Renal Flashcards

Question

How calculate daily sodium intake

Answer 1

Daily input=output

Answer 2

23-(.03age)+(.5weight)-(.62xBMI)

Answer 3

-18.37-(.09age)+(.34weight)+(.25height)

Answer 4

-10.5-(.01age)+(.2weight)+(.18height)

Answer 5

-16.71-(.05age)+(.22weight)+.24height Height cm and weight kg

Answer 6

TBWx(desired Na-serum Na)

Answer 7

Usually near 1% Na excreted/Na filtered= UxV/PxGFR=Cna/Ccr

Answer 8

Acute tubular necrosis (damage to kidney parenchyma so urine is more of an extracelular fluid ooze-cant concentrate)specific granite <1.01 Low protein intake Starvation Severe liver disease

Answer 9

Pre renal acute kidney injury (small amount of concentrated urine, specific gravity >1.02) High protein intak e After GI bleed

Answer 10

Small amount of normal uring Imaging will show accumulation upstream from block Relief of obstruction can lead to post obstructive diuresis, can be life threatening Blood uring

Answer 11

UproxV Uprox(24hrUcr/Ucr)

Answer 12

UcrxV V=24 hr U Cr/UCr

Answer 13

Grams/day of protein excreted

Answer 14

Detect small amounts in urine (trace amounts)

Answer 15

Hydrochlorothiazide Metolazone Chlorthilidone

Answer 16

Furosemide Torsemide Bumetanide Ethacrynic acid

Answer 17

Na channel blocker - amigo ride - triamterene Aldosterone antagonist - spironolactone - eplerenone

Answer 18

Conivaptan | Tolvaptan

Answer 19

Acetazolamide

Answer 20

Substance that promotes the renal excretion of sodium

Answer 21

Substance that produces free water clearance

Answer 22

V-Cosm V-(UosmxV/Posm)

Answer 23

No arterial anastomoses Ischemia and death downstream

Answer 24

Osmotic diuretics Carbonic anhydrase inhibitors

Answer 25

Osmotic diuretics

Answer 26

Loop diuretics

Answer 27

Thiazide diuretics

Answer 28

Na channel blockers spironolactone

Answer 29

Essential hypertension Edema associatedwith - congestive heart failure - liver failure - kidney failure

Answer 30

Triamtrene, amiloride...Na channel blockers Spironolactone-aldosterone antagonist

Answer 31

Thiazides-Na Cl cotransporter blockers Loop diuretics-Na K 2Cl cotransporter blockers Carbonic anhydrase inhibitors (seldom used) Osmotic diuretics-non reabsorbable solutes

Answer 32

Thick segment

Answer 33

Hypo-neurons don’t fire hyperpolarized Hyper-depolarizes maybe lethal since Na channels cant reactivation

Answer 34

Hypokalemia increases the toxicity of the digitalis

Answer 35

Tall T wave Prolonged PR interval Wide QRS interval Flattened P waves Arrhythmias including bradycardia, ventricular tachycardia or fibrillation Sinus arrest or nodal rhythm with possibl easystole

Answer 36

Flattened T waves ST segment depression Prolonged QT interval Tall U waves* Atrial arrhythmias Ventricular tachycardia or ventricular fibrillation

Answer 37

Inhibits reabsorption of sodium and chloride in the thick ascending limb of the loop by blocking Na K 2Cl cotransporter Inhibits paracellular reabsorption of Ca and Mg by the TAL due to loss of K backleak responsible for lumen+transepithelial potential

Answer 38

Causes increased excretion of water, sodium, K, Cl, Mg, and Ca

Answer 39

Edema, heart fail, hepatic disease, renal disease, acute pulmonary edema by decreasing preload (decrease EC vol, rapid dyspnea relief), HTN(works with low GFR)

Answer 40

Hypokalemia, hyponatremia, hypocalcemia, hypomagnesia, hypochloremic metabolic alkalosis, hyperglycemia, hyperureicemia, hyperuricemia, ototoxicity (vertigo), hypersensitivity BC IT IS A SULFONAMIDE

Answer 41

Similar to furosemide with longer T1/2 better oral absorption and some evidence that is works better in heart failure

Answer 42

Sulfonamide similar to furosemide,but more predictable oral absorption ethacrynic acid: non sulfonamide loop diuretic reserved for those with sulfa allergy

Answer 43

Max doses_>profound diuresis! From dissatisfaction of the medullary interstitial gradient —irrespective of whether urine was dilute or concentrated, get large volume of isotonic urine

Answer 44

PO, IV, IM IV 5 min last 2 hours PO 30-60 min lasts 8 hours

Answer 45

When rapid and massive fluid removal is needed (edema, cardiac, renal origin), acute pulmonary edema, HTN that is unresponsive to other diuretics (still works with RBF and GFR are low)

Answer 46

Rapid effects <5min that are though to be due to prostagladin mediated venodilaion that reduces preload

Answer 47

HypoNa, hypoCl, hypoK, which lead to hypovolemia and hypotension HypoMg HypoCa

Answer 48

K H exchange at cells try to maintain plasma K Also Na K exchange

Answer 49

Kidney stones (OPPOSITE OF THIAZides

Answer 50

Hyperglycemia Hyperuricemia (gout) Decrease HDL, increase LDL, increase TG (atherosclerosis

Answer 51

Frequent interactions since both drugs are often used to treat heart failure and the risk of digoxin toxicity is increased by low K due to the diuretic

Answer 52

Increased chance of hearing loss if combined with drugs having similar toxicity

Answer 53

Can counterbalance potassium wasting effects

Answer 54

Lithium toxicity, potentialte effects of other antihypertensive agents and have diuretic effects antagonized by NSAIDS

Answer 55

More predictable absorption

Answer 56

Long T1/2 better for absorption, may work better in heart failure

Answer 57

Among the few diuretics that can be used by people who are allergic to sulfa drugs

Answer 58

Hydrochlorothiazide-sulfa drug 12 others often ending in thiazide

Answer 59

Inhibitors Na reabsorption in the DT via blockade of NaCl cotransporter

Answer 60

Increases urinary excretion of Na and H2O Increases urinary excretion of K and Mg K losing

Answer 61

HTN (not effective in patients with low GFR) Edema Calcium nephorlithiasis

Answer 62

Orthostatis hypotension Hypo k, mg, na, cl, metabolic alkalosis Hyper ca, hyperglycemia, hyperuricemia Sulfa-hypersensitivity

Answer 63

Similar to HCTZ but poor oral absorption

Answer 64

Similar to HCTZ but half life of f40-60 hrs..prolonged/stable response with proven benefits is reason it is preferred by some hypertension specialists

Answer 65

Another long acting thiazide diuretic, this’s is a favorite of cardiologists for use as an adjunct diuretic in the treatment of CHF

Answer 66

Block Na Cl cotransporter More Ca reabsorption in PT bc of volume contraction Mg only reabsorbed in TALH.distal nephron ...loss greater with thiazides than loop diuretics

Answer 67

Don’t work

Answer 68

HCO3 Impairs distal nephron H secretion

Answer 69

Diuresis begins < 2 hours after oral ingestion with peak at 406 hours and effects lasting 12 hours.. in other works shouldn’t take this one at bedtime Drug is exceed unchanged in uring

Answer 70

primary HTN and edema Nephrotoxicity diabetes insipidus Decreases Ca excretion, day decraese risk of kidney stones (opposite of loop diuretics( Can be added to loop diuretics to increase diuresis

Answer 71

Hypovolemia K losing (downstream Na K exchanger tried to salvage Na at hte expense of K) Hypochloremic metabolic alkalosis Hypomagnesia

Answer 72

Combined with antiHTN meds K loss can be offset by combining K sparing diuretics Increase risk of digoxin and lithium toxicity

Answer 73

1-2 x more potent Different structure Longer HL Larger volume of distribution than HCTX, prescribed much less commonly in the US

Answer 74

Reduce CVD mortality and morbidity

Answer 75

Cortical collecting duct

Answer 76

Triamterene, amiloride..Na channel block | Spironolactone..aldosterone antagonist

Answer 77

Blocks the luminal Na channels in CT

Answer 78

Blocks aldosterone receptor in CD

Answer 79

Small increase in Na excretion Blocks major pathway for K elimination so K is retained H Mg Ca excretion also decreased

Answer 80

Counteracts K loss induced by other diuretics in the treatment of HTN or heart failure Ascites, pediatric HTN

