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PBL SEM 4 > CASE 7 > Flashcards

CASE 7 Flashcards

1
Q

at what 2 main sites do diuretics work?

A

loop of henle and DCT

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2
Q

what part of the nephron is impermeable to water?

A

ascending limb of LoH

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3
Q

name a loop diuretic

A

furosemide

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4
Q

how do loop diuretics work?

A
  • block the NaKCl transporter in the thick ascending limb of the loop of Henle and inhibit chloride reabsorption
  • this thus prevents Na+ reabsorption — so less water is reabsorbed via osmosis
  • results in increased loss of salt and water
  • high loss of fluid
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5
Q

when are loop diuretics used?

A

pulmonary oedema, HF, renal insufficiency, or resistant hypertension

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6
Q

unwanted effects of loop diuretics

A

hypotension, hypovolaemia, hypokalaemia, metabolic alkalosis

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7
Q

name a thiazide diuretic

A

indapamide

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8
Q

how do thiazide diuretics work?

A
  • inhibit the NaCl transporter in the distal convoluted tubule (DCT), preventing the removal of Na+ and Cl- from the tubular fluid, along with the water that would have travelled with the ions to maintain osmolarity
  • has a vasodilator action — BP falls initially due to renal action, reduced blood volume stimulates renin secretion which limits the effect on BP, vasodilation maintains the antihypertensive effect
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9
Q

when are thiazide diuretics given?

A

given as an add one when other drugs are not efficient on their own — potentiates the effect of other drugs

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10
Q

unwanted effects of thiazide diuretics

A

more frequent urination, hypokalaemia, erectile dysfunction

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11
Q

what is spironolactone an example of?

A

potassium sparing diuretic

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12
Q

how do K sparing diuretics work?

A

blocks the mineralocorticoid receptor, preventing the action of aldosterone, thereby causing increased excretion of Na+ and water, while preventing K+ ions in the circulation

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13
Q

what part of the nephron does aldosterone work at?

A

DCT and collecting duct

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14
Q

when are K sparing diuretics used?

A

in treatment of HF, hyperaldosteronism, resistant HT (especially w low renin)

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15
Q

what do K sparing diuretics prevent when given with a loop pr thiazide diuretic?

A

hypokalaemia

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16
Q

unwanted effects of K sparing diuretics

A

potentially fatal hyperkalaemia, GI upset, gynaecomastia, menstrual disorders and testicular atrophy due to actions at other steroid receptors

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17
Q

K sparing diuretics prevent action of ______ on kidney, (stimulate aldosterone release), resulting in vasodilation and reduced plasma volume

A

angiotensin 2

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18
Q

what is mannitol?

A

osmotic diuretic

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19
Q

what do osmotic diuretics do?

A

• work in the late PCT and the descending loop of Henle
• promotes water excretion without increasing the loss of electrolytes

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20
Q

unwanted effects of osmotic diuretics

A

acute hypovolaemia

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21
Q

All diuretics can disturb the plasma electrolyte balance, with ___ a particular concern. Diuretics can also cause loss of ______ function as a consequence of hypovolaemia. For these reasons, serum ________ and _________ levels are monitored during treatment.

A

All diuretics can disturb the plasma electrolyte balance, with K+ a particular concern. Diuretics can also cause loss of renal function as a consequence of hypovolaemia. For these reasons, serum electrolyte and creatinine levels are monitored during treatment.

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22
Q

what type of diuretics are more likely to cause hypokalaemia?

A

loop

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23
Q

why are thiazide and thiazide-like diuretics safer than loop?

A

dont cause such profound salt and water loss

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24
Q

what diuretics work at the NCC in the distal tubule?

A

thiazide eg. indapamide

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25
Q

what diuretics work at the NKCC co-transporter in the loop of henle?

A

loop. eg furosemide

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26
Q

what does urine analysis look for?

A

proteinuria, albuminuria, haemoglobinuria, haematuria, WBC, glucose

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27
Q

what is GFR?

A

= glomerular filtration rate

  • rate in millilitres per minute at which substances in plasma are filtered throguh the glomerulus ie. the clearance of a substance from the blood
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28
Q

what is normal GFR for an adult male?

A

90 to 120 ml per min

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29
Q

according to the Kidney Disease Improving Global Outcomes (KDIGO), what are the stages of chronic kidney disease in terms of GFR?

A
  • Stage 1 GFR greater than 90 ml/min/1.73 m²
  • Stage 2 GFR-between 60 to 89 ml/min/1.73 m²
  • Stage 3a GFR 45 to 59 ml/min/1.73 m²
  • Stage 3b GFR 30 to 44 ml/min/1.73 m²
  • Stage 4 GFR of 15 to 29 ml/min/1.73 m²
  • Stage 5-GFR less than 15 ml/min/1.73 m² (end-stage renal disease)
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30
Q

what are normal albumin levels in urine?

A

very little — less than 30mg/g — anything above this may mean you have kidney disease, even if your GFR number is above 60

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31
Q

what levels of albumin:creatinine ratio are normal, show microalbuminuria and albuminuria?

A

<30 is normal, 30-300 is microalbuminuria, above 300 is albuminuria

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32
Q

what are the divisions of the nephron and what happens at each?

A

• glomerulus — filtration (provides a size and charge barrier - large or negatively charged molecules are repelled)
• proximal convoluted tubule — selective reabsorption of water, ions, and all organ nutrients
• descending limb of loop of Henle — selective reabsorption of water
• ascending limb of loop of Henle — selective reabsorption of Na+ and Cl-
• distal convoluted tubule — secretion of ions, acids, drugs, toxins / variable reabsorption of water, Na+ and Ca++
• collecting tubule — variable reabsorption of water and reabsorption/secretion of Na+, K+, H+ and HCO3-

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33
Q

what is the first stage of RAAS?

A

release of renin

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34
Q

where is renin released from?

A

granular cells of the renal juxtaglomerular apparatus (JGA)

35
Q

what 3 things stimulate renin release?

A
  1. reduced Na+ delivery to the DCT detected by macula densa cells
  2. reduced perfusion pressure in the kidneys detected by baroreceptors in the afferent arteriole
  3. sympathetic stimulation of the JGA via B1 adrenoreceptors
36
Q

what is the release of renin inhibited by?

A

atrial natriuretic peptide (ANP) = released by stretched atria in response to increases in BP

37
Q

angiotensinogen is a precursor produced by the ______ and cleaved by renin to form __________

A
  • liver
  • angiotensin I
38
Q

how is angiotensin I converted to angiotensin II?

A

converted to angiotensin II by angiotensin converting enzyme (ACE

39
Q

where does most of the angiotensin I to II converison occur and why?

A

occurs mainly in the lungs where ACE is produced by vascular endothelial cells, although ACE is generated in smaller quantities within the renal epithelium

40
Q

