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Renal > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

List the different types of diuretic

A

Loop
Thiazide
Osmotic
Carbonic anhydrase inhibitors

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2
Q

How to diuretics work (generally)

A

They cause the excretion of electrolytes (particularly Na and Cl)
This triggers the excretion of water by osmosis

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3
Q

List diseases that produce oedema

A

Nephrotic syndrome
Congestive heart failure
Hepatic cirrhosis with ascites

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4
Q

What causes oedema

A

An imbalance between the rate of formation and absorption of interstitial fluid

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5
Q

How does nephrotic syndrome lead to oedema

A

In this condition, large proteins are allowed into the filtrate from blood
This causes fluid to also move out of blood - enters interstitium
The lower blood volume and renal perfusion activates the RAAS system
This leads to further water retention

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6
Q

How does congestive heart failure lead to oedema

A

In HF there is reduced cardiac output and therefore reduced renal perfusion
This activates RAAS which leads to water and Na retention

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7
Q

How does cirrhosis lead to oedema (ascites)

A

Fibrosis in the liver produces a resistance to blood flow, increased liver pressure and decreased albumin
This causes fluid to be lost to the peritoneal cavity = ascites
RAAS is again activated

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8
Q

How do diuretics mobilize the oedema fluid

A

Diuretic causes excretion of salt and water – blood in kidney becomes more concentrated which draws water from the interstitial fluid (reduced oedema)

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9
Q

Where in the nephron do carbonic anhydrase inhibitors work

A

Proximal convoluted tubule and the early distal convoluted tubule
Work on the Na/H exchange
Weak diuretic

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10
Q

Where in the nephron do loop diuretics work

A

Loop diuretics block the triple transporter in the loop of Henle – very strong action

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11
Q

Where in the nephron do thiazide diuretics work

A

Early distal convoluted tubule

Act on the Na/Cl co-transporter

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12
Q

Where in the nephron do potassium sparing diuretics work

A

Collecting tubule and duct

Block Na/K exchange

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13
Q

Diuretics usually work at the basolateral membrane of tubular cells - true or false

A

False

They mostly act on the apical membrane as this is where the transporters are

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14
Q

How do diuretics enter the filtrate

A

If not bound to large proteins they can enter by glomerular filtration
Organic anion transporters move acidic drugs into the filtrate
Organic cation transporters move basic drugs into the filtrate

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15
Q

Which diuretics are acidic

A

Thiazide and loop agents

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16
Q

Which diuretics are basic

A

triamterene and amiloride

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17
Q

How does the organic anion transporter (OAT) work

A

Na+/K+ works at basolateral membrane
Allows Na to move down the conc gradient – a-KG is co-transported by this
This movement drives OA to enter the cell in exchange for the a-KG leaving the cell again
OA is actively pumped out of apical membrane by a transporter using ATP (primary active transport)
Some OA can be reabsorbed on another antiport system – exchange of OA and a-KG

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18
Q

How does furosemide increase your risk of gout

A

It reacts with urate in the tubular cells

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19
Q

How does the organic cation transporter work

A

OC enters the cell against a chemical gradient – driven by electrical gradient
OC is pumped out by primary active transport
Also in the apical membrane the MATE transporter which moves OC out in exchange for H+ ions

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20
Q

How are calcium and magnesium absorbed in the kidney

A

The negative charge created by the triple transporter drives their movement
They are moved through specific proteins into the interstitium - paracellular route

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21
Q

How does the triple transporter work

A

2 Cl- move downhill by the triple transporter
Cl leaves the basolateral membrane via a chloride channel
K+ must move uphill – energy comes from Na+ movement
K+ re-enters the tubule and also moves out of the BL membrane via a channel
Movement of 1 Na and K and 2 Cl

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22
Q

How does the triple transporter end up giving the cell negative potential

A

positive move in and so do 2 negatives. However, the K+ is recycled back into tubule so cell has negative potential

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23
Q

How do loop diuretics work

A

They block the triple transported in the ascending loop of Henle
This alters the electrolyte balance (less reabsorption) and reduces water reabsorption

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24
Q

Loop diuretics have a venodilator effect - true or false

A

True

This is useful in treating pulmonary oedema

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25
Q

Loop diuretics have rapid action - true or false

A

True
Especially with IV administration
Used in emergency treatment of acute pulmonary oedema

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26
Q

What are the clinical indications for loop diuretics

A 
Acute pulmonary oedema 
Chronic heart failure 
Chronic kidney failure 
Hepatic cirrhosis with ascites 
Nephrotic syndrome 
Hypertension 
Increase urine volume in acute kidney failure 
Reduce acute hypercalcaemia
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27
Q

which loop diuretic is best for those with heart failure

A

Bumetanide

Furosemide absorption can be unpredictable in CHF

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28
Q

How are loop diuretics processed by the body

A

Absorbed in the GI tract
Strongly bind to plasma proteins
Enter nephron by the OAT mechanism

