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Body in Balance Unit 3 > Week 9 > Flashcards

Week 9 Flashcards

1
Q

components of urinary system

A
  • kidneys (2)
  • ureters (2)
  • bladder
  • urethra
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2
Q

retroperitoneal space

A

space that lies posterior to the peitoneum (lining of GI tract and other abdominal organs) in abdomen

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3
Q

positioning of kidneys in body

A

left kidney = T11 - L2

right kidney = T12 - L3

Upper half of kidney is protected by the rib cage

Right kidney positioned lower due to liver

located lateral to vertebral bodies in paravertebral gutters

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4
Q

why is it more common to biopsy the inferior pole of the kidney rather than the superior pole?

A

Biopsy of superior pole could cause pneumothorax

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5
Q

supporting structures around the kidneys

A
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6
Q

hilus of kidney contains (anterior to posterior order):

A
  • renal vein
  • renal artery
  • ureter
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7
Q

3 major sections on kidney (internal)

A
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8
Q

interdigitations of cortex and medulla of kidney include:

A
  1. renal columns
  2. medullary rays
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9
Q

renal sinus in kidney is made up of:

A

minor calyx

major calyx

renal pelvis

order is from medulla to ureter

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10
Q

how to tell right kidney from left kidney

A

from anterior to posterior the hilus of the kidney goes renal vein, renal artery, then ureter; hilus points toward medial aspect; can figure out direction of kidney by location of ureter

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11
Q

“lobe” of the kidney

A

renal pyramid and its associated cortex

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12
Q

“lobule” of kidney

A

one central collecting duct and associated nephrons that drain filtrate into the central duct

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13
Q

smallest functional unit of the kidney

A

nephron

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14
Q

how many nephrons per kidney

A

1-4 million

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15
Q

components of renal corpuscle

A
  • glomerulus (tuft of capillaries)
  • glomerular capsule (Bowman’s capsule)
    • visceral layer – completely surrounds tuft of capillaries; podocytes
    • parietal layer
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16
Q

afferent vs efferent arteriole and glomerulus

A

afferent brings blood that needs to be filted to the glomerulus; efferent arteriole bringing filtered blood away from glomerulus

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17
Q

the two poles of a renal corpuscle

A

afferent pole and urinary pole

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18
Q

podocytes of nephron

A

specialized epithelial cells

have primary and secondary processes

pedicals envelop the endothelium

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19
Q

blood in kidney is being filtered through what 3 components?

A
  • fenestrated endothelium – capillary with lots of openings, allows molecules to leave the bloodstream
  • basement membrane
    • Combined basal lamina of both the endothelium and the podocytes
  • Filtration slits between the pedicels
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20
Q

Proximal Convoluted Tubule (PCT) of nephron anatomy

A
  • At urinary pole of renal corpuscle
  • Modified simple cuboidal cells
  • Cells have “brush border”
    • Abundant microvilli and canaliculi
    • Absorb macromolecules
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21
Q

anatomy: Loop of Henle in nephron

A
  • Extends into the medulla

Thick descending limb

  • Similar cells to PCT (simple cuboidal cells with brush border)

Thin limb

  • Simple squamous epithelium

Thick ascending limb

  • Simple cuboidal cells without brush border
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22
Q

anatomy: macula densa of nephron

A
  • Region of densely concentrated nuclei at end of thick ascending loop
  • Adjacent to afferent arteriole
  • Cells are sensitive to filtrate flow and ion content
    • Part of juxtaglomerular apparatus
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23
Q

anatomy: Distal Convolueted Tubule (DCT)

A
  • Begins after macula densa
  • Simple cuboidal cells without brush borders
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24
Q

anatomy: collecting duct

A
  • Drains filtrate from many nephrons
  • Center of the lobule
  • Simple cuboidal cells
  • Traverses medulla to renal papillae
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25
Q

histology of collecting system components of kidney: Minor calyx; major calyx; renal pelvis

A
  • ALL transitional epithelium
  • “Urothelium”
  • Cells can break and reform junctions
  • Cells store plasmalemma intracellularly that can be added to cell surface as needed
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26
Q

histology of ureter

A
  • Transitional epithelium
  • Contraction propagated by surrounding smooth muscle in minor calyces
  • peristaltic wave continues through ureter
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27
Q

anti-reflux mechanism in urinary bladder

A

as bladder fills, the hole where ureter is entering closes up in response to the weight; prevents urine from moving back up the system

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28
Q

trigone of urinary bladder

A

triangle between ureteric orifice and urethral orifice

does not stretch/contract

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29
Q

detrusor muscle of urinary bladder

A

smooth muscle found in the wall of the bladder. The detrusor muscleremains relaxed to allow the bladder to store urine, and contracts during urination to release urine.

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30
Q

histology of urethra

A

Distally, the urothelium transitions to nonkeratinized stratified squamous epithelium

Female urethras are much shorter, UTIs are more common

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31
Q

Urethral sphincters

A

Internal urethral sphincter

  • Base of bladder
  • Smooth muscle
  • Autonomic

External urethral sphincter

  • Perineum of pelvis
  • Skeletal muscle
  • Somatomotor
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32
Q

how much of blood supply from aorta do kidneys receive?

A

Receive ~ 25% of the blood supply from the aorta

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33
Q

kidneys receive blood supply from what vessels?

A

left and right renal artery (paied branch of abdominal aorta) then to lobar (segmental) arteries – 70% of population

30% of population – polar arteries; remnants of ascent of kidney into abdomen from pelvic from development

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34
Q

blood supply to adrenal glands (suprarenal glands)

A

Superior suprarenal artery

  • Branch of inferior phrenic a.

