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Physiological Toxicology > Exam 2 > Flashcards

Exam 2 Flashcards

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?

A
  1. protection of gastric mucosa
  2. increasing GFR and normal sodium and water elimination
  3. Balance vascular tone and platelet aggregation
25
Q

Chronic dosing of NSAIDs can lead to what?

A

Cardiovascular effects

26
Q

NSAID overdose creates a risk for adverse effects on ….

A

GI tract and kidneys

27
Q

How would GI and renal effects from NSAID activity be lessened?

A
28
Q

What are RBF and GFR?

A

Renal blood flow and glomerular filtration rate (finish later)

29
Q

What determines RBF and GFR?

A

Afferent and arteriolar tone

30
Q

What happens when hydrostatic pressure in the glomerulus increases?

A

GFR increases

31
Q

Where does the problem with acute NSAID overdose -> AKI begin? What occurs here?

A

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
Q

What results from chronic NSAID overuse in the kidneys?

A

A decline in kidney function due to a chronic decrease in RBF which leads to hypoxia and further damage to the papillae (necrosis)

33
Q

What are the three functions of PGE2?

A

To protect the gastric lining by increasing the secretion of mucus, bicarbonate release, and mucosal blood flow

34
Q

What happens to PGE2 functions with NSAID exposure?

A

These functions diminish, putting the body at risk for gastic ulceration

35
Q

Why would the papillae of the kidneys be affected first with NSAID overdose or chronic use?

A

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
Q

What would encourage better blood flow in the kidneys?

A

Administration of IV fluids - increasing vascular volume and subsequently increasing renal perfusion

37
Q

How would we replenish prostaglandins from acute NSAID overdose?

A

Misoprostol administration - this is a PGE1 analog and would result in the decrease of gastric HCL release and increase mucus production

38
Q

What is the primary cause of the signs of EG toxicosis?

A

The metabolites of EG formed in the liver that later move to the kidneys via the bloodstream

39
Q

What is the end product of EG metabolism and how does it damage the kidneys?

A

Calcium oxalate precipitates (solidifies) in the renal tubules

40
Q

How do EG metabolites cause polyuria?

A

They increase the osmotic pressure in the tubules causing the cells to begin to lose their ability to properly concentrate the urine

41
Q

How does oliguria occur?

A

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
Q

What are the two possible treatments for EG toxicosis?

A

Ethanol and Fomezipole*

43
Q

What is the least effective way to remove EG and EG metabolites?

A

Hemoperfusion - AC does not bind to EG

44
Q

Where is canthardin absorbed and excreted?

A

Absorbed in the GI tract -> renal excretion

45
Q

What is the primary effect of cantharidin toxicosis and what is the mechanism of effect?

A

Cantharidin causes fluid filled vesicles by crossing cell membranes, releasing protein enzymes that damage cell desmosomes and allow intracellular fluid to accumulate

46
Q

What is cadmium and what is the #1 exposure route?

A

A heavy metal - food is the primary exposure route, unless you smoke

47
Q

Describe the kinetics of cadmium

A

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
Q

What is another molecule that binds metals for transport and distribution, similar to metallothionein?

A

Glutathione

49
Q

Cadmium nephrotoxicity is due to what two factors?

A

Tubular damage and glomerular damage

50
Q

What should you consider when dealing with proteinuria in a patient?

A

The potential of tubular and glomerular damage

51
Q

What are the three neurons (minimum) involved in the efferent autonomic pathways?

A

Preautonomic, preganglionic autonomic, and postganglionic autonomic

52
Q

What neuroglia are present in the CNS? (4)

A

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
Q

What neuroglia are present in the PNS? (2)

A

Schwann cells and satellite cells

54
Q

What are the functions of astrocytes?

A

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
Q

fdwTetradoxin (TTX) blocks what kind of channels?

A

Sodium channels

56
Q

What is the mechanism of action for TTX?

A

Prevents the depolarization of neurons

57
Q
A
58
Q
A
59
Q
A

Physiological Toxicology (3 decks)

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