the excessive synthesis and decreased breakdown of the ECM, which may result from a normal wound-healing response becoming deregulated, with an uncontrolled inflammatory response and myofibroblast proliferation
• including dysregulated apoptosis
• both can l/t CKD in untreated obstructive uropathy

Question 3

What happens when one kidney is obstructed d/t obstructive disease?

Answer 3

• Opposite kidney compensates for loss fx => hypertrophy and hyperfunction

Question 4

Relief of obstruction?

Answer 4

• postobstructive diuresis and may cause fluid and electrolyte imbalance

Question 5

Kidney stones

Answer 5

• caused by supersaturation of urine w/ precipitation of stone-forming substances, changes in urine pH, or UTI. Most stones are unilateral
• pain and bleeding can occur
• block flow
• ureters (ureteral stone) or bladder (bladder stone)

Causes -
* Have too much calcium (a mineral) or other substances in your urine
* Have certain medical problems, including certain cancers
* Have people in your family who’ve had kidney stones
* Eat certain foods
* Are middle-aged or older
* Are male

sx -
* bladder stones => lower abdomen (belly pain)
* stones in kidney or ureter may cause back pain, usually in between ribs and hip + also maybe across your belly and down your legs [severe and comes and goes]
* nausea/vomiting
* reddish-brown or bloody urine
* urgency
* burning or pain when you pee
* if infection => cloudy or smelly + possible fever

tx-
small stone - pass on its own may need pain med
* Larger stones - pain med, lithrotripsy (sound waves to break up stone into tiny pieces
* Or use a scope via urethra or scope into kidney through a small cut in your back [once inside, the stone can pulled out with the scope; or may need a laser or another method such as shock wave lithrotripsy
* once broken into small pieces => can be peed out => use strainer to identify stones

prevention-
calcium diet (minimize) but eat enough
avoid red meat, organ meats, and shellfish (high purines => uric acid)
avoid high oxalate content (spinach, berries, wheat bran, nuts, tea, rhubarb
Moderate protein
avoid salts
avoid high dose of vitamin C => l/t oxalate when excess of 1000mg/day

most common kidney stone => calcium oxalate and most often causes obstruction in the ureter

Question 6

Neurogenic bladder

Answer 6

• neural lesion that interrupts innervation of the bladder
• PMC or pontine micturition center coordinates mechanical process of micturition, thus the sphincter and detrusor muscle activites of urinary bladder
• **Upper motor neron lesions above the PMC result in detrusor hyperreflexia **(uninhibited or reflex bladder)
  1) Upper motor neuron d/o in which bladdder empties automactically when full and external sphincter functions nokrmally [PMC still intact therefore there is coordination between detrusor muscle contraction and relaxation of urethral sphincter]
  2) Causes: stroke, brain injury, dementia, brain tumor
• Upper motor neuron lesiosn between C2 and S1 l/t overactive or hyperreflexive bladder function [below PMC but above sacral micturition center]
  1) loss of pontine coodriation of detrusor muscle contraction + external shicter relaxation => both contracting at same time causing functional obstruction of bladder
  2) Detrusor hyperreflexia with detrusor sphincter dyssnergia (loss of coordinated neuromuscular contraction)
  3) Diminished bladder relaxation during storage w/ small urine volumes and high intravesicular (inside bladder) pressures
  4) resulting in overactive bladder syndrome w/ urgency, frequency, urge incontinence, increased urethral turbulence and UTI
  Causes - spinal cord injury, MS, guillain barre syndrome, intervetebral disk problems
• managed by a-adrenergic blocking (antimuscarinic) medications or botulinum toxin A + bladder neck incision (remove contraction) + intermittent catherization (w/ aboves meds for proper evacution) + condom catheter + transurethral resection or sphincterotomy (remove sphincter tissue)
• Lower motor neuron lesions below S1 result in detrusor areflexia with underactive, hypotonic, or atonic bladder function (involve the sacral micturition)
  1) acontractile detrusor or atonic bladder w/ retention of urine and distention; if sensory innervation of bladder intact, full bladder may be sensed but the detrusor may no contract
  2) Underactive bladder syndrome w/ stress and overflow incontinence
  3) causes - myelodysplasia (blood cells in bone marrow - immature cancer), MS, tabes dorsalis (degenrating nerves in dorsal columns of the spinal cord and carry info regarding proprioception), peripheral polyneuropathies
  4) intermittent catherization w/ antimmuscarinic drugs, long-term catherization, augmentation enterocystoplasty (enlarge low compliant bladder with piece of small bowel), urinary diversion (new way for urine to exit)