Middle suprarenal artery

  • Branch of aorta

Inferior suprarenal artery

  • Branch of renal a.
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35
Q

how are adrenal glands associated with kidneys

A

Anatomically, but not functionally, related to kidneys

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36
Q

pathway of arterial blood supply to the kidney

A

arteries: renal, lobar, interlobar, arcuate, interlobular

No collateral circulation/anastomoses in the kidney

Occlusion of a lobar artery will cause pyramid(s) to become necrotic

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37
Q

afferent arteriole to glomerulus comes from which artery?

A

interlobular artery

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38
Q

venous return from kidneys

A
  • IF efferent arteriole is closer to capsule, it will enter peritubular capillaries in the cortex
  • IF efferent arteriole is closer to medulla, it will enter the vasa recta in the medulla
  • interlobular vein, arcuate evin, interlobar vein, lobar vein, renal vein
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39
Q

difference betwen left and right renal veins

A

IVC runs down right side of midline; to get to the IVC the left renal vein has to cross the midlinel

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40
Q

pathway of left renal vein

A
  • left side has some veins that drain into the left renal vein so that they don’t also have to cross the midline: left suprarenal vein, left gonadal vein
  • left renal vein runs underneath the SMA (superior mesenteric artery); Travels between superior mesenteric artery (SMA) and abdominal aorta
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41
Q

Nutcracker syndrome

A

Left renal vein travels between superior mesenteric artery (SMA) and abdominal aorta

If vein is compressed, patient will present with hematuria, left flank pain, varicosities, could present with pelvic congestion

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42
Q

blood supply to the bladder - pathway/branching

A

abdominal aorta

  • Internal iliac artery
    • Umbilical artery
      • Superior vesicle artery
        • Superior bladder (males and females)
    • Inferior vesicle artery (males)
      • Inferior bladder, prostate
    • Uterine artery (females)
      • Uterus, inferior bladder, vagina
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43
Q

sympathetic innervation to the abdominal organs

A
  • Thoracic and lumbar splanchnic nerves will synapse in collateral ganglia (prevertebral, preaortic )
    • Celiac ganglion, SMA and IMA ganglion
  • Postganglionic sympathetic fibers travel to target organ (kidney, ureter)
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44
Q

sympathetic innervation to pelvic organs

A

Lumbar splanchnic nerves synapse in superior hypogastric plexus (collateral ganglia)

Sacral splanchnic nerves synapse in inferior hypogastric plexus

Plexuses communicate with each other via left and right hypogastric nerves

From autonomic plexus the postganglionic sympathetic fibers travel to target organ (bladder, urethra)

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45
Q

parasympathetic innervation to abdominal organs

A
  • Vagus nerve provides parasympathetics to majority of abdominal organs
    • Preganglionic parasympathetic fibers
  • Terminal ganglia in organ
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46
Q

parasympathetic inneration to pelvic organs

A
  • Cell bodies in lateral horn at S2-S4 levels
  • Pelvic splanchnics
    • Preganglionic parasympathetics run through inferior and superior hypogastric plexus to synapse on terminal ganglion of organ.
    • Bladder, urethra, urethral sphincters
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47
Q

Autonomic plexus

A

A nerve plexus of sympathetic or parasympathetic axons, often containing autonomic neurons or ganglia. Such a plexus typically extends along major arteries and is named for its underlying artery

  • Preganglionic sympathetic fibers (sacral splanchnics)
  • Postganglionic sympathetic fibers
  • Preganglionic parasympathetic fibers (pelvic splanchnics)
  • Viscerosensory
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48
Q

sacral plexus

A
  • Lumbosacral trunk (L4- L5) and sacral spinal nerves
  • 3 S’s (somatomotor, somatosensory, sympathetic)
  • NOT autonomic
  • S2-S4 of sacral plexus
  • Pudendal nerve
  • External urethral sphinctor
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49
Q

definition of Chronic Kidney Disease (CKD)

A

When kidneys do not work as they should

condition characterized by a gradual loss of kidney function over time

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50
Q

definition of End State Renal Disease (ESRD)

A

no kidney function

need dialysis or a transplant to survive

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51
Q

fraction of people in US with kidney disease

A

1 out of 9 people

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52
Q

risk factors associated with CKD

A

age >50

males

smoking

hypertension

diabetes

abdominal obesity

pre-term birth

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53
Q

Seven Major Functions of the Kidney

A
  1. Regulation of water and electrolyte balance
  2. Regulation of acid base balance
  3. Excretion of metabolic waste and bioactive substances
  4. Maintenance of blood pressure
  5. Regulation of red blood cell production
  6. Regulation of Vitamin D production
  7. Gluconeogenesis
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54
Q

glomerular filtration

A

Fluid flows from area of high pressure to area of lower pressure • Inorganic ions filtered • Proteins left behind • 180 L per day

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55
Q

cells that make up the juxtaglomerular apparatus

A
  1. Granular cells (secrete renin); also called juxtaglomerular cells
  2. Macula densa cells (detect Na+ flow, can help regulate blood flow); distal part of thick ascending loop
  3. Mesangial cells (phagocytic/contractile)
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56
Q

glomerulus and blood flow

A

each glomerulus has the ability to change the amount of blood coming to the glomerulus – can modify how much filtration is going on

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57
Q

amount of fluid filtered by kidney that is reabsorped into system

A

99% of filtered

(rest is secreted/excreted)

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58
Q

two types of nephrons

A

cortical nephrons and juxtamedullary nephrons (descend deep into medulla, role in concentration)

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59
Q

percentage of glucose reabsorbed in healthy person in kidneys

A

100% should be reabsorbed (none excreted)

