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Step 1 > Renal > Flashcards

Renal Flashcards

1
Q

Prosnephros

A

Week 4 then disintegrates

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2
Q

Mesonephros

A

functions as interim kidney for 1st trimester

later contributes to make genital system

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3
Q

Metanephros

A

permanent
appear in 5th week
nephrogenesis continues through weeks 32-36

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4
Q

Ureteric bud

A

derived from causal end of mesonephric duct

gives rise to ureter, pelvis, calyces, collecting duct, fully canalized by 10th week

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5
Q

Metanephric mesenchyme

A

ureteric bud interacts with this tissue

interaction induced differentiation and formation of glomerulus through to distal convoluted tubule

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6
Q

Aberrant interaction between these 2 tissues may result in several congenital malformations of the kidney

A

Ureteropelvic junction- last to canalize –> congenital obstruction
Cause of prenatal hydronephrosis
detected by US

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7
Q

Potter Sequence

A

Oligohydramnios –> compression of developing fetus –> limb deformities, facial anomalies, lack of amniotic fluid aspiration into fetal lungs –> pulmonary hypoplasia
Caused by ARPKD, obstructive uropathy, bilateral renal agenesis, chronic placental insufficiency

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8
Q

Horseshoe kidney

A

inferior poles of both kidneys fuse abnormally
get trapped in Inferior mesenteric artery and stay in low abdomen
Associated with hydronephrosis, renal stones, infection and increased risk of renal cancer
Higher incidence in chromosomal aneuploidy

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9
Q

Unilateral renal agenesis

A

ureteric bud fails to induce differentiation of metanephric mesenchyme –> complete absence of kidney and ureter

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10
Q

Multicycstic dysplastic kidney

A

ureteric bud fails to induce differentiation of metanephric mesenchye –> nonfunctional kidney with cysts and connective tissue
Nonhereditary and unilateral
Bilateral –> potter sequence

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11
Q

Duplex collecting system

A

Bifurcation of ureteric bud before it enters the metanephric blastema creates a Y shaped bifid ureter. Duplex collecting system can occur through 2 ureteric buds reaching and interacting with metanephric blastema
Associated with vesicoureteral reflux and ureteral obstruction
increase risk of UTI

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12
Q

Posterior Urethral valves

A

membrane remnant in the posterior urethra in males
persistence –> urethral obstruction
Dx prenatally by bilateral hydronephrosis and dilated or thick walled bladder on US
associated with oligohydramnios in severe obstruction

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13
Q

Renal blood flow

A

renal A –> segmental A –> interlobar A ==> arcuate A –> interlobular A –> afferent arteriole –> glomerulus –> efferent arteriole –> vasa recta –> venous outflow

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14
Q

Course of ureters

A

arise from renal pelvis –> under gonadal A –> over common iliac A –> under uterine A/vas deferens

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15
Q

Blood supply to ureter

A

proximal- renal A
Middle- gonadal A, aorta, common and internal iliac A
Distal- internal iliac and superior vesical A

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16
Q

3 common points of reteral obstruction

A

ureteropelvic junction, pelvic inlet, ureteropelvic junction

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17
Q

Fluid Compartments

A 
60% total body water
40% ICF (K+, Mg2+, organic phosphates)
20% ECF (Na+, Cl-, HCO3-, albumin)
Plasma volume measured via radiolabeling albumin
ECF measured with inulin or mannitol
Plasma volume= TBV x (1-Hct)
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18
Q

Glomerular filtration barrier

A

Fenestrated capillary endothelium (prevent >100 nm from entering)
BM iwth Type 4 collagen and heparan sulfate
Visceral epithelial layer with podocyte foot processes (prevent >50-60 nm from entering)
All three layers have - charged glycoproteins that prevent - charged molecules entry

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19
Q

Renal clearance equations

A

C= (UV)/P
If C < GFR –> net tubular resorption or not freely filtered
If C > GFR –> net tubular secretion of X
C = GFR –> no net secretion or reabsorption

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20
Q

GFR equations

A

Inulin clearance
C = GFR = U x V/P = K (PGC- PBS) - (piGC- piBS)
piBS = 0 usually
Normal GFR = 100
Creatinine is approximate (slightly overestimates because a little secreted)

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21
Q

Effective renal plasma flow

A 
PAH clearance (100% excretion)
eRPF = U x V/P = C
RBF = RPF/ (1-Hct) = usually 20-25% cardiac output
underestimates true renal flow slightly
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22
Q

