Lecture 9 (Renal)-Exam 5

Question 1

Nighttime Enuresis in Children
* What age does this occur at?
* When does normal successful bladder control begin?
* Often dry when? With what?

Answer 1

• Involuntary loss of urine after age 5
• Normal successful bladder control begins between 24 and 36 months
• Often dry during day with nighttime enuresis

Question 2

Nighttime Enuresis in Children
* Primary=
* Secondary=
* Who should not be investigated?

Answer 2

• Primary = patient never had period of complete control
• Secondary = dry for ≥ 6 months
• Children < 5 years should not be investigated

Question 3

Nighttime Enuresis in Children
* What do you need to rule out?
* What type of diary?

Answer 3

• UA and culture to rule-out UTI
• Voiding and fluid intake diary

Question 4

Nighttime enuresis-Common comorbidities
* What is most common?
* What are some other issues? (4)

Answer 4

• Constipation (33 to 75%) – treatment resistance common
• Urinary tract infection (18 to 60%)
• Obstructive sleep apnea (10 to 54%)
• Overactive bladder or dysfunctional voiding (up to 41%)
• Attention-deficit/hyperactivity disorder (12 to 17%)

Question 5

Nighttime enuresis
* What are the risk factors?(5)

Answer 5

• Younger age
• Male sex
• Black race
• Family history of enuresis
• History of recurrent UTIs

Question 6

Fill in for dx and treatment approach

Answer 6

Question 7

Diagnostic and treatment approach
* Fill in if the child wants treatment?

Answer 7

Question 8

Desmopressin - DDAVP
* What is it also called?
* What does vasopresin increase and cause?
* Where does ADH travel?
* What does it signals?
* Increasing cAMP increases what?
* What does it allow?

Answer 8

AKA vasopressin / antidiuretic hormone (ADH)
* Increased osmolarity triggers the hypothalamus to release more ADH into the blood
* ADH travels to the kidneys to act on vasopressin 4 receptors in the DCT and collecting duct of the nephron
* Signals adenylyl cyclase to convert ATP to cAMP
* Increased cAMP – increases aquaporin production and stimulates vesicles containing aquaporin to fuse to the apical side cell membrane
* Allows H20 to move from the renal tubule into the blood

Question 9

What age does children get desmopressin?

Answer 9

Children ≥ 6 years and adolescents

Question 10

Desmopressin - DDAVP
* What is the dose?
* When do you limit fluid?

Answer 10

• 0.2 to 0.6mg PO at bedtime
• Limit fluid starting at least one hour before dose and until next morning (at least 8 hours after administration)

Question 11

Desmopressin - DDAVP
* What are the drug reactions?
* What are the black box warning (2)?

Answer 11

Adverse Drug Reactions:
* Hyponatremia
* Xerostomia

Black Box Warning:
* Severe hyponatremia
* Monitor serum sodium within 7 days of treatment initiation and periodically thereafter (at least monthly)

Question 12

Alternative therapy / monitoring for nighttime enuresis
* What is second line? Similar efficacy but what?
* What happens after stopping?

Answer 12

• Tricyclic antidepressants second-line therapy
• Similar efficacy but increased adverse effects including anticholinergic side effects and potential cardiac toxicity
• Relaspe MC after stopping TCAs

Question 13

Answer 13

Question 14

Answer 14

Question 15

Kidneys-Physiology, Pharmacodynamics and Pharmacokinetics
* Major function to do what?
* What is filtration? What is too large to be filtered in normal healthy kidneys?

Answer 15

• Major function is to eliminate excess ions and wastes from the blood
• Filtration: water and small molecular weight ions and molecules diffuse across the glomerular capillary membrane in Bowman’s capsule and enter the proximal tubule
• Proteins are too large to be filtered in normal healthy kidneys

Question 16

Kidneys-Physiology, Pharmacodynamics and Pharmacokinetics
* What is secretion?
* What is reabsorption?