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60
Q

proximal tubule reabsorption of filtrate

A

reabsorbs about 2/3 of filtrate; mainly sodium and water

major site of reabsorption of sodium and water

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61
Q

major characteristic of thick ascending limb of nephron

A

impermeable to water; sodium, potassium, and chloride ions can be reabsorped

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62
Q

highlight channel of distal convoluted tubules

A

sodium-chloride transporter

lot of the energy in tubular system used here

here about hydrochlorothiazide in context here

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63
Q

collecting duct system clinical significances

A

where aldosterone and ADH work

this is where blood pressure is adjusted; via control of amount of sodium reabsorped vs excreted

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64
Q

Compare the differential blood supply of the renal cortex and medulla

A

all blood first goes to the cortex; the osmolarity of the cortical interstitium matches rest of body

Small percentage flows into the medulla (<10%); restricted flow borders on hypoxia and allows interstitial fluid composition to be varied

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65
Q

renal blood flow vs. renal plasma flow

A

take blood flow and calculate plasma flow using hematocrit; gives us the RPF which is used to calculate the filtration fraction

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66
Q

filtration fraction

A

filtration fraction = GFR / RPF

GFR: glomerular filtration rate; plasma going to bowman space

RPF: renal plasma flow

filtration fraction usually 20% (about 125 mL/min.)

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67
Q

significance of low pressure in peritubular capillaries?

A

this is the location of reabsorption; low pressure allows for reabsorption whereas high pressure would make it hard

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68
Q

site of largest vascular resistance in renal blood flow

A

the afferent and efferent arterioles are the site of largest vascular resistance due to their smooth muscles

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69
Q

role of afferent and efferent arterioles on blood pressure control in glomerular capillary blood pressure

A

glomerular capillary blood pressure can be cahgned by changes in arteriole diameter of afferent and efferent arterioles

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70
Q

glomerular filtration definition

A

movement of fluid (plasma) across filtration barrier

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71
Q

layers that fluid passes through/between in filtration barriert to get to Bowman space from capillary

A

capillary

between capillary endothelial cells

pass glomerular basement membrane

Bowman Space (now fluid gets referred to as “filtrate”

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72
Q

charge of filtration barrier

A

filtration barrier is negatively charge

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73
Q

effect of high blood sugar (i.e. diabetes) on glomerular filtration

A

glycoproteins can attach to the negative charge on filtration barrier leading to clumping and decreased glomerular filtration

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74
Q

features of filtration barrier that allow us to keep cells and proteins within glomerular capilarries (keep them from getting filtered)

A

Size Barrier

  • <7,000 daltons can be filtered easily
  • up to 70,000 daltons has some filtration

Electrical Charge

  • filtration barrier has (-) charge; lots of plasma proteins also have negative charge which causes repulsion of charge and, therefore, decreased filtration of negatively charged proteins
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75
Q

glomerular filtration of substances that bind to plasma proteins

A

plasma proteins don’t really get filtered, so substances that bind to plasma proteins are also not filtered (some calcium, hydrophobic hormones)

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76
Q

equation for Glomerular Filtration Rate

A

GFR = Kf x NFP

Kf = hydraulic permeability x surface area

NFP = net filtration pressure in glomerulus (sum of starling forces)

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77
Q

equation for Net Filtration Pressure (NFP

A

NFP = PGC - PBC - πGC

PGC: glomeruluar capillary blood pressure

PBC: Bowman Space hydrostatic pressure

πGC: osmotic force from protein in plasma

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78
Q

values for starling force components of net filtration pressure

A

PGC = 60 (constant)

PBC = 15 (constant)

πGC = variable; increases along the length of the glomerular capillary (due to plasma protein conc increasing); usually average 29 mmHG

πBC = 0

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79
Q

how does filtration coefficient in glomerular capillaries compare to typical systemic capillaries?

A

100 times greater in glomerular capillaries – due to fenestrations allowing more to filter through capillary walls

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80
Q

what changes the glomerular filtration rate? (general variables)

A

GFR = Kf x NFP

changing either these variables change GFR

NFP includes PGc, PBC, and πGC

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81
Q

factors that can change filtration coefficient in glomerular filtration

A
  • contraction of mesangial cells reduces surface area (not a muscle but has contractile properties); decrease in Kf
  • decrease in functioning nephrons due to age and disease decrease Kf
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82
Q

factors that can change glomerular capillary pressure (PGC)

A

Increases

  • increase in renal artery pressure
  • increase in efferent arteriole resistance
  • dilation of afferent arteriole (decrease resistance)

Decreases

  • increase in afferent arteriole pressure
  • dilation in efferent arteriole pressure (decrease resistance)
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83
Q

factors that change pressure of bowman’s space (PBC) in glomerular filtration

A

altered in pathophysiology when there is urinary tubule occlusion; examples are prostate hypertrophy, benign tumor, kidney stones

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84
Q

factors that change oncotic pressure of glomerular capillaires (πGC) in glomerular filtration

A

decrease in protein conc (such as in liver disease) increase NFP

decrease in renal plasma flow –> concentrated plasma protein = decreases NFP

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85
Q

what is filtered load?

