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Kidney > Apex- Renal > Flashcards

Apex- Renal Flashcards

1
Q

At what vertebral levels do the kidneys lay

A

between T12-L3 in the retroperitoneal space

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2
Q

The kidney can be divided into what 2 parts and what does each contain (4/2)

A

Renal Cortex

  • Glomerulus, bowmans capsule
  • Proximale and distal tubules

Renal Medulla

  • loop of henle
  • collecting duct

(the two things that drop down)

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3
Q

functional unit of the kidney

A

nephron

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4
Q

What substance is produced by the juxtaglomeular apparatus

A

renin

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5
Q

Where is erythropoietin synthesized and what is it secreted in response to?

A

In the kidney

-secreted in response to hypoxia

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6
Q

The kidney produces : (select 3)

  • Calcitrol:
  • ADH:
  • Aldosterone:
  • Renin:
  • Erythropoietin:
  • Angiotensinogen:
A

-Calcitrol: parathyroid tells kidneys to convert inactive vitamin D3 to active vitamin D3 (calcitrol)

  • ADH: supraoptic nuclei and paraventricular nuclei in the hypothalmus- released from posterior pitutiary gland
  • Aldosterone: adrenal cortex

-Renin: by the juxtaglomerular apparatus in response to decreased perfusion

-Erythropoietin: secreted in response to hypoxia

-Angiotensinogen: liver

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7
Q

Where is angiotensinogen manufactured

A

in the liver

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8
Q

Where is aldosterone synthesizied

A

in the adrenal cortex

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9
Q

Where is ADH produced/released from

A

produced in the hypothalmus (supraoptic and paraventricular nuclei)

released from posterior pitutiary gland

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10
Q

Where is erythropoietin syntheized

A

in the kidney

(in response to hypoxia)

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11
Q

What is calcitrol

A

the active form of vitamin D3

synthesized in the kidney under influence of parathyroid hormone

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12
Q

where is renin produced from?

A

the kidney - the juxtaglomerular apparatus

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13
Q

What organs are the regulators of acid base balance

A

lungs and kidney

lungs- rid body of volatile acids (CO2)

kidneys- rid body of non-volatile acids (Bicarb)

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14
Q

someone is anemic bc of chronic kidney diseae - why are they anemic?

A

bc the kidney produces erythropoietin (stimulates RBC production), less RBCs = less hgb

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15
Q

Renal blood flow decreases ____% per decade after the age of ____

A

10% /decade after 50yo

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16
Q

In the neonate, RBF doubles when and reaches adult function when

A

*rule of 2’s

  • RBF doubles in first 2 weeks of life
  • adult levels by 2 years
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17
Q

Difference between aldosterone and ADH (vasopressin)

A

aldosterone controlls extracellular fluid volume (sodium and water reabsorption)

ADH manipulates plasma osmolarity (water is absorbed by sodium is not)

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18
Q

T/F- the kidney is capable of phase 1 and phase 2 metabolism

A

true

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19
Q

Why do people hgb become elevated when “dry”

A

bc if they are intravascularly dry, the kidneys sense reduced o2 delivery to them, they secrete erythropoietin to make more RBCs, more RBCs = more hemoglobin to try and carry more o2 to the kidneys

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20
Q

Why cant you give NSAIDs to people with impaired renal function

A

bc they block prostagladins and prostagladins control blood flow to the renal arteries

  • PGE2 and PGI2 vasodilate the renal arteries (afferent)
  • Thromboxane A2 consticts the renal arteries (efferent)
  • blocking this, impairs filtration time
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21
Q

____ & ____ vasodilate the afferent arterioles

_____constricts the efferent arterioles

(prostagladins subtypes)

A

PGE2 & PGI2 vasodilate

Thromboxane A2- constricts

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22
Q

What is the vitamin D3 that is sythesized by the skin upon exposure to ultraviolet light?

A

Calciferol (like a feral cat outside)

-it’s INACTIVE

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23
Q

2 ways we get vitamin D

-how does it become activated?

A

Sunlight (calciferol, skin) & Diet

(both inactive forms)

  • liver converts calciferol to 25-hydroxycholecalciferol (biotransformation- makes orginal word root longer)

25-hydroxychloecalciferol is converted to

1,25- dihydroxycholecalciferol (calcitriol) - active form of vitamin D 3

PTH regulates this process - increase serum PTH, increases serium calcitrol level

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24
Q

Active form of Vitamin D3

A

Calcitriol

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25
Q

T/F- the renal medulla receives 90% of the renal blood flow

A

FALSE- renal cortex

-think - cortex = higher level functions = more o2 needed

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26
Q

How do the kidneys prevent hypoglycemia during fasting?

