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Pharm II > Lecture 9 (Renal)-Exam 5 > Flashcards

Lecture 9 (Renal)-Exam 5 Flashcards

1
Q

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

A
  • Involuntary loss of urine after age 5
  • Normal successful bladder control begins between 24 and 36 months
  • Often dry during day with nighttime enuresis
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2
Q

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

A
  • Primary = patient never had period of complete control
  • Secondary = dry for ≥ 6 months
  • Children < 5 years should not be investigated
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3
Q

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

A
  • UA and culture to rule-out UTI
  • Voiding and fluid intake diary
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4
Q

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

A
  • 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%)
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5
Q

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

A
  • Younger age
  • Male sex
  • Black race
  • Family history of enuresis
  • History of recurrent UTIs
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6
Q

Fill in for dx and treatment approach

A
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7
Q

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

A
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8
Q

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?

A

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

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9
Q

What age does children get desmopressin?

A

Children ≥ 6 years and adolescents

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10
Q

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

A
  • 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)
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11
Q

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

A

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)

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12
Q

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

A
  • Tricyclic antidepressants second-line therapy
  • Similar efficacy but increased adverse effects including anticholinergic side effects and potential cardiac toxicity
  • Relaspe MC after stopping TCAs
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13
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A
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14
Q
A
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15
Q

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

A
  • 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
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16
Q

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

A
  • 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
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17
Q

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

A
  • 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
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18
Q

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

A
  • 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

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19
Q

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

A
  • GFR cannot be measured directly; several exogenous and endogenous markers used
  • Exogenous: inulin, radiolabeled markers
  • Endogenous: serum creatinine, cystatin C
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20
Q

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

A

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

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21
Q

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

A
  • 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)
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22
Q

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

A
  • 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
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23
Q

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

A

Pediatric patients < 18 years – Bedside Swartz Equation

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24
Q

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

A

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

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25
Q

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

A
  • 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)
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26
Q

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

A
  • 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
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27
Q

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?

A
  • 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
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28
Q

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

A
  • 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)
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29
Q

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

A
  • Prerenal
  • Intrinsic
  • Postrenal
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30
Q
A
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31
Q

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

A

Hypoperfusion of renal parenchyma
* Intravascular volume depletion
* Hemorrhage
* GI losses
* Burns

Reduction of effective circulating volume
* Decreased cardiac output
* Systemic vasodilation

Functional
* Medications

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32
Q

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

A

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

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33
Q

What is the RAAS pathway? (general)

A
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34
Q

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

A
  • 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
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35
Q

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

A

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

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36
Q

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

A

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

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37
Q

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

A

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

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38
Q
A
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39
Q

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

A
  • 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
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40
Q

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

A
  • 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
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41
Q

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

A

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

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42
Q

What are the beta one effects when blocked?

A

Effects Cardiac:
* Decrease HR and contractility
* Decrease oxygen demand
* Decrease blood pressure
* Decrease conduction effects

Effects Renal:
* Decrease renin and decrease BP

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43
Q

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

A
  • Afferent arteriole dilation – mediated by vasodilatory prostaglandins, bradykinin, nitric oxide plus
  • Efferent arteriole constriction – mediated by angiotensin II
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44
Q

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

A
  • 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
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45
Q

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

A

Fractional excretion of sodium (FENa)

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46
Q

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

A

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

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47
Q

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

A
  • Tubular dysfunction
  • Intrinsic AKI
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48
Q
A
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49
Q

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

A
  • Assess volume status
  • Remove potential nephrotoxins
  • Dose adjust medications as necessary
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50
Q

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

A

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

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51
Q
A
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52
Q

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

A

Fluid resuscitation->Isotonic fluids or blood

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53
Q

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)

A

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

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54
Q

Prerenal AKI treatment
* Consider what for perisistently low MAPs?

A

Consider vasopressor support for persistently low MAPs

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55
Q

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

A

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

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56
Q
A
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57
Q

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

A
  • Acute interstitial nephritis
  • Acute tubular necrosis
  • Acute glomerulonephritis
  • Vascular damage - rare
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58
Q

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

A

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

59
Q

These were all the stared ones

What are the drugs that are associated with acute intersitial nephritis? (9)

A
  • B lactam drugs
  • Fluroquinolones
  • Rifampin
  • Sulfa based drugs
  • Proton pump inhibitor
  • NSIADs
  • Phenytoin
  • Allopurinol
  • 5-aminosalicylates

5-barns ppf

60
Q

Acute Interstitial Nephritis
* What is the classic presentation?

A
  • 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

61
Q

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

A
  • 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%
62
Q

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

A
  • Supportive therapy
  • Removal of offending agent
  • Corticosteroids: Prednisone 1 mg/kg/day for 2 to 4 weeks followed by a taper
63
Q

AIN Treatment
* Closely monitor what?

A

BUN, SCr, proteinuria if present

64
Q

AIN Treatment
* What are supportive care measures?

A
65
Q

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

A
  • MCC intrinsic AKI
  • Acute destruction and necrosis of the renal tubules of the nephron
  • Reversible (recovery in 7 to 21 days)
66
Q

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

A
  • 50% due to renal ischemia->Extended prerenal AKI MC
  • 35% secondary to exogenous and/or endogenous nephrotoxins
67
Q

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

A

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

Exogenous
* drugs
* contrast dyes

68
Q

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

A

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

69
Q

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

A
  • 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
70
Q

Note to self: Come back to this question after asking Dr.V a qustion

What is the treatment of ATN?