Question 7

Overactive bladder, also called OAB

Answer 7

• uncontrollable or premature contraction of bladder that results in urgency with or without incontinence, frequency, and nocturia

Question 8

Anatomical obstructions for urine flow

Answer 8

• prostatic enlargement (BPH) - nonmalignant adenomatous overgrowth of the periurethral prostate gland. Symptoms are those of bladder outlet obstruction—weak stream, hesitancy, urinary frequency, urgency, nocturia, incomplete emptying, terminal dribbling, overflow or urge incontinence, and complete urinary retention
  1) growth of multiple fibroadenomatous nodules develop from periurethral region (tissue around the urethra) starting from glands rather than true fibromuscular prostate (surgical capsule)
  2) as urethra narrows + lengthens => urine outflow is progressively obstructed
  3) Increased pressure r/t micturition and bladder distention => l/t hypertorphy of bladder detrusor, trabeculation (thickening of bladder walls), diverticula (small, bulging pouches develop in the digestive tract)
  4) incomplete emptying => stasis and predisposes to calculus formation

====================
urinary calculi
* Hyperoxaluria can be primary or caused by excess ingestion of oxalate-containing foods (eg, rhubarb, spinach, cocoa, nuts, pepper, tea) or by excess oxalate absorption due to various enteric diseases (eg, bacterial overgrowth syndromes, Crohn disease, ulcerative colitis, chronic pancreatic or biliary disease) or ileojejunal (eg, bariatric) surgery.
* Hypocitruria (urinary citrate < 350 mg/day [1820 micromol/day]), present in about 40 to 50% of calcium calculi–formers, promotes calcium calculi formation because citrate normally binds urinary calcium and inhibits the crystallization of calcium salts.
* patients have normal serum calcium, but urinary calcium is elevated > 250 mg/day (> 6.2 mmol/day) in men and > 200 mg/day (> 5.0 mmol/day) in women.
* Uric acid calculi most commonly develop as a result of increased urine acidity (urine pH < 5.5), or very rarely with severe hyperuricosuria (urinary uric acid > 1500 mg/day [> 9 mmol/day]), which crystallizes undissociated uric acid. Uric acid crystals may comprise the entire calculus or, more commonly, provide a nidus on which calcium or mixed calcium and uric acid calculi can form.

=============

Some patients present with sudden, complete urinary retention, with marked abdominal discomfort and bladder distention. Retention may be precipitated by any of the following:

• Prolonged attempts to postpone voiding
• Immobilization
• Exposure to cold
• Use of anesthetics, anticholinergics, sympathomimetics, opioids, or alcohol
• Avoidance of anticholinergics, sympathomimetics [Sympathomimetic agents may cause or worsen urinary difficulty in patients with prostate enlargement due to smooth muscle contraction in the bladder neck (internal sphincter) via stimulation of alpha-1 adrenergic receptors.], and opioids
• Use of alpha-adrenergic blockers (eg, terazosin, doxazosin, tamsulosin, alfuzosin, silodosin), 5 alpha-reductase inhibitors (finasteride, dutasteride), or the phosphodiesterase type 5 inhibitor tadalafil, especially if there is concomitant erectile dysfunction
• Transurethral resection of the prostate or an alternative bladder outlet procedure
• BONUS
  1) Sympathetic - B-adrenergic (NE) => bladder expansion or relaxes? [detrusor muscle] + a-adrenergic (NE) => internal urethral sphincter constriction
  2) voluntary skeletal muscle => external urethral sphincter
  3) Parasympathetic - Muscarinic repceptor (Ach) => bladder contraction and internal urethral sphincter relaxation

• **urethral stricture **(scarring that narrows the tube that carries urine out of your body (urethra). A stricture restricts the flow of urine from the bladder and can cause a variety of medical problems in the urinary tract, including inflammation or infection, injury)
  tx-
  Urethrotomy, or cutting the stricture through a scope. Urethroplasty, or surgical reconstruction of the urethra; which is often the most effective approach.
• ** pelvic organ prolapse** in women - cystolecele, uterine prolapse, rectocele

Question 9

Partial obstruction of bladder

Answer 9

• overactive bladder contractions w/ urgency
• dposition of collagen in bladder wall over time => result in decreased bladder wall compliance and ineffective drtusor muscle contraction