Filtration

A

FF= GFR/RPF (Normal = 20%)
filtered load= GFR x plasma conc
Prostaglandins dilate afferent arteriole
Ang II constricts efferent arteriole

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23
Q

Afferent arteriole constriction

A

decrease GFR and RPF

No change FF

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24
Q

Efferent arteriole constriction

A

increase GFR
decrease RPF
FF increases

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25
Q

increase plasma conc

A

decrease GFR
No change RPF
decrease FF

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26
Q

Constriction of ureter

A

decrease GFR
no change RPF
decrease FF

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27
Q

Dehydration

A

decrease GFR
DECREASE RPF
Increase FF

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28
Q

Calculation of reabsorption and secretion rate

A 
Filtered load = GFR x P
Excretion rate = V x U
Reabsorption = filtered- excreted
Secretion rate = excreted - filtered
(V x UNa) / (GFR/ PNa)
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29
Q

Early PCT

A

contains brush border
Reabsorb glucose and AA, HCO3, Na, Cl, PO4, K, H2O, uric acid
PTH –> inhibit Na+/ PO4 cotransport –> increase PO4 excretion
ATII –> stimulate Na+/H+ exchanger –> increase Na+, H2O and HCO3 reabsorption

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30
Q

Thin descending loop of Henle

A

passively reabsorbs H2O via medullary hypertonicity
Concentrating segment
Make urine hypertonic

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31
Q

Thick ascending loop of Henle

A

reabsorbs Na, K and Cl
indirectly induces paracellular reabsorption of Mg and Ca via + lumen potential
impermeable to H2O
Make urine less concentrated as it ascends

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32
Q

Early DCT

A

reabsorbs Na, Cl
impermeable to H2O
Makes urine hypotonic
PTH –> increase Ca/Na exchange –> increase Ca reabsorption

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33
Q

Collecting tubule

A

reabsorbs Na in exchange for secreting Na and K (aldosterone)

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34
Q

Aldosterone

A

mRNA –> protein synthesis
principal cells increase apical K+ conductance, increase Na/K pump, increase ENaC –> lumen negative –> K secretion
a intercalated cells lumen negative –> increase H ATPase –> increase H secretion –> increase HCO3/Cl exchanger

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35
Q

ADH

A

V2 receptor –> insert aquaporin H2O channels on apical side

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36
Q

Fanconi syndrome

A

generalized reabsorption defect in PCT –> increase excretion of AA, glucose, HCO3, PO4
Lead to metabolic acidosis, hypophosphatemia, osteopenia
Causes: Hereditary defects, ischemia, multiple myeloma, nephrotoxins, lead poisoning

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37
Q

Bartter Syndrome

A

reabsorption defect in TAL (Na/K/Cl transport)
Metabolic alkalosis, hypokalemia, hypercalciuria
AR
Like loop diuretics

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38
Q

Gitelman Syndrome

A

Reabsorption defect of NaCl in DCT
Metabolic alkalosis, hypoMg, hypoK, hypocalciuria
AR
Like thiazide diuretic

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39
Q

Liddle Syndrome

A

Gain of function mutation –> decrease Na channel degradation –> increase Na reabsorption in collecting duct
Metabolic alkalosis, hypoK, HTN, low aldosterone
AD

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40
Q

Syndrome of Apparent Mineralcorticoid Excess

A

cortisol activate mineralcorticoid receptors
Hereditary 11B HSD deficiency –> increase cortisol –> increase mineralcorticoid receptor activity
metabolic alkalosis, hypoK, HTN, low serum aldosterone
AR
Treat with K sparing diuretics

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41
Q

Renin

A

secreted by JG cells in response to low renal perfusion pressure, increase renal sympathetic discharge and decrease NaCl delivery to macula densa

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42
Q

AT II

A

maintain blood volume and blood pressure

affects baroreceptor function, limits reflex brady

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43
Q

ANP and BNP

A

released from atria and ventricles in response to high volume, inhibit RAAS, relax vascular smooth muscle via cGMP –> increase GFR, decrease renin
Dilates afferent arteriole

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44
Q

ADH

A

regulate serum osmolarity and respond to low blood volume states. Simulates reabsorption of water in collecting ducts and reabsorption of urea in collecting ducts to maximize osmotic gradient

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45
Q

Aldosterone

A

regulate ECF volume and Na content
increase release in low blood volume states
Responds to hyperK by increase K excretion