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29
Q

When are loop diuretics contraindicated

A

Severe hypovolaemia or dehydration

Must take caution with severe hypokalaemia or hyponatraemia, hepatic encephalopathy and gout

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30
Q

What are the adverse affects of loop diuretics

A 
Hypokalaemia 
Metabolic alkalosis - more H+ is secreted 
Hypocalcaemia and hypomagnesaemia 
Hypovolaemia and hypotension - elderly 
Hyperuricaemia - may precipitate gout 
Dose related loss of hearing
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31
Q

How do thiazide diuretics work

A

Inhibit the Na/Cl carrier
Prevents dilution of filtrate in the distal tubule
Increases the load of Na in the collecting tubule - causes K loss
Causes more Na excretion = modest diuresis

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32
Q

Thiazide diuretics have a vasoconstrictor effect - true or false

A

False

It is a vasodilator effect which helps with hypertension treatment

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33
Q

How are thiazide diuretics absorbed

A

Well absorbed in GI tract

Enter nephron by OAT mechanism

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34
Q

What are the clinical indications for thiazide diuretics

A 
Mild heart failure 
Hypertension 
Severe resistant oedema - with a loop 
Renal stone disease - reduces amount of Ca in filtrate 
Nephrogenic diabetes insipidus?
35
Q

List examples of thiazide diuretics

A

Bendroflumethiazide

Indapamide, metolazone - thiazide like

36
Q

When are thiazide diuretics contraindicated

A

Hypokalaemia

Must be cautious in hyponatraemia and gout

37
Q

What are the adverse effects of thiazide diuretics

A 
Hypokalaemia 
Metabolic alkalosis 
Hypovolaemia and Hypotension 
Hyperuricemia - may precipitate gout 
Erectile dysfunction 
Impaired glucose tolerance in diabetics
38
Q

How can thiazide diuretics be used in osteoporosis

A

They help reabsorb calcium

39
Q

How does aldosterone act in the kidney

A

It acts on cytoplasmic receptors to active the ENaC channel
This allows more Na reabsorption
Aldosterone also increases abundance of Na/K ATPase so you can also pump the excess Na out of the cell as well

40
Q

How do the potassium sparing diuretics work

A

Amiloride and Triamterene - block apical sodium channel and decrease its reabsorption
Spironolactone and eplerenone - compete with aldosterone to prevent it activating ENaC

41
Q

How do loop and thiazide diuretics cause K+ loss

A

The increase the load of Na in the filtrate
Some is reabsorbed which makes the lumen more negative
These both increase driving force for K+ secretion into filtrate and it is lost in the urine

42
Q

How are spironolactone and eplerenone absorbed by the body

A

Well absorbed from GI tract

Spironolactone is rapidly metabolised to canrenone which is the active part

43
Q

How are amiloride and triamterene absorbed in the body

A

T is well absorbed in the GI tract, A is not

Enter nephron via OCT in proximal tubule

44
Q

When are potassium sparing diuretics contraindicated

A

Severe renal impairment
Hyperkalaemia
Addison’s disease

45
Q

What are the clinical indications for potassium sparing diuretics

A

Used alongside other diuretics to counteract potassium loss

Heart failure
Hyperaldosteronism - Conns
Resistant hypertension
secondary hyperaldosteronism (due to hepatic cirrhosis with ascites)

46
Q

How do osmotic diuretics work

A

They enter the nephron by glomerular filtration
Increase the osmolarity of the filtrate which opposes the absorption of water
They also decrease sodium reabsorption in the proximal tubule - higher fluid volume so Na conc decreased

47
Q

Where is the major site of action of osmotic diuretics

A

Proximal tubule

As this is where most isosmotic reabsorption of water occurs

48
Q

When are osmotic diuretics used

A

In prevention of acute hypovolaemic renal failure - maintains urine flow
In urgent treatment of raised intracranial and intraocular pressure

49
Q

How do osmotic reduce intracranial and intraocular pressure

A

Solute itself doesn’t get into eye or brain (due to BBB) but increases plasma osmolarity
This creates a osmotic gradient that draws fluid into the blood – reducing pressure

50
Q

what are the adverse effects of osmotic diuretics

A

Transient expansion of blood volume

Hyponatraemia

51
Q

When else might osmotic diuresis occur (without use of diuretics)

A

In hyperglycaemia - the excess glucose in the urine means the filtrate retains fluid
As a consequence of iodine radiocontrast dyes - dye is excreted and takes some water with it