A

the quantity of a substance that gets filtered to the glomerular capillaries per unit time; what get’s presented to the nephron to handle (some can be reabsorped)

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86
Q

equation for filtered load

A

GFR x [S]plasma where [S] is our substance of interest that is being measured

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87
Q

defintion of renal autoregulation

A

the process by which kidneys resond to changes in systemic pressure in order to maintain GFR and keep a constant flow by adjusting resistance

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88
Q

two mechanisms for renal autoregulation of RBF and GFR

A

1. Arteriole Myogenic Mechanism

  • Increase in mean arterial pressure => increase in smooth muscle stretch in afferent arteriole => triggers channels to release calcium to smooth muscle => contraction

2. Tubuloglomerular Feedback

  • macula densa cells in juxtaglomerular apparatus have transporters for salts
  • in increased pressure more salts get filtered to nephron; macula densa cells working harder to reabsorp these (Na+, Cl-, K+) => Na+/K+ pump working harder leads to incrase in ADP and adenosine
  • ADP and adenosine bind to receptors on smooth muscle surrounding afferent arteriole => increase in intracellular calcium => vasoconstriction
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89
Q

reabsorption in the proximal convoluted tubule

A

HUGE reabsorption of Na+, Cl- , K+, HCO3 - , and water back into peritubular caps; about 67% of what was filtered

filtration is iso-osmotic; reabsorbing a proportional amount of water with the solutes (300mOsm)

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90
Q

amount of filtrate that goes past PCT per dau (proximal convoluted tubule)

A

60 L/Day

about 180 L/day enters glomerulus but 2/3 is reabsorbed through the PCT so only 60 L/day goes past the PCT

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91
Q

apical membrane of epithelial cells around nephron tube

A

the apical membrane is the mebrane of the epithelial cell that faces toward the lumen of the nephron tube

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92
Q

basolateral membrane of epithelial cells around nephron tube

A

the basolateral membranes are the membranes of the epithelial cell that are not the apical membrane

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93
Q

mechanism of paracellular reabsorption at nephron tube epithelial cells

A

absorption occurs between the epithelial cells; passive transport down electrochemical gradient through tight junctions that filter for size and charge (selectivity of tight junctions varies – depends on the nephron segment); proximal tubule tight junctions are leaky

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94
Q

Epithelial Salt and Water Reabsorption in the Proximal Tubule

A

Step 5: Bulk flow into peritubular capillaries favored by low Pc, high Pisf and high peritubular capillary πc.

Exit of water concentrates many solutes, like urea, K+ , Cl- , Mg2+, and Ca2+; they then diffuse down their concentration gradients through tight junctions

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95
Q

limits to tubule reabsorption

A

Gradient-Limited:

If a solute can leak back through the paracellular path, that limits the size of the gradient that can be generated (e.g., Na+)

Tubular Maximum-Limited

If a solute cannot leak through the paracellular path, the limit on transport is set by the number and activity of transporters (glucose, Glu for example)

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96
Q

Osmole

A

Number of moles of free solute particles in the solution

97
Q

Osmolarity

A

Number of osmoles of solute per liter of solution

98
Q

Osmolality

A

Number of osmoles of solute per kilogram of solvent

99
Q

equation for osmolality

A

Osmolality ≈ 2[Na] + [glucose]/18 + [BUN]/2.8

100
Q

division of water in the body

101
Q

substance that is the main contributor to osmolality in the blood

A

sodium contributes the most

102
Q

how to calculate total body water?

A

take the patient’s and multiply by a fraction

  1. 60 x weight in men
  2. 50 x weight in women
103
Q

osmolality between body compartments

A

have consistent osmolality

104
Q

Properties of the Intracellular Fluid (ICF)

A
  • water content in person determines ICF volume
  • 2/3 of total body water
  • major solutes are K+, phosphates and proteins
105
Q

how does ICF affect osmolality in body?

A

osmolality = total osmoles in body / total water in body

total water in body is proportional to ICF; increases in ICF means a decrease in osmolality

106
Q

major properties of ECF

A
  • All fluid outside the cell
  • Major solutes include Na, Cland HCO3
  • Changes in sodium content (NOT concentration) affect ECF
107
Q

components of the ECF

A

intrvascular volume (plasma) and extravascular volume (interstitial)

108
Q

signs and symptoms of low ECF

A

Symptoms:

  • Thirst
  • Lightheadedness
  • Palpitations

Signs

  • Orthostasis
  • Urine output
  • Dry mouth/moist membranes
  • Dry axilla
  • Low JVP/high JVP
  • Skin turgor/edema
109
Q

which part of the nephron is the most susceptible to change in absorption of sodium (in terms of percentages)

A

collecting duct

110
Q

how does chloride absorption relate to sodium absorption?

A

Chloride absorption is dependent on sodium reabsorption and the percentages of filtered chloride absorbed are the same as that of sodium

111
Q

minimal urinary water loss we need to get rid of solutes in body

A

0.4 liters/day

112
Q

in which party of the nephron is the most water reabsorbed?

A

proximal tubule

113
Q

If you drink a gallon of water, where would the reabsorption of water be affected (in terms of percentages)?

A

Collecting duct

114
Q

types of transporter for sodium in proximal tubule

A

Sodium passes from the lumen to epithelial cell via a Sodium-Hydrogen antiporter (H+ balances the charge of moving Na+)

Also, Organic nutrient reabsorption with Na+ via a variety of specific transporters

115
Q

where the second most sodium absorbed in the nephrone loop?

A

thick ascending limb (25%)

116
Q

sodium absorption on distal convoluted tubule

A

5% of total sodium that’s reabsorbed

Sodium-Chloride cotransporter

117
Q

sodium reabsorption in collecting duct system

A

70% of the cell are called principal cells. Reabsorb sodium via epithelial sodium channels

Aldosterone influences Na absorption here

118
Q

water reabsorption in collecting duct system

A

The cortical collecting duct cells are not permeable to water unless aquaporins are present. Aquaporins are controlled by ADH secretion

119
Q

what are the effects of adding an isotonic solution to the body?