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46
Q

JG apparatus

A

JG (afferent arteriole) and macula densa (distal loop of henle)
JG cells secrete renin in response to low renal blood pressure and increase sympathetic tone
Macula densa sense low NaCl delivery to DCT –> increase renin release –> efferent arteriole vasoconstriction –> increase GFR

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47
Q

Erythropoietin

A

released by interstitial cells in peritubular capillary bed in response to hypoxia. Stimulate RBC proliferation in bone marrow

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48
Q

Calciferol

A

PCT cells convert 25OH vit D3 –> 1,25OH vit D (1a hydroxylase)

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49
Q

prostaglandins

A

paracrine secretion vasodilates the aferent arteriolesto increase RBF

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50
Q

Dopamine

A

secreted by PCT cells, promotes natriuresis
low doses –> dilate interlobular arteries, afferent arterioles and efferent arterioles –> increase RBF
At high doses –> vasoconstrictor

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51
Q

ANP

A

secreted in response to high atrial pressure
increases GFR and Na filtration with no Na reabsorption in distal nephron
NET EFFECT: Na loss and volume loss

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52
Q

Ang II

A

in response to low BP
Efferent arteriole constriction –> high GFR and FF with Na reabsorption in proximal and distal nephron
NET EFFECT: preserve FF in low volume state and Na reabsorption to maintain volume

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53
Q

PTH

A

low plasma Ca, high plasma PO4 or low plasma 1,25OH vit D

increases reabsorption of Ca (DCT), decrease PO4 reabsorption (PCT) and increase 1,25OH vit D production

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54
Q

Aldosterone

A

low blood volume and hyperK

NET: increase Na reabsorption, increase K secretion, increase H secretion

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55
Q

ADH

A

high plasma osmolarity and low blood volume
Bind to principal cells –> increase aquaporins and water reabsorption
increase reabsorption of urea in collecting ducts to maximize corticopapillary osmotic gradient

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56
Q

Shift K into cell –> hypoK

A

hypo osmolarity
alkalosis
B adrenergic agonist
Insulin

57
Q

Shift K out of cell –> Hyper K

A 
Digitalis
hyperosmolarity
lysis of cells
acidosis
B blocker
Insulin deficiency
succinylcholine
58
Q

Sodium electrolyte imbalance

A

Low: nausea, malaise, stupor, coma, seizures
High: irritability, stupor, coma

59
Q

Potassium electrolyte imbalance

A

Low: U wave and flattened T wave on ECG, arrhythmia, muscle cramps, spasm, weak
High: Wide QRS and peaked T, arrhythmias, muscle weakness

60
Q

Calcium electrolyte imbalance

A

Low: tetany, seizures, QT prolong, twitching, spasm
High: stones, cones, groans, thrones, psychiatric overtones

61
Q

Mg electrolyte imbalance

A

Low: tetany, torsades de pointes, hypokalemia, hypocalcemia
High: low DTRs, lethargy, brady, hypotension, cardiac arrest, hypocalcemia

62
Q

Phosphate electrolyte imbalance

A

Low: bone loss, osteomalacia, rickets
High: renal stones, metastatic calcifications, hypocalcemia

63
Q

Respiratory acidosis

A 
Hypoventilation High bicarb, high PCO2
airway obstruction
acute/chronic lung disease
opioids
weak respiratory muscles
64
Q

High anion gap Metabolic acidosis

A 
low PCO2, low bicarb, anion gap >12
Methanol
uremia
DKA
propylene glycol
Iron
Lactic acidosis
Salicylates
65
Q

Normal anion gap Metabolic acidosis

A 
Low PCO2, low bicarb, anion gap = 8-12
HyperCl
Addison
RTA
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
66
Q

Respiratory Alkalosis

A 
Hyperventilation: low bicarb, low PCO2
anxiety
Hypoxemia
Salicylates (early)
Tumor
PE
67
Q

Metabolic Alkalosis

A 
High PCO2 and high bicarb
loop diuretics
vomiting
antacid use
hyperaldosteronism
68
Q

RTA 1

A

Distal
a intercalated cells unable to secrete H –> no new HCO3 –> metabolic acidosis
urine pH= basic
Serum K low
caused by amphotericin B, congenital anomalies, SLE
Associated with increase stones and increase bone turnover

69
Q

RTA 2

A

Defect in PCT HCO3 reabsorption –> excrete in urine –> metabolic acidosis
urine pH= basic when resorptive threshold exceeded, acidic when depleted
Serum K low
Causes: fanconi, multiple myeloma, carbonic anhydrase inhibitors
Associated with risk of rickets