Answer 81

``` Hyper K Hypo Na Hypo vol HyperCl metabolic acidosis Dizzy, fatigue, headache ``` Nauseas vom

Answer 82

Similar to amiloride for edema and off label HTN rapidly absorbed, duration of 6-9 hrs, eliminated as drug metabolites

Answer 83

Competitive antagonist of aldosterone receptors Partial agonist at androgen receptors

Answer 84

Counteracts K loss induced by other diuretics in the treat of HTN, heart failure, ascites Hyperaldosteronism Reduce fibrosis post MI Hirsutism

Answer 85

HyperK Amenorrhea, hirsutism, gynecomastia, impotence

Answer 86

More selective aldosterone antagonist, approved for use in post MI heart failure and alone or in combination for HTN

Answer 87

Increase Decrease If Na cant get into the cell, K cant get out of the cell into the tubular lumen

Answer 88

Channel is blocked directly, effects are seen more rapidly than with spironolactone but smaller and therefore harder to detects lasts 12-16 hours

Answer 89

HTN, edema, often in combo with loop of thiazide diuretic

Answer 90

Hyperkalemia | Nausea, vom, leg cramps, dizzy, bloody dyscrasias rare

Answer 91

Blocks ability of aldosterone to bind to its receptor and increase Nareabsorption int he CCD Leads to increased Na accretion

Answer 92

Can take 48 hours to work Steroid hormones produce effects with a slow onset

Answer 93

HTN and edema, often in combination with a loop or thiazide diuretic Primary hyperaldosteronism Reduce mortality rate in patients with severe heart failure

Answer 94

HyperK, endocrine effects include gynecomastia, importance’s, menstrual irregularities, hirsutism and deepening voice

Answer 95

Often combined with thiazide and loop diuretics to counteract their K loss Should NEVER be given with drugs that increase plasma potassium levels, but used cautiously with ACE inhibtiors

Answer 96

Block antidiuretic hormone receptor in the CD

Answer 97

Non peptide arginine vasopressin receptor antagonist V1A and V2

Answer 98

Promotes excretion of free water Decreasing Uosm Increasing Posm

Answer 99

Euvolemic and hypervolemic hyponatremia in patients that are hospitalized, symptomatic, not responsive to fluid restriction

Answer 100

Too rapid serum sodium correction can lead to seizures, osmotic demyelination, coma, or death

Answer 101

Orthostatic hypotension, fatigue, thirst | Polyuria, bedwetting

Answer 102

Selective V2 receptor antagonist given ORALLY Initiate and reinitiate tolvaptan in patients ONLY IN A HOSPITAL where plasma sodium can be closely monitored Must use <30 days for hyponatremia, longer use can kill by hepatoxicity

Answer 103

Prevents ADH mediated insertion of the aquaporin water channels into luminal membrane of principle cells in collecting duct Prevents the reabsorption of water, therefore increases water excretion Decrease plasma volume and increase plasma osmolality primarily due to an increase in plasma sodium

Answer 104

Conivaptan-t1/2 5.3-8.1 hours Tolvaptan effects increase to peak at 4 hrs, lasts 4-8hours

Answer 105

Hypervolemic or euvolemic hyponatremia AD polycystic kidney disease

Answer 106

Orthostatic hypotension Fatugue Thirst Polyuria, bedwetting

Answer 107

Metabolized by CYP3A4, so inhibitors and inducers of this enzyme can alter its half life and potential for toxicity Selective water loss means - possibility of hypovolemia - other electrolytes and drugs can become concentrated..hyperNa, K uricemia Toxic levels

Answer 108

Tin descending limb

Answer 109

Acetazolamide-sulfa drug Causes metabolic acidosis and alkaline urine

Answer 110

Na bicarbonate diuresis Bicarbonate remains in early proximal tubule H cyclone lose, inhibiting Na/H exchange Hyperchloremic acidossi

Answer 111

Urinary alkalinization Metabolic alkalosis Glaucoma:acetazolamide, dorzalamide Acut mountain sickness

Answer 112

Hyperchloremic metabolic acidosis Nephrolithiasis: renal stones Potassium wasting

Answer 113

Mannitol Also use urea, glycerin and isosorbide

Answer 114

Non metabolized 6 carbon sugar, freely filtered with minimal reabsorption The inability to reabsorbed. This keeps water water in the proximal tubular lumen; this water is delivered to the distal portions of the nephron where much of it is excreted Pull water out of cells Excrete TBW in excess of plasma electrolytes

Answer 115

Distributes in ECF, must give IV large amounts 50-2000 g Effects are noticeable within 30-60 minutes and mannitol is eliminated unchanged in the urin over a period of 6-8 hours

Answer 116

EC volume is acutely increased bc mannitol sucks water out of the cells which can exacerbate heart failure Headache, nausea, vomiting and fluid electrolyte imbalances also occur

Answer 117

Prophylaxis of renal failure Reduction of intracranial pressure Reduction of intraocular pressure

Answer 118

Some more MOST

Answer 119

More, smoke,some

Answer 120

Many souls ith claims that they are effective Some can Probably OK by themselves BUT DO NOT MIC WITH CONVENTIONAL DIURETICS bc of potential for adverse effects

Answer 121

Contains sweet glycyrrhizic acid , potentials aldosterone effects in kidney and dose-dependently increases systolic blood pressure

Answer 122

Loop diuretic Add thiazide according to ClCr Add distal diuretic

Answer 123

Spironolactone ClCr >50 add HCTZ ClCr<50 do to loop diuretic and treat like renal insuff or nephrotic syndrome

Answer 124

Treat like renal insufficiency or nephrotic syndrome if not mild Mild and ClCr <50 treat like “” Mild and ClCr>50 add HCTZ then treat like rest

Answer 125

Incorrect diagnosis (venous or lymphatic edema) Inappropriate NaCl or fluid intake ) Inadequate drug reaching tubule lumen in active form -poor absorption (uncompensated HF) -decreased RBF (HF, cirrhosis, old) Decreased functional renal mass (AKI, CKD, old Inadequate renal response -low GFR (AKI, CKD) , decreased effective arterial volume (edema) -activation RAAS (edema -nephron adaptation (prolonged diuretic therapy -NSAIDS(indomethacin, asprin

Answer 126

Thiazide diuretics, furosemide, K sparring diuretics

Answer 127

ACE I or ARB or CCB not black Black thiazide

Answer 128

Stage C-HF Diuretics to relieve congestion Aldosterone antagonists

Answer 129

Excesssice passing of urine , tasteless Central-lack of ADH Can treat with ADH agonist Nephrogenic-unresonveness to ADH Treat with thiazide diuretic

Answer 130

Desmopressin, a synthetic V2 agonist if central If lack of ADH response frominterstitial fibrosis, Li, antagonism of ADH in principal cells Thiazide diuretics

Answer 131

Appearance of DI symptoms in this case coincides with use of Li to treat bipolar disorder

Answer 132

Li induced DI bc Li reabsorption-like Na reabsorption is increased in the proximal tubule and can cause Li toxicity

Answer 133

Amiloride..blocks influx of Li into CCD cells Very dilute urine->urine of appropriate concentration to maintain water homeostasis bc amiloride blocks Li influx into principal cells, allowing ADH to work

Answer 134

It is NOT caused by lithium

Answer 135

Plasma least, more intracellularly, most IN THE BONE

Answer 136

Muscle contraction Intracellular signaling Bone formation Neuronal excitation

Answer 137

Hyper-raise threshold Hypo-lowers threshold

Answer 138

Decreases total serum calcium without affecting ionized. If serum albumin is abnormal, clinical decisions should be based on ionized calcium levels

Answer 139

Measured total Ca (mg/dL)+.8 (4-serum albumin )

Answer 140

Calcitrion (1,25 OH vitamin D3) PTH Calcitonin Sites of regulation—-kidney, bone, intestine

Answer 141

Lowers blood Ca levels in three ways: -inhibits Ca absorption by the intestines -inhibits osteoclast activity in bones -inhibits renal tubular reabsorption of Ca (increase Ca excretion) Like PTH it inhibits tubular phosphate reabsorption

Answer 142

Increase plasma Ca, decrease plasma PO4–>increased ionized plasma Ca - acts in distal nephron to increase Ca reabsorption - inhibits PO4 reabsorption int he proximal tubule - enhances bone release of Ca

Answer 143

Serum Ca acting on calcium sensing receptors on Parathyroid cells in a negative feedback manner Activated by low Ca

Answer 144

Renal synthesis from 25-OH vitamin D3 is stimulated by PTH Acts through calcitrion receptor Increases blood Ca levels

Answer 145

Promotes absorption of dietary calcium from GI tract Increases renal tubular reabsorption of filtered Ca Stimulates release of Ca from bones...acts on osteoblasts to activate osteoclasts

Answer 146

65 Paracellular, but some active transport

Answer 147

Paracellular | 20

Answer 148

8 Active transport along electrical and chemical gradients Renal epithelial Ca channel(TRPV5)-along with calbindin, regulated by calcitriol

Answer 149

Enzyme that can break down complex carbs, disruption leads to premature aging...has a direct stimulators effect on TRPV5

Answer 150

PTH and locally synthesized tissue kallikrein

Answer 151

Decreased Ca absorption Increased Caexcretion Decrease bone resorption NORMOCALCEMIA

Answer 152

*entry of calcium into ECF by bone resorption and intestinal absorption Primary hyperparathyroidism, thiazide diuretics, milk alkali syndrome, familial hypocalciuric hypercalcemia, malignancy, immobilization syndrome, granulomatous disease, VD intoxication

Answer 153

Mild-asymptomatic Severe-neurologic (weak, fatigue, confusion, stupor, coma) and GI (anorexia, nausea, vomiting and constipation) NV cause hypovolemia —impaired calcium excretion—worsening

Answer 154

Increasing calcium excretion Decreasing resorption Decreasing absorption —-ECF volume replacement with .9% saline ——furosemide —-calcitonin

Answer 155

Bisphosponates

Answer 156

Decreased calcium absorption from GI or decreased resorption Hypoparatyroidism, chronic kidney disease,familial hypocalcemia, rhabdomyolysis, septic shock, VD defiency, parathyroidectomy, acute pancreatitis (Ca soaps)

Answer 157

When ionized calcium concentration is reduced

Answer 158

Neuromuscular irritability (fatigue, paresthesia, circumpolar, twitching, tetany, chvostek, trousseau, laryngeal and bronchial spasm) Altered central nervous system function (emotional disturbances, depression, coma, seizures, papilledema, cerebral calcifications) CVD (lengthen QT, dysrhythmias, hypotension, CHF) Derm(dry skin, coarse hair, brittle nails, cataracts)

Answer 159

IV calcium

Answer 160

Oral calcium supplements +/- VD

Answer 161

Calcium and VD supplements

Answer 162

Bone formation, cellular energy metabolism, regulation of protein/enzyme function

Answer 163

85% bone rest in cells 1% ECF 2/3 organic phosphate 1/3 inorganic

Answer 164

Decrease by carbohydrate or glucose infusion Increase by high phosphate meal

Answer 165

Decreases serum by increases renal excretion

Answer 166

Decreases serum PO4 by increases renal excretion

Answer 167

Increase serum PO4s..increases intestinal phosphate absorption

Answer 168

Decrease serum PO43..shirt phosphate into cells

Answer 169

Phosphatonin released by bone that promote PO43 excretion by the kidney...familial problems also can be secreted by tumor to cause phosphate wasting

Answer 170

70kg man filters 200 molecules PO42 per day with 12.5 excreted int he urine - contrast with 1% of filtered Na excreted in urine - corresponds to 900 mg/day or 64% of dietary intake/day that needs to be laminated by kidneys Becomes problematic when GFR falls

Answer 171

3 Na dependent PO43 transporters NaPi2 is responsible for 85% transport, highly regulated FGF-23 and PTH regulate

Answer 172

PTH and FGF-23

Answer 173

Chronic kidney disease stages 3-5 Acute renal failure/acute kidney injury Hypoparathyroidism, pseudohypoparathyroidism Acromegaly Tumoral calcinosis FGF-23 inactivating gene mutation GALNT3 mutation with aberrant FGF-23 glycosylation KLOTHO inactivating mutation with FGF-23 resistance Bisphosphonatesc

Answer 174

Ingestion of phosphate, phosphate-containing enemas IV phosphate delivery

Answer 175