Answer 16

• Secretion = active process that take place in the proximal tubule; facilitates elimination of compounds from the renal circulation into the tubular lumen
• Reabsorption = water and solutes; occurs throughout the nephron; medication reabsorption primarily in the distal tubule and collecting duct

Question 17

Kidneys-Physiology, Pharmacodynamics and Pharmacokinetics
* What is renal clearance?
* What is the rate of excretion?

Answer 17

• Renal clearance = ability of the kidneys to remove molecules from blood plasma by excreting them into urine. Molecules/ions dissolved in plasma can be filtered via glomerulus. Those ions not reabsorbed are then eliminated in the urine and cleared from the blood
• Rate of excretion = filtration rate + secretion rate - reabsorption rate

Question 18

Measurement of kidney function
* What is gold standard? What does it refect?
* What is normal for male and female?

Answer 18

• Gold standard = glomerular filtration rate (GFR) -> aka creatinine clearance
• Reflects the ability of the kidneys to filter fluids and various substances, including medications

Normal
* Healthy men 127 ± 20 ml/min/1.73m2
* Healthy women 118 ± 20 ml/min/1.73m2

Question 19

Measurement of kidney function
* What cannot be measured directly? What are the markers?

Answer 19

• GFR cannot be measured directly; several exogenous and endogenous markers used
• Exogenous: inulin, radiolabeled markers
• Endogenous: serum creatinine, cystatin C

Question 20

Estimation of GFR
* What is the traditional equation?
* What is good and bad?

Answer 20

Cockcroft-Gault = “traditional” equation
* Good correlation when quick estimate is required – readily calculate
* Created prior to new standardized serum creatinine assays; not revised
* Generally overestimates glomerular filtration rate (GFR) and is no longer recommended

Question 21

Modification of Diet in Renal Disease (MDRD)
* Recommeded for use in what?
* Not recommended for what?
* Calculates what?

Answer 21

• Recommended for use in chronic kidney disease (CKD) only
• Not recommended for acute kidney injury (AKI)
• Calculates a higher GFR for AA patients (same creatinine value)

Question 22

Chronic kidney disease epidemiology (CKD-EPI)
* What is not a factor?
* Better estimate of what?

Answer 22

• 2021 CKD-EPI equation current recommended standard – does not use race as a factor
• CKD-EPI better estimate of GFR for patients with creatinine clearance > 60 ml/min/1.73m2

Question 23

Estimation of GFR
* What is used in pediatric patients?
* What is this equation?

Answer 23

Pediatric patients < 18 years – Bedside Swartz Equation

Question 24

GFR and Medication dosing
* Many medications require what?
* What are the GFR cut offs?

Answer 24

MANY medications require dose reduction based on GRF

GFR cut offs for dose adjustment vary by drug; typical cutoffs include:
* < 60 ml/min/1.73 m2
* 30 to 60 ml/min/1.73 m2
* < 30 ml/min/1.73 m2

Question 25

GFR and Medication dosing * What is bottom line? * Standard labs help with what? * What is a renal function panel?

Answer 25

* BOTTOM LINE – verify need for dosage adjustments for all patients with a GFR of < 60 ml/min/1.73m2 * Standard labs that help with assessment of GRF should be drawn at least annually in most patients * Renal function panel (BUN, SCr, hemoglobin-A1C, albumin-creatinine ratio, urinalysis)

Question 26

How to adjust dosages by renal function: * Red flag patients? * What do you need to document and treat accordingly?

Answer 26

* Red flag patients: patients of older age 70+ and diabetic patients * If patient answers “no” to having any kidney history or having seen a nephrologist and appears a good historian and healthy, then document and treat accordingly

Question 27

How to adjust dosages by renal function * If patient unsure or has risk factors; obtain what? * If inpatient, get who involve? * What do you need to do?