70
Q

RTA 4

A

hypoaldosteronism –> decrease ammonium secretion
acidic urine pH
high serum K

71
Q

RBC casts

A

glomerulonephritis, HTN emergency

72
Q

WBC casts

A

tubulointerstitial inflammation, acute pyelonephritis, transplant rejection

73
Q

Granular casts

A

Acute tubular necrosis

74
Q

Fatty casts

A

Nephrotic syndrome

75
Q

Waxy casts

A

end stage renal disease

76
Q

Hyaline casts

A

nonspecific

77
Q

Nephritic syndrome

A

glomerular inflammation –> GBM damage –> loss of RBCs into urine (hematuria)
low GFR –> oliguria, azotemia, increase renin release, HTN
Protein <3.5

78
Q

Nephrotic Syndrome

A

podocyte damage –> impaired charge barrier –> proteinuria (>3.5)
hypoalbuminemia edema
frothy urine with fatty casts

79
Q

Nephritic- Nephrotic syndrome

A

severe GBM damage –> loss of RBC and impaired charge barrier
>3.5 proteinura
Can occur with any form of nephritic syndrome

80
Q

Acute poststrep GN

A

Nephritic
Children 2-4 weeks after group A strep
resolve spontaneously
TYPE III hypersensitivity
peripheral periorbital edema, tea colored urine, HTN, decrease levels of C3
glomeruli enlarged and hypercellular, starry sky granular appearance, subepithelial IC humps

81
Q

PRGN

A

Nephritic
poor prognosis
Crescent shaped (fibrin and plasma protein with glomerular parietal cells, monocytes and macrophages)
Linear IF –> good pasture (anti GBM) Type 2 hypersensitivity
Negative IF, Pauci immune- granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis or microscopic polyangiitis
Granular IF- PSGN or DPGN

82
Q

Diffuse proliferative GN

A

Nephritic
SLE (wire lupus)
IF granular
subendothelial IgG with C3 deposition

83
Q

IgA nephropathy

A

Nephritic
episodic hematuria that occurs with respiratory or GI infection. Henoch Schnlein
Mesangial proliferation
IgA deposits

84
Q

Alport Syndrome

A

Nephritic
Mutation in COL4 –> thin/ split glomerular BM
X linked Dominant
eye problems, GN, sensorineural deafness
basket weave appearance due to irregular thickening of GBM

85
Q

MPGN

A

Nephritic + Nephrotic
Type 1- secondary to Hep B/C infection = sunendothelial deposits with granular IF
Type 2- C3 nephritic factor –> decrease C3 factors = intramembranous deposits

86
Q

Minimal change disease

A

Nephrotic
children
triggered by recent infection, immunization, immune stimulus
Normal glomeruli, neg IF, effacement of podocyte foot processes

87
Q

FSGS

A

Nephrotic
Secondary to HIV, SCD, heroin, obese, interferon tx, congenital malformations
segmental sclerosis, hyalinosis, neg IF, effacement of foot processes

88
Q

Membranous nephropathy

A

Nephrotic
secondary to drugs, infections, SLE, solid tumors
diffuse capillary and GBM thickening, IF granular, spike and dome appearance (subepithelial deposits)

89
Q

Amyloidosis

A

Nephrotic
Congo red stain with polarized light
Associated with chronic conditions that predispose to amyloid deposition

90
Q

Diabetic GN

A

Nephrotic
mesangial expansion, GBM thickening and increased permeability
glomerulosclerosis eosinophilic

91
Q

Calcium oxalate hypocitraturia

A

dumbbell shaped
most common
via ethylene glycol, vit C abuse, hypocitraturia, malabsorption

92
Q

Calcium phosphate stoes

A

high pH

wedge shaped prism

93
Q

Struvite

A

high pH
coffin lid
Proteus, Staph saprophyticus, klebsiella
Staghorn caliculi

94
Q

Uric acid

A

low pH
rhomboid/ rosettes
Risk: low urine volume, arid climate, acidic pH
associated with hyperuricemia, leukemia

95
Q

Cystine

A

low pH
hexagon
Cystine reabsorbing PCT transporter lose function
Nitroprusside +

96
Q

Hydronephrosis

A

distention/ dilation of renal pelvis and calyces
caused by urinary tract obstruction
Dilation occurs proximal to site of pathology
Cr elevated

97
Q

Stress incontinence

A

outlet incompetence –> leak with high intra abdominal pressure
+ bladder stress test
Obese, vaginal delivery, prostate surgery
pelvic floor muscle strengthening, weight loss