``` Respiratoy acidosis/metabolism acidosis Tumor lysis syndrome Rhabdomylosis Hemolytic anemia Catabolic state ```

Answer 176

Hyperglobulinemia, hyperlipidemia, hemolysis, hyperbilirubinemia

Answer 177

Deposition of Calvclium in soft tissues and resultant fall in ECF ionized calcium Calciphylaxis

Answer 178

Renal osteodystrophy

Answer 179

Acute-saline diuresis | End stage kidney disease-reduce dietary intake/intestinal absorption (phosphate binder)

Answer 180

CKD causes decreased 1,25 (OH)2D3 and increased phosphorus causing decreased calcium and increased FGF-23...increases PTH Both FGF-23 and PTH are phosphatic

Answer 181

Bone demineralization due to chronic kidney disease Can cause bonejoint pain, bone deformation or fracture

Answer 182

Hyperparathyroidism secondary to hyperphosphatemia...kidney is unable to excrete phosphate

Answer 183

Kidney unable to activate vitamin D to calcitrion needed for Ca absorption from diet

Answer 184

Ca/VD supplement Restriction of dietary phosphate, use of phosphate binders Hemodialysis/renal transplantation China cal et (calcium sensitized drug, lowers PTH)

Answer 185

Redistribution of extracellular phosphate into the intracellular space Decrease in intestinal absorption of phosphate Decrease in renal reabsorption of phosphate

Answer 186

Can be cause of death in starving people/anorexics as hexokinase phosphorylation glucose taken into cells

Answer 187

Tend to be malnourished so re feeding syndrome partially responsible

Answer 188

When treated with large doses of insulin

Answer 189

Tumor makin FGF23

Answer 190

Muscular abnormalities-weak, rhabdomyolysis, impaired diaphragmatic function, respiratory failure, heart failure Neurologic abnosmalities-paresthesia, confusion, stupor, dysarthria, seizures, and coma Hemolysis and platelet dysfunction Chronic hypophosphatemia-rickets, in kids, stromal Asia in adults

Answer 191

Asymptomatic and requires no therapy except treatment of the underlying cause

Answer 192

Oral phosphate

Answer 193

IV phosphate therapy espicially when associated with serious clinical manifestations

Answer 194

Kalemic | Magnesemic

Answer 195

50% mineralized in bone 49% intracellularly 10% ionized but has crucial role as cofactors in many biological processes such as ATPases, regulation of ion channels and translational processes 1% extracellular with 60% of that ionized , 30% bound albumin, 10% complexed with phosphatase

Answer 196

Paracellular and follows Na

Answer 197

Driven by the transepithelial gradient generated by Na K 2Cl cotransporter

Answer 198

Via TRPM6 channels

Answer 199

PCT not major site of reabsorption

Answer 200

Mg concentration same inside and outside, so electrical potential is primary driver of cellular Mg influx, intracellular shuttling is not well understood Hormonal regulation is uncertain and thought to be indirect, EGF is only hormone identified thus far

Answer 201

Decreased nutrition, diuretics, decreased albumin, aminoglycosides, decreased reabsorption (PPI)

Answer 202

Alcoholism, malabsorption, parenteral nutrition, PPI, familial hypomagnesia with secondary hypocalcemia Increased losses Redistribution -hungry bone syndrome

Answer 203

Neuromuscular manifestations(weak, tremor, seizures, tetany, positive chvostek and trousseau (but think Ca first), nystagmus CVD-T wave changes, U waves, prolonged QT and QU, repolarized alternans, premature ventricular contractions, v fib, monomorphic ventricular tachycardia, enhanced digitalis toxicity) Metabolic-hypoK and Ca

Answer 204

Oral or IV Mg

Answer 205

End stage renal disease Massive intake..epsom salt Magnesium infusion..administration to limit neuromuscular excitability in pregnant women with pre-ecclampsia/ecclampsia

Answer 206

<3.6 asymptomatic 4. 8-7.2-nauseas flushing headache 7. 2 to 12 somnolence, hypoca, absent DTR, hypotension, bradycardia >12 -muscle paralysis-flaccid

Answer 207

Normal renal function-stop administration and wait and/or add loop or thiazide diuretic Reduced renal function -stop administration and wait and/or add loop thiazide diuretic then ADD SALINE End stage kidney disease-dialysis

Answer 208

Side effects

Answer 209

``` Family history Age Males Black Diabetes ```

Answer 210

92%, no cause found, chronic and progressice, use drugs that lower BP but DONT treat underlying cause Low renin Normal renin High renin

Answer 211

Primary cause identified, less, can be cured by treating cause

Answer 212

``` Chronic kidney disease Renovascular OC Coarctation Primary aldosteronism Cushing ```

Answer 213

COxperipheral resistance

Answer 214

8nl/pir^4 N-viscosity L length R radius

Answer 215

Reflex circuit keeps arterial pressure at present level on a second by second basis

Answer 216

Stretch receptors located in the carotid sinus and aortic arch

Answer 217

Attempts to reduce arterial reassure with drugs Innervated the heart and travel along the blood vessels, forming multiple synapses such that the nerves resemble a string of beads

