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Renal Module > Lecture 10 - Effects Of Drugs And Chemcials On The Nephron Part 2 > Flashcards

Lecture 10 - Effects Of Drugs And Chemcials On The Nephron Part 2 Flashcards

1
Q

How else apart from toxins can inflammation occur?

A

As a result of chronic conditions like diabetes

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2
Q

What does inflammation of the kidneys tubules do?

A

Leads to damage to the glomerular filtration barrier. Either due to edema or by infiltration of the inflammatory cells

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3
Q

What is edema?

A

It is swelling due to too much fluid

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4
Q

What happens when the filtration barrier loses its integrity due to inflammation?

A

Start to see large molecules like proteins appearing in the tubular fluid and into the urine

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5
Q

What happens to long term damage of the glomerular due to inflammation?

A

Get thickening of the Barrier as a result of fibrotic tissue (kidney fibrosis) which reduces the GFR rate

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6
Q

What could kidney fibrosis also cause?

A

Could become too thick and block the glomerular all together - meaning there is less space for the plasma to flow through capillaries - resulting in glomerulus death

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7
Q

What is an example for a toxin that gets taken by the podocytes?

A

Bucillamine - cells that wrap around the basal laminar - kill podocytes

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8
Q

What is the collecting duct surrounded by?

A

Tight junctions - water can not move in and out normally it has additional processes that help

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9
Q

What can amphotericin B do in the loop of henle?

A

It can form smaller pores in the apical membrane of the loop of henle.

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10
Q

What happens to amphotericin B as filtrate volume drops?

A

It increases rapidly

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11
Q

What happens when you start to see amphotericin B pores in the membrane? - Amphotericin treatment

A

causes leakages of K+ and Mhg2+ in the PCT, loss of the ability to excrete protons in the collecting cut

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12
Q

What is lithium usually given to people for?

A

Treatment for bipolar disorder. It interferes with the vasosupressin system

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13
Q

What does ADH (vasosupressin do)?

A

Inserts water pores in the collecting duct cells membrane to enable reabsorption of solute free water from the collecting duct

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14
Q

Where is ADH released from?

A

Pituitary

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15
Q

What happens when ADH binds to the collecting duct cells?

A

It triggers a second mechanism system which triggers the release of water pores from storage vesicles, aquaporin 2 can then exocytose the vesicle (now have a gate way for water to move)

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16
Q

What does lithium do that is bad for the collecting duct?

A

When it enters the collecting duct cell it directly interferes with the second messenger signal.

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17
Q

What are the 3 fates of tubular handling?

A

Filtered,
filtered then reabsorbed,
filtered and secreted

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18
Q

What is the filtered fate?

A

It is left untouched by the nephron - amount excreted = amount filtered e.g. inulin creatinine

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19
Q

What is the filtered and reabsorbed fate?

A

Amount excreted less then amount filtered e.g. glucose amino acids Na+

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20
Q

What is the filtered and secreted fate?

A

Amount excreted is more than amount filtered e.g. PAH drug molecular and metabolic end products

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21
Q

What converts chemicals from small to high MW?

A

Small lipid chemicals

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22
Q

How this process done? - small lipid molecules converting chemicals from small to high MW

A

2 step process:
1 - cytochromosomes p450, ADH and esterases introduce a functional group into the chemical
2 - transferases attach covalently a large water soluble molecule eg sulphate - creating conjugation

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23
Q

What is the down side of the process? - small lipid molecules converting small to high MW?

A

The activated chemical can turn a non toxic chemical into a toxic one. Introducing a functional group can make the compound more reactive and bind to proteins. Alterations the function

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24
Q

What is an example for heavy metal?

A

Mercury

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25
Q

What organ is the principle site of action for toxicity of mercury and other heavy metals?

A

The kidneys

26
Q

What happens once mercury is inside you?

A

Easily oxidised to the inorganic form which can be absorbed through various routes and is very damaging

27
Q

What happens if mercury is methylated?

A

If it becomes methyl mercury it is very toxic and can pass through cell membranes more easily

28
Q

What is glutathione?

A

Is one of the water soluble high molecular compounds that is used for metabolism but also as an antioxidant (designed to protect against reactive oxygen species)

29
Q

What type of peptide is glutathione?

A

It is tripeptide - reacting with anti oxygen species or electrical chemicals - heavy metals as well

30
Q

What does mercury target once in the body?

A

It takes the par recta which contains the metabolic activity

31
Q

How does mercury in the target the pars recta?

A

It binds to glutathione by the sub hydrol groups in the liver, it is then taken up into the PCT from reabsorption as it looks like a small protein

32
Q

What occurs when mercury is in the pCT?

A

Acute toxicity - cellular necrosis in the pars recta

33
Q

What is cadmium?

A

It is used in the electronic industry - present as an environmental contamination

34
Q

What is cadmium excreted as?

A

As metallothionein complex

35
Q

Where is cadmium synthesised?

A

In the liver and this is where it makes the metallomethionein complex

36
Q

Where does the complex go?

A

It gets taken up by the kidneys and cadmium is broken down from the complex

37
Q

What happens when cadmium is free from the complex?

A

It can cause damage leading to toxicity

38
Q

What are many haloalkenes?

A

They are nephrotoxins producing proximal renal tubular damage

39
Q

What is an example of haloalkenes?

A

1,1 dichloroethene

40
Q

What are haloalkenes associated with?

A

The bio activation via the cysteine conjugate Beta lyase pathway

41
Q

What is hexachlorobutadiene?

A

It is an electrophilic Chemical so glutathione binds to it — synthesis in the liver ( a water soluble chemical ) pumped into the bile

42
Q

Where does the bile end up?

A

In the GI tract as bile is an emulsifier it is released in the GI tract upstream of the absorption site

43
Q

What happens once the bile is in the GI tract?

A

It ends up in the kidney in the PCT cells - an enzyme called beta lyase converts it into DNA reactive metabolite which causes damage to the PCT cells

44
Q

What is aristolochic acid (AA) characterised by?

A

Interstitial nephritis - associated with upper urinary tract cancers at later stages of

45
Q

What is AA believed to be?

A

A causative agent and is secreted by PCT cells

46
Q

What is the mechanism for AA?

A

Caused by local metabolism in the kidney and in the liver - leading to formation of a number of active metabolites

47
Q

What is a key active metabolite?

A

Artisolactam I or II

48
Q

What is vasodilation mediated by in the control of GFR?

A

Mediated by prostaglandin release

49
Q

What is vasoconstriction mediated by in the control of GFR rate?

A

Renin-angiotensin system

50
Q

What do calcineurin inhibitors do?

A

Increase renin synthesis and decrease PGE2 and COX2

51
Q

What do NSAIDS do?

A

Decrease PEG2 release

52
Q

What do ACE inhibitors do?

A

Decrease all synthesis

53
Q

What is related to ischaemic cells death?

A

NSAIDS

54
Q

What gives a measure of renal function?

A

Creatinine clearance

55
Q

Where is the basal Lamar?

A

The mesh of the filtration barrier which sites between the endothelial cells and the podocytes

56
Q

What is the basal Lamar made of?

A

It is made of collagen

57
Q

What does it mean if you detect collagen in the urine?

A

The glomerular is damaged

58
Q

Where is the alpha sub family found?

A

In the pars recta

59
Q

Where is the gamma sub family found?

A

In the distal tubule

60
Q

What is the kidney injury molecule -1 (KMI-1)?

A

A transmembrane glycoprotein

61
Q

What is a novel biomarkers for the glomerulus?

A

The basal Lamar

Renal Module (10 decks)

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