A

by synthesizing glucose from amino acids

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27
Q

How does active vitamin D3 increase serum calcium levels? (3 ways)

A
  1. stimulates intenstines to absorb more CA++ from food
  2. instructs kidney to reduce CA++ and phos exretion
  3. Increases deposition of CA++ into the bone (increases bone turnover time- no clue)
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28
Q

What hormone controls plasam osmolarity?

A

ADH

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29
Q

What hormone controls extracellular fluid volume?

A
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30
Q

Where do the kidneys receive SNS innervation from?

A

T8-L1

(Lies at T12-L3)

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31
Q

How much of the CO do the kidneys receive

A

20-25%

1,000 - 1250ml/min

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32
Q

Of the blood flow delivered to the kidney, only ____% is filtered at the glomerulus

A

20%

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33
Q

Renal blood flow is (directly/inversely) propotional to the difference between MAP and renal venous pressure and (directly/inversely) propotional to renal vascular resistance

A

directly proportional to difference between MAP and renal venous pressure (greater pressure gradient = greater RBF)

-inversel ypropotional to RVR (increases resistance = decreased RBF)

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34
Q

Autoregulation maintains renal blood flow between a MAP of ____ - _____

A

50- 180mmHg

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35
Q

the blood in the peritubular capillaries returns to the IVC by way of what?

A

the renal veins

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36
Q

How to calculate RBF

A

(MAP-Renal venous pressure)/ Renal vascular esistance

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37
Q

Renal cortex recieves ___% of RBF (PO2)

Renal medulla recieves ___% of RBF (PO2)

which is more sensitive to ischemia?

A

Cortex - 90% renal blood flow (PO2 50)

Medulla - 10% RBF (PO2 10)

*medulla is most sensitive to ischemia

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38
Q

T/F - UOP is autoregulated

A

false- it is linearly related to a MAP > 50

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39
Q

What is the myogenic mechanism and how does it relate to RBF

A

If pressure is too high through the renal artery, the myogenic mechanism constricts the afferent arteriole to protect the glomerulus from excessive pressure

-

-when the pressure is too low, the mygoenic mechanism dilates the afferent arteriole to increase blood flow going to the nephron

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40
Q

Where in the kidney specifically is the juxtaglomerular apparatus located?

A

in the distal tubule (specifically the region that passes through the afferent and efferent arterioles)

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41
Q

What renal structures are innervated by the SNS?

A

The afferent and efferent arterioles

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42
Q

Which factor increases renin release?:

A. PEEP

B. Hypervolemia

C. Angiotensinogen

D. Increased chloride delivery to the macula densa

A

A. PEEP

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43
Q

Increase or decrease renin release:

-Beta 1 stimulation

A

Increase (Beta receptors on the juxtaglomerular apparatus)

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44
Q

(Increased/decreased) sodium and chloride delivery to the distal tubule increases renin release

A

decreased

(decreased solutes, release renin > vasoconstriction)

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45
Q

Aldosterone is a ______ hormone that is produced by the zona ________ of the adrenal gland.

A

steroid hormone, zona glomerulosa

NA+ reabsorption, K+ and H+ excretion

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46
Q

T/F- Aldosterone does not meaningully affect serum os

A

true- it manipulates absopriton and excretion of solutes; whereas ADH mainpulates reabsopriton of water (osmolarity) and not solutues

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47
Q

Aldosterone facilitates reabsoprtion and exretion of what?

A

absorpiton of sodium (and water)

exretion of K & H

think NA has two ++ , so in addition to K+ , it also excretes H+ to balance the scale

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48
Q

Angiotension 2 causes constriction of the (efferent/afferent) arteriole, which (increases/decreases) GFR

A

efferent

increases

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49
Q

What happens when renin is released

A

it converts angiotensinogen from the liver to angiotension 1

angiotension 1 is converted to angiotension 2 by ACE in the lungs (also breaks down bradykinins)

  • angiotension 2 is the most potent vasoconstrictor in the body: peripheral vessels, efferent arteriole, triggers release of aldosterone (na and water reabosprtion, k & H extretion- DT), relase of ADH (post. pit) - water reabsorption (CD) ; signals sodium to be reabsoprtied in the proximal tubule, and triggers thirst
  • wow that was extra
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50
Q

6 mechanisms by which angiotension 2 increases BP

A
  1. peripheral vasoconstriction
  2. constriction of the efferent arteriole
  3. aldosterone release
  • from the adrenal gland (zona glomerulosa)
  • steroid hormone
  • promotes NA+ reabsoprtion, K+ exretion
  • distal tubule
  1. ADH release
  • Posterior pituitary
  • water reabsoprtion
  • collecting duct
  1. Na+ reabsoprtion
    * proximal tubule
  2. Thirst
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51
Q

What causes aldosterone to be released (3) things

A

RAAS activation

Hyperkalemia (takes sodium, gets rid of K)

Hyponatremia (takes sodium, gets rid of K)

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52
Q

Conn’s disease occurs with (too much/too little) aldosterone production

A

too much

  • causes sodium retention and potassium loss
  • aldosterone = conn man, takes sodium for k

*too little aldosterone production is uncommon

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53
Q

ADH agonizes the (V1/V2) receptor and (increases/decreases) cAMP

A

agonizes the V2 receptor (increases aquaporin channels in the CDs)

increases cAMP

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54
Q

T/F ADH increases water reabsorption in the proximal tubules

A

false- collecting ducts

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55
Q

What is the principle determinate of osmolarity

What 2 other things play a role?