Answer 27

* If patient unsure or has risk factors; obtain basic labs that include BUN and SCr prior to starting therapy that requires dos adjustment for renal impairment * Inpatient-Get Pharmacy involved * Documentation, Documentation, Documentation

Question 28

Acute Kidney Injury (AKI) * What happens in GFR? * Results in what? What is that?

Answer 28

* Abrupt and usually reversible decline in the glomerular filtration rate (GFR) – hours to days * Results in azotemia-> Elevation of renal waste products including serum blood urea nitrogen (BUN), creatinine (SCr), and other metabolic waste products that are normally excreted by the kidney (azotemia)

Question 29

Acute Kidney Injury (AKI) * What are the Three main categories based on anatomic location of injury?

Answer 29

* Prerenal * Intrinsic * Postrenal

Question 30

Answer 30

Question 31

Prerenal AKI * Hypoperfusion of renal parenchyma: What are the 3 subgroups and their causes?

Answer 31

Hypoperfusion of renal parenchyma * Intravascular volume depletion * Hemorrhage * GI losses * Burns Reduction of effective circulating volume * Decreased cardiac output * Systemic vasodilation Functional * Medications

Question 32

Pre-renal AKI * Patients with mild reduction in volume, do what to compensate? * Work together to increase?

Answer 32

Patients with mild reduction in volume usually able to compensate by activating compensatory mechanisms * Sympathetic nervous system * Renin-angiotensin-aldosterone * Release of antidiuretic hormone Work together to increase blood pressure and thirst – increases fluid intake and sodium and water retention

Question 33

What is the RAAS pathway? (general)

Answer 33

Question 34

RAAs: * What causes a decrease in blood volume? * What happens down stream due to blood volume dropping? (stop at ATII)

Answer 34

* Dehydration, low sodium, or hemorrhage causes a decrease in blood volume * Decrease in blood volume -> decreased blood pressure * Decreased blood pressure -> stimulates JG cells of kidney to release renin * Renin cleaves angiotensinogen to angiotensin I * Angiotensin converting enzyme converts angiotensin I into angiotensin II

Question 35

RAA System * Angiotensin II: What does it stimulate at the adrenal gland? What does that cause?

Answer 35

Stimulates cells in the zona glomerulosa of the adrenal gland -> increases aldosterone * Aldosterone increases sodium and water reabsorption in the kidneys * Increases blood volume -> increases blood pressure

Question 36

RAA System * Where does AT II bind and what does it stimulate?

Answer 36

Binds AT II receptors in blood vessels * Stimulates vasoconstriction -> increases blood pressure

Question 37

RAAS: Angiotensin II * What does it stimulate at the posterior pituitary? What does it cause?(2)

Answer 37

Stimulates posterior pituitary to release anti-diuretic hormone in the renal collecting ducts (CD) * Increase DCT / CD aquaporins -> increase water reabsorption * Increases blood volume -> increases blood pressure

Question 38

Answer 38

Question 39

Adrenergic Nervous system (SNS)-Beta Receptor * Found where? * What are the two types? * What is the normal physiology?

Answer 39

* Found on multiple different target organs and beta receptors * Beta-1 and beta-2 receptors * Normal physiology: norepinephrine and epinephrine stimulate beta receptors during a flight or fight situation

Question 40

Adrenergic Nervous system (SNS)-Beta blockers * Competitive what? * Counter the effects of what? * Decrease what type of effects?

Answer 40

* Competitive inhibitors of beta-adrenergic receptors * Counter the effects of catecholamines (epinephrine / norepinephrine) on the sympathetic nervous system * Decreased sympathetic effects on the cardiovascular system

Question 41

Where is beta one receptors? What is the normal response to stimulation?

Answer 41

Location: Heart and kidneys Effects cardiac: * Increase HR (conduction) = Increased blood pressure * Increased contractility = Increased SV=increase CO = Increase BP Effects kidney: * Stimulates JG cells to release renin

Question 42

What are the beta one effects when blocked?