Answer 218

On bc to cause vasoconstriction to maintain venous return with changes in posture

Answer 219

Act both in the brain and in the periphery in a presynaptic receptors act in both the brain and in their periphery in a presympathetic tone

Answer 220

Increase heart rate and contractility, and stimulate renin secretions by the kidneys

Answer 221

Dilate skeletal muscle vasculature | -important during fight or flight response with concomitant a1 receptor vasoconstriction blood shunted to msucles

Answer 222

Renal blood volume, it is slow! But keep in mine, high salt intake causes hormonal changes that shift the intrinsic renal relationship between arterial pressure and urinary output of Na to the left, low salt to the right

Answer 223

Salt resistant, not changes in slope but increases Salt sensitive, bo up in dose response

Answer 224

Vascular smooth muscle Vascular a1 receptors Renal tubules (B1 juxtagloerular cells, angiotensin converting enzyme, angiotensin II receptors, aldosterone receptors) Brainstem Sympathetic ganglia Adrenergic terminals Cardiac B1 receptors

Answer 225

Thiazide diuretics, ACEI or ARB, and CCB

Answer 226

Do not prevent MI, heart failure, or death as well as other therapies Associated with a significantly higher incidence of stroke than other therapies

Answer 227

Angiotensin I cleaved from angiotensinogen by renin is cleaved by angiotensin converting enzyme to form angiotensin II.

Answer 228

Vasoconstrictor, increases total peripheral resistance Acts to increase extracelllular fluid volume - stimulating thirst - stimulating aldosterone secretion - stimulating ADH secretion

Answer 229

Follow an initial increase in cardiac output In some cases TPR increase is initiating event

Answer 230

Weight reduction Na restriction Alcohol restriction Exercise Smoking cessation Maintence of K and Ca intake Stress management

Answer 231

Aliskirin ARBS ACEI

Answer 232

Serum creatinine increases (preserves kidney function in hyperfiltering diabetics, can also alarm. Physicians) Ang II tone helps maintain resistance in efferent arterioles

Answer 233

Competitive inhibitor of ACE

Answer 234

Prevents conversion of angiotensin I to II Lowers levels of angiotensin II Increase renin and decrease aldosterone Lowers bp

Answer 235

Hypertension, add thiazide or loop diuretic if additional lowering is needed at max recommended dose Acute HTN HF with reduced ejection fraction LV dysfunction following MI Diabetic nephropathy

Answer 236

Cough Angioedema Hypotension Headache

Answer 237

Another early ACEI, a prodrug with active form available for IV

Answer 238

ACE inhibitor, longer half life permitting 1 dose a day

Answer 239

Now widely used ACE inhibitor, longer half life permitting 1 dose a day

Answer 240

Angioedema can be deadly CHOKE AND SWALLOW ON OWN TONGUE

Answer 241

Competitive nonpeptide angiotensin II receptor antagonist for AT1

Answer 242

Blocks vasoconstrictor and aldosterone-secreting effects of angiotensin II Induces a more complete inhibition of the renin angiotensin system than ACE inhibitors Does not affect the response to bradykinin

Answer 243

Treatment of diabetic nephropathy with increased Scr and proteinuria in type 2 diabetes and HT HT, Akon or in combination with other antihypertensives Hypertension with left ventricular hypertrophy to reduce risk of stroke CKD and HT regardless of race or diabetes status, to improve kidney outcomes Heart failure if intolerant of ACE inhibtiors Off label Marian

Answer 244

More common in diabetic nephropathy Hypotension, first dose hypotension, orthostatic hypotension Fatigue, dizzy Hypoglycemia, hyperkalemia Diarrhea, gastritis, nausea, weight gain Anemia Weakness, back/knee Cough

Answer 245

T1/2 6-10 hrs, noteworthy in that not a prodrug requiring activation, excreted primarily in feces as unchanged drug

Answer 246

T1/2 is 5-9 hrs, noteworthy for its relatively irreversible binding

Answer 247

Direct renin inhibitor, resulting in black of the conversion of angiotensinogen to angiotensin I

Answer 248

Decreases the formation fo angiotensin II, a potent blood pressure elevating peptide elevating peptide viavasoconstriction, aldosterone release and Na retention ACE inhibitor and ARB therapy can be offset by increases in plasma renin activity (PRA), which is blocked by direct renin inhibitors

Answer 249

Treatment of HTN alone or in combination with other antihypertensive agents

Answer 250

Few Rash Cough Diarrhea

Answer 251

2 weeks see effects | T1/2=24hrs

Answer 252

Age, race, Conor I’d conditions

Answer 253

Asthma B2 agonists are used for bronchodilator Diabetes..B2 receptor effects offset hypoglycemia and alert patient via palpitations

Answer 254

Heart failure

Answer 255

HTN at earlier age Average bp higher Worse disease severity More stroke, heart disease, and stage KIDNEY disease, heart failure

Answer 256

B blockers, ACE inhibitors and ARBS Diuretics , calcium channel blockers

Answer 257

Diuretic Should be used first line combinations herapy if SBP>15 and DBP>10

Answer 258

Identify cause and treat

Answer 259

ACE inhibitors ARBS

Answer 260

Efferent tone Precipitate renal failure in patients with bilateral renal stenosis Can help preserve renal function in diabetic patients

Answer 261

Pregnancy | All trimesters

Answer 262

Asymptomatic incidental RAS Renovascular hypertension Accelerated CV disease CHF, stroke, scndoary aldosteronism Ischemic nephropathy

Answer 263

Flash pulmonary edema, progressive renal failure, refractory congestive cardiac failure

Answer 264

Renovascular has more abdominal bruit, blood urea, potassium, duration, urinary casts and proteinuriia

Answer 265

Reduced renal perfusion Increase RAAS, impaired Na and water excretion ->volume exmpasion inhibitors RAAS Overall-reduced arterial pressure only after volume depletion may lower GFR Detect with renin plasma

Answer 266

Reduced arterial pressures Enhanced lateralization of diagnostic tests GFR fallelevated plasma renin

Answer 267

Vasoconstriction, Na retention, aldosterone secretion, vascular, sympathetic nervous system, Myocardial effects

Answer 268

Not surgery it fails to materially recover kidney function Use drugs to block the RAAS and statin therapy

Answer 269

Pyuria +/- bacteria

Answer 270

Rhubarb and blueberries

Answer 271

Methylene blue in viagara

Answer 272

Riboflavin (BIRGHT yellow)-can be used to turn it yellow if drinking a lot of water to pass a drug test

Answer 273

AR maple syrup I urine disease Buildup of branched chain aa (leucine, isoleucine, valine) and their toxicity by products (ketoacidosis) in the blood and the urine unless dietary intake is carefully managed