98
Q

Urgency incontinence

A

Detrusor overactivity
UTI
Kegel, bladder training, antimuscarinics

99
Q

Overflow incontinence

A

incomplete emptying
polyuria, bladder outlet obstruction, neurogenic bladder
catheterize, relieve obstruction

100
Q

Acute cystitis

A

inflammation of bladder
Sx: suprepubic pain, dysuria, urinary frequency, urgency
Risk: female, sex, catheter, DM, impaired bladder emptying
Bacteria: E coli, staph sap. Klebsiella, proteus mirabilis
Neg urine culture, + leukocyte esterase and nitrites

101
Q

Acute pyelonephritis

A

Neutrophils infiltrate renal interstitium
affect cortex spare glomeruli
fever, flank pain, nausea/ vomiting, chills
via ascending UTI
Risk: catheter, UTI, vesicouteral reflux, DM, pregnancy

102
Q

Chronic pyelonephritis

A

recurrent acute pyelonephritis
Coarse asymmetric corticomedullary scarring, blunted calyx
Tubules contain eosinophilic casts

103
Q

Xanthogranulomatous pyelonephritis

A

orange nodules that mimic tumor
widespread kidney disease
via Proteus infection

104
Q

Prerenal azotemia

A

hypovolemia, low CO, low effective circulating volume
low RBF –> low GFR –> increased reabsorption of Na+/H2O and urea
urine osm >500
urine Na < 20
Fe(Na) <1%
BUN:Cr >20

105
Q

Intrinsic Renal Failure

A 
acute tubular necrosis, acute GN, vasculitis, Malignant HTN, TTP-HUS
ATN --> low GFR, granular casts
urine osm <350
Urine Na >40
FE (Na) >2%
BUN:Cr <15
106
Q

Postrenal azotemia

A

stones, BPH, Neoplasm, Congenital anomalies
outflow obstruction
urine osm <350

107
Q

Acute interstitial Nephritis

A

acute interstitial renal inflammation
Pyuria and azotemia after administration of drugs that act as haptens, inducing hypersensitivity
Fever, rash, hematuria, pyruria, CVA tenderness

108
Q

Acute tubular necrosis

A

increase FE (Na)
1. inciting event
2. Maintenance - oliguria 1-3 weeks
3. Recovery- polyuria, BUN and Cr fall
Ischemic- secondary to low renal blood flow –> death of tubular cells (PCT and TAL susceptible)
Nephrotoxic- secondary to injury with toxins, crush injury, hemoglobinemia (Proximal tube susceptible)

109
Q

Diffuse cortical necrosis

A

acute generalized cortical infarction of bowth kidneys
Vasospasm + DIC
Associated with obstetric catastrophes, septic shock

110
Q

Renal papillary necrosis

A

Sloughing of necrotic renal papillae –> gross hematuria and proteinuria
triggered by recent infection or immune stimulus
Associated with SCD, Acute pyelonephritis, Analgesics, DM

111
Q

Consequences of renal failure

A

decline in renal filtration –> excess nitrogenous waste products and electrolyte disturbances
Metabolic acidosis, dyslipidemia, high potassium, uremia, Na+ / H2O retention, growth retardation, EPO deficiency, renal osteodystrophy.

112
Q

Renal osteodystrophy

A

Hypocalcemia, hyperphosphatemia and failure of vit D hydroxylation associated with CKD –> hyper PTH
PO4 bind with Ca and deposit –> low Ca, 1,25 vit D –> low intestinal Ca absorption
subperiosteal thinning of bones

113
Q

ADPCKD

A

Cysts in cortex and medulla –> bilateral enlarged kidneys
flank pain, hematuria, HTN, urinary infection, progressive renal failure
PKD1 mut (chr 16) or PKD2 mut (chr4)
complications: CKD, HTN
Associated with berry aneurysms, MVP, benign hepatic cysts, diverticulosis

114
Q

ARPCKD

A

cystic dilation of collecting ducts
infants
Associated with congenital hepatic fibrosis
lead to potter sequence
systemic HTN, progressive renal insufficiency, portal HTN

115
Q

AD tubulointerstitial kidney disease

A

causes tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine
Medullary cysts
SMALLER kidneys of US