Answer 42

Effects Cardiac: * Decrease HR and contractility * Decrease oxygen demand * Decrease blood pressure * Decrease conduction effects Effects Renal: * Decrease renin and decrease BP

Question 43

Presental AKI * GFR may also be maintained by what? (2)

Answer 43

* Afferent arteriole dilation – mediated by vasodilatory prostaglandins, bradykinin, nitric oxide plus * Efferent arteriole constriction – mediated by angiotensin II

Question 44

Prerenal AKI * What certain drugs upset the compensatory renal mechanisms? Explain (3)

Answer 44

* Angiotensin converting enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARBS) decrease efferent arteriole resistance * NSAIDS – inhibit renal prostaglandin production and afferent arteriolar vasodilation * Contrast dyes

Question 45

Differentiating AKI etiologies * What helps differentiate the causes of AKI?

Answer 45

Fractional excretion of sodium (FENa)

Question 46

Differentiating AKI etiologies * Low (<1%)-low urine sodium concentration: * Assoicated with what? * Stimulation of what? * Intact what? * Common with what?

Answer 46

Low (<1%) – low urine sodium concentration * Associated with oliguria * Stimulation of Na retention mechanisms has occurred * Tubular function intact * Common with prerenal AKI

Question 47

Differentiating AKI etiologies * High (> 2%) – high urine sodium concentration: * What type of dysfunction? * _ AKI

Answer 47

* Tubular dysfunction * Intrinsic AKI

Question 48

Answer 48

Question 49

Prerenal AKI treatment * Assess what? * Remove what? * What is neccesary?

Answer 49

* Assess volume status * Remove potential nephrotoxins * Dose adjust medications as necessary

Question 50

Prerenal AKI treatment * Monitor and correct what? What is mc?

Answer 50

Monitor and correct electrolyte abnormalities * Hyperkalemia MC with prerenal AKI -> 90% potassium renally eliminated

Question 51

Answer 51

Question 52

Prerenal AKI treatment * What type of resuscitation? What type?

Answer 52

Fluid resuscitation->Isotonic fluids or blood

Question 53

Prerenal AKI treatment: isotonic fluids * What are the different types of isotonic fluids? * Specific volume recomendations depend on what? What are the different types? What is the goal?(3)

Answer 53

NS or LR or plasmalyte Specific volume recommendations depend on etiology of AKI and urine output * Bolus – 1 to 3 L (1L over 15 min to 1 hour) * Continuous infusion – 75 to 125 mL/hour * Goal – replace fluid deficit, improve urine output, improve blood pressure / MAP

Question 54

Prerenal AKI treatment * Consider what for perisistently low MAPs?

Answer 54

Consider vasopressor support for persistently low MAPs

Question 55

Prerenal AKI treatment – Renal replacement therapy * Indicated for what? * Requires who? * What are the differnet types? Which one is MC for AKI?

Answer 55

Indicated for no or inadequate response to first-line therapies * Requires Nephrology consultation * Intermittent – hemodialysis / peritoneal-> MC for chronic situation * Continuous renal placement therapies-> MC for AKI

Question 56

Answer 56

Question 57

Intrinsic Kidney Injury * What are the differenly ones? (4)

Answer 57

* Acute interstitial nephritis * Acute tubular necrosis * Acute glomerulonephritis * Vascular damage - rare

Question 58

Acute Interstitial Nephritis: * What is it? * What type of response? what does it cause? * What is the MCC? * When does it occur?

Answer 58

Inflammatory or allergic response in the interstitium; spares the glomeruli * Allergic hypersensitivity response – interstitial infiltration of lymphocytes, eosinophils, and polymorphonuclear neutrophils * **Most common cause – Drug Hypersensitivity ~70%** * Usual presentation -> 14 days after therapy initiation

Question 59

# These were all the stared ones What are the drugs that are associated with acute intersitial nephritis? (9)

Answer 59

* B lactam drugs * Fluroquinolones * Rifampin * Sulfa based drugs * Proton pump inhibitor * NSIADs * Phenytoin * Allopurinol * 5-aminosalicylates ## Footnote 5-barns ppf

Question 60

Acute Interstitial Nephritis * What is the classic presentation?