A

Sodium concentration

Glucose and BUN

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56
Q

Normal serum osmolarity

A

280-290mOsm/L

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57
Q

In what 2 instances is ADH released into the systemic circ?

A
  1. increased osmolarity of ECF (will promote water reabsoprtion to dilute solutes)
  2. decreased blood volume/ RAAS activation
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58
Q

2 ways by which ADH restores blood pressure

A

1. V1 receptor stimulation in vasculature causes vasoconstriction (increased SVR)

  • Gq ⇒ increased IP3, DAG, CA +

2. V2 receptor stimulation in the collecting ducts causes water retention

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59
Q

(Osmolality/Osmolarity) measures the number of osmoles per (liter/kg) of solvent

A

Osmolality - osmoles per kg

OsmolaRity- osmoles per liteR

(differences are so minuscule that they can be used interchangably but just incase you get questions on this bullshit)

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60
Q

Half life of ADH

A

5-15 minutes

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61
Q

All of hte following enhance renal perfusion EXCEPT:

  • fenoldopam
  • PGE2
  • Naturitic peptide
  • Thromboxane A2
A

Thromboxane A2

(vasoconstrictor and increases in time of ischemia)

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62
Q

What do naturitic peptides do to the kideny

A
  • well they are released in response to increased blood volume
  • so they inhibit RAAS, promoting sodium and water exretion
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63
Q

What does the stimulation of D1 vs D2 receptors result in

A

D1 ⇒ vasodilation, increased renal blood flow, increased GFR, diuresis, sodium exretion

D2 ⇒ decreased NE release from the presynaptic SNS nerve terminal

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64
Q

3 things that promote renal vasodilation

A
  1. prostagladins
  2. naturitic peptide
  3. dopamine receptors
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65
Q

Where are prostagladins produced?

A

inthe afferent arteriole of the kidney

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66
Q

When is arachidonic acid liberated from the cell membrane (4) & How

A

in response to

  1. ischemia
  2. hypotension
  3. NE
  4. Angiotension 2

(well thats confusing)

Phospholiapse A2 convers phospholipid in the cell membrane to arachidonic acid

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67
Q

What two things are produced by arachidonic acid and by what 2 pathways

A

1. Cyclic endoperoxides: (Cyclooxygenase pathway)

  1. ​Vasodilators: PGI2 ♦ PGE2 ♦ PGD2
  2. Vasoconstrictors: Thromboxane A2 ♦ PGF2

2. Leukotrienes (Lipooxygenase pathway)

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68
Q

How do NSAIDS reduce renal blood flow?

A

By inhibiting cyclooxygenase and the production of vasodilating prostagladins

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69
Q

Vasodilator or vasoconstrictor:

PGI2

A

Vasodilator

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70
Q

Vasodilator or vasoconstrictor:

PGE2

A

Vasodilate

(D2, I2,E2)

-when you DIE, you vasodilate

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71
Q

Vasodilate or constrict

PGD2

A

Vasodilate

(D2, I2, E2)

-when you DIE, you vasodilate

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72
Q

Vasodilate or vasoconstrict:

Thromboxane A2

A

Vasoconstrict

(+PGF2)

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73
Q

Vasodilate or constrict: PGF2

A

Constrict

(D-I-E = vasodilate)

(F = fuck that, i’m gonna try to help you not die and constrict)

(+thromboxane A2)

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74
Q

Where are D1 receptors located (2 places)

A

on the kidney and in splanchic circulation

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75
Q

Where are D2 recpetors present

A

on the presynaptic adrenergic nerve terminal

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76
Q

(D1/D2) receptor stimulation results in (increased/decreased) cAMP

A

D1 = increased cAMP (vasodilation, increased RBF, increased GFR, diuresis (bc of the increased RBF), sodium exretion

D2 = decerased cAMP (decreased NE release from presynaptic nerve terminals)

i’m confused

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77
Q

What is Fenoldopam

A

a selective D1 agonist that increases renal blood flow

  • low doses 0.1-0.2mcg/kg/min
  • may offer renal protection during aortic surgery and during CPB
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78
Q

2 effects natruetic peptide has on the kidneys

A
  1. inhibits renin release
  2. promotes sodium and water exretion in the collecting ducts
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79
Q

Normal GFR

A

125mL/min

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80
Q

3 determinants of glomerular hydrostatic pressure

A
  1. Arterial pressure
  2. afferent arteriole resistance
  3. efferent arteriole resistance
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81
Q

T/F - The Glomerular hydrostatic pressure if the most important determinant of GFR

A

True

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82
Q

Constriction of the efferent arteriole (increases/decreases) RBF and GFR

A

decreased RBF but increases GFR

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83
Q

Where does MOST of hte sodium reabsopriton occur in the nephron?