52
Q

Give an example of an osmotic diuretic

A

Mannitol

53
Q

Give an example of a carbonic anhydrase inhibiter

A

Acetazolamide

54
Q

What are carbonic anhydrase inhibitors used for

A

Not used as diuretics anymore
Reducing intraocular pressure - glaucoma
Prophylaxis of altitude sickness
Some forms of infant epilepsy

55
Q

How do carbonic anhydrase inhibitors work (in kidney)

A

Inhibit carbonic anhydrase
This increases excretion of HCO3 with Na, K and H20
Gives an alkaline diuresis

56
Q

How is alkalising the urine useful

A

It can relive dysuria
Prevents crystallisation of weak acids - decreases formation of uric acid stones
Enhances secretions of weak acids

57
Q

How does vasopression (ADH) work

A

Released from posterior pituitary
Binds to G protein coupled receptor = increased cAMP
This increases insertion of aquaporin 2 channels into the apical membrane
More water is reabsorbed

58
Q

What causes neurogenic diabetes insipidus

A

Caused by lack of vasopressin secretion from the posterior pituitary

59
Q

How do you treat neurogenic diabetes insipidus

A

Desmopressin
Synthetic analogue of vasopressin but selective for V2 receptor
Doesn’t cause the vasoconstriction

60
Q

What substances can affect vasopressin secretion

A

Ethanol inhibits secretion

Nicotine enhances it

61
Q

What causes nephrogenic diabetes insipidus

A

Mutations in the V2 gene - usually recessive and X linked
This prevents the nephron from responding to vasopressin
No current treatment

62
Q

How do aquaretics work

A

Act as competitive antagonists of vasopressin receptors

This causes excretion of water without accompanying Na

63
Q

Give examples of aquaretics

A

Tolvaptan

Conivaptan

64
Q

How is tolvaptan used

A

Syndrome of inappropriate ADH secretion

Role in HF being investigated

65
Q

Where is SGLT2 expressed

A

In the proximal tubule of the kidney

66
Q

How do SGLT2 inhibitors work

A

Block SGLT2 to prevent reabsorption of glucose
Leads to glycosuria - glucose excreted
This decreases HbA1c and leads to weight loss
Used in diabetes treatment

67
Q

Name some SGLT2 inhibitors

A

Dapagliflozin

Canagliflozin

68
Q

SGLT2 inhibitors cause a diuresis - true or false

A

True

A mild one

69
Q

What are the functions of prostaglandins that are made in the kidney

A

Vasodilators

They are produced in response to ischaemia, mechanical trauma, angiotensin II, ADH and bradykinin

70
Q

How do prostaglandins affect GFR

A

Only affect GFR if there is widespread vasoconstriction or decreased blood flow
They cause vasodilation of the afferent arteriole and trigger renin release

71
Q

Why might NSAIDs precipitate renal failure

A

They inhibit COX which decreases prostaglandins

Can lead to issues if the kidneys need to prostaglandin mediated vasodilation

72
Q

What is an adverse drug reaction

A

Any undesirable reaction (whether expected or not) that leads to detriment in the wellbeing of the patient in the absence of another explanation

73
Q

Give examples of drugs with a low therapeutic index

A

gentamicin, lithium, digoxin, warfarin, vancomycin, theophylline

74
Q

Adverse drug reactions are common in which groups

A

The elderly and frail
Those with multiple morbidities - renal/hepatic impairment
Polypharmacy
Drugs with low therapeutic index

75
Q

What is a Type A adverse drug reaction

A

Due to augmented pharmacological effect

Dose dependant and predictable

76
Q

Give examples of Type A adverse drug reactions

A

Diuretics can cause pre-renal failure and dehydration if too high a dose is given
ACEi shouldn’t be taken if you have D&V
Drug-drug interaction
Drug-food interaction
Drug disease interaction

77
Q

What is a Type B adverse drug reaction

A

Includes bizarre, unpredicted effects of a drug
Not dose dependent
These are the dangerous ones - can be fatal

78
Q

Give examples of Type B adverse drug reactions

A

Drug rashes
Bone marrow aplasia
Hepatic necrosis

79
Q

What is a Type C adverse drug reaction

A

Chronic effects of the drug
Occurs with prolonged therapy
Need to monitor these drugs and tell patients about them

80
Q

Give examples of Type C adverse drug reactions

A

Steroids in Cushing’s - osteoporosis

NSAIDs can lead to hypertension

81
Q

What are Type D adverse drug reactions

A

Delayed effects of a drug
May occur years after stopping treatment
Often cardiogenic or teratrogenic

82
Q

Give examples of Type D adverse drug reaction

A

Secondary malignancy post-chemo

83
Q

What are Type E adverse drug reactions

A

End of treatment effects

Occurs with abrupt withdrawal of a drug as you can get rebound effects

84
Q

What is a Type F adverse drug reaction

A

Failure of therapy

Renal (18 decks)

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