Answer 60

* Fever (27 to 80%) * Maculopapular rash (15 to 25%) * Eosinophilia (23 to 80%) * Arthralgia (45%) * Oliguria (50%) * Tubular dysfunction may manifest as metabolic acidosis, hyperkalemia, salt wasting and concentration defects | Other causes – infection, autoimmune, idiopathic

Question 61

NSAID induced AIN * Different clinical presentation compared to other agents? Explain (4)

Answer 61

* Delayed onset - 6 months after therapy initiation * Patients > 50 years (older) * Lower incidence of fever, eosinophilia (< 10%) * Concomitant nephrotic syndrome (proteinuria > 3.5 gm/day) >70%

Question 62

AIN Treatment * What type of therapy? * Remove what? * What do you need to give?

Answer 62

* Supportive therapy * Removal of offending agent * Corticosteroids: Prednisone 1 mg/kg/day for 2 to 4 weeks followed by a taper

Question 63

AIN Treatment * Closely monitor what?

Answer 63

BUN, SCr, proteinuria if present

Question 64

AIN Treatment * What are supportive care measures?

Answer 64

Question 65

Acute Tubular Necrosis (ATN) * MCC of what? * What is it? * Reversible or nonreversible?

Answer 65

* MCC intrinsic AKI * Acute destruction and necrosis of the renal tubules of the nephron * Reversible (recovery in 7 to 21 days)

Question 66

Acute Tubular Necrosis (ATN) * 50% due to what? What is MC? * What is the cause 35% of the time?

Answer 66

* 50% due to renal ischemia->Extended prerenal AKI MC * 35% secondary to exogenous and/or endogenous nephrotoxins

Question 67

Acute Tubular Necrosis (ATN) * What are the endogenous and exogenous nephrotoxins?

Answer 67

Endogenous * Myoglobin (rhabdomyolysis) * Hemoglobin (hemolytic anemia) * Uric acid (tumor lysis syndrome) * Myeloma light chains (multiple myeloma) Exogenous * drugs * contrast dyes

Question 68

ATN * What goes into the tubule? * What does this cause? What are the effects? (4)

Answer 68

Dead tubular cells sluff off into tubule Plugs the tubule and increases tubule pressure * Less fluid able to be filtered * GFR decreases -> less blood filtered through glomerulus * Less urine produced -> oliguria * Less urea and creatinine filtered out -> azotemia

Question 69

ATN * Dead tubular cells not good at what? * Dead tubular cell plugs eventually does what?

Answer 69

* Dead tubular cells not good at filtering electrolytes and they accumulated in the blood -> potassium / acids * Dead tubular cell plugs eventually excreted -> muddy brown cast

Question 70

# Note to self: Come back to this question after asking Dr.V a qustion What is the treatment of ATN?

Answer 70

* Remove offending agent * Supportive care

Question 71

What are the most common medications/toxins associated with ATN?

Answer 71

Question 72

Acute Glomerulonephritis: * What is it caused by? * Immune mediated damage to the what?

Answer 72

* Inflammation of the glomerulus * Immune-mediated damage to the basement membrane, the mesangium, or capillary endothelium

Question 73

Acute Glomerulonephritis * What is damaged? What leaks out? * What is the cause?

Answer 73

Podocytes damaged -> large gaps between cells -> increased permeability to large molecules * Proteins * Blood Leaky basement membrane decreased pressure across glomeruli

Question 74

Acute Glomerulonephritis * What is the result due to less fluid being filtered? (3) * AGN can arise from what?

