Nephrology Flashcards
(121 cards)
1
Q
What is the common causative organism of UTI in women?
A
E. coli
2
Q
What is the most common organism of UTI in men?
A
Proteus species
3
Q
What does upper UTI consist of?
A
Kidney & ureter. Pyelonephritis and renal abscess.
4
Q
What are the s/s of upper UTI?
A
- flank pain
- CVA tenderness
- temp >38
- hematuira
- N/V
- malaise
- mental status change
5
Q
What is the treatment of complicated and uncomplicated upper UTI?
A
- inpatient treatment
- caftriaxone if uncomplicated
- gentamycin, ampicillin, cefazolin in complicated infections.
6
Q
What does a lower UTI consist of ?
A
Bladder and urethra. Cystitis, urethretitis, and prostatitis.
7
Q
What are the s/s of lower UTI?
A
- dysuria
- frequency
- urgency
- suprapubic pain
- hematuria with bacteriuria
- incontinence
8
Q
What are the common treatment of lower UTI?
A
Bactrim and Macrobid
9
Q
What are the common causes of UTI?
A
- Ascending infection from genital and GI tract.
- incomplete bladder emptying
- bladder outlet obstruction
- urethral strictures
- renal failure
- DM
- vesicoureteral reflux
- fistula
- urinary diversion infected stones
- age
- pregnancy
- instrumentation
- poor patient compliance
- foley catheters
10
Q
What are the antibiotics of choice for acute pyelonephritis?
A
Ampicillin, Gentamicin, Cipro, Levofloxacin, Bactrim
11
Q
What are the antibiotics of choice for acute cystitis?
A
Cephalexin, Cipro, Levofloxacin, Nitrofurantoin, Norfloxacin, Bactrim.
12
Q
What is the antibiotics of choice for chronic bacterial prostatitis and nonsexually transmitted acute epididymitis?
A
Cipro, Levofloxacin, Bactrim.
13
Q
What is the treatment of STD associated UTI?
A
Rocephin chot 250mg x1 and doxy 100mg q12hrs.
14
Q
What are the antibiotics of choice for pregnant women with UTI?
A
Nutrofurantoin (Macorbid), bactrim, and beta lactam (PCNs & cephalosporins (cephalexin).
** sulfonamides cannot be given near delivery.
15
Q
What is the definition of recurrence UTI?
A
- two or more symptomatic UTIs over a 6 month peroid or 4 or more over a 12 month period.
- Unresolved infection, abnormal vaginal colonization by original strain, or reinfection with a new strain.
16
Q
What is the management of recurrent UTIs?
A
- antibiotic prophylaxis (macorbid, cephalexin, and bactrim)
- intermittent self treatment
- postcoital prophylaxis antibiotics
- possible anatomic eval
17
Q
What is the definition of oliguria?
A
- 100-400ml/24 hours
2. urinary output of less than 400-500 ml/fay or less than 20ml/hr
18
Q
What is the definition of GFR?
A
- Glomerular filtration rate (GFR) measures the amount of plasma ultra-filtered across the glomerular capillaries and correlates with the ability of the kidneys to filter fluids and various substances.
- Measured indirectly by determining the renal clearance of plasma substance that are not bound to plasma proteins are freely filterable across the glomerulus and are neither secreted nor absorbed along the renal tubules.
19
Q
What is the normal GFR range?
A
150-250L/ 24hr OR 100-120ml/min/1.73m2 of BSA
20
Q
What is the formula of GFR?
A
renal clearance = urine concentrationx urine flow rate (ml/min) divided by plasma concentration
21
Q
What is creatinine clearance?
A
- estimates GFR when kidney fx is stable. Creatinine production and secretion are equal.
- Creatinine clearance is how kidney dosing is determined.
- Creatinine clearance is age and gender dependent.
- males - 97-137 and females 88-128
- Urea clearance is used also to determine GFR, it underestimates, where as creatinine clearance overestimates, as person reaches ESRD the average of both is used.
22
Q
What is the causes of increased GFR?
A
- increased blood volume and increased blood pressure.
- In stage 1 of CKD, GFR may initially be increased due to compensatory mechanisms due to hyperfiltration at the glomerulus or disease at a different segment of the nephron, interstitium, or vascular supply.
23
Q
What is the cause of decreased GFR?
A
Due to dehydration or volume loss, or is related to loss of nephrons due to continued kidney insult.
24
Q
How to calculate FeNA?
A
Urine Na X plasma Cr X 100 divided by plasma Na X Urine Cr.
25
What is the Fena precentage compared to AKI phase?
less than 1% - prerenal
greater than 1% - intrinstic
greater than 2-4% - postrenal.
26
What are the common causes of hypercalcemia?
1. neoplasia (bone-primary, myeloma, acute leukemia, nonbone solid tumors, breast, lung, squamous nonpulmonary, kidney, neoplasm secretion of parathyroid hormone related protein.