A

ECF osmolality increases

TBW increases by the amount of fluid given

ECF volume increases

ICF volume and osmolality does not change

120
Q

what effect does adding salt to the body have on body fluid compartments?

A

ECF osmoles increases

ECF volume increases

ICF volume decreases

osmolality in both ICF and ECF increases (and equal each other)

121
Q

what effect does adding pure water have on the body fluid compartments of the body?

A

osmolality decreases (same osmolality for ECF and ICF)

both ICF and ECF increase

(2/3 of added water to ICF, 1/3 to ECF)

122
Q

equation for filtered load

A

Px x GFR

Px = PX is the plasma concentration of X (mg/mL)

GFR is the glomerular filtration rate (mL/min)

123
Q

equation for Excreted Load (mg/min)

A

UX x V

Ux = UX is the urinary concentration of X (mg/mL)

V is the rate of urine formation (mL/min).

124
Q

fractional excretion

A

Fractional Excretion = Excreted Load/Filtered Load

125
Q

what is renael plasma clearance (RPCx)?

A

the amount of blood plasma from whicht the kidney completely removes a substance

126
Q

equation for RPCx (renal plasma cleraance)

A

(Ux x V) / Px

PX is the plasma concentration of X (mg/mL)

UX is the urinary concentration of X (mg/mL)

V is the rate of urine formation (mL/min).

127
Q

Uses for knowing the Renal Plasma Clearance (RPCx) in a patient

A
  1. determine how well a kidney is functioning by looking at the RPC of a substance that is well-studied and normal values are known for
  2. determine how a healthy kidney handles a novel substance (like new drug)
128
Q

how can inulin be used to determine GFR?

A

the excreted load of inulin exiting the body via the urine derives entirely from that portion of the plasma filtered at Bowman’s capsule. So if you determine the RPC for inulin, you have simultaneously determined the GFR

Inulin isn’t secreted or reabsorbed in nephron

This method is problematic for clinical assessments, however, because it is rather invasive; inulin must be administered at a constant rate via intravenous infusion to achieve a steady plasma concentration, and a urinary catheter must be inserted to get an instantaneous measure of urine flow rate and inulin concentration

129
Q

creatine and calculation of GFR

A

A single measurement of plasma creatinine concentration, accompanied by a 24-hour determination of urinary flow rate and creatinine concentration, can give a fairly good estimate of GFR.

130
Q

most commonly used clinical method to measure GFR

A

measure plasma concentration of creatinine; if function is cut into half then the plasma concentration would be doubled to compensate

131
Q

measuring renal blood flow using PAH (para-aminohippuric acid)

A

RPCPAH = (UPAH x V)/ PPAH= Renal Plasma Flow

P = plasma concentration

U = urine concentration

V = rate of urine formation

Then to calculate RBF: (RPF) / (1-HCT)

hematocrit

132
Q

what does the RPC tell us about absorption and secretion of a substance by the nephron?

A

the RPC can only tell us the net movement, not how much of each process was involved

133
Q

type of drugs favored for elimination by kidneys and liver

A

kideys – favor elimination of hydrophilic drugs, nonionic, protein-bound

liver – favors elimination of lipophilic drugs; cannot be protein-bound

134
Q

kidney ability to clear synthetic drugs

A

Most synthetic drugs are ~ 500 daltons or less, so potentially can be cleared by the kidney because small enough, but need to be hydrophilic and not highly bound to protein

135
Q

definition of biotransformation

A

the alteration of a substance, such as a drug, within the body to make it easier to process/eliminate

136
Q

primary site of biotransformation in the body and why

A

liver

Liver enzymes convert substances to more polar, more hydrophilic metabolites that enhance renal elimination

Polar substances can cross cell membranes and the filtration barrier in the kidney easier than non-polar substances

137
Q

Name two drug-binding proteins in plasma and their drug-binding characteristics

A

Albumin binds acidic compounds (major blood protein contributing to drug binding)

α-1 acidic glycoprotein binds basic compounds

138
Q

Proximal tubular secretion of drugs

A

Drugs that are not filtered at the glomerulus can be transported into the lumen of the proximal tubule • Protein bound drug dissociates, then the drug can be transported

  • Renal organic acid (anion) transport system
  • Renal organic base (cation) transport system
139
Q

Renal organic acid (anion) transport system

A

Active transport of negatively charged acidic drug across basolateral membrane, then efflux across apical membrane into tubular lumen

140
Q

Renal organic base (cation) transport system

A

Passive movement of positively charged basic drug across basolateral membrane, then active transport across apical membrane into tubular lumen

141
Q

mechanisms of Tubular reabsorptionof substances (vitamins, drugs, enzymes)

A
  • Passive reabsorption
    • Lipophilic substances (undissociated molecules of weak bases and acids) can move from lumen into tubular cell, then into interstitium
    • Ionized drugs are trapped in the lumen and eliminated in the urine
    • Urine pH can be altered to facilitate urinary elimination
  • Active reabsorption
    • Vitamins e.g. ascorbic acid
  • Endocytosis (active)
    • Insulin
142
Q

normal urine pH physiological range

A

4.5 to 8.5

143
Q

effect of urinary pH on a weak acid drug

A

Weak acid

RCOOH (lipid soluble) ↔ RCOO- (trapped) + H+

As urine pH rises above pKa of drug, percentage ionized form increases, trapping drug in urine

Acidifying urine will enhance reabsorption; alkalinizing urine will enhance elimination

144
Q

effect of urinary pH on weak base drug

A

RNH3 + (trapped) ↔ RNH2 (lipid soluble) + H+

As urine pH falls below pKa of drug, percentage ionized form increases, trapping drug in urine