116
Q

simple cysts

A

filled with ultrafiltrate

asymptomatic

117
Q

Complex cysts

A

require follow up or remove due to RCC risk

118
Q

Renavascular disease

A

renal impairment due to ischemia from renal A stenosis or microvascular disease
low renal perfusion –> high renin –> high Ang –> HTN
caused by atherosclerotic plaques or fibromuscular dysplasia
asymmetric renal size, epigastric/ flank bruits

119
Q

RCC

A

polygonal clear cells (chr 3) filled with accumulated lipids and carbohydrates
originate in PCT –> invade renal V –> IVC –> hematogenous spread –> metz to lung and bone
hematuria, palpable masses, polycythemia, glank pain, fever, weight loss
men 50-70
risk: obese, smokers
Paraneoplastic: PTHrP, EPO, ACTH, Renin

120
Q

Renal oncocytoma

A

Benign epithelial cell tumor from collecting ducts
Large eosinophilic cells with abundant mitochondria without perinuclear clearing.
painless hematuria, flank pain, ab mass

121
Q

Wilms tumor

A

childhood
embryonic glomerular structures
large, palpable, unilateral flak mass, hematuria HTN

122
Q

WAGR

A

wilms, aniridea, genitourinary malformations, retardation (WT1 deletion)

123
Q

Denys Drash

A

wilms, diffuse mesangial sclerosis, dysgenesis of gonads

WT1 mut

124
Q

Beckwith Wiedemann

A

Wilms, macroglossia, organomegaly, hemihyperplasia, omphalocele
WT2 mut

125
Q

Urothelial carcinoma of the bladder

A

painless hematuria

associated with phenacetin, smoking, amiline dyes and cyclophosphamide

126
Q

SCC of bladder

A

chronic irritation of bladder –> squamous metaplasia –> dysplasia and SCC
Risk factors: schistosoma, chronic cystitis, smoking, chronic kidney stones
painless hematuria

127
Q

Mannitol

A

osmotic diuretic, increase tubular fluid osmolarity –> increase urine flow
used in drug overload, elevated intracranial or intraocular pressure
Adverse: PE, Na imbalance, contra in anuria and HF

128
Q

Acetazolamide

A

carbonic anhydrase inhibitor, alkalinizes urine
used in glaucoma, met alk, altitude sickness, intracranial HTN
Adverse: proximal renal tubular Acidosis, paresthesias, NH3 tox, sulfa allergy, hypoK, calcium phosphate stone

129
Q

Loop diuretics

A

Furosemide, bumetanide, torsemide
sulfa- inhibit Na/K/Cl of TAL, abolish hypertonicity of medulla –> prevent concentrated urine
use in edema, HTN, hyperCa
Adverse: ototox, hypoK, hypoMg, Dehydration, allergy, met alk, nephritis, gout

130
Q

Ethacrynic acid

A

nonsulfa Na/K/Cl inhibitor
used in diuresis in patients allergic to sulfa
Adverse: more ototox

131
Q

Thiazaide diuretics

A

hydrochlorothiazide, chlothalidone, metolazone
inhibit NaCl reabsorption in DCT
used for HTN, HF, hyperCalciuria, neph DI, osteporosis
Adverse: hypoK, met alk, hypoNa, hypoglycemia, HypoCa, sulfa

132
Q

K sparing diuretics

A

Spironolactone- aldosterone antag
Amiloride- Na block
used for hyperaldosteronism, K= depletion, HF, neph DI, antiandrogen
Adverse: hyperK

133
Q

Diuretics Urine NaCl

A

increase with diuretics

serum NaCl decrease

134
Q

Diuretics urine K

A

increase in loop and thiazide diuretics

135
Q

Diuretics blood pH

A

acidemia- carbonic anhydrase inhibitor, spironolactone and hyperkalemia
Alkalemia- loop diuretics and thiazides

136
Q

Diuretics urine Ca

A

increase with loop diuretics

decrease with thiazides

137
Q

ACEi

A

-opril
inhibit ACE –> low Ang II –> low GFR
used in HTN, HF, proteinuria, diabetic nephropathy
Adverse: cough, angioedema, teratogen, creatinine increase, hyperK, hypotension

138
Q

ARBs

A

-sartan
block AngII to AT1 receptor- DO NOT DECREASE BRADYKININ
used in HTN, HF, proteinuria, CKD, with ACEi intolerance
Adverse: hyperK, low GFR, hypotension, teratogen

139
Q

Alliskiren

A

renin inhibitor (block Ang I –> Ang II)
used in HTN
Adverse: hyperK, low GFR, hypotension, angioedema, contra in patients taking ACEi or ARBS or pregnant.

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