2. primary hyperparathyroidism
3. thiazide diuretics
4. tertiary renal hyperparathroidism
5. idiopathic
6. spurious (artifactual)
7. dehydration
8. serum protein elevation
9. Milk-alkali syndrome
10. Vitamin D or Vit A excess
11. Acromegaly
12. Adrenal insufficiency
13. Pheochromocytoma
14. Thyrotoxicosis
15. Granulomatous diseases (production of calcitriol)
16. Paget disease of bone
17. Hypophosphatasia
18. Immobilization
19. Familial hypocalciuric hypercalcemia
20. Complications of kidney transplant
27
What are the causes of hypermagnesium?
1. renal failure and decreased renal excretion secondary to salt depletion
2. abuse of antacids and laxatives
3. endocrinopathies (deficiency of mineralocorticoids or thyroid hormones)
4. increased tissue breakdown (rhabdo)
5. redistribution: acute DKA, pheochromocytoma
6. IV mag given to preeclampsia and exlampsia pts
7. lithium, volume depletion, familial hypocalciuric hypercalcemia
28
What is the GFR pathophysiology?
Stage I: GFR > 90, kidney damage but normal or increased GFR
Stage II: GFR 60-89, kidney damage w/mild or slightly decreased GFR
Stage III: GFR 30-59, mod decrease in GFR w/mod complications
Stage IV: GFR 15-29, severe complications & severe decrease in GFR
Stage V: (KIDNEY FAILURE): ESRD, GFR <15 or on HD/PD, uremia, CVD
Renal replacement (HD/PD) indicated if GFR < 5-10 Ferri has dialysis needed at 10-15, CMDT at 10 or less.
29
Risk factors for developing hyponatremia?
1. CHF
2. cirrhosis
3. nephrotic syndrome
4. blood loss
5. NGT suctioning
6. emesis
7. diarrhea
8. excess sweating
9. burns
10. SIADH
11. diuretics (especially thiazides in elderly females)
12. renal failure
13. cortisol deficiency
14. hypothyroidism
15. increased H2O ingestion
16. beer potomania
30
What is the predisposing factors of isotonic (serum osmo 275-295) or pseudohyponatremia? What is the treatment?
1. hyperlipidemia and hyperproteinemia.
| 2. no treatment needed but confirmed with lab.
31
What is the predisposing factors of hypertonic (>295 serum osmo) or translocational hyponatremia? What is the treatment?
1. hyperglycemia and mannitol administration
| 2. high glucose - need for correction formula. manage glucose correction and discontinue mannitol.
32
What is the predisposing factors of hypervolemic hypotonic? What is the treatment?
1. Involves excess total body Na that stimulates the ADH secretion: CHF, cirrhosis, nephrotic syndrome, CKD (predialysis)
2. loop diuretics or dialysis to correct total body water.
33
What is the predisposing factors of hypovolemic hypotonic? What is the treatment?
1. Stimulates ADH secretion causing losses of water and salt to be replaced by only water: blood loss, GI loss (vomiting, NG suction, diarrhea), excess diuresis, aldosterone deficiency, excess sweating, burns.
2. Give NS or LR to replete volume and to suppress ADH
34
What is the predisposing factors of euvolemic hypotonic? What is the treatment?
1. involves autonomous ADH secretion or reduced renal water formation: SIADH, cortisol deficiency, hypothyroidism, diuretics (thiazides), acute/chronic renal failure, HIV patients (multiple factors), psychogenic polydipsia and force water intake (marathon runners), beer potomania (lot of fluid with not a lot of salt).
2. should respond to free water restriction alone
35
Acute hyponatremia (exercised induced) with severe neuro manifestations can be reversed by?
Rapidly with 100ml of 3% hypertonic saline infused over 10 mins.
36
Chronic hyponatremia correction rates are?
low (6meq/24hrs for high risk pts for demyelination and those reversed to quickly can receive DDVAP and D% to relower Na.
37
How to calculate sodium deficit to determine the ml/hr of 3% saline?
sodium deficit = TBW x (desired Na-actual Na)
70kg female, na 124, desired 130
35x(130-124)=210
or 3% saline infusion of 0.25ml/kr/hr, no higher than 0.5ml/kg/h
38
Drugs used to treatment hyponatremia?
1. Demeclocycline (300-600 BID) for those struggling to restrict water.
2. Vasopressin antagonist (vaptans) are good 2nd line agent and those with heart failure.
39
What are the cause of low urine K+?
<20 mEq/L as result of extrarenal causes
| diarrhea, vomiting, laxative abuse, Villous adenoma, Zollinger-Ellison syndrome
40
What are the causes of high urine K+?
> 40 mEq/L with renal loss (mineralocorticoids, primary hyperaldosteronism, Bartter syndrome, Gitelman syndrome, Cushing syndrome etc. table 21-3)
41
What is hypokalemia in the presence of acidosis?
Profound K depletion and requires urgent treatment
42
What is the risk of hypokalemia and dig?
digitalis toxicity.
43
What are the s/s of mild to moderate hypokalemia?
1. Muscular weakness
2. tenderness
3. fatigue
4. muscle cramps
5. Gastrointestinal smooth muscle involvement may result in constipation or ileus.
44
What are the s/s of severe hypokalemia?