Alkalinizing urine will enhance reabsorption; acidifying urine will enhance elimination

145
Q

bioavailability

A

mathematically representation of how much of a drug dose reaches the systemic circulation; extent of absorption

Bioavailability (F) is the fraction of administered dose that is delivered to the systemic circulation

146
Q

pharmokinetics parameters

A

Bioavailability

Volume of distribution

Elimination rate constant

Half-life

Clearance

147
Q

bioavailability difference in IV dosing vs. oral dosing

A

Intravenous (IV) dosing bypasses GI absorption and yields 100% bioavailability

Oral drug formulations need to pass multiple barriers before getting into the systemic circulation – less bioavailability

148
Q

Volume of distribution (Vd) of a drug and how to calculate it

A

Vd determines the dose that should be given to a patient

Published Vd (L/kg) x patient weight (kg) = Vd (L) for the patient

After the first dose of a drug, the Vd(L) can be estimated for the drug in the individual patient:

Vd(L) = Dose (mg) / Cpost

Where Cpost is the highest concentration achieved after the first dose

149
Q

Zero Order drug:

percentage of drugs of this order, plasma conc over time, characteristic, rate, general example of drug

150
Q

First Order Drug

percentage of drugs of this order, plasma conc over time, characteristic, rate, general example of drug

151
Q

Elimination rate constant in first order drug and how it can be altered by changes in clearance

A

The amount of drug in the body diminishes logarithmically over time (first order elimination); Ke is the elimination rate constant

Ke = Cl/Vd

t1/2 = 0.693/Ke

If 𝐶𝑙↑, then 𝐾e will ↑ and 𝑡𝑡 ½ will ↓

152
Q

rate of elimination relating to clearance and plasma concentration

A

Rate of Elimination = Cl x Cp

where Cp is plasma conc and Cl is clearance

153
Q

steady state of a drug

A

when the rate of drug infusion becomes equal to rate of elimination

drug in = drug out

154
Q

how long to reach the steady state of a drug?

A

about 3 to 5 half lives if there is not loading dose

155
Q

way to reach a steady state sooner in drugs with a long half life

A

can give a loading dose – a dose of higher concentration/frequency to front load and try to reach therapeutic state sooner

156
Q

how to calculate a loading dose

A

loading dose = (Vd)(Cp) / (F)

where F is bioavailability

Cp is desired plasma concentration

Vd is volume of distribution in liters

Vd = populatio Vd x patient weight in kg

157
Q

when to use intermittent infusions

A

Drugs that work by maximizing plasma concentration for a short period of time (for efficacy) but require the drug to clear from the plasma (to prevent toxicity) require intermittent infusions

158
Q

when to use continuous infusion

A

Drugs that need constant exposure at receptors in the body will

require a continuous infusion

159
Q

Steady state relationship to time and dosase

A

time to steady sate independent to dosade; the dosage applied will determine how high the steady state is, but not how long it takes to reach the steady state, no matter what level it happens to be at

160
Q

sodium regulation in a response to body volume

A
  • Volume status mediates sodium balance
  • Body: Volume status is up
    • Kidney: Response is to waste sodium
  • Body: Volume status is low
    • Kidney: Response is to reabsorb sodium
161
Q

baroreceptors that can effect sodium reabsorption

A
  • arterial baroreceptors
  • cardiopulmonary baroreceptors
  • intrarenal baroreceptors
162
Q

where is renin secreted from?

A

granular cells in the juxtaglomerular apparatus

163
Q

triggers for renin release

A
  1. sympathetic nervous system actiation of B1 adrenergic receptors
  2. decrease in afferent arteriole stretch
  3. macula densa sensing less sodium in filtrate
164
Q

Renin-Angiotensin system: renin release to formation of Angiotensin II

165
Q

effects Angiotensin II has on the body

166
Q

what is the rate-limiting step of the renin-angiotensin system?

A

Release of Renin is the rate-limiting step

167
Q

role of Natriuretic Peptides in kidney and blood pressure maintenance (where produced, what it’s produced in response to, effects on body, purpose)

A

produced in the heart; response to stretch

effects natriuretic peptide has on the body: vasodilation, decrease PCT reabsorption of Na+, offset effect of aldosterone

purpose: get rid of excess sodium

168
Q

pressure natriuresis mechanism

A

high blood pressure leads to increases in renal perfusion pressurelead to decreases in sodium reabsorption and increases in sodium excretion.

169
Q

effect of volume contraction on body (overview map)

170
Q

systemic effects of volume expansion (overview map)

171
Q

Assessment of Volume Status: history and physical exam

A
  • Thirst, diarrhea, vomitting
  • JVP (venous bed)
  • Skin turgor and presence/absence of edema (interstitial bed)
  • Low BP (arterial bed)
  • Urine sodium and chloride for effective circulating volume
172
Q

effect of aldosterone level on urine sodium and chloride

A

high serum aldosterone would lead to low sodium and chloride in patient’s urine

173
Q

where are plasma proteins synthesized

174
Q

the effects of Na depletion on effective circulating volume, ECF volume, plasma volume, and cardiac output

175
Q

the effects of heart failure on effective circulating volume, ECF volume, plasma volume, and cardiac output

176
Q

the effects of advanced hepatic cirrhosis on effective circulating volume, ECF volume, plasma volume, and cardiac output

177
Q

In the setting of a high sodium diet, what would happen to total extracellular fluid volume

A

Will Increase

178
Q

In the setting of a high sodium diet, what would happen to Effective Circulating Volume

A

Will Increase

179
Q

In the setting of a high sodium diet, what would happen to urine sodium excretion

A

Will Increase

180
Q

In the setting of an acute myocardial infarction, what will happen to the total extracellular fluid volume?