Answer 274

DI Glomerulonephritis Pyelonephritis Can’t concentrate urine Highly concentrated

Answer 275

6 ——fixed acid is being excreted as ammonium

Answer 276

A high power field likely has 3-5 neutrophils

Answer 277

``` MYOGLOBINURIA Intravascular hemolysis Nephrotic syndrome Urine contains a dye Nephrotic syndrome Analgesi nephropathy ```

Answer 278

Gram negative organism?

Answer 279

Diabetic ketoacidosis

Answer 280

Liver disease

Answer 281

Hemolytic disease

Answer 282

Bcence Johnson protein in multiple myeloma

Answer 283

Filtered load of glucose is greater than PCT reabsorption capacity

Answer 284

Urine infected with ammonia producing organisms ALKALINE

Answer 285

Acidic urine Metabolic origin

Answer 286

Damage to the glomerular endothelial cells Form when the tubule cells die and slough off WBC casts form HTN there is tubulointerstitla nephritis

Answer 287

Encase/lubricate junk in the tubular lumen to facilitate elimination Keep distal tubules from collapsing if GFR ceases Sop up waste products secreted by the proximal tubule that bind to protein so that my protein transporters and channels continue to function properly

Answer 288

Capillary membrane

Answer 289

Cell membrane

Answer 290

IC>IS>plasma

Answer 291

Na Cl HCO3

Answer 292

K, PO43 protein

Answer 293

Liver, lymphocytes

Answer 294

Maintains cell volume constant With protein inside the cell and na outside

Answer 295

Increased capillary hydrostatic pressure Excess kidney retention of salt and water (acute or chronic kidney fail, mineralocorticoid excess) High venous pressure (heart failure, venous obstruction , failure of venous pumps) Decreased arteriolar resistance (excessive body heat, insuffiency of the sympathetic nervous system, vasodilator drugs)

Answer 296

Loss of protein (nephrotic syndrome) Loss of protein from denuded skin areas (burns, wounds) Failure to produce proteins (liver disease, severe protein or caloric malnutrition)

Answer 297

Immune reactions that cause release of histamine, toxins, bacterial infections, vitamin defiency, espicially vitamin C, prolonged ischemia, burns

Answer 298

Cancer, infections(filariasis, nematodes), surgery, congenital absence or abnormality of lymphatic vessels

Answer 299

Interstitial normally has low compliance Lymph flow can increase 10-50 fold Increased amounts of protein poor capillary fluid flow wash protein out from the interstitial space, decreasing net capillary filtration pressure

Answer 300

Depression of metabolic systems of tissues Lack of adequate nutrition to the cells *cells lack the resources to drive the NaKATPase pump, so Na accumulates in cells and they expand and water follows sodium into the cells

Answer 301

Too little extracellular Na or too much water

Answer 302

Brain cell swell

Answer 303

Yup Na content and concentration are not the same thing

Answer 304

Sensed by effective vascular volume, stretch receptors AngII Aldo SNS ANF

Answer 305

Plasma osmolality Osmoreceptors ADH

Answer 306

Autoregulated | MAP

Answer 307

Increased delivery of solute to juxtaglomerular apparatus Increased resistance of afferent arterioles Decreased RBF and GFR

Answer 308

Creatinine increases This presernves kidney function in hyperfiltering diabetics can also alarm physicians

Answer 309

Small increase in GFR dueto increased MAP, get increase Pc, ensuring that there is proportional reabsorption of filtrate. More is reabsorbed but more is also delivered to the thin limbs and more reaches the distal portions With volume expansion, dilution of plasma proteins+ increased RBF leads to these changes in the peritubular capillary

Answer 310

Create gradient of 2 across the transported is multiplied along the length of the transporter array due to countercurrent flow In TAL to provide solute for the hypertonic renal medullary interstitial while simultaneously diluting the tubular fluid

Answer 311

Generated hypertonic renal medullary interstitial

Answer 312

Neededfor the possible excretion of excess water

Answer 313

Vascular Low pressure-cardiac atria, pulmonary vasculature High pressure-carotid sinus, aortic arch, juxtaglomerular apparatus of kidneys

Answer 314

Angiotensin II NE E

Answer 315

Aldosterone | ANP

Answer 316

Ability to retain na will become maxed out and arterial pressure then falls to a level where intake=output on the curve

Answer 317

Hormones minimal values and Na dumping hormones are a maximal values, and further increases in Na intake will cause arterial pressure to increase to a value where intake=output

Answer 318

Decreased sympathetic activity, increased ANP, decreased pi, decreased RAAS All leading to increased excretion of Na

Answer 319

Dilation of afferent arterioles Decreased Na reabsorption

Answer 320

Constriction of efferent arterioles | Decreased Na reabsorption

Answer 321

Decreased Na reabsorption

Answer 322

Decreased reabsorption

Answer 323

``` Decreased skin tumor Thirst Dry mucous membranes Sunken eyes Oliguria As worsens get tachycardia, hypotension, tachypnea, confusion ```

Answer 324

Edema, bounding pulse

Answer 325

Decrease ECFV and increase in total body sodium

Answer 326

Severe nephrotic syndrome

Answer 327

Diuretics, Na wasting tululopathies, genetic or acquired tubulointerstitila disease, Obstructive uropathy/postobstructive diuresis, hormone defiency, hypoaldosteronism, adrenal insuffiency

Answer 328

Oliguric acute renal failure, acute glomerulonephritis, severe chronic renal failure, nephrotic, nephrotic syndrome, primary hyperaldosteronism, Cushing, liver disease, conn, gordon, Liddell

Answer 329

Plasma >145

Answer 330

2xNa in plasma More accurate 2plasma Na+glucose in plasma/18+ BUN plasma/2,8

Answer 331

Plasma osmolality up and blood pressure or volume decrease

Answer 332

Increase plasma osmolality Decrease blood volume Decrease blood pressure Nausea, hypoxia Morphine, nicotine, cyclophosphamide

Answer 333

Decreased plasma osmolality Increased blood volume Increased blood pressure Alcohol, clonidine, haloperidol

Answer 334

Increased osmolality Decreased blood volume Decreased blood pressure Increased angiotensin II Dry mouth

Answer 335

Decreased osmolality Increased blood volume Increased blood pressure Decreased angiotensin II Gastric distention

Answer 336

Inhibits osmoreceptors in anterior hypothalamus—THIRST decreased Decrease ADH Decrease H2O permeability in late distal tubule and CD Decrease H2O reabsorption Decrease urine osmolarity and increase volume Increase plasma osmolarity toward normal

Answer 337

Stimulates osmoreceptors in anterior hypo->increase thirst Increase ADH from PP Increase H2O permeability in late DT and CD Increase H2O reabsorption Increase urine osmolarity Decrease urine vol Decrease plasma osmolarity toward normal

Answer 338

Lose volume from ECF

Answer 339

Lose volume os ICF and ECF | Increase osmolarity in ICF and ECF

Answer 340

Lose volume ECF gain volume ECF lost osmolarity in ICF and ECF

Answer 341

Gain volume in ECF

Answer 342

Increase volume ECF lose volume ICF | Gain osmolarity in ICF and ECF

Answer 343

Gain volume ECF, ICF, lose osmolarity ICF and ECF

Answer 344

Hyponatremia <135 mEq/L In 15-20% of hospitalized patients!!!

Answer 345

CHF Liver disease sepsis Nephrotic syndrome Prego

Answer 346

``` Stupor/coma Anorexia, nausea, vom Tendon reflexes decreased Limp muscles (weak Orthostatic hypotension Seizures/headache Stomach cramping ```

Answer 347

Fluid restriction

Answer 348

Vaptans or hypertonic NaCl

Answer 349

Hypertonic NaCl

Answer 350

NaKCli and H2O

Answer 351

NaKCl and INCREASED H2O

Answer 352

NaKCL and H2O decrease

Answer 353

Increase na and decrease H2O

Answer 354

Ptweightxdesired correction rate

Answer 355

Osmotic demyelination syndrome Can do 2.5 mEq/L/hr in acute In chonic .5?

Answer 356

Desmopressin, oxytocin, NSAIDS, MDMA, tumors producing vasopressin , brain tumors, HIV, traumatic brain injury

Answer 357

1% associated with high mortality and morbidity in the elderly See in people that live alone and fall Indicator of neglect in nursing home Ppl in desert

Answer 358

Administration of hypertonic saline, hypertonic sodium bicarbonate Hypertonic dialysis Hypertonic feedings Primary hyperaldosteronism Cushing

Answer 359

Diabetes insipidus Hypodipsia Insensible dermal and skin loses

Answer 360

Lack of access to water broken thirst MOA

Answer 361

Twitching tremors, hyperreflexia Restlessness, irritable, confusion I intense thirst, dry mouth, decreased urine output Pulmonary and peripheral and peripheral edema

Answer 362

Isotonic saline

Answer 363

Hypotonic IV solutions

Answer 364

.6% body weightx (1-140/Na)

Answer 365

Will cause brain edema Correct over 48 hours at .5mEq/L/hr

Answer 366

<3.7 mEq/L

Answer 367

Cells stay refractory since Na channels are not deactivated High T wave, prolonged PR interval, v fib

Answer 368

Hyperpolarized Low T wave High U wave low ST

Answer 369

ICF takes in H Low ECF pH<7,35 High H buffered by raising ECFK

Answer 370

ICF donates H so ECF has ph>7.45 Low H, bufferented by lowering ECF K

Answer 371

K into ECF could lead to fatal hyperkalemia if not for its rapid redistribution into the ICF; insulin is most important

Answer 372

``` Insulin!!!!! B2 agonist Aldosterone defiency A blockers Alkalosis Hypoosmolarity ```

Answer 373

``` A agonist (NE, EPI) Insulin defiency Aldosterone B2 blockers Acidosis Hyperosmolarity Exercise Lysis ```

Answer 374

Increase Na in | K out at principal cells of collecting duct

Answer 375

``` Plasma K Aldosterone ADH Acid base balance Tubular fluid flow rate ``` DISTAL NEPHRONNNN

Answer 376

Limit Na permeability in distal nephron, and without Na influx, do not have K secretion/excretion

Answer 377

Combine to promote increased K secretion/excretion

Answer 378

Due to redistribution or extrearenal k losses

Answer 379

With renal or extrarenal K loss

Answer 380

Love K excretion High Cl excretion -BP normal diuretics -BP high hyperaldosteronism

Answer 381

Due to RBC cell lysis

Answer 382

GI losses (vomit, diarrhea) Renal tubular acidosis (types I and II) Aldosterone Paralysis Hypothermia Insulin excess Cushing Insufficient intake Diuretics Elevated beta adrenergic activity Alkalosis

Answer 383

CNS-drowsi Neuromuscular-weak skeletal and weak smooth (ileus and constipation) CV-ventricular arrhythmias, hypotension, cardiac arrest Renal-impaired concentrating ability causes polyuria and nocturnal Metabolic?