Answer 74

Less fluid filtered * Less blood flow -> less urine -> oliguria * More fluid in body -> edema -> hypertension * Less electrolyte filtered -> azotemia AGN can arise from a primary kidney injury or a secondary illness

Question 75

Acute Glomerulonephritis * Most are what? * Can be classifed based on what?

Answer 75

* Most are progressive and **require intervention** to prevent progression to chronic GN, CKD and ultimately ESRD * Can be classified based on clinical presentation - nephrotic vs nephritic presentation

Question 76

KNOWWWW

Answer 76

Question 77

Treatment-AGN * What is treatment for secondary disease? * What is the treatment for primary disease?

Answer 77

## Footnote Early intervention key to preventing disease progression

Question 78

AGN treatment

Answer 78

Question 79

Answer 79

Question 81

Role of ACEis and ARBs * Control what? * Reduce what? * Indicated if what? * Start how?

Answer 81

* Control blood pressure * Reduce proteinuria – slow progression of kidney disease * Indicated if urine albumin > 30 mg/24 hours * Start at lowest dose and titrate to: Urine albumin < 30 mg/24 or 30 to 50 % decrease in urine albumin or side effects ## Footnote REDUCING PROTEINURIA IS COMPLETELY SEPARATE OF HTN

Question 82

Role of ACEis and ARBs * Expect increased in what? When should you continue and discontinue?

Answer 82

Expect increased serum creatinine and potassium after initiation – usually by 20% * If stable, continue therapy * If increase > 30% consider holding and consulting expert – nephrologist

Question 83

Role of ACEis and ARBs * Not contrainated for who? * Benefits for who?

Answer 83

* Not contraindicated for a specific creatinine level * Benefits for Stage 4 or 5 CKD studies ongoing

Question 84

* What are the three primary ways to block activiity of ATII?

Answer 84

Block the conversion of angiotensin I to angiotensin II * Angiotensin converting enzyme inhibitors (ACEI) Block angiotensin II from binding its receptors in blood vessels * Angiotensin II receptor blockers Inhibit renin release

Question 85

What are the examples and indications of ace-i?

Answer 85

Question 86

What are the SE and CI of acei?

Answer 86

SE: * Increased potassium * Hypotension * Cough * Angioedema CI * PREGNANCY! * Angioedema * Bilateral renal artery stenosis * Severe chronic kidney disease

Question 87

Ace-inhibitors -“prils” * What do you monitor? * For fun/review: what do you monitor for Statins?

Answer 87

* Monitoring: electrolytes, SBP > 100 mmHg, renal function * Statin: LDLs

Question 88

Side effects of ACEI * Normally, ACE breaks down what? * What happens when ACE inhibitors are given? * What drug does not cause this?

Answer 88

* Normally, ACE breaks down bradykinin into inactive metabolites * ACE inhibitors  prevent the breakdown of bradykinin * Angiotensin receptor blockers generally do not have these effects

Question 89

What happens when ACEi prevent the breakdown of bradykinin?

Answer 89

Increased levels of bradykinin resulting in * Accumulation of protussive mediators in the respiratory tract – dry cough * Increased capillary permeation and vasodilation – edema and swelling

Question 91

Angiotensin receptor blockers -“sartans” * What are examples? * What are the indications?

Answer 91

Question 92

Angiotensin receptor blockers -“sartans” * What are the SE and CI?

Answer 92

SE: * Increased potassium * Hypotension * Cough – less than ACEI * Angioedema – less than ACEI CI * PREGNANCY! * Bilateral renal artery stenosis * Severe chronic kidney disease

Question 94

Diuretics * What is the purpose of diuretics?

Answer 94

Increase production of urine; decrease water from the body

Question 95

What are the five main classes of diuretics?