A

Will remain unchanged

181
Q

In the setting of an acute myocardial infarction, what will happen to the effective circulating volume?

A

Will decrease

182
Q

In the setting of an acute myocardial infarction, what will happen to the urine sodium excretion?

A

Will decrease

183
Q

In the setting of heart failure, what would happen to total extracellular fluid volume

A

Will Increase

184
Q

In the setting of heart failure, what would happen to Effective Circulating Volume

A

Will decrease

185
Q

In the setting of heart failure, what would happen to urine sodium excretion

A

Will decrease

186
Q

Treatment of Volume Contraction

A

priority is to replace volume

give isotonic solution

(increases the ECF without increasing the ICF bc same tonicity)

will provide sodium

187
Q

Treatment of Volume Overload

A

Treatment = Remove sodium

decrease intake and/or increase output (furosemide)

188
Q

If a patient has low blood pressure and high edema, how should you treat them?

A

priority would be to address blood pressure at first and then look at how to treat edema

189
Q

definition of diuretic vs natriuretic

A

Diuretic: A compound that increases the excretion of urine (volume)

Naturetic: A compound that increases the renal excretion of sodium

note – The action of most diuretics is to increase renal sodium excretion

190
Q

main action of diuretics

A

Decrease reabsorption of filtered sodium by blocking sodium transporters

191
Q

three main types of diuretics

A
  • Loop diuretics
  • Thiazide diuretic
  • Potassium sparing diuretics
192
Q

normal mechanism of reabsorption in thick ascending loop of henle

193
Q

mechanism of loop diuretic

A

NET EFFECT: Na+, K+, Cl- , Ca2+, Mg2+ lost in urine

Inhibit Na-K-2Cl carrier in the thick ascending LOH (Compete with Cl- at its binding site (within the tubular lumen)

Decrease urinary Ca2+ reabsorption in the LOH

194
Q

examples of loop diuretic meds

A

Furosemide (Lasix), bumetanide (bumex)

195
Q

indications for loop diuretics

A

HTN, edema

Hypercalcemia

196
Q

major side effects of loop diuretics

A
  • large reduction of effective circulating volume
  • hypokalemia and metabolic alkalosis
  • hypocalcemia
  • ototoxicity (Na/2CL/K channels in ear also blocked by med)
197
Q

mechanism of reabsorption in the distal convoluted tubule

A
  1. ) Decrease in intracellular [Na+], increase in intracellular [K+]
  2. ) Decrease in intracellular [K+] and [Cl-] via basolateral channels
  3. ) Reabsorption of filtered Na+ and Cl- down their concentration gradients via NCC channel

NET EFFECT: Na+, Cl- reabsorbed

198
Q

mechanism of thiazide diuretics

A

Inhibit NaCl transport in distal tubule

Compete with Cl- at its binding site (within the tubular lumen)

Can theoretically lead to excretion of 5-7% of filtered Na+

 Increase urinary calcium reabsorption

Likely due to mild volume depletion

Increased passive reabsorption of calcium in proximal tubule

199
Q

examples of thiazide diuretics medications

A

Chlorothiazide, hydrochlorothiazide, chlorthalidone, metolazone

200
Q

indications for thiazide diuretics

A

hypertension, hypercalcuria, diabetes insipidus (a condition characterized by large amounts of dilute urine and increased thirst)

201
Q

major side effects of thiazide diuretics

A
  • volume depletion
  • hypokalemia and metabolic alkalosis
  • hypercalcemia
202
Q

mechanism of reabsorption in the distal tubule/collecting duct

203
Q

mechanism of potassium sparing diuretics

A

two types of potassium sparing diuretics

  1. mineralocorticoid receptor blocker
  • aldosterone never gets to bind to its receptor in the cell
  • Na+ not absorbed, K+ and H+ not secreted
  1. block ENaC channels
  • blocks Na+ channel on basal lumenal membrane
  • Na+ not absorbed, K+ and H+ not secreted
204
Q

examples of medications that are potassium sparing diuretics

A

type 1: spironolactone

type 2: amilioride, triamterene

205
Q

indications of potassium sparing diuretics

A

hypertension

hypokalemia

metabolic alkalosis

206
Q

major side effects of potassium sparing diuretics

A
  • hyperkalemia
  • metabolic acidosis
  • nephrotoxicity (triamterene)
  • systemic anti-adrogen (spironolactone)
207
Q

mechanism of carbonic anhydrase reabsorption in the proximal tubule

208
Q

effect and mechanism of carbonic anhydrase inhibitors

A

NET EFFECT: Na+ and HCO3- are lost in the urine

Inhibits carbonic anhydrase enzyme (catalyst) (Critical enzyme involved in movement of CO2 in/out of cells)

209
Q

example medication of carbonic anhydrase inhibitor

A

Acetazolamide (Diamox)

210
Q

main indications for carbonic anhyrase inhibitors

A
  • Edema in a patient with metabolic alkalosis (rare)
  • Extra-renal
  • glaucoma, altitude sickness, epilepsy
211
Q

Major Side Effects of Carbonic Anhydrase Inhibitors

A
  • METABOLIC ACIDOSIS
  • Sedation
  • Paresthesias
  • Bone marrow depression
212
Q

mechanism of action for osmotic diuretics

A

 Increases osmolality of tubular lumen
 Prevents water and (and some sodium) reabsorption

213
Q

example of used osmotic diuretic

A

Mannitol (Freely filtered, non-reabsorbable polysaccharide)

214
Q

major side effects of mannitol (osmotic diuretic)