Question 10

Renal cell carcinoma

Answer 10

• most common renal neoplasm
• larger neoplasms metastasize to lung, liver, and bone

Question 11

Bladder tumors

Answer 11

• composec of transitional cells w/ papillary appearance (ong, thin “finger-like” growths. These tumors grow from tissue that lines the inside of an organ.) and high rate of recurrence

Question 12

Host defenses that protect against UTI

Answer 12

• high osmality (more particles in serum, dehydrated in a sense) in urine and acidic PH of urine
• uromodulin (regulation of ion transport in the thick ascending limb, immunomodulation and protection against urinary tract infections and kidney stones)
• mucus – Periurethral mucus-secreting glands surround the distal 2/3’s of female urethra (mucus from these glands trap bacteria before it can ascend proximal urethra) // while for males, long of male urethra and secretions from prostate and accessory periurethral gland combine to form a protective barrier
• other antimicrobrial proteins that activate immune response, sphincters that prevent reflux, and urine flow that washes out bacteria

Question 13

Virulent uropathogens

Answer 13

• pili (short hair like structure (mvmt, adherence to surfaces) or fimbriae (thin, protein tubs similar to pili; all gram neg. but not many gram + bacteria) or both
• bind to uroepithelium and retrograde mvmt in the urinary tract
• form biofilms to enhance colonization and rest host defense + antimicrobial therapy

Question 14

Cystitis

Answer 14

• inflammation of bladder
• d/t bacteria (acute or chronic)
• frequency, urgency, and dysuria are caused by inflammation

=================

• interstitial cystitis & bladder pain syndrome => chronic bladder problem - It is a feeling of pain and pressure in the bladder area. Along with this pain are lower urinary tract symptoms which have lasted for more than 6 weeks, without having an infection or other clear causes.
• could be an autoimmune injury w/ increased permeability of glycosaminoglycan layer of bladder mucosa (In a healthy bladder there is a natural barrier that protects the bladder lining from the urine. This barrier is called the glycosaminoglycan (GAG) layer)

Question 15

Pyelonephritis

Answer 15

• acute or chronic inflammation of renal pelvis (The kidney pelvis acts like a funnel, collecting the urine produced in the kidney and leading to a central “stem,” the ureter)
• r/t ascending infection and obstructive uropathies
• can l/t abscess formation and scarring w/ acute or chronic kidney injury
• 90% of cases is d/t escherichia coli (usually in large intestine) among who are not hospitalized or living in nursing home
• infections tend to ascend from genital area through uretha to bladder, up to ureters, to the kidneys
• kidney stone and enlarged prostate gland can exacerbate that
• increased during pregnancy too (enlarging uterus puts pressure on ureters => partially obstructs normal downard flow of urine)
• additionally, risk of reflux during preg d/t likelihood of increasing ureter dilation and reducing muscle contractions needed to expel urine
• cathether indwelling is another risk
• staphylococcal skin infection (5%) of transmitting to kidneys

sx:
* chills/fever
* pain in lower part of back either side (tenderness on affected side at back)
* n/v
* 1/3 of people will have sx of cystitis (bladder infection) - frequent, painful urination
* one or both kidneys may be enlarged and painful
* renal colic (intense periods of pain)
* abdomen tightly contracted
* irritation from infection or passing kidney stone => ureter spasms

tx -
Antibiotics
Occasionally surgery (to correct abnormality of urinary tract) [chronic pyelonephritis => undergo kidney transplantation]

Question 16

Glomerular d/o’s

Answer 16

• group of related diseases of glomerulus
• can be primary d/t immune injury, infection, ischemia, toxins/drugs, or vascular disorders
• secondarily - systemic diseases

Question 17

Acute glomerulonephritis

Answer 17

• d/t inflammatory dmage to glomerulus d/t immune responses

1) deposition of circulating immune complexes (glomerular capillaires [type III])

2) antibodies reacting in situ to planted antigens (type II - reaction of antibodies in situ against planted antigens within the glomerulus) — glomerular injury occurring with complement deposition and activation and release of immunologic substances that lyse cells and increase membrane permeability

3) antibodies directed against the glomerular basement membrane (type II) – immune response that causes crescent formation and a linear pattern of immunofluorescence; generally associated with rapidly progressive renal failure such as Goodpasture syndrome (type II hypersensitivity reaction)