Answer 384

Prevent life threatening conditions Replace K Diagnose/correct underlying cause

Answer 385

Renal disease: ARF, CKD, type iV RTA Excessive intake: food, K+IV fluids, blood transfusion Drugs: K sparing diuretics, K salts of penicillin Fictitious: prolonged use of tourniquet, hemolysis Endocrine: Addison’s Tissue release: rhabdomysis, burns, hemolysis, cytotoxic therapy Shift out of cell: acidosis, B antagonist, insulin defiency, tissue damage

Answer 386

Abnormal heart rhythm, bradycardia, v fib, peaked T wave

Answer 387

Numbnesss, weakness

Answer 388

NSAIDS, COX2 inhibitors , aliskiren beta blockers ACEI ARBS Spironolactone Amiloride

Answer 389

Antagonize cardiac effects (IV Calcium) Redistribute K into cells (give insulin and glucose, B2 agonist such as albuterol) Facilitate K elimination (administer K losing diuretic consider mineralocorticoid (if have hypoaldosteronsm , cation exchange resin, dialysis)

Answer 390

Hemolysis Thrombocytopenia Leukocytosis

Answer 391

``` Acidosis. Decreased insulin B block Arginine infusion Digitalis overdose Periodic paralysis ```

Answer 392

GFR<5 mL/mim oliganuria >20 impaired K secretion -low or normal aldosterone

Answer 393

Addison disease Hyporeniinemic Drugs

Answer 394

Primary tubular disorders | Drugs-spironolactone, amiloride, triamterene

Answer 395

``` Cystitis Prostatis Pyelonephritis Renal damage in young children Pre term birth Complications from frequent antibiotic use -antibiotic resistance, C diff ```

Answer 396

Asymptomatic bacteriuria

Answer 397

Contamination of the periurethral area with a uropathogen from the gut Colonization of the urethra and migration to the bladder Colonization and invasion of the bladder, mediated by pili and adhesins Neutrophil invasion Bacterial multiplication and immune system subversion Biofilm formation Epithelial damage by bacterial toxins and proteases Ascension to the kidneys Colonization o the kidneys Host tissue damage by bacterial toxins Bacteraemia

Answer 398

Acute cystitis or pyelonephritis -likely in nonpregnant outpatient women without an atomic abnormalities or instrumentation of the urinary tract Cystitis Pyelonephritis

Answer 399

Compromised urinary tract or host defense - urinary obstruction - urinary retention caused by neurological disease - immunosuppression - renal failure - renal transplantation - pregnancy - foreign bodies (calculi, indwelling catheters)

Answer 400

Fibrinogen

Answer 401

EPUC | Uropathogenic E. coli

Answer 402

Biofilm like intracellular bacterial communities Type 1 pili*, antigen 43, curli

Answer 403

Produce urease Calcium crystals and magnesium ammonium phosphate precipitates Crystalline biofilm

Answer 404

Microcolony formation by changing hydrophobicity of P aeruginosa surface Lectins, rhamnolipids

Answer 405

Fibrinogen

Answer 406

Asymptomatic bacteriuria Cystitis Pyelonephritis Complicated UTIprostatis

Answer 407

Urine screen unrelated to GU tract symptoms Bacteriuria

Answer 408

Dysuria, urinary frequency, urgency Nocturia, hesitancy, suprapubic discomfort, gross hematuria

Answer 409

Likely a young, non pregnant female with above symptoms

Answer 410

Nitrofurantoin, TMP-SMX, fosfomycin Oral beta lactam (amoxicillin, cefpodoxime, cefdinir, cefadroxil) Fluoroquinolones (ciprofloxacin, levofloxacin, ofloxacin)

Answer 411

Nitrofurnation

Answer 412

Not fully understood Conversion of nitrofurantoin into highly reactive intermediates by bacterial reductase Toxic intermediates react nonspecifically with many ribosomal proteins and disrupt synthesis of proteins, RNA, DNA, and metabolic processes

Answer 413

Metabolized and excreted so quickly that no systemic antibacterial action is acheived

Answer 414

Anorexia, nausea, vomiting Antagonizes nalidixic acid (synthetic quinolone antibiotic)

Answer 415

Glucose 6 phosphate DH defiency Antagonizes nalidixic acid (synthetic quinolone antibiotic)

Answer 416

CELl wall synthesis inhibitor Inhibits the cytoplasmic enzyme enolpyruvate transferase by covalently binding to the cysteine residue of the active site and blocking the addition of phosphoenolpyruvate to UDP-N-acetylglucosamine

Answer 417

Due to inadequate transport of drug into the cell

Answer 418

Only oral form approved in USA, oral bioavailability is 40%

Answer 419

Limited (headache and diarrhea)

Answer 420

Safe in pregnancy!

Answer 421

Nitrofurnation and fosfomycin TMP-SMX

Answer 422

No doesn’t achieve adequate renal tissue levels

Answer 423

If prevalence of resistance is known to exceed 20%

Answer 424

Amoxicillin-aminopenicillin Cefpodoxime-3rd generation cephalosporin Cefdinir-3rd generation ceph Cefadroxil-1st gen cephalosporin Less effective than fluoroquinolones (more side effects) and TMP-SMX

Answer 425

Ciprofloxacin Levofloxacin Ofloxacin Moxifloxacin is NOT RECOMMENDED bc attains lower urinary levels than other fluoroquinolones

Answer 426

Disabling and potentially irreversible adverse effects of systemic fluoroquinolones outweighs their benefits in treating uncomplicated cystic Tendinitis and tendon rupture Peripheral neuropathy CNS effects

Answer 427

Resistance

Answer 428

Espicially among outpatients with uropathogenic E. coli

Answer 429

Ertapenem (a car ape EM)

Answer 430

As a class carbapenems have a wide spectrum with good activity against gram negatives (including p aeruginosa), gram positive, and anaerobes Ertapenem specifically is insufficiently active against P aeruginosa

Answer 431

Unilateral back or flank pain, fever Mild-low grade fever with or without lower back pain or costovertebral angle pain Severe-high fever, rigors, nausea, vomiting, and flank andor loin pain Development of bacteremia

Answer 432

Fever (not present in cystitis), low back pain May or may not have symptoms of cystitis

Answer 433

Fluoroquinolones (ciprofloxacin, levofloxacin) TMP-SMX, oral beta lactam, aztreonam

Answer 434

Ciprofloxacin or levofloxacin Give for severe pyelonephritis or risk factors for resistance -administered with parenteral broad spectrum antibiotic until susceptibility data is available Aminoglycosides used are gentamicin and tobramycin

Answer 435

Gram negative and P aeruginosa

Answer 436

Irreversible protein synthesis inhibitos, binds to 30s ribosomal subunit Interference with the initiation complex of peptide formation Misreading of mRNA leading to production of non functional proteins

Answer 437

Cleared by kidneys

Answer 438

8th CN toxicity: vertigo, hearing loss Renal toxicity Neuromuscular blockade

Answer 439

TMP SMX, oral beta lactams, aztreonam

Answer 440

Fluoroquinolone patient hypersensitivity or fluoroquinolone resistance

Answer 441

Amoxicillin cefpodoxime Cefdinir Cefadroxil

Answer 442

Monobactam, monocyclic beta lactam ring

Answer 443

Activity against aerobic gram negatives (P aeruginosa)

Answer 444

Little cross reactivity with bicycling beta lactams

Answer 445

Cell wall synthesis inhibitor, transpeptidase inhibitor

Answer 446

IV formulation, 1-2 hour half life, prolonged in renal failure

Answer 447

Limited, neutropenia (children 3-11%) , pain at injection (children 12%)

Answer 448

Similar to uncomplicated cystitis and pyelonephritis | Can by cystic, pyelonephritis or both

Answer 449

Severe dysuria | 70-80% of all complicated UTI are due to an indwelling catheter

Answer 450

Organisms causing complicated UTIs are more likely to be resistant to commonly used oral agents recommended for empiric treatment of uncomplicated cystitis

Answer 451

Ciprofloxacin or levofloxacin

Answer 452

Ceftriaxone, ciprofloxacin, levofloxacin or azteronam

Answer 453

Beta lactam and beta lactamase inhibitor or a carabapenem

Answer 454

Ciprofloxacin or levofloxacin Covers p aeruginosa MOXIFLOXACIN is not recommended -attains lower urinary levels than other fluoroquinolones

