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Physiological Toxicology > Exam 2 > Flashcards

Exam 2 Flashcards

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1
Q

Which parts of the nephron are in the cortex? …. The medulla?

A

Cortex - Distal and proximal tubule, glomerulus, bowman’s capsule
Medulla - Descending and ascending limp of loop of Henle, collecting duct

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2
Q

What is the job of the macula densa?

A

“Salt sensor” - senses sodium levels and exerts local and endocrine control over glomerular blood flow in response

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3
Q

What are the 5 roles of the kidneys?

A
  1. Regulating electrolyte levels
  2. Maintaining ECF volume and blood pressure
  3. Regulating blood pH
  4. Excreting metabolic waste products and xenobiotics
  5. Endocrine -renin, calictrol, erythropoietin, prostaglandins
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4
Q

Where does renal blood supply get routed (in order)?

A

First, the glomeruli, then the vasa recta, then the interstitium of the cortex and medulla

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5
Q

Route renal blood supply from entrance - exit.

A

Renal artery - segmental arteries - interlobar arteries - arcuate arteries - afferent arterioles - glomerular capillaries - efferent arterioles - peritubular capillaries and/or vasa recta - interlobular veins - arcuate veins - interlobar veins - segmental veins - renal vein

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6
Q

Vasa recta establishes _________

A

A countercurrent exchange mechanism

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7
Q

What are the three main processes for xenobiotic elimination via the urine?

A
  1. Glomerular filtration
  2. Active secretion into proximal tubule vs. active reabsorption
  3. Passive diffusion into tubules vs. out of tubules
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8
Q

How much cardiac output do the kidneys receive?

A

20-25%

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9
Q

Which segment of the PCT has the highest level of oxygen consumption?

A

S1

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10
Q

Which PCT segment is the longest?

A

S2

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11
Q

This segment has the highest levels of P450s, but the least amount of mitochondria?

A

S3

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12
Q

What kind of toxic damage would S1 tubular cells be prone to?

A
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13
Q

What are the implications of the S3 segment cell make-up?

A
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14
Q

Loop of Henle receives less ______, but higher levels of ______________.

A

blood flow; luminal levels of xenobiotics

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15
Q

Which segment of the nephron would you rather be if you wanted to keep relatively safe from xenobiotics?

A
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16
Q

Eicosanoids are what kind of molecules? What are the three main kinds?

A

Signaling molecules (lipid derived) - prostaglandins (PGs), thromboxanes, leukotrienes

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17
Q

What is the role of eicosanoids?

A

Local paracrine signaling - playing important roles in normal physiology and inflammation

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18
Q

What enzyme is responsible for mediating the formation of prostaglandins and thromboxanes?

A

COX enzymes - COX-1 and COX-2

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19
Q

How do PGs and TXs exert their effects?

A

By binding their receptors

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20
Q

Do PGs and TXs have the same effect or multiple effects?

A

Multiple effects, benefical or harmful

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21
Q

Which COX enzyme is not constitutively expressed and how is it expressed?

A

COX-2 is not consitutively expressed and is instead induced in response to inflammatory mediators

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22
Q

What occurs with PGs and TXs with inflammation?

A
  1. Higher levels of PGs and TXs
  2. There are PGs and TXs in tissues that do not constitutively produce them
  3. Inflammation is perpetuated
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23
Q

What inhibits COX enzymes and therefore PGs and TXs?

A

NSAIDS

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24
Q

What physiologic effects do PGs carry out?