A
  • Remove offending agent
  • Supportive care
71
Q

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

A
72
Q

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

A
  • Inflammation of the glomerulus
  • Immune-mediated damage to the basement membrane, the mesangium, or capillary endothelium
73
Q

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

A

Podocytes damaged -> large gaps between cells -> increased permeability to large molecules
* Proteins
* Blood

Leaky basement membrane decreased pressure across glomeruli

74
Q

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

A

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

75
Q

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

A
  • 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
76
Q

KNOWWWW

A
77
Q

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

A

Early intervention key to preventing disease progression

78
Q

AGN treatment

A
79
Q
A
80
Q
A
81
Q

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

A
  • 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

REDUCING PROTEINURIA IS COMPLETELY SEPARATE OF HTN

82
Q

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

A

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

83
Q

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

A
  • Not contraindicated for a specific creatinine level
  • Benefits for Stage 4 or 5 CKD studies ongoing
84
Q
  • What are the three primary ways to block activiity of ATII?
A

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

85
Q

What are the examples and indications of ace-i?

A
86
Q

What are the SE and CI of acei?

A

SE:
* Increased potassium
* Hypotension
* Cough
* Angioedema

CI
* PREGNANCY!
* Angioedema
* Bilateral renal artery stenosis
* Severe chronic kidney disease

87
Q

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

A
  • Monitoring: electrolytes, SBP > 100 mmHg, renal function
  • Statin: LDLs
88
Q

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

A
  • Normally, ACE breaks down bradykinin into inactive metabolites
  • ACE inhibitors prevent the breakdown of bradykinin
  • Angiotensin receptor blockers generally do not have these effects
89
Q

What happens when ACEi prevent the breakdown of bradykinin?

A

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

90
Q
A
91
Q

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

A
92
Q

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

A

SE:
* Increased potassium
* Hypotension
* Cough – less than ACEI
* Angioedema – less than ACEI

CI
* PREGNANCY!
* Bilateral renal artery stenosis
* Severe chronic kidney disease

93
Q
A
94
Q

Diuretics
* What is the purpose of diuretics?

A

Increase production of urine; decrease water from the body

95
Q

What are the five main classes of diuretics?

A
  • 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
96
Q
A
97
Q

Where is most of the Na reabsorbed?

A
98
Q

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

A
99
Q

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

A
100
Q

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

A
101
Q
A
102
Q

Potassium sparing diuretics
* Where do they work?

A

Work in the DCT and CD

103
Q

Potassium sparing diuretics
* What happens in the prinicpal cells?

A

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

104
Q

Potassium sparing diuretics
* What happens in the intercalated cells?

A

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

105
Q

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

A

Movement of all these electrolytes is controlled by aldosterone

106
Q

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

A

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

107
Q

What happens to intercalated cells when aldosterone is present?

A

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

108
Q

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

A
  • Blocking the steroid receptor -> aldosterone cannot bind
  • Blocking ENaC channels on the cell membrane
109
Q

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

A
  • Increased excretion of Na+
  • Increased water loss through urine
  • Decreased excretion of H+ and K
110
Q

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

A
111
Q

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

A
112
Q

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

A
113
Q

What are the SE and CI of potassium sparing diuretics?

A
114
Q
A
115
Q

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

A
116
Q

Thiazide diuretics
* What is the MOA?

A
117
Q

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

A
118
Q

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

A
119
Q

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

A
120
Q

Osmotic diuretics
* What are the SE and CI?

A
121
Q

Carbonic anhydrase inhibitors
* MOA? What does it cause?

A

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

122
Q

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

A
  • Weak diuretic
  • Causes urine alkalinization
  • Decreases the production of aqueous humor
  • Decreases the production of CSF
  • Used for high altitude sickness
123
Q

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

A
124
Q

Carbonic anhydrase inhibitors
* What is the MOA and Indications?

A
125
Q

Carbonic anhydrase inhibitors
* What are the SE and CI?

A
126
Q

AGN treatment: IgA nephropathy
* What is the txt?

A
127
Q

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

A
128
Q

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

A
129
Q

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

A
130
Q

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

A
131
Q

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

A
132
Q
A
133
Q

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

A
  • Narrowing of the renal artery which brings blood to kidneys
  • Decreases downstream renal blood flow
  • Detected as low blood pressure
134
Q

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

A
  • Kidneys increase the blood pressure to compensate
  • Renin continues to be released because the blockage prevents improved blood flow to the kidneys
135
Q

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

A

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

136
Q

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

A
  • Blood pressure control with ACEI / ARB if NO bilateral disease or status post revascularization
  • Revascularization via renal catheter arteriography
137
Q

What are the causes of Post-renal AKI?

A
  • 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
138
Q

Post-renal AKI
* What is the treatment?

A

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

139
Q

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

A
  • 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
140
Q

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

A
  • 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
141
Q

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?

A
142
Q

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

A
143
Q

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?

A

Pharm II (14 decks)

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