  • proximal tubule
  • distal tubule
  • collecting duct
  • ascending loop of henle
A

Proximal tubule

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84
Q

Define:

Reabsoprtion:

Secretion:

Excretion:

A

Reabsoprtion - substance is transfered from the tubule > peritubular capillaries

Secretion - substance transferred from the peritubular capillaries > tubules

Excretion - substance is removed fromo the body in the urine

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85
Q

Which part of the loop of henle (ascending vs descending) is highly permeable vs impermeable to water

A

Descending = highly permeable (think taking a deep dive into a pool of water)

Ascending - impermeable to water

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86
Q

Primary site of reabsorption in the nephron

A

proximal convuluted tubule

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87
Q

T/F - reabsorption of solutes and water is proportional in the proximal convuluted tubule

A

True

65% sodium, (followed by) 65% water

+ 65% K, Cl-, HCO3-

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88
Q

Primary goal of the loop of henle

A

handles sodium and water to form concnetrated or dilute urine

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89
Q

What part of the nephron “fine-tunes” solute concentration

A

the distal convoluted tubule

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90
Q

T/F- the late distal tubule is impermeable to water

A

True - except i nthe presence of aldosterone or ADH which fine-tune the final urine concentration

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91
Q

What does the collecting duct do?

A

regulates the final concentration of the urine

92
Q

Where does aldosterone act on the nephron?

A

In the DCT & collecting ducts

93
Q

Where does ADH act on the nephron?

A

in the DCT and collectin ducts

94
Q

Where in the nephron does parathyroid hormone promote CA+2 reabsoprtion?

A

Distal tubules

95
Q

Which part of hte nephron is impermeable to water?

A

The ascending loop of henle

96
Q

match

A
97
Q

What specifically in the kidney do most diuretics target?

A

The NA/K- ATPase pumps that allows sodium to move from the tubule to the peritubular capillaries that allows for maintenance of the concnetration gradient

98
Q

What is the function of carbonic anhydrase in the proximal tubule?

A

So

  1. CO2 and water diffuse into the PCT where carbonic anhydrase is
  2. Carbonic anhydrase facilitates the formation of carbonic acid (H2CO3)
  3. H2CO3 then dissocitates into:

H+ (Stays in the tubular lumen)

HCO3 - (Diffuses back into the blood)

-so with people on carbonic anhydrase inhibitors, HCO3- stays in the urine, making it more basic, and produces a mild hyperchloremic metabolic acidosis

99
Q

Why wouldn’t you want to give acetazolamide (diamox) to a COPD patient or someone with an elevated CO2 level

A

elevated CO2 level = hydrogen ion excess /acidosis

if you give diamox - your going to lose HCO3- in the urine and take away the kidneys ability to try and buffer that excess H+ in the blood (worsens hypercapnia/sleepiness)

100
Q

What diuretic may be given for those with central sleep apnea and why?

A

acetazolamide (diamox) - bc it will prodice a mild metabolic acidosis and the excess H++ ions will stimulate respiratory drive

101
Q

Dose of acetazolamide

A

250-500mg

102
Q

Which diuetic can be used to treat open-angle glaucoma

A

acetazolamide (diamox)

-inhibition of carbonic anhydrase reduces aqueous humor production and decreases IOP

103
Q

T/F- carbonic anhydrase inhibitors can produce hypokalemia

A

True - not sure why though….

104
Q

Where do osmotic diuretics work?

A

in the proximal tubule (primary) and loop of henle

105
Q

Why is mannitol thought to protect the kidney

A

Bc it’s going to enhance renal blood flow by pulling fluid into the intravascular space

106
Q

If your giving mannitol, what should you think of in terms of pt history

A

mycoardial function - if poor; it can preciptate heart failure and pulmonary edema bc the heart cant handle the increase in volume

107
Q

What is isosorbide

A

an osmotic diuretic

108
Q

What diuretics inhibit water reabsoprtion in the proximal tubule and loop of henle?

A

Osmotic diuretics

-mannitol, glycerin, isosorbide

109
Q

what is glycerin

A

an osmotic diuretic

  • i think this is what they are talking about with TUR syndrome and using glycerin as the fluid - if it gets into a venous sinus, it can increase intravascular volume and lead to pulm edema? maybe? lol who knows
110
Q

Dose of mannitol

A

0.25-1g/kg

111
Q

Mannitol can be used as a differential diagnosis of acute oliguria - how?