Study These Flashcards
A
  1. protection of gastric mucosa
  2. increasing GFR and normal sodium and water elimination
  3. Balance vascular tone and platelet aggregation
25
Chronic dosing of NSAIDs can lead to what?
Cardiovascular effects
26
NSAID overdose creates a risk for adverse effects on ....
GI tract and kidneys
27
How would GI and renal effects from NSAID activity be lessened?
28
What are RBF and GFR?
Renal blood flow and glomerular filtration rate (finish later)
29
What determines RBF and GFR?
Afferent and arteriolar tone
30
What happens when hydrostatic pressure in the glomerulus increases?
GFR increases
31
Where does the problem with acute NSAID overdose -> AKI begin? What occurs here?
The afferent arteriole, the vessel constricts and decreases GFR and RBF which results in a lack of sufficient blood supply for the nephron, damaging the cells and leading to necrosis if severe enough
32
What results from chronic NSAID overuse in the kidneys?
A decline in kidney function due to a chronic decrease in RBF which leads to hypoxia and further damage to the papillae (necrosis)
33
What are the three functions of PGE2?
To protect the gastric lining by increasing the secretion of mucus, bicarbonate release, and mucosal blood flow
34
What happens to PGE2 functions with NSAID exposure?
These functions diminish, putting the body at risk for gastic ulceration
35
Why would the papillae of the kidneys be affected first with NSAID overdose or chronic use?
The papillae have the least amount of blood flow, so the resultant decrease in renal flow that occurs with NSAID use is detrimental to the papillae
36
What would encourage better blood flow in the kidneys?
Administration of IV fluids - increasing vascular volume and subsequently increasing renal perfusion
37
How would we replenish prostaglandins from acute NSAID overdose?
Misoprostol administration - this is a PGE1 analog and would result in the decrease of gastric HCL release and increase mucus production
38
What is the primary cause of the signs of EG toxicosis?
The metabolites of EG formed in the liver that later move to the kidneys via the bloodstream
39
What is the end product of EG metabolism and how does it damage the kidneys?
Calcium oxalate precipitates (solidifies) in the renal tubules
40
How do EG metabolites cause polyuria?
They increase the osmotic pressure in the tubules causing the cells to begin to lose their ability to properly concentrate the urine
41
How does oliguria occur?
Damaged tubular cells create an increased back pressure from the tubules to the glomeruli, making it difficult to pass filtrate through the tubules, resulting in decreased urine output
42
What are the two possible treatments for EG toxicosis?
Ethanol and Fomezipole*
43
What is the least effective way to remove EG and EG metabolites?
Hemoperfusion - AC does not bind to EG
44
Where is canthardin absorbed and excreted?
Absorbed in the GI tract -> renal excretion
45
What is the primary effect of cantharidin toxicosis and what is the mechanism of effect?
Cantharidin causes fluid filled vesicles by crossing cell membranes, releasing protein enzymes that damage cell desmosomes and allow intracellular fluid to accumulate
46
What is cadmium and what is the #1 exposure route?
A heavy metal - food is the primary exposure route, unless you smoke
47
Describe the kinetics of cadmium
Cadmium is absorbed in the respiratory tract - if inhaled - or the GI tract - if ingested. Cadmium binds to albumin and metallothionein for transport and deposited into he liver and kidneys
48
What is another molecule that binds metals for transport and distribution, similar to metallothionein?
Glutathione
49
Cadmium nephrotoxicity is due to what two factors?
Tubular damage and glomerular damage
50
What should you consider when dealing with proteinuria in a patient?
The potential of tubular and glomerular damage
51
What are the three neurons (minimum) involved in the efferent autonomic pathways?
Preautonomic, preganglionic autonomic, and postganglionic autonomic
52
What neuroglia are present in the CNS? (4)
Astrocytes - (several functions) Oligodendrocytes - wraps multiple axons in myelin Microglia - macrophage like immune cells Ependymal cells - line spinal cord and ventricles to form CSF
53
What neuroglia are present in the PNS? (2)
Schwann cells and satellite cells
54
What are the functions of astrocytes?
1- form BBB by encasing endothelial cells 2 - regulate vascular tone 3 - store glucose and provide to neurons as lactate 4 - buffer K+ and pH in interstitial fluid 5 - clear glutamate and GABA NT from synapses 6 - facilitate water and gas transport antioxidant role 7 -guide axon migration
55
fdwTetradoxin (TTX) blocks what kind of channels?
Sodium channels
56
What is the mechanism of action for TTX?
Prevents the depolarization of neurons
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Physiological Toxicology (3 decks)

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