1. cardiac rhythm changes including premature atrial or ventricular beats
2. Flaccid paralysis
3. hyporeflexia
4. hypercapnia
5. tetany
6. rhabdomyolysis
45
What is transtubular K+ gradient (TKKG)?
1. Simple and rapid eval of net K secretion.
| 2. hypokalemia with a TTKG more than 4 suggest renal potassium loss with increased distal K secretion
46
What are the causes of hypokalemia?
1. Decreased potassium intake
2. Potassium shifts into the cells:
Alkalosis
Barium intoxication
Beta-adrenergic agonist
Increased postprandial secretion of insulin
Periodic paralysis (hypokalemic)
Trauma (via beta adrenergic stimulation?)
3. Renal potassium loss
Increased aldosterone effects: Primary hyperaldosterone, Secondary aldosteronism
(dehydration, heart failure)
Bartter’s syndrome
Gitelman syndrome
Cushing’s syndrome
ectopic ACTH-producing tumor
Congenital abnormality of steroid metabolism (adrenogenital syndrome, 17-alpha-hydroxylase defect, apparent mineralocorticoid excess, 11-beta-hydroxylase deficiency)
Renin-producing tumor
Renovascular HTN
malignant HTN
4. Increased flow to distal nephron: Diuretics (lasix, thiazides), Salt-losing nephropathy, polyuria
Hypomagnesemia
Renal tubular acidosis (type I/II)
Liddle Syndrome
5. Extrarenal potassium ions- Vomiting, diarrhea, laxative abuse, Villous adenoma, Zollinger-Ellison syndrome
47
What is the treatment of mild to moderate hypokalemia?
Oral potassium supplementation is the safest and easiest treatment. Acute- Max single oral dose of 40-60 mEq with repeat measurement of serum K in 4 hr then repeat PRN; Chronic- 10-40 mEq/day in 1-2 doses.
48
What are the important notes of dietary K?
1. entirely coupled to phosphate rather than chloride and is not effective in correcting potassium loss associated with chloride depletion from diuretics or vomiting.
2. high potassium diet: nuts, dried fruits, tomatoes, potatoes, oranges
49
What is the treatment of kidney function and mild to moderate hypokalemia?
20 mEq/day of oral K+ is generally sufficient to prevent hypokalemia, but 40-100 mEq/day over a period of days to weeks is needed to treat hypokalemia and fully replete potassium stores
50
What is the treatment of severe hyperkalemia?
1. IV potassium
| 2. pts with cardiac arrhythmias or hepatic encephalopathy, or those unable to take oral supplements
51
What are the complications of severe hypophosphatemia?
1. less than 1.5mg/dl (normal 2.5-4.5)
2. rhabdo
3. paresthesias
4. encephalopathy (irritability, confusion, dysarthria, seizures, and coma)
5. Resp failure from diaphragmatic weakness
52
What are the causes of hypophosphatemia?
1. Loss of urinary phosphorus- Diuresis, DKA, Hyperparathyroidism, Renal tubule defects (Fanconi’s syndrome, Amphotericin B toxicity)
2. Cellular uptake- Increased glucose utilization (treatment of DKA or alcohol withdrawal, total parenteral nutrition), Acute respiratory Alkalosis, Burns
3 Deficient GI intake or absorption- Calcium salts (PhosLo, Os-Cal), polymer gels (Renagel), Lanthanum Chloride (Fosrenol), Malabsorption syndromes
53
What are the treatment options for hypophosphatemia?
1. Phosphat repletion and maintainance fluids - rapid depletion of Ca can occur with parental admin so oral is preferred.
2. Moderate hypophosphatemia (1.0-2.5) usually asymptomatic and does not require treatment.
3. DKA with hypophosphatemia - usually corrected with normal dietary intake.
4. Chronic hypophosphatemia - oral phosphate (phos packet).
5. IV sodium or potassium phos 2mg over 6 hours or 5mg over 12 hours.
6. Plasma phos, calcium, and K monitored Q6.
7. Mag deficiency treated
54
What is contraindications of phos replacement?
hypoparathyroidism, advanced CKD, tissue damage and necrosis, and hypercalcemia.
55
What are the side effects of parenteral administration of phos?
hypotension and rapid decline in calcium levels.
56
What are the causes of prerenal AKI?
1. Decreased intravascular volume (hemorrhage, GI losses, dehydration, excessive diuresis, extravascular space sequestration, pancreatitis, burns, trauma, peritonitis)
2. Change in vascular resistance (vasodilatory) - (sepsis, anaphylaxis, anesthesia, and afterload-reducing drugs)
3. Low cardiac output (cardiogenic shock, heart failure, MI, pulmonary embolism, pericardial tamponade, positive pressure ventilation, arrhythmias, and valvular disorders).
4. NSAIDs minimize afferent arteriolar vasodilation by inhibiting prostaglandin-mediated signals. In cirrhosis and heart failure, NSAIDs have deleterious effects.