A

if the issue is pre-renal, UOP will increase (kindey still works fine)

if the issue is intrinsic- there will be no increase in UOP (kidney is damaged and not fucntioning as it should)

112
Q

Mannitol in TBI- yes or no

A

NO - the BBB can be disrupted and if mannitol enters the brain it will worsen cerebral edema

113
Q

Loop diuretics disrupt the __________ transporter in the medullary region of the (thick/thin) portion of the (ascending/descending) loop of henle.

A
  • NA-K-2CL transporter
  • Thick portion of ASCENDING loop (impermeable to water)
  • increased amount of sodium remains in the tubule

…idk i dont get it

114
Q

Dose of furosemide

A

20-200mg

115
Q

What is Bumetanide?

Dose?

A

Bumex - loop diuretic

0.5-2mg

116
Q

What is ethracrynic acid ?

A

Edecrin

-loop diuretic

117
Q

What diuretics inhibit the Na-Cl co-transporter in the distal tubule

A

Thiazides

118
Q

Which type of diuretics can cause hyperglycemia?

A

Thiazide diuretics

-speculated poss decrease insulin release from pancreas or impair glucose utilization in the body .

119
Q

What is chlorthalidone

A

Thiazide diuetic

(DCT)

120
Q

What is metolazone

A

thiazide diuretic

(DCT)

121
Q

What is indapamide

A

thiazide diuretic

(DCT)

122
Q

What is spironolactone?

A

K-sparing diuretic

aldostone antagonist

-inhibits K secretion and NA reabsportion in the collecting ducts

123
Q

What is amiloride?

A

K-Sparing diuretic

(collecting duct)

124
Q

What is triamterene?

A

K-Sparing diuretic

(Collecting duct)

125
Q

Why would K-sparing diuretics be used in someone with secondary hyperaldosteronism?

A

increased aldosterone = hypernatremia, hypokalemia

-K-sparing diuretics do the opposite.

126
Q

Which K-sparing diuretic antagonizes aldosterone at the mineralocorticoid receptors?

A

Spironolactone

127
Q

3 drug classes the increase the risk of hyperkalemia in a patient on K-sparing diuretics

A
  1. NSAIDS
  2. betablockers
  3. ACE inhibitors
128
Q

What does the tubular function of the kidney assess?

A

concentrating ability

129
Q

3 tests of glomerular function

A
130
Q

Normal BUN

A

10-20mg/dL

131
Q

Normal serum creatinine

A

0.7-1.5mg/Dl

132
Q

normal creat clearance

A

110-150ml/min

133
Q

4 tests of tubular function (concentrating ability)

A
  1. Fractional excretion of sodium (1-3%)
  2. Urine os (70-1400mOm/L)
  3. Urine sodium concentration (130-260mEq/day)
  4. urine SG (1.003- 1.030)
134
Q

what is creatinine?

A

a metabolic byproduct of creatine breakdown

(levels should be normal if your kidneys functioning normally, they can filter it out)

135
Q

Best indicator of GFR

A

creatine clearance

(110-150ml/min)

136
Q

Normal fractional exretion of sodium

A

1-3%

137
Q

Normal urine os

A

70-1400 mOsm/L

138
Q

Normal urine sodium concentration

A

130-260 mEq/day

139
Q

normal urine SG

A

1.003- 1.030

140
Q

What is the primary metabolite of protein metabolism in the liver?

A

urea

(amino acids ⇒ ammonia ⇒ urea)

141
Q

Why would somone have a BUN < 8mg/dL

(2 causes)

A
  1. overhydration (diluted out)
  2. Decreased urea production
  • malnutrition - not taking in enough protein (gets broken down to ammonio > urea)
  • severe liver disease - liver can’t metabolize ammonia into urea
142
Q

What BUN level would signify to you that your patient may be dehydrated

A

20-40 range

143
Q

Why would a BUN of 20-40 be something present in a patient with a GIB?

A

because BUN increases after a high digestion of protein or blood

144
Q

creatine production is constant and (directly/inversely) proportional to muscle mass

A

directy propotional

women and elderly have lower creat levels bc they have decreased muscle mass

145
Q

a 100% increase in creatinine indicates a ___% reduction in GFR

A

50%

146
Q

Normal BUN:Cr ratio

A

10:1

147
Q

What does a BUN:Cr ratio of > 20:1 suggest?

A

PRE-renal azotemia

148
Q

If Fe(NA+) [fractional exretion of sodium] is <1% - what does that suggest?

what if it’s > 3%?

A

<1% - prerenal (more sodium is conserved relative to amount of creatinine cleared)

>3% = imparied tubular function )more sodium is excreted relative to the amount of creatinine cleared

149
Q

T/F- failing kidneys waste sodium

A

True

150
Q

What does a large amount of protein in the urine indicate?