Answer 455

Mpicillin or amoxicillin

Answer 456

Nitrofurantoin TMP SMX Fosfomycin Oral beta lactams (amoxicillin, cefpodoxime, cefdinir, cefadroxil) Use these drugs only is uropathogenic is known to be susceptible

Answer 457

Urinary analgesic with unknown mechanism, can cause significant nausea Colors urine orange/red

Answer 458

Ceftriaxone, ciprofloxacin or levofloxacin - covers P aeruginosa - moxifloxacin is NOT recommended - attains lower urinary levels than other fluoroquinolones Aztreonam

Answer 459

Cefepime Piperacillin+ tazobactam -if P aeruginosa suspected a higher dose can be used Ceftolozane+tazobactam Ceftazidime+avibactam Meropenem -if p aeruginosa suspected a higher dose can be used Imipenem Doripenem

Answer 460

B lactamase inhibtiors

Answer 461

Piperacillin+tazobactam Ceftolozane+tazobactam Ceftazidime+avibactam

Answer 462

By companion beta lactam

Answer 463

Resemble B lactam molecules, very weak antibacterial action Protect hydrolysable B lactams from inactivation by these enzymes ``` Good inhibtors of amber class A B-lactamase -these b lactamase are produced by staphylococci, H influenzae, N gonorrhea, salmonella, shigella, E. coli* and K pneumoniae* ``` ``` Poor inhibtiors of class C b lactamase -these B lactamase are produced by enterobacter app, citrobacter spp, S marcescens, and P aeruginosa ```

Answer 464

Limited (<10%), diarrhea, constipation, vomiting, skin rash

Answer 465

E. coli, K pneumoniae, enterobacter, P aeruginosa

Answer 466

Imipenem, doripenem, meropenem, ertapenem (resistant cystitis)

Answer 467

Wide spectrum with good activity against gram negatives (including p aeruginosa), gram positives, and anaerobes - doripenem and meropenem have greater activity against gram negatives and slightly less activity against gram positives - ertapenem insufficiently active against P aeruginosa

Answer 468

B lactamases

Answer 469

Inhibit transpeptidase, similar to penicillins and cephalosporins

Answer 470

Metabolized by dihydropeptiase in kidney

Answer 471

Not metabolized by dihydropeptidase

Answer 472

Nausea, vomiting, diarrhea, skin rashes, infusion site reactions, seizures

Answer 473

Less likely to cause seizures

Answer 474

Piperacillin-anti-pseudomonas penicillin Ceftazidime-3rd gen cephalosporincefepime-4th gen cephalosporin Ceftolozane-5th gen ceph

Answer 475

Piperacillin Ceftazidime Ceftolozane

Answer 476

Cell wall synthesis inhibitors, bind and inhibit transpeptidase

Answer 477

B lactam hypersensitivity

Answer 478

E. coli (most), proteus, P aeruginosa Enterobacteriaceae including klebsiella, enterobacter, and seratia spp

Answer 479

Fever, chills, malaise, myalgia, dysuria, lower urinary tract symptoms (frequency, urgency, urge incontinence), pelvic of perineal pain and cloudy urine

Answer 480

Patient is acutely ill with spiking fever, possible complaint of pain During the exam, a prostate will be warm, firm, edematous and tender

Answer 481

TMP SMX Ciprofloxacin Levofloxacin

Answer 482

Most common cause of acute nephritis in kids -97% of cases occur in regions with poor ppl Caused by prior infection with group A beta hemolytic strep(gram+)

Answer 483

Asymptomatic, microscopic hematuria Acute nephritic syndrome (red/brown urine, proteinuria, edema, HTN, elevation in serum creatinine)

Answer 484

Management-loop diuretic, anti HTN agent, dialysis Recurrent group A beta hemolytic strep infection -antibiotics

Answer 485

With agents greater B lactamase stability Penicillin G -IM injection if adherence to previous antibiotic uncertain Cephalexin or cefadroxil -1st gen cephalosporins Cefpodoxime or cefdinir -3rd gen cephalosporins Amoxicillin or clindamycin

Answer 486

Streptococci, staphylococci, and pneumococci - enterococci and gram negative aerobes resistant - very effective against anaerobes

Answer 487

Protein synthesis inhibitor, binds 50S ribosomal subunit

Answer 488

Penetrates most tissue (not brain and CSF) Metabolized in the liver and excreted int he urine

Answer 489

Diarrhea, nausea, skin rashes Risk factor for C diff induced diarrhea and colitis -GI filled with anaerobes

Answer 490

Obstruction

Answer 491

Interrupted stream, frequency, hesitation, fullness, dribbling, urgency, weak stream

Answer 492

Don’t pick it-doesn’t go into urine

Answer 493

Terazosin, doxazosin, tamsulosin, silodosin, alfuzosin

Answer 494

Relax muscle tone Rapid relief of symptoms

Answer 495

Muscle contraction Bladder outlet obstruction

Answer 496

Detruser instability

Answer 497

Reduce spasm Promote muscle relaxation Improve urine flow

Answer 498

A1>>a2 Take 1 hours prior

Answer 499

Postural hypotension, dizziness fatigue

Answer 500

PDE-5 inhibitors (sildenafil, vardenafil)

Answer 501

A1a=a1D>a1B

Answer 502

Yes | A1a-a1D

Answer 503

Reduced ejactulation, IFIS

Answer 504

PDE inhibitors (sildenafil, vardenafil) Increase concentration of CYP3A4

Answer 505

Non specific | A1 selective

Answer 506

Yes (functional)

Answer 507

QT prolongation

Answer 508

PDE-5 inhibitors (sildenafil, vardenafil) Increase concentration of CYP 3A4 substrates

Answer 509

- best monotherapy for prompt relief of symptoms (days) - all have comparable clinicalefficacy - alfuzosin has functional uroselectivity - distributes into the prostate>serum - avoid in hepatic impairment - take immediately after the same meal every day Tamsulosin-FDA approved as generic

Answer 510

Finasteride, dutasteride Prevents enlargement and shrinks prostate Delayed action -shrinkage takes 3-6 months

Answer 511

Aging+dihydrotestosterone

Answer 512

Androgenic steroids, testosterone, and DHT

Answer 513

Steroid 5a reductase type 1 and type 2

Answer 514

Epithelial atrophy, shrinkage, and gradual relief of LUTS

Answer 515

T accumulation DHT depletion

Answer 516

Androgen receptor less occupied No gene transcription

Answer 517

Specific inhibitors SAR2

Answer 518

Dual inhibitorSAR1 and 2

Answer 519

SAR2 SAR2>>1 90% decreased PSA 50% decreased 15-20% increased 70% decreased

Answer 520

SAR 1 and 2 SAR2>>1 90% decreased 50% decreased 15-20% increased 90% decreased

Answer 521

Take 3 months for measurable effect to be observed Have similar efficacy - improved LUTS - reduced prostate volume and reduced serum PSA - reduced need for surgery Have similar AE - erectile dysfunction - gynecomastia - depressed libido - ejaculation disturbance No dosage adjustment necessary for: Age, renal insuffiency No established clinically significant drug interactions Use caution with liver abnormalities -metabolized by hepatic CYP3A

Answer 522

For severe symptoms of BPH, known to have large prostate, no response from monotherapy Long term combination therapy significant improves patient symptoms versus either drug alone

Answer 523

PDE-5 inhibtors tadalafil | -for patients with both BPH and ED

Answer 524

Consistent or recurrent inability to acquire or sustain an erection of sufficient regidity and duration for sexual intercourse

Answer 525

Obesity, smoking, stress, CVD, adverse drug effect (diuretics, antidepressants SSRI)

Answer 526

Blood flows into corpora cavernous and corpus spongiosum (glans penis) NO facilitates smooth msucle relaxation - maximize blood flow - penile engorgement Relaxed smooth muscle leads to blood in sinusoids and a rigid organ

Answer 527

Increase in cGMP, decreases in iCa, smooth muscle relaxation and erection

Answer 528

Competitive inhibitors of the PDE-5 enzyme

Answer 529

Take 1 hour prior, 4 hours, empty, 4, hepatic CYP3A4

Answer 530

Take 1 hour prior, 4-5 hours, empty, 4, hepatic CYP3A4

Answer 531

Take 1 hour prior, 36 hours(1 weekend), doesn’t matter, 18, hepatic CYP3A4

Answer 532

Take 15 min prior (high dose)** Take 30 min prior (normal dose) 4 hours, doesn’t matter, 4 hours, hepatic CYP3A4