4) complement activation

• urine sediment contain large amounts of protein (nephrotic sediment) or have red and WBC w/ protein (nephritic sediment)
• This condition often associated with immune complex deposition in glomerulus or in situ formation

=======

• streptococcal infection (poststreptococcal glomerulonephritis) [2-10 y/o] after recovery from infection
• Staphylococcus and pneumococcus, viral infections (e.g chickenpox), parasitic (malaria for e.g) => postinfectious glomerulonephritis
• also caused by noninfection d/o
  1) IgA-assocaited vasculitis (HSP or henoch-schonlein purpura) – antibody IgA collect in small blood vessels => inflamed and leak blood [red-purple rash link]
  2) systemic lupus erythematosus (lupus)
  3) cryoglobulinemia (most common w/ hepatits C, abnormal proteins in blood)
  4) good pasture syndrome – uncommon autoimmune disorder in which bleeding into the lungs and progressive kidney failure occur (Corticosteroids, cyclophosphamide (a chemotherapy drug), and plasma exchange are used to try to prevent permanent lung and kidney damage) // may cough up blood
  5) granulomatosis with polyangiitis –inflammation of small- and medium-sized blood vessels and tissues in the nose, sinuses, throat, lungs, or kidneys (cause unknown // beigins with nosebleeds, nasal gongestion, sinusitis, hoarseness, ear pain, fluid in middle ear, eye redness + pain, and coughing) ===> resembles infection w/o identifying an organism

=======
sx
typically none
first ones
1) edema d/t fluid retention, low urine volumen, and dark urine output with blood
2) puffiness of face + eyelids then legs
3) BP increases
4) drowy or confused
5) n/v, malaise common as well

rapid progressive
* weakness, fatigue, fever
* loss of appetite, n/v, abdominal pain, joint pain
* flu-like illness in month where kidney failure develops
* little urine production

for chronic form
* when acute doesn’t resolve, can be caused by hereditary nephritis (inherited genetic disorder)
* undetected for awhile while edema may occur + high BP common => l/t kidney failure (itchiness, decreased appetite, n/v, fatigue, difficulty breathing)

====
tx
acute form
1) low protein and Na+ diet
2) diuretics; tx high bp
3) Antibx usually ineffective b/c nephritis begins 1-6 weeks after infection, which has resolved; if bacterial infection still present then start (antimalarial if malaria)
4) corticosteroid for autoimmune d/o

rapid progressive
1) corticosteroids (cyclophosphamide - immunosuppressant)
2) plasma exchange to remove antibodies from blood
3) kidney transplant - last resort

chronic
1) ACE inhibtor (-pril) or ARB (-sartan) slows progression by reducing blood pressure and excretion of protein
2) sodium intake reduction including protein
3) end stage => dialysis or kidney transplant

Question 18

Lupus nephritis

Answer 18

• formation of autoantibodies against double-stranded DNA (dsDNA) and nucleosomes in the glomerulus => l/t inflammation and injury
• causing blood, protein in urine, high BP, impaired kidney fx or kidney failiure + characterized by abnormally high levels of nitrogen-containing compounds (such as urea, creatinine, various body waste compounds, and other nitrogen-rich compounds (azotemia)
• d/t lupus (primarily women in childbearing age or black)

=======
sx
edema, HTN, or combination

tx
1) ACE inhibitor or ARB (angiotensin II receptor blocker) for HTN or proteinuria
2) corticosteroid (myophenolate mofetil or cyclophosphamide)
3) kidney transplant for patients w/ ESKD

• 50% of patients s/ systemic lupus erythematosus (SLE) and develop within 1 year usually

Question 19

IgA nephropathy

Answer 19

• binding of abnormal IgA to mesangial cells in the glomerulus l/t injury and mesangial proliferation (may present w/ nephrotic syndrome, which is group of sx iincluding proteinuria, low blood protein levels, high cholesterol elvels, high triglyceride levels, and swelling) + hematuria
• increased number of mesangial of cells w/ damage to glomeruli
• mesangial cells – structural support of glomerular capillaries, regulation of the glomerular filtration rate, mesangial matrix formation, phagocytosis, and monitoring of capillary lumen glucose concentration

Question 20

Focal segmental glomeurlosclerosis

Answer 20

• scarring lesion involving not all glomeruli (focal) and some but not all of the glomerular capillaries (segmental)

=========
* Known causes include:

1. Drugs such as heroin, bisphosphonates, anabolic steroids
2. Infection
3. Inherited genetic problems
4. Obesity
5. Reflux nephropathy (a condition in which urine flows backward from the bladder to the kidney)
6. Sickle cell disease
7. Some medicines

Symptoms may include:

• Foamy urine (from excess protein in the urine)
• Poor appetite
• Swelling, called generalized edema, from fluids held in the body
• Weight gain

tx
corticosteroids
immunosuppresive drugs
plasmapheresis

Question 21

Membranous nephropathy

Answer 21

complement-mediated glomerular injury with increased glomerular permeability and glomerulosclerosis.