5. Epi, Norepi, high dose dopamine, anesthetic agents, and cyclosporine - renal vasoconstriction.
6. Uncontrolled hypertension/atherosclerosis
7. Liver disease (advanced hepatic disease that may cause hepatic renal syndrome due to vasoconstriction in the kidneys).
8. Renal artery stenosis causes increased resistance and decreased renal perfusion.
57
What is prerenal AKI?
1. Most common.
| 2. Cause by hypoperfusion of the kidneys
58
What labs correlate with prerenal AKI?
1. BUN:creat ratio >20:1
2. FeNa <1%
3. urine Na <20
4. urine osmo >500
5. UA - benign or hyaline casts.
6. urine specific gravity >1.020
7. Fe Urea <35%
59
What is postrenal AKI?
1. Least common reason for AKI.
| 2. Associated with conditions that cause obstruction of urinary flow and consequently a decrease in GFR.
60
What is the treatment of prerenal AKI?
1. Depends entirely on the causes but achievement of euvolemia, attention to serum electrolytes, and avoidance of nephrotoxic drugs are benchmarks for therapy. (Volume status, cardiac function, diet, and drug usage).
61
What are the causes of postrenal AKI?
1. urethral obstruction
2. bladder dysfunction or obstruction
3. neurogenic bladder
4. diabetic neuropathy
5. spinal cord disease
6. obstruction of both ureters or renal pelvises
7. benign prostatic hyperplasia (most common in men)
8. anticholinergics (urinary retention)
9. obstruction by bladder, prostate, and cervical cancers
10. retroperitoneal fibrosis
11. neurogenic bladder.
12. blood clots
13. bilateral ureteral stones
14. urethral stones or strictures
15. occluded foley catheter
16. bilateral papillary necrosis.
62
What are the signs and symptoms of postrenal AKI?
1. anuric or polyuric
2. may complain of lower abdominal pain.
3. Polyuria can occur in the setting of partial obstruction with resultant tubular dysfunction and an inability to appropriately reabsorb salt and water loads.
4. enlarged prostate, distended bladder, or mass detected on pelvic exam.
63
What are the labs of postrenal AKI?
1. urine Na >40
2. urine osmo <350
3. urine specific gravity fixed 1.0008 to 1.012
4. fena variable.
5. BUN: creat >20:1
6. UA - normal or red cells, white cells, or crystals.
64
What test should be order for suspected postrenal AKI?
1. bladder catheterization
2. US
3. xray
4. CT or MRI
65
What is intrinsic renal AKI?
1. Account for up to 50% of all cases of AKI referred to a nephrologist
2. Considered after prerenal and postrenal causes have been excluded.
3. Sites of injury are the tubules, interstitium, vasculature and glomeruli.
4. Abrupt decrease in glomerular filtration rate due to tubular cell damage that results from renal ischemia or nephrotoxic injury
5. Acute tubular necrosis: accounts for most hospital associated cases of intrinsic acute renal failure
66
What are the causes of intrinsic AKI?
1. Ischemic
~ decreased CO, prolonged hypotension, volume depletion, catecholamines, volume shift, liver disease (hepatorenal syndrome).
2. Nephrotoxic
~ Endogenous -hemoglobinuria (hemolysis), myoglobinuria (rhabdomyolysis), hyperuricemia, and multiple myeloma.
~ Exogenous - aminoglycoside, contrast, ethylene glycol, amphotericin B, cyclosporine, antineoplastics, and heavy metals.
~ Drug induced tx - stop offending drug or needs to renally dosed based on creatinine clearance.
~Contrast related treatment & prevention - fluids, N-acetylcysteine, sodium bicarb, and metformin hold 48 hours before contrast.
3. Acute tubulointerstitial nephritis
~ Bacterial pyelonephritis: infectious causes may include strep, leptospirosis, cytomegalovirus, histoplasmosis, and rocky mountain spotted fever.
~ Drug-induced hypersensitivity to penicillins, cephalosporins, sulfonamides, NSAIDs, Rifampin, Phenytoin, Allopurinol
~ Immunologic disorders - Lupus, Sjogren syndrome, sarcoidosis, cryoglobulinemia.
67
What is the lab results of acute tubular necrosis - intrinsic AKI? (ischemia, nephrotoxins)
1. BUN:creatine ratio <20:1
2. urina Na >20
3. Fe urea >1
4. urine osmo 250-300
5. UA - granular (muddy brown) cast, renal tubular cast
68
What is the lab results of acute glomerulonephritis - intrinsic AKI? (immune complex-mediated, pauci-immune, antiGBM related).
1. BUN: creat ratio >20:1
2. Urine Na <20
3. fe Na <1
4. urine osmo variable
5. UA - red cells, dysmorphic red cell, and red cell cast
69
What is the lab results of acute interstitial nephritis? (allergic reaction, drug reaction, infection, collagen vascular disease).
1. BUN:creat <20:1
2. urine Na variable
3. fe Na <1 >1
4. urine osmo variable
5. UA - white cells, white cell casts, with or with out eosinophils
70
What is the causes of hyperkalemia?