Answer 533

PDE-5 enzymes

Answer 534

Blue vision and blurred vision PDE-5 1 fold in corpus cavernosum PDE-6 10 fold in retina

Answer 535

But little significance

Answer 536

Negligible

Answer 537

Reasonably well tolerated PDE-5

Answer 538

Well tolerated PDE-5 related -headache, dyspepsia, nasal congestion PDE-6 related (sildenafil, vardenafil, and avanafil) -blurred blue vision Specific to tadalafil -back pain, myalgia, limb pain

Answer 539

* organic nitrates - extreme and dangerous Specific to vardenafil -patient needs to be hemodynamically stable Specific to tadalafil -when used for BPH, concurrent a1 blockers not recommended Specific to sildenafil -concurrent a blockers initiated at lowest recommended dose

Answer 540

Vacuum erection devices -try first, l,ess expensive and non invasive Penile injections with alprostadil -prostagladin E1

Answer 541

Leads to increase in cAMP, decreases in iCa, smooth muscle relaxation, and erection

Answer 542

Prolonged erection (priapism)-medical emergency, need to evacuate clogged blood - can result in permanent corporal fibrosis and ED - 6% of men using intrapenile alprostadil injection (can also occur with PDE-5 inhibitors )

Answer 543

Sympathomimetic (phenylephrine)+aspiration

Answer 544

Thick active Thin passive

Answer 545

PCT Filtered glucose, aa, uric acid, phosphate, and bicarbonate are passed into the urine instead of being absorbed Not considered to be a defect in a specific channel, but a more general defect in the function of the proximal tubules

Answer 546

``` Polyuria, polydipsia, hypovolemia Hypophosphatemia rickets Growth failure Type 2 renal tubular acidosis Hypokalemia Hyperchloremia Hypophosphatemia/phosphaturia Glycosuria -recall this also can be caused by the sodium glucose co transporter 2 SGlT2 inhibtors (the gliflozins such as canaglofloxin) -proteinuria/aminoaciduria -hyperuricosuria ```

Answer 547

Treat underlying causes Replace substances water in the urine - HCO3 (can use citrate), phosphate+vitamin D to promote bone growth - if genetic causes, minimize intake of substance that is not handled properly (cysteine, tyrosine, galactose, copper)

Answer 548

Bartter syndrome type I Bartter syndrome type II Barter syndrome III Bartter syndrome type IV Bartter syndrome IVB Bartter syndrome type V Gitelman Syndrome

Answer 549

Concentrating capacity reduced and diluting capacity reduced

Answer 550

Concentrating capacity normal.near normal and diluting capacity reduced

Answer 551

Dysfunction inNKCC2 , ROMK, CLC-kB ,CLC-Ka

Answer 552

CLCNKB gene | Defect in Cl channel

Answer 553

AR Rare Presents in childhood

Answer 554

Seen 24-30 weeksof gestation as polyhydramnios;polyuria/polydipsia with hypercalcuria after birth

Answer 555

No noticeable symptoms until school agi - polyuria/polydipsia - vomiting, growth retardation

Answer 556

Loop diuretics

Answer 557

Life long increases in dietary Na and K and K sparing diuretics to limit K loss -also PGE2 directly stimulates renin release from juxtaglomerular cells and contributes to the electrolyte abnormalities that are seen in bartter syndrome..NSAIDS can help correct this

Answer 558

Normal to low BP Polyuria/polydipsia Elevated plasma renin and aldosterone Hypokalemia Hyponatremia Hypocalcemia Hypomagnesia Hypochloremic alkalosis Hyperglycemia Hyperuricemia Increased cholesterol and triglycerides ISOTONIC URINE

Answer 559

Defect in. NaCl symporter-defective in gitelman syndrome

Answer 560

AR less rare than bartter Mutations in the gene coding for the thiazide sensitive NaCl cotransporter in distal tube

Answer 561

Late childhood or adulthood, may be more severe in females Mimics chronic use of thiazide diuretics May get htn at later stage

Answer 562

``` Polyuria/polydipsia Hypokalemia Hyponatremia Hypercalcemia Hypomagnesemia Hypochloremic metabolic alkalosis Hyperglycemia Hyperuricemia Increased cholesterol and triglycerides ``` And can DILUTE OR CONCENTRATE URINE

Answer 563

Life long Cornerstone is taking NaCL to avoid sodium depletion (which would increase Aldo) and providing supplementation of K and Mg -but supplementation->side effects Aim for asymptomatic stable hypokalemia and borderline hypomagnesemia -an aldosterone antagonist can stabilize the hypokalemia, but it competes with compensatory secondary hyperaldosteronism NSAIDS are ineffective in gitelman syndrome (defect is downstream from macula densa)

Answer 564

Exclusion Made in someone who presented with unexplained hypokalemia and metabolic alkalosis with a moral or low bp

Answer 565

Gitelman-dilute Bartter-isotonic

Answer 566

Bartter-hypocalcemia/hypercalciuria, opposite of gitelman

Answer 567

Chloride Patients who secretively take diuretics have a variable urine chloride concentration correlations with or without diuretic effect..so a urine diuretic screen should be obtained

Answer 568

Bartter | Gitelman

Answer 569

ENaC channel doesn’t degrade properly

Answer 570

Rare AD Mutation changes ENaC Chen also so that they are not degraded correctly by ubiquitin proteasome system->increased Na reabsorption with K loss —early and often severe hypertension associated with -low plasma renin activity, low aldosterone -metabolic alkalosis -hypokalemia

Answer 571

Low Na diet and K sparing diuretics

Answer 572

Caused by a failure of response to aldosterone, leading to renal tubular acidosis and hyperkalemialevevls of aldosterone are actually elevated due to a lack of feedback inhibition

Answer 573

Large amounts of Na

Answer 574

Due to unmeasured anions (anion gap) Normal 8-16 mEq/L

Answer 575

Renal loss of HCO3(cant reabsorbed) Normal anion gap Hyperchloremia

Answer 576

Decrease excretion of H as titratable acid and HN4 Decrease ability to acidity urine Normal anion gap

Answer 577

Hypoaldosteronism Decreased excretion of NH4 Hyperkalemia inhibits NH3 synthesis Normal anion gap

Answer 578

Acidemia, normal anion gap, normal serum creatinine, no diarrhea

Answer 579

Distal Impaired H secretion <15 HCO3 Urine pH>5.5 Low K Autoimmune disorder related Severe

Answer 580

Proximal tubule Impaired proximal HCO3 reabsorption Plasma HCO3 12-20 Ph urine under 5.5, over 7 when give alkali therapy Los plasma K Related to faconi, multiple myeloma, drugs

Answer 581

Combo of 1 and 2, very rare genetic form (carbonic anhydrase II defiency)

Answer 582

ADRENAL Hyperkalemia Lack of Aldo or failure of kidney to respond to it Plasma HCO3>17 Urine pH <5.5 High plasma K Related to diabetic nephropathy, drugs (ACEI, ARB, heparin, NSAIDS) Normal anion

Answer 583

Accumulation of acid in the body due to a failure if the kidneys to properly acidity the urine

Answer 584

H secretion by a intercalated cells is somehow impaired Recall this is how new HCO3 is generated to maintain acid base homeostasis Phosphate and ammonia buffer this H

Answer 585

Untreated->growth retardation in kids, progressive kidney and bone disease in adults Restore normal growth and preventing kidney stones are the major goals of therapy - sodium bicarbonate or sodium citrate to treat acidosis (1-2 mEq/kg/day) - >correction of low k, salt depletion and Ca leakage..without Ca leakage, also decrease kidney stone development

Answer 586

HCO3, the major buffer in the body, is among the good stuff normally reclaimed by the proximal tubules

Answer 587

Identify the correcting the underlying causes of acquired forms of proximal RTA Children with this disorder would likely receive large doses of potassium citrate, and oral alkali (10-15 mEq/kg/day) - correcting acidosis and low potassium levels restores normal growth patterns, allowing bone to mature while preventing further renal disease - vitamin D supplements may also be needed to help prevent bone problems

Answer 588

Low Aldo High K Low NH3 synthesis by pT Recall how new HCO3 is generated by having NH3 accept H->NH4 to maintain acid base homeostasis

Answer 589

Type 4 (most common; hyperkalemia from no Aldo or failure to respond to it) - patients may require alkaline agents to correct acidosis, but therapy is aimed primarily at reducing serum K - low K diet and a loop diuretic - alter drug doses and/or change drugs (spironolactone, ACE inhibitors, angiotensin receptor blockers, NSAIDS)

Renal Flashcards

(671 cards)