Question 22

Rapidly progressive glomerulonephritis (RPGN)

Answer 22

associated with injury that results in the proliferation of glomerular capillary endothelial cells and a rapid loss of renal function.

Question 23

Mesangial proliferative glomerulonephritis

Answer 23

usually idiopathic and involves deposits of immune complex in the mesangium with mesangial cell proliferation.

Question 24

Mebranoproliferative glomerulonephritis

Answer 24

• mesangial cell proliferation
• complement deposition
• crescent formation (proliferation of parietal epithelium of Bowman’s capsule with the presence of macrophages, lymphocytes, neutrophils, fibrin, and collagen ==> two or more layers of proliferating cells in bowman’s capsulte)

Question 25

Chronic glomerulonephritis

Answer 25

• r/t variety of diseases that cause deterioration of glomerulus and progressive loss of renal fx over months to years – diabetic neuropathy and lupus nephritis

Question 26

Deiab

Diabetic nephropathy

Answer 26

• develops from metabolic, inflammatory, microvascualr complciations d/t chronic hyperglycemia

Question 27

Nephrotic syndrome

Answer 27

• excretion of at least 3.5 g of protein (primarily albumin) in urine per day b/c of glomerular injury w/ increased capillary permeability and loss of membrane negative charge

principal signs
1) hypoproteinemia
2) hyperlipidemia (probably increased hepatic lipogenesis, a non-specific reaction to falling oncotic pressure secondary to hypoalbuminemia)
3) edema (kidney unable to secrete salt and unrelated to systemic factors)
* liver cannot produce enough protein to compensate for loss

Question 28

Nephritic syndrome

Answer 28

• hematuria and red blood cell casts in urine and less severe proteinuria

Question 29

Acute kidney injury

Answer 29

• sudden decline in kidney fx w/ decreased glomerular filtration and increase in serum creatinine (waste production of creatine - chemical used by body to supply energy to mostly muscles), cystatin C (biomarker of kidney fx), and BUN levels (amount of urea nitrogen found in your blood. Urea nitrogen is a waste product made when your liver breaks down protein. It’s carried in your blood, filtered out by your kidneys, and removed from your body in your urine)
• BUN (5-20 mg/dl), creatinine (0.7-1.3 for men, 0.6 to 1.1 for women), cystatin c (0.6-1.1), GFR >60 is normal

3 categories
1) prerenal – decreased renal perfusion with a decreased GFR, ischemia, and tubular necrosis
* main causes – extracellular fluid volume deleption (low fluid intake, diarrheal illness, sepsis), CV disease (heart failure, cardiogenic shock), decompensated liver disease
* usually hypoperfusion severe and prolonged (however healthy kidney will reabosrb sodium and h2o, l/t oliguria w/ high urine osmolality and low urine sodium

2) intrarenal – assocaited with several systemic diseases or to drug toxicity but commonly related to acute tubular necrosis (kidney disorder involving damage to the tubule cells of the kidneys, which can lead to acute kidney failure. The tubules are tiny ducts in the kidneys that help filter the blood when it passes through the kidneys)
* other causes: acute glomerulonephritis, nephrotoxins (OTC, prescription)
* glomerular disease l/t decreased GFR, increased GFR permeability to proteins + RBC => may l/t inflammtory (glmoerulonephritis) or vascular damage d/t ischemia or vasculitis
* tubule damage can d/t ishcemia, obstruction from cellular debris, protein or crystal deposition + cellular/interstitial edema /// interstitial inflammation? => immunologic or allergic

3) postrenal – associated with diseases that obstruct flow of urine from kidneys
* causes – crystalline or proteinaceous material precipitates
* further reducing GFR d/t obstructed ultrafiltrate (bladder outlet obstruction most common for men)
* obstruction can affect renal blood flow => initially increase flow and pressure in glomerular capillary d/t reduced afferent arteriolar resistance => within 3-4 hrs l/t reduced blood flow and by 24 hours renal flow is less than 50% normal l/t increased resistsance of renal vasculature => may take up to a week to recover after relief of 24 hour obstruction

sx:
Symptoms of uremia may develop later as nitrogenous products accumulate. Such symptoms include