A

Glomerular injury

(>750mg/day or +3 by UA)

151
Q

T/F- specific gravity is a better test of tubular function than urine osmolality

A

false

urine os is superior

152
Q

T/F- prerenal azotemia can canuse acute tubular necrosis

A

True

153
Q

T/F- hydroxyethyl startches are assoicated with an increased risk of renal mobidity

A

True

-whatever the fuck that is

154
Q

What is the most common cause of perioperative kidney injury?

A

ischemia-reperfusion injury

155
Q

Your argument if somone is saying they arent making much urine

A
  • well surgical stress increases ADH release and the body will hold onto fluid
  • just because they arent making a huge amount of urine doesn’t indicate that their kidneys are taking a hit; MAP is >65, they are being perfused, its fine lol
156
Q

Cause of prerenal injury

A

decreased perfusion to the kidneys

*restore RBF with IVF, blood, and pressors to halt progression to ATN

157
Q

What can cause ATN? (2)

A

ischemia and nephrotoxic drugs

-supportive treatment

158
Q

What is postrenal injury do to?

A

an obstruction between anywhere between collecting system and urtethra

159
Q

t/f- efforts should be made to convert oliguric to nonoliguric aki with diuretics

A

false- increases renal injury and mortality

160
Q

t/f- renal dose dopamine does not prevent or treat aki

A

true

161
Q

T/F- vasopressin maintains GFR and UOP better than NE or neo

A

true

162
Q

Vasopressin preferentially constricts the (afferent/efferent) arteriole

A

efferent

163
Q

What are the 2 most common causes of CKD?

A
  1. Diabetes
  2. HTN
164
Q

Pathophysiologic considerations for ESRD include (select 3):

  • Secondary hyperparathyroidism
  • Increased PT
  • Megoblastic anemia
  • Obstrictive ventilatory defect
  • Gap metabolic acidosis
  • Increased bleeding time
A
  • Secondary hyperparathyroidism
    • ​From impaired active vitamin D3 production and hyperphosphatemia
  • Increased PT
    • PT, PTT, and platelets are normal
  • Megoblastic anemia
    • erythropoietin production is reduced
    • contribut4es to normocytic normochromic anemia
    • megoblastic anemia is associated with nitrous oxide
  • Obstrictive ventilatory defect
    • Fluid overload creates a restrictive ventilatory defect (not obstructive)
  • Gap metabolic acidosis
    • ​from the accumulation of non-volatile acids
  • Increased bleeding time
    • ​uremia increases bleeding time
165
Q

What is bleeding time a measure of?

A

Platelet function

-it is elevated by uremia and is the most accurate predictor of bleeding risk

166
Q

What is demopressin?

why would it be given?

A

von Willebrand factor 8

(first line treatment to decrease risk of bleeding in the uremic patient)

167
Q

What is the first line treatment in the anemic patient with CKD?

A

Erythopoietin + iron

*NOT PRBC - increases risk of HLA sensitization and future rejection of a transplanted kindey

168
Q

Why are you not suprised if a CKD patient has a pericardial effusion and/or tamponade?

A

bc elevated uremic levels in the blood can lead to pericarditis (inflmattion of the heart sac) - the irritation can lead to fluid accumulation

169
Q

gap acidosis is the result of accumulation of ___________;

non-gap acidosis is hte result of a loss of __________.

A

gap acidosis - accumulation of non-volatile acids

non-gap - results from loss of HCO3 ions

170
Q

Normal GFR

A

>/= 90

171
Q

Drugs to avoid in the patietn on HD (select 2):

  • Vecuronium
  • Meperidine
  • Sux
  • Dex
A

Vec ⇒ 3-OH Vec

Meperidine ⇒ Normeperidine (accumulation > seizures)

Sux is only contraindicated if the K is high

172
Q

Which is better for the renal patient, atracurium or cistatricurium

A

Cisatracurium

(AHHHHtracurium produces more laudanosine - CNS stimulant and also releases histamine - risk of hypotension)

173
Q

Why is fluids and bicarb indicated in rhabdo patients

A

fluids bc myglobin is nephrotic and can cause ATN

sodium bicarb to alkalize the urine

  • Aciditic urine causes myoglobin to precipitate in the proximal tubule causing tubular obstruction and ATN
174
Q

Where is compound A vs free fluride ions produce with sevo?

A

compound A is produced in the breathing circuit (soda lime)

free flouride ions are produced by the liver

175
Q

5 heavy hitters abx on renal fx

A

gentamycin

vancomycin

tobramycin

amikacin

amphotericin B

176
Q
A
177
Q

3 Aminoglycoside antibiotics

A

Gentamycin, tobramycin and amikacin

*give plenty of fluids with these agents

178
Q

match

A

Their in the correct order

179
Q

Why should you limit your fluid with TURP procedures

A

bc the irrigation fluid is abosrbed through the open venous sinuses of the prostate > risk of overload of toxicity from the irrigation solutes

180
Q

How much irrigant can be absorbed into systemic circulation during a TURP?