Answer 95

* Carbonic anhydrase inhibitors - **acetazolamide** * Loop diuretics – **furosemide, bumetanide**, torsemide, ethacrynic acid * Thiazide diuretics – **chlorothiazide, chlorthalidone, hydrochlorothiazide,** metolazone * Osmotic diuretics - **mannitol** * Potassium-sparing diuretics – **spironolactone, amiloride, triamterene**

Question 96

Answer 96

Question 97

Where is most of the Na reabsorbed?

Answer 97

Question 98

Loop diuretics: * What are the examples? * Where is the site of action?

Answer 98

Question 99

Loop diuretics * What is the MOA? * What are the indications?

Answer 99

Question 100

Loop diuretics * What are the SE? (3) * What is CI?(2)

Answer 100

Question 101

Answer 101

Question 102

Potassium sparing diuretics * Where do they work?

Answer 102

Work in the DCT and CD

Question 103

Potassium sparing diuretics * What happens in the prinicpal cells?

Answer 103

Two pumps on apical side: * ATP-dependent K+ pump -> pushes K+ into the tubule * Epithelial Na+ channel (ENac) ->push Na+ into cell One pump on basal lateral surface * Na+-K+ ATPase pump -> moves two K+ into cell for every three Na+ out

Question 104

Potassium sparing diuretics * What happens in the intercalated cells?

Answer 104

Primarily remove H+ from blood Two pumps on apical side: * H+ ATPase -> H+ into the tubule * H+-K+ ATPase -> H+ into tubule in exchange for K+ into cell One pump on basal lateral surface * Na+-K+ ATPase pump -> moves two K+ into cell for every three Na+ out

Question 105

Potassium sparing diuretics * Movement of these electrolytes is controlled by what?

Answer 105

Movement of all these electrolytes is controlled by aldosterone

Question 106

Potassium sparing diuretics * how does aldosterone affect the prinicpal cells?

Answer 106

Aldosterone enters cells -> binds to steroid receptor ->upregulates the synthesis of Na+-K+ ATPase pumps -> net effect is more K+ secreted into urine and more Na+ secreted into blood

Question 107

What happens to intercalated cells when aldosterone is present?

Answer 107

Aldosterone enters cell -> binds to a steroid receptor -> upregulates the synthesis Aldosterone increases the synthesis of H+ -K+ ATPase -> increases hydrogen secretion

Question 108

Potassium sparing diuretics * Work by either doing what? (2)

Answer 108

* Blocking the steroid receptor -> aldosterone cannot bind * Blocking ENaC channels on the cell membrane

Question 109

Potassium sparing diuretics * What is the net effect? (3)

Answer 109

* Increased excretion of Na+ * Increased water loss through urine * Decreased excretion of H+ and K

Question 110

Potassium sparing diuretics * What are the examples? * Where is the site of action?

Answer 110

Question 111

Potassium sparing diuretics * What is the MOA of aldosterone blockers and ENac/Na/K-ATPase?

Answer 111

Question 112

What are the indications for potassium sparing diuretics?(3)

Answer 112

Question 113

What are the SE and CI of potassium sparing diuretics?

Answer 113

Question 114

Answer 114

Question 115

What are the examples of thiazide diuretics? What is the site of action?

Answer 115

Question 116

Thiazide diuretics * What is the MOA?

Answer 116

Question 117

Thiazide diuretics * What are the indications?(4) * What are the SE? (2) * What is CI?(2)

Answer 117

Question 118

Osmotic diuretics * What are the examples? * What is the Site of action?

Answer 118

Question 119

Osmotic diuretics * What is the MOA? * What are the indications?

Answer 119

Question 120

Osmotic diuretics * What are the SE and CI?

Answer 120

Question 121

Carbonic anhydrase inhibitors * MOA? What does it cause?

Answer 121

Bind to and inhibit carbonic anhydrase enzymes * Decreased bicarbonate and sodium reabsorption in the PCT * Increased excretion of sodium, bicarbonate, and water

Question 122

Carbonic anhydrase inhibitors * Strong or weak diuretic? * Causes what? * Decreases what? (2) * Used for what?