• Anorexia
• Nausea
• Vomiting
• Weakness
• Myoclonic jerks
• Seizures
• Confusion
• Coma
• Asterixis is a clinical sign that describes the inability to maintain sustained posture with subsequent brief, shock-like, involuntary movements
• Hyperreflexia
• chest pain
• fluid accumulation in lungs or pericardial tamponade (when enough fluid accumulates in the pericardial sac compressing the heart and leading to a decrease in cardiac output and shock.)
• cola colored urine in glomerulonephritis or myoglobinuria

prodromal phase (normal urine output with varying duration) => oliguric phase (urine output 50-500 ml/day) => postoliguric phase (urine ouput goes to normal => serum creatinine and urea levels may not fall for several more days // tubular dysfunction may persist for few more days and manifested by sodium wasting, polyuria unresponsive to vasopressin, or hypercholremic metabolic acidodis (d/t Na+ loss))

tx

• Immediate treatment of pulmonary edema and hyperkalemia
• Dialysis as needed to control hyperkalemia, pulmonary edema, metabolic acidosis, and uremic symptoms
• Adjustment of drug regimen for degree of renal dysfunction
• Usually restriction of water, sodium, phosphate, and potassium intake, but provision of adequate protein
• Possibly phosphate binders (for hyperphosphatemia) and intestinal potassium binders (for hyperkalemia)
• Pulmonary edema is treated with oxygen, IV vasodilators (eg, nitroglycerin), diuretics (often ineffective in AKI), or dialysis.
• Hyperkalemia is treated as needed with IV infusion of 10 mL of 10% calcium gluconate, 50 g of dextrose, and 5 to 10 units of insulin. These drugs do not reduce total body potassium, so further (but slower-acting) treatment is needed (eg, sodium polystyrene sulfonate, diuretics, dialysis).
  (Calcium is given intravenously to protect the heart, but calcium does not lower the potassium level. Then insulin and glucose are given, which move potassium from blood into cells, thus lowering the potassium level in blood. Albuterol (used mainly to treat asthma) may be given to help lower the potassium level) [Albuterol is an adrenergic agonist that has an additive effect with insulin and glucose, which may in turn help shift potassium into the intracellular space. ]
• correction of the nonanion gap portion of severe metabolic acidosis (pH < 7.20) is often recommended and may be treated with IV sodium bicarbonate in the form of a slow infusion (≤ 150 mEq [or mmol] sodium bicarbonate in 1 L of 5% D/W at a rate of 50 to 100 mL/hour). Because variations in body buffer systems and the rate of acid production are hard to predict, calculating the amount of bicarbonate needed to achieve a full correction is usually not recommended. Instead, bicarbonate is given via continuous infusion and the anion gap is monitored serially.

====
Hemodialysis or hemofiltration is initiated when

• Severe electrolyte abnormalities cannot otherwise be controlled (eg, potassium > 6 mmol/L)
• Pulmonary edema persists despite drug treatment
• Metabolic acidosis is unresponsive to treatment
• Uremic symptoms occur (eg, vomiting thought to be due to uremia, asterixis, encephalopathy, pericarditis, seizures)

Question 30

oliguria

Answer 30

• urine output of <400 cc per day and be d/t alteration in renal blood flow, tubular obstruction, or tubular fluid backleak or by a combo

Question 31

Chronic kidney disease

Answer 31

• progressive loss of renal fx
• plasma creatinine gradually increase as GFR declines
• sodium is loss in urine, K+ retained (depend on aldosterone being less effective?)
• acidosis develops + vitamin D activation declines
• calcium + phosphate metabolism altered
• erythropoietin (stimulate RBC production production decreased

symptomatic changes not obvious until renal fx declines to less than 25%
* conditions that contribute to progression – glomerular HTN, hyperfiltration (glomeruli produce excessive amounts of pro-urine), tubulointerstitial inflammation, and fibrosis
* pathologic changes of chronic renal injury? angiotensin II and proteinuria

Question 32

uremic syndrome

Answer 32

• proinflammaotry state with urea accumulated and other nitrogenous compounds + toxins // including alterations in fluid, electrolyte, and acid-base balance that result in CKF