-recetion time should be limited to what?

A

10-30ml/min

30 mins - 300mls -900mls of fluid

60 minutes - 600 - 1080mls of fluid

limited to 1 hour

181
Q

Which fluid irrigant for TURPs is associated with TURP syndrome ?

what is the classic triad of sxs

A

hypo-osmolar irrigant (distilled water)

*HTN, bradycardia (reflex), and change in MS

182
Q

which irrigant for TURP can lead to transient blindness?

A

Glycine

  • it’s an inhibitory neurotransmitter in the eye
  • no treatement is required (transient)
183
Q

Treatment for TURP syndrome

A

hemodynamic support

  • correct sodium levels (will be diluted down)
  • monitor for seizures and treat with midaz
184
Q

Your main concerns for TURPs (4)

A
  1. TURP syndrome (htn,brady, change ms)
  2. Bladder perforation (abdominal and shoulder pain)
  3. bleeding
  4. hypothermia (need bair hugger)
185
Q

What level is required for a spinal for a TURP

A

T10

186
Q

The height of the irrigating soluation should be no more than ____cm above the OR table

A

60cm

(60/2.54 = 24inches/2feet)

187
Q

Why aren’t NS or LR used for TURP irrigation?

A

bc they are highly ionized, making them good conductors of electricity

-ok for bipolar but not okay for monopolar

188
Q

Which TURP irrigant fluid increases ammonia levels and can lead to decreased LOC?

A
189
Q

which irrigant solution for TURP can lead to hyperglycemia

A

Sorbitol

190
Q

What should you do if your suspect TURP syndrome (pt becomes HTN and bradycardic?)

A
  • support hemodynamics
  • tell surgeon
  • get labs: sodium, hct, creat, glucose, ekg
  • if NA > 120, restrict fluids and give furosemide

if NA < 120, give 3% saline at < 100mls/hr and d/c once NA 120

191
Q

What’s your concern during a TURP if the surgon is saying he’s not getting return of irrigation fluid

A

-early sign of bladder rupture

*monitor hemodynamics, open fluids, H&H

*prepare for emergent suprpubic systostomy or possible ex. lap

192
Q

how do you figure out blood loss with TURPs since it mixes with the irrigation fluid

A

rough estimate = 2-5ml/min of resection time

30 mins = 60-150mls of blood

193
Q

At what serum sodium concentration are seizures likely to occur?

A

<110

194
Q

2 Absolute contraindication to extracorporeal shock wave lithotripsy

A

Pregnancy & bleeding disorders/anticoagulation

*VERYIFY NEGATIVE URINE HCG FOR FEMALES

195
Q
A
196
Q

What is lithotripsy?

A

a procedure that breaks up stones in the kidney, urteter, or bladder

197
Q

What the ESWL shock wave timed with

A

the R-wave to minimize R-on-T phenomonon

198
Q

Nephrolithiasis =

Ureterolithasis =

Cystolithiasis =

A

Nephrolithiasis = kidney stone

Ureterolithasis = ureter stone

Cystolithiasis = bladder stone

199
Q

Relative contraindications to ESWL (5)

A
  1. Pacemaker/ICD
  2. Calcified aneurysm of the aorta or renal artery (can break off?)
  3. UTI (untreated)
  4. obstruction beyond the renal stone (cant elminate fragments)
  5. morbid obesity (further distance from energy source to stone
200
Q

Why is it super important to keep the patient still during ESWL

A

bc any internal organ in the path of the shock wave is at risk for perforation

201
Q

T/F: hematuria is a common side effect of ESWL

A

True

202
Q

How is a percutaneous nephrolithotripsy done?

A

pt is prone- surgeon places urtetheral stents

neph tube is placed to access the stone

  • irrigation considerations
  • PTX is a possible complication
203
Q

concern with perc nephrolithotripsy

A

-irrigation fluids and PTX

204
Q

4 complications assoicated with ESWL

A

arrhythmias

organ perforation

skin bruising

hematuria

205
Q

Which of the following are increased in the serum of the patient with renal osteodystrophy (select 2)

  • phosphate
  • PTH
  • calcitrol
  • calcium
A

Phosphate and PTH

“Two P’s increased in pts with renal osteodystoPhy”

  • Calcitrol - the active form of vitamin D3 is protuced by the kidney; when kidney fails to produce calcitrol, the body absorbs less calcium from the GI tract and serum CA falls
  • Decreased calcium levels signal the anterior pituitary to release PTH in attempt to correct calcium levels via:
    • demineralization of the bone ⇒ increased risk of fxs
    • As GFR declines, phosphate clearance is reduced –> increased serum phosphate concentration
206
Q