1. Decreased K+ excretion
- Kidney disease, acute and chronic
- Renal secretory defects (may or may not have reduced kidney function): kidney transplant, interstitial nephritis, systemic lupus erythematosus, sickle cell disease, amyloidosis, obstructive nephropathy
-Hyporeninemic hypoaldosteronism (often in diabetic patients with mild to moderate diabetic nephropathy) or selective hypoaldosteronism (eg, AIDS patients)
-Drugs that inhibit potassium excretion: spironolactone, eplerenone, drospirenone, NSAIDs, ACE inhibitors, angiotensin II receptor blockers, triamterene, amiloride, trimethoprim, pentamidine, cyclosporine, tacrolimus
2. Shift of K+ from within the cell
-Massive release of intracellular K+ in burns, rhabdomyolysis, hemolysis, severe infection, internal bleeding, vigorous exercise
-Metabolic acidosis (in the case of organic acid accumulation—eg, lactic acidosis—a shift of K+ does not occur since organic acid can easily move across the cell membrane)
-Hypertonicity (solvent drag)
-Insulin deficiency (metabolic acidosis may not be apparent)
-Hyperkalemic periodic paralysis
-Drugs: succinylcholine, arginine, digitalis toxicity, beta-adrenergic antagonists
-Alpha-adrenergic stimulation?
3. Excessive intake of K+
-Especially in patients taking medications that decrease
potassium secretion (see above)
-ACE, angiotensin-converting enzyme; NSAIDs, nonsteroidal anti-inflammatory drugs.
71
What are the EKG changes related to hyperkalemia?
1. ECG changes in hyperkalemia include bradycardia, PR interval prolongation, peaked T waves, QRS widening, and QRS-T complexes.
2. Conduction disturbances, such as bundle branch block and atrioventricular block, may occur
72
What is the management of hyperkalemia?
1. EKG normal:
Lasix 40-80mg IV to increase renal excretion
Kayexalate 15-45 grams with osmotic cathartic (33% sorbitol or lactulose) to increase GI potassium excretion, must establish bowel activity by abdomen exam
Hemodialysis or peritoneal dialysis to remove potassium in renal failure
2. EKG abnormal, monitor ekg until normal
~ Absent P waves, QRS widening or sine wave
Calcium gluconate 10% 1 gram IV infusion over 1-2 min to antagonize hyperkalemic effect; Immediate onset; Effects last for minutes only.
~ Regular insulin 10 units IV over 2-5 mins to increase cellular potassium uptake; Add glucose D50% 25-50 grams if euglycemic; Effect in 15-30 mins, lasts for 30-60mins.
~ Albuterol 10-20mg via inhalation over 10mins to increase cellular potassium uptake, effect in 15-30 mins; Effect lasts for 60-120mins
~ Sodium bicarbonate 50 mEq IV over 1-2 mins
May cause hypernatremia with repeated doses; Effects lasts for 2-6 hours
~ Diuretic, resin, dialysis as above to enhance removal after above measures
3. Peaked t waves
Insulin/glucose or albuterol
Diuretic, resin, dialysis
73
What is proteinuria in CKD?
1. Angiotensin–converting-enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) reduce proteinuria and slow progression of CKD, especially in hypertensive diabetic patients.
2. Persistent proteinuria are diagnostic of CKD even when eGFR is normal.
3. ACE inhibitors and Calcium channel blockers may be superior to conventional tx in decreasing proteinuria and reducing glomerular HTN.
4. the presence of proteinuria is associated with more rapid progression of CKD and with increased risk of cardiovascular mortality.
74
What are the causes of hypovolemic hypernatremia? What is the tx?
1. extrarenal causes - sweating, GI loss, respiratory, burns
2. renal causes - diuretics, glycosuria, mannitol, urea, renal failure.3
3. Hypo/isotonic fluid
75
What are the causes of euvolemic hypernatremia? What is the treatment?
1. DI, hypodipsia, insensible, respiratory, skin.
| 2. Free water
76
What are the causes of hypervolemic hypernatremia? What is the treatment?
1. iatrogenic (hypertonic saline), mineralcorticoid, cushing disease, hypertonic dialysis
2. Water plus diuretics
77
What is the treatment of acute pyelonephritis?
1. First-line therapy:
Penicillin (Ampicillin 1 g q6h) AND Aminoglycoside (Gentamicin or Tobramycin) prior to obtaining sensitivities---Fevers may persist for up to 72 hrs even with appropriate abx; failure to respond w/in 48 hrs =CT or US to exclude complications.