Answer 122

* Weak diuretic * Causes urine alkalinization * Decreases the production of aqueous humor * Decreases the production of CSF * Used for high altitude sickness

Question 123

Carbonic anhydrase inhibitors * What is the example? * What is the Site of action?

Answer 123

Question 124

Carbonic anhydrase inhibitors * What is the MOA and Indications?

Answer 124

Question 125

Carbonic anhydrase inhibitors * What are the SE and CI?

Answer 125

Question 126

AGN treatment: IgA nephropathy * What is the txt?

Answer 126

Question 127

AGN treatment: Post strept * What is the treatment? How many recover? What can it progress to?

Answer 127

Question 128

AGN treatment: Rapidly progressive GN * What are the two types and the treatments?

Answer 128

Question 129

AGN treatment: minimal change nephropathy * What is the txt? * Common in who?

Answer 129

Question 130

AGN treatment: Focal segmental glomerulosclerosis * What is the txt? * Most common in who? * What is the prognosis? * What is common?

Answer 130

Question 131

AGN treatment: Membranous nephropathy * What is the txt? * What is generally not effective? * What are secondary causes?

Answer 131

Question 132

Answer 132

Question 133

Renal artery stenosis * Narrowing of what? * Decreases what? * Detected as what?

Answer 133

* Narrowing of the renal artery which brings blood to kidneys * Decreases downstream renal blood flow * Detected as low blood pressure

Question 134

Renal artery stenosis * Kidneys increase what? * Renin continues to be released because why?

Answer 134

* Kidneys increase the blood pressure to compensate * Renin continues to be released because the blockage prevents improved blood flow to the kidneys

Question 135

Renal artery stenosis (RAS) * MCC? * How do you Dx?

Answer 135

MCC – atherosclerosis and fibromuscular dysplasia DX – high suspicion based on presentation * HTN in patients < 55 yrs * Rapid onset * Azotemia after ACEI or ARB initiation * Peripheral artery disease

Question 136

Renal artery stenosis (RAS) * What is the treatment?

Answer 136

* Blood pressure control with ACEI / ARB if NO bilateral disease or status post revascularization * Revascularization via renal catheter arteriography

Question 137

What are the causes of Post-renal AKI?

Answer 137

* Bladder outlet obstruction MCC * Obstructive uropathy secondary to prostatic cause – BPH, tumors, infection * Ureteral obstruction – nephrolithiasis, malignancy * Renal pelvis / tubular obstruction – nephrolithiasis, drugs * Neurogenic bladder * Anticholinergic medications

Question 138

Post-renal AKI * What is the treatment?

Answer 138

Treatment: Treat the cause * Urgent Urology consult for complete obstruction when urine catheter possible or complicated

Question 139

CKD - Treatment * Control what? How? * Decrease what? How? * Control what? (2)

Answer 139

* Control blood pressure – ACE-I or ARBs – do this early in disease! * Decrease / minimize proteinuria – same – ACE-I or ARBs – early * Control diabetes if present * Control lipids if hyperlipidemia exists

Question 140

CKD - Treatment * What can happen? * Replace what? * Dialyses indicated for what? * AVOID what? * What is last line?

Answer 140

* Renal osteodystrophy – Calcium, phosphate binders (calcium usually low, phosphorus usually high) * Replace Vit D and calcium if deficient * Dialyses indicated for GFR less than 10ml/min or if serum creatinine 8 or greater * AVOID nephrotoxic agents!!! * Transplantation

Question 141

Medication managment and patient safety in CKD * We recommend that prescribes should take what? * How should you measure GFR? * We recommend temporary discontinuation of what?

Answer 141

Question 142

CKD * CKD patient should seek medical or pharmacist advise before what? * We recommend not using what? * When should metformin be continued?

Answer 142

Question 143

CDK * We recommend that all people taking what should have labs mointor? * People with CKD should not be denied therapies for other conditions such as what?

Answer 143