What are the MOST potent stimulators of ADH secretion (2):

  • Hypernatremia
  • Hypovolemia
  • Hyponatremia
  • hypovolemia
A
  • hypovolemia
  • hypernatremia
207
Q

BUN/Crt ratio of 30 most likely suggests (select 2):

  • Acute tubular necrosis
  • intersistial nephritis
  • UGIB
  • dehydration
A

-UGIB & Dehydration

  • creatinine is a waste product of muscle metabolism
  • urea is a waste product of protein metabolism
  • ratio distinguishes between pre-renal and intrinsic kindey injury
  • normal = 10:1
  • BUN and creat both freely filtered at glomerulus
  • BUN can undergoreabsorption in the renal tubules & creat does not
  • When kidneys conserve more water, they pull BUN back into the blood
  • Because BUN is returned to the blood but creat is not, the BUN/Creat ratio increases
208
Q

Normal GFR:

-125ml/min

-275ml/min

-450ml/min

-650ml/min

A

125ml/min

209
Q

Renal blood flow to each kidney in ml/min

A

650ml/min

  • kidney gets 20%-25% of cardiac output
    • 1,000-1,250ml/min to BOTH
    • 500-650ml/min to each kidney
210
Q

normal filtration fraction

A

20% of renal blood flow

(125GFR/650 RBF to each kidney)

211
Q

T/F: The fraction of ultrafiltrate excreted as urine is 10%

A

False- 1%

212
Q

Creat clearence

  • Normal =
  • Mild dysfx=
  • Mod dysfx=
  • Severe dysx=
A
  • Normal = 95- 150ml/min
  • Mild dysfx= 50-80ml/min
  • Mod dysfx=10-25ml/min
  • Severe dysx= <10ml/min
213
Q

How to calculate creat clearance for a man

vs woman 8

A

Man: (140-age) x (weight kg) / (Serum creatinine x 72)

Woman: 0.85 x [(140- age) x (weight kg) / (Serium creat x 72)]

214
Q
A
215
Q

What is the BEST method of renal protection following major muscle trauma?

  • mannitol
  • norepi
  • acidyfing the urine
  • N-Acetylcystine
A

Mannitol

  • The best way to prevent AKI is to maintain UOP between 100-150mls/hr
  • Best accomplished with osmotic diuresis with mannitol
216
Q

NSAIDS inhibit _____________ which reduces __________ leading to increased renal vascular resistance and decreased renal blood flow

A

inhibit cyclooxygenase

> reduced renal prostaglandin synthesis

217
Q

T/F: When antagonizing Roc in a patient with ERSD, the dose of neostigmine should be decreased by 25%

A

False - same as non-ERSD pt

218
Q

Presence of U waves on an EKG - what 2 drugs are the MOST likely cause for this finding (select 2):

  • Amiloride
  • Metolazone
  • Bumetanide
  • Spironolactone
A

Metolazone & Bumetanide

  • amiloride and spironolactone = K sparing
  • Bumetanide = bumex = loop - yes
  • Metolazone = zaroxyln = thiazide = yes
219
Q

What kind of diuretic is zaroxolyn?

Generic?

Does it cause hypokalemia?

A

Metolazone

  • Thiazide
  • yes
220
Q

Pt presents for b/l mastectomy and has n/v/polyuria and short QTc, which of the following agents will worsen this patient’s condition?

A. Mannitol

B. Hydrochlorothiazide

C. Furosemide

D. Triamterene

A

B. Hydrochlorothiazide

  • Symptoms suggestive of high calcium levels
  • Also makes sense bc b/l mastectomy = breast cancer
  • cancer = cause of hypercalcemia
  • other EKG changes = prolonged PR, wide QRS, short QTc
  • TX = IV hydration with NSS and furosemide
    • Thiazide diruetics inhibit the NA-Cl exchangeer in the distal tubule which activates the NA-Ca antiporter and increases CA reasoprtion
221
Q

which of the following should be avoided in the diabetic patient?

A. Spironolactone

B. Triamterene

C. HCTZ

D. Ethacrynic acid

A

C. HCTZ

-thazides cause hyperglycemia (mechanism not completely understood- poss decreased insulin realease from pancrease or imparied glucose utilization in body)

222
Q

What class of diuretic is triameterene

A

potassium sparing

223
Q

What class of diuretic is indapamide?

A

Thiazide diuretic

(Distal tubule)

224
Q

3 unique side effects of thiazide diruetics

A
  • Hyperglycemia (caution in diabetics)
  • Hypercalcemia (caution in hypercalcemia)
  • Hyperuricemia (caution in gouty arthritis)
225
Q
A

Kidney (2 decks)

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