2. Avoid Aminoglycosides in patients with pre-existing renal disease (Aminoglycosides= NEPHROTOXIC)
3. Cephalosporin (Cephalosporin 1-2 g q8h)-not routinely used for empiric tx
4. Other IV abx options include:
Sulfonamides (TMP/SMX) (DO NOT GIVE NEAR TIME OF DELIVERY IN PREGNANCY)
Aminoglycosides (Amikacin)
Antipseudomonal penicillins (Piperacillin)
Penicillin-β-lactamase inhibitor combos (Piperacillin/tazobactam)
Cephalosporins (Cefotaxime, Ceftriaxone, Cefepime, Ceftazidime, Cephalexin) CEPHALEXIN OK IN PREGNANCY)
Quinolones (Ciprofloxacin, Levofloxacin)- DO NOT USE DURING PREGNANCY
5. Pseudomonas coverage:
Ceftazidime 1-2 g IV q8h, Piperacillin/tazobactam, or Carbapenems for resistance to Cipro
6. Gram-positive cocci coverage (Enterococci, Staphylococci):
Vancomycin 1 g IV q12h, Linezolid 600 mg IV/PO q12h, Daptomycin 4-6 mg/kg IV daily
7. PO abx options include:
Ciprofloxacin 750 mg q12h x 7-14 days ($$) OR
Levofloxacin 750 mg daily x 5 days ($$$) OR
Trimethoprim-sulfamethoxazole 160/800 mg q12h x 3 days ($)
78
What is the management of pyelonephritis?
1. Patient considered ACUTE and should be hospitalized if: Toxic, Complicated Infections, Diabetes or otherwise Immunocompromised, or Suspected bacteremia
2. F/u urine cultures are mandatory following completion of tx
3. No radiologic tests needed for healthy patients with uncomplicated pyelonephritis if therapeutic response after 48 hrs of abx therapy
4. If no response within 48 hrs, abdominal CT is study of choice
5. Inpatient care includes supportive care, monitoring of culture results, adjustment of abx regimen, and IVF repletion until clinically improved, then conversion to PO abx regimen for TOTAL duration of 10-14 days
6. Pyridium 200 mg TID x 2 days for burning/discomfort with urination
7. Treat all diabetics as complicated acute pyelonephritis
79
What is calcium kidney stone? What is the treatment?
1. hypercalciuric calcium nephrolithiasis.
2. Caused by absorptive (caused by increased absorption of calcium at the small bowel, diet dependent, renal phosphate leak that causes increased Vit D synthesis and increased small bowel absorption of Ca). Tx is hydrochlorothiazides or decrease in calcium diet.
3. resorptive - hyperparathyroidism, tx surgical resection of adenoma.
4. renal leak - renal tubules unable to reabsorb filtered Ca.
80
What is hyperuricosuric Ca nephrolithiasis?
1. Caused by dietary excess or uric acid metabolic defects
| 2. tx purine dietary restrictions or allopurinol or both
81
What is hyperoxaluric Ca nephrolithiasis?
1. due to primary intestinal disorders
2. chronic diarrhea, oftne with IBS or steatorrhea
3. Ca is unavailable to bind to oxalate promoting stone formation.
4. Tx: increase fluid intake and oral Ca supplements with meals, reduce diarrhea or steatorrhea
82
What is hypocitraturic Ca nephrolithiasis?
1. Chronic diarrhea, type 1 renal tubular acidosis, chronic or aggressive thiazide diuretics
2. tx potassium citrate supplements
83
What is uric acid calculi?
1. urinary pH <5.5, increasing pH to levels higher than 6.5 can dramatically increase dissolving large stones.
2. tx potassium citrate
3. decrease protein intake
4. hyperuricemia present? allopurinol
84
What is struvite calculi?
1. mag-ammonium-phos stones
2. women with recurrent UTIs caused by urease producing organisms
3. Percutaneous nephrolithotomy or extracorporeal shock wave lithotripsy.
4. antibiotics
5. acetohydroxmine acid
85
What is cystine calculi?
1. abnormal excretion of cystine, ornithine, lysine, and arginine.
2. increase fluid intake, alkalinize the urine to ph great than 7.5 or 8, and admin penicillamin, or tiopronin MPG
86
What is the management of obstructing stone with associated infection?
1. medical emergency requiring urology consult and prompt drainage by ureteral catheter or percutaneous nephrostomy tube. abx alone are inadequate unless the obstruction is drained.
87
When to admit for renal stone?
1. intractable N/V and pain
| 2. obstructing stone with signs of infection
88
What is the most common caused of ESRD?
DM, HTN, chronic glomerulonephritis
89
What is acute tubular necrosis?
1. form of acute kidney injury (AKI) characterized by acute tubular cell injury and dysfunction.
2. most common form of AKI.
3. secondary to ischemic injury, nephrotoxic injury, or septic injury or may be multifactorial.
4. Suspect ischemic ATN in the setting of hemorrhage, hypotension, recent surgery, and/or sepsis.
5. Suspect nephrotoxic ATN in the setting of iodinated radiocontrast imaging, nephrotoxic medications, rhabdomyolysis, hemolysis, or multiple myeloma
90
What is the contributing factors of ATN?
ISCHEMIA - caused by inadequate renal blood flow due to hypotension, hypoxemia, volume depletion, shock, sepsis, major surgeries with prolonged times of hypoperfusion (which can be exacerbated by vasodilating anesthetic agents.)
EXOGENOUS NEPHROTOXINS: Medications such as Aminoglycosides, Amphotericin B, Vancomycin, intravenous acyclovir, and several cephalosporins, Radiographic contrast media, Cyclosporine
ENDOGENOUS NEPHROTOXINS: Heme-containing products, uric acid, paraproteins, Myoglobinuria (a consequence of rhabdomyolysis crush injury), or muscle necrosis from prolonged unconsciousness, seizures, cocaine, and alcohol abuse. Dehydration and acidosis, Hyperuricemia
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What is the physical findings of ATN?
1. Nonspecific symptoms
Symptoms often due to uremia or its underlying cause - uremia can cause:
2. Nausea
3. Vomiting
4. Malaise
5. Altered sensorium
6. Pericardial effusions can occur with uremia, and pericardial friction rub can be present.
Symptoms r/t electrolyte imbalances
1. Arrhythmias (hyperK)
2. AKI can cause nonspecific diffuse abd pain and ileus, as well as platelet dysfunction
3. asterixis and confusion
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What is the radiologic technique for ATN?
CT or US
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What are the common causes of elevated anion gap?
1. Lactic Acidosis - increased production of lactate - shock, end organ ischemia, inadequate circulating O2, Sz (grand mal), Cyanide, impaired lactate clearance (liver failure, metformin, isoniazid), CHF, IV contrast, sepsis, CHF, IV contrast
2. Ketones - DKA, ETOH ketoacidosis, starvation
3. Carbon monoxide and cyanide
4. Renal failure
5. Severe Rhabdo
6. Toxins metabolized to acids - toxic alcohol, Toluene, ASA, Paraldehyde
7. Isoniazid toxicity
8. Salicylate toxicity
9. Iron toxicity
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What are the common causes of normal anoin gap metabolic acidosis?
1. Not as immediately dangerous - gastric loss of bicarb
2. GI HCO3 loss - diarrhea, colostomy, ileostomy, enteric fistulas, iron exchange resins (kayexalate)
3. Renal HCO3 loss - renal tubular acidosis, tubulointerstitial renal disease, Hyperparathyroidism
4. Rapid NS infusion
5. Urologic procedures - ureterosigmoidostomy, ureteroileal conduit
6. Ingestions - acetazolamide, CaCl, Mag sulfate
7. Other - Hypoaldosteronism, Hyperkalemia, Toluene
8. Rapid infusion of NS
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What is red blood cell cast associated with?
Glomerulonephritis and vasculitis
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What is white blood cell cast associated with?
interstitial nephritis and pyelonephritis.
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What is epithelial cell cast associated with?
acute tubular necrosis, interstitial nephritis, glomerulonephritis.
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What is granular cast associated with?
renal parenchymal disease (nonspecific)
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What is waxy, broad cast associated with?
advanced renal failure
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What is hyaline cast associated with?
normal findings in concentrated urine
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What is fatty cast associated with?
heavy proteinuria.
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What is the cockcroft and Gault formula?
1. CrCl = (140-age) x kg x (0.85 if female)/ 72 x PCr
2. PCr is serum creatinine
3. .85 for women because of decreased muscle mass
4. Assess renal function and prescribing a drug that is renally excreted.
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What is the S/S of acute bacterial prostatitis?
1. fever
2. irritative voiding symptoms
3. perineal or suprapubic pain
4. exquisite tenderness common on rectal exam
5. positive urine culture.
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What is the general considerations of acute bacterial prostatitis?
1. usually caused by gram-negative rods, especially e coli and pseudomonas species and less commonly by gram-positive organisms (ex. enterococci).
2. most likely routes of infection include ascent up the urethra and reflux of infected urine into the prostatic ducts.
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What is the lab results of acute bacterial prostatitis?
1. CBC shows leukocytosis and a left shift.
| 2. UA shows pyuria, bacteriuria, and varying degrees of hematuria.
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What is the treatment of acute bacterial prostatitis?
1. hospitalization may be required and parenteral abx (ampicillin and aminoglycoside) should be initiated until organism sensitives are available.
2. after the pt is afebrile for 24-48 hours, oral abx (ex, quinolones) are used to complete 4-6 weeks of therapy.
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What is the s/s of chronic bacterial prostatitis?
1. irritative voiding symptoms
2. perineal or suprapubic discomfort (often dull and poorly localized)
3. positive expressed prostatic secretions and culture
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What is the general considerations of chronic bacterial prostatitis?
1. Gram-negative rods are the most common etiologic agents, but only one gram-positive organism (enterococcus) is associated with chronic infection.
2. most likely routes of infection include ascent up the urethra and reflux of infected urine into the prostatic ducts.
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What is the labs associated with chronic bacterial prostatitis?
1. UA is normal unless secondary cystitis is present.
| 2. positive expressed prostatic secretions and culture
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What is the treatment of chronic bacterial prostatitis?
1. Trimethoprim-sulfamethoxazole is associated with the best cure rates however increasing resistance to this abx up to 20% has been noted.
2 Other effective agents include quinolones, cephalexin, erythromycin and carbenicillin.
3. optimal duration of therapy remains controversial, ranging from 6-12 weeks.
4. Symptomatic relief may be provided by anti-inflammatory agents and hot sitz baths.
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What is the classification of saline responsive metabolic alkalosis?
1. Uses the urine Cl- as a marker for volume status
2. A sign of normotensive extracellular volume contraction and hypokalemia
3. Much more common
4. Hypotension and orthostasis may be seen
5. Vomiting or NG suction
6. Contraction alkalosis
7. Posthypercapnia alkalosis
8. Urine Cl- < 25 mEq/L
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What is the treatment of saline responsive metabolic alkalosis?
1. Correction of the extracellular volume deficit with isotonic saline
2. Diuretics should be discontinued
3. H2-blockers or PPIs may be helpful in patients with alkalosis from NG suction
4. Acetazolamide will increase renal bicarb excretion for pts w/ pulm or cardio disease that prohibits adequate resuscitation
5. Severe cases: May require dialysis w/ low-bicarb dialysate
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What is the classification of saline unresponsive metabolic alkalosis?
1. Excessive total body bicarb with either euvolemia or hypervolemia
2. Hyperaldosteronism
3. Alkali administration with ↓GFR
4. Urine Cl- > 40 mEq/L
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What is the treatment of saline unresponsive metabolic alkalosis?
1. Surgical removal of a mineralocorticoid-producing tumor
2. Blockage of aldosterone effect with an ACE-I or with spironolactone
3. Primary aldosteronism can be treated ONLY with K+ repletion
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What is the screening techniques and diagnostic standards of renal artery stenosis?
1. Screening offered for those with new onset hypertension <30 y.o or severe HTN in >55y.o (CMDT states females <40y.o); those with malignant, accelerated, or resistant HTN; unexplained pulm edema or atrophic kidney; azotemia following initiation of ACEI/ARB; kidney size differing by >1.5cm
2. Screening includes U/S, CTA, MRA depending on pt specific contraindications (MRA-metal, CTA-contrast) are noninvasive screening techniques but renal angiography is the diagnostic gold standard used after positive screening
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What is polycystic kidney disease?
1. Most common single genetic cause of CKD
2. autosomal dominant PKD
3. present typical with localized flank pain, fevers, and nausea and vomiting, similar to pyelonephritis.
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What is the nonpharm therapy of PKD?
- <2 g sodium diet/24 h and calories is recommended
- Increased water consumption > 3L/day suppress vasopressin if preserved renal function. (cAMP = cyst formation & vasopressin stimulates the production of cAMP).
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What is the acute treatment of PKD?
- Gross hematuria supportive care (bed rest, hydration, analgesics, stop antihypertensive meds at this time).
- Small obstructive kidney stones - lithotripsy <2 cm in renal pelvis or calyces or percutaneous nephrolithotomy is another potential option.
- Infections are treated with antibiotics that penetrate cysts fluoroquinolones, bactrim, vancomycin, and chloramphenicol.
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What is the chronic treatment of PKD?
- Younger patients: strict BP control in younger individual <110/75 w/ intact kidney function (w/slower increase in TKV, reduced urinary albumin excretion, greater reduction in LV mass index)
- All ADPKD patients: BP <130/80
- ACE ARB are first choice drug for treatment for HTN
- HLD tx aggressively w/ LDL target <80
- Pretransplant uni or bil nephrectomy w/ recurrent infections, significant kidney enlargement causing limitation of daily activities and malnutrition
- ESRD, peritoneal or HD can be bridge to transplant
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Lab findings of PKD?
H/H elevated d/t increased erythropoietin, UA shows microscopic hematuria, and proteinuria >1g per day.
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What are the CT contrast considerations?
1. Contrast nephropathy is the 3rd leading cause of new onset AKI in hospitalized pts.
2. Predisposing factors include advanced age, pre-existing kidney dz (serum creatinine >2), volume depletion, diabetic nephropathy, HF, plasma cell myeloma, repeated doses of contrast, and recent exposure to other nephrotoxic agents like NSAIDS and ACEIs.
3. Toxicity usually occurs within 24-48hrs after the study
4. Mainstay of therapy is 1L of NS over 10-12hrs both before and after contrast
5. Isotonic is superior over hypotonic, and both are superior to oral
6. Some studies have shown sodium bicarb IV is a better volume expander than NS, but other studies show something else so I doubt they’ll ask this one.
7. Neither mannitol nor lasix offer benefit over NS… lasix may lead to increased renal dysfunction
8. N-acetylcysteine is a drug that is not well understood and may or may not prevent kidney injury (diff studies say different things). Acetylcysteine is an antioxidant w/ little toxicity but MOA is not understood
9. Nephrotoxic agents should be avoided the day before and after exposure
10. CT scans w/ gadolinium can cause nephrogenic systemic sclerosis in pts w/ eGFRs<30 (CMDT p.927)
11. Diabetic pts with a serum creatinine of 1.5-2.5 should be adequately hydrated before and after
12. Contrast should not be given to a pt with a serum creatinine >3 unless the potential benefit outweighs the high risk of AKI