A

Causes water loss in excess of sodium (water moves without sodium)

  • Hypernatremia

Can cause increases in ECV due to increased serum osmolality

215
Q

conditions to consider if a patient is demonstrating refractory edema

A

Poor GI absorption

  • Bowel wall edema can impact oral medications intestinal absorption

Decreased drug entry into the tubular lumen

  • Renal failure – competition with organic anions for luminal secretion
  • Nephrotic syndrome – tubular protein binding and third spacing

Heart failure – poor renal perfusion increases proximal Na+ reabsorption

216
Q

how to treat patient with refractory edema

A

Use combination of diuretics with different site of action

Different classes of diuretics work at different segments of the nephron

Remember: Blocking sodium reabsorption proximally causes increased sodium reabsorption distally

217
Q

diuretics used together in combonation for diuretic synergy

A

Loop + thiazide

• Most potent diuretic effect

Loop + K+ sparing

• Help limit alkalosis and hypokalemia

Thiazide + K+ sparing

• Help limit alkalosis and hypokalemia

218
Q

can you assess a patient to see if they need to restrict their sodium intake?

A

Can be assessed by 24 hour urinary collection for sodium

If UNa+ is > 100-150 mEq/day, need better dietary control

219
Q

magnitude of effectiveness of different diuretic types

A

Loop diuretics – Most effective – ~30% of sodium reabsorbed in LOH

Thiazide diuretics – Moderately effective – ~7% of sodium reabsorbed in distal tubule

Potassium Sparing diuretics – Mildly effective – ~2% of sodium reabsorbed in collecting duct

220
Q

general properties of organic solute transport

A
  • each organic solute does not have its own designated channel; one channel can move many different solutes
  • majority of organic solute transport happens in the proximal tubule – Organic solutes not reabsorbed there are (almost) always excreted
  • transport cascade always starts with Na-K ATPase
    • Neutral or negatively charged organic solutes reabsorbed with sodium via symporters
    • Positively charged organic solutes reabsorbed along electrical gradient
221
Q

glucose reabsorption in the kidney

A

all glucose is reabsorbed when plasma glucose is less than 375 mg/min; if higher than 375 then glucose will be excreted (found in urine)

Transporter capacity is overwhelmed so excess glucose ends up in the urine

222
Q

glucose transport inhibitors in kidney

A

SGLT2 channel inhibitors used to block glucose reabsorption (increase excreted glucose) for people with excess glucose

rarely used; interesting concept

223
Q

how larger filtered proteins, such as albumin, reabsorbed back into circulation?

A
  • albumin binds to receptor
  • gets endocytosed
  • vesicle merges with lysozyme in cell
  • enzyme degrades protein to its amino acids
  • amino acids transported out of cell across basolateral membrane via transporters
  • **normally no protein ends up in urine but this process can be easily saturated
224
Q

how are filtered peptides reabsorbed back into circulation?

A
  • Peptides are catabolized within the lumen via peptidases on apical membrane
  • Amino acids are transported into cell via transporters on apical membrane
  • Amino acids are transported out of cell across basolateral membrane via transporters
225
Q

changes in concentration of peptide hormones as a result of kidney disease

A

Kidneys are a major site of catabolism of many peptide hormones

decreased rates of degradation in kidney disease may increase plasma concentrations

226
Q

the three mechanisms of proteinuria

A

Glomerular

  • increased filtration of proteins due to loss of charge/size selectivity; Tm is reached and excess protein excreted

Overflow

  • excess amounts of plasma proteins increase amount in filtrate (more being made); Tm is reached and excess protein is excreted

Tubular

  1. tubular damage or dysfunction inhibits normal reabsorption
  2. protein released from damaged tubular cells
227
Q

Organic cation secretion (where occurs, nature of transporters, mechanism)

A
  • Primarily in the proximal tubule
  • Transporters are generally non-selective

high Tm

228
Q

Organic anion secretion (where occurs, nature of transporters, modifications, process)

A

Primarily in the proximal tubule

Transporters are generally non-selective; high Tm

Many anions are poorly water soluble

  • Dependent on conjugation with glucoronate or ulfate
  • Occurs in liver
  • Conjugated anion removed by kidney
229
Q

properties of urate

A
  • Freely filterable
  • Reabsorbed, secreted, and again reabsorbed
  • Blood levels are normally maintained relatively constant; secretion can increase to keep levels normal
230
Q

what is urate and what is it’s significance?

A
  • Organic anion, base form of uric acid
  • elevated serum levels can cause gout
  • removal from the blood by kidneys is important for preventing disease
231
Q

elevated serum urate/uric acid can be caused by:

A

decreased GFR

excessive reabsorption

decreased secretion

232
Q

pH of typical western diet

A

generally more acidic

233
Q

what is urea?

A

converted from ammonium in the liver

byproduct of amino acid metabolism

not toxic, but is osmotically active

must be excreted

234
Q

properties of urea

A
  • freely filtered
  • polarized – cannot cross lipid bilayer
  • can cross tight junction in some segments of nephrons
  • reabsorbed, secreted, reabsorbed
    • urea recycling is important in countercurrent mechanism
235
Q

what is BUN?

A

blood urea nitrogen; a reflection of plasma urea concentration

236
Q

proportion of urea in urine

A

makes up about half the solute in urine

237
Q

how much of filtered urea ends up in the urine?

238
Q

what does urea excretion try to match?

A

tries to match hepatic production

239
Q

definition/purpose of .Countercurrent multiplication in the kidneys

A

the process of using energy to generate an osmotic gradient that enables you to reabsorb water from the tubular fluid and produce concentrated urine

Body in Balance Unit 3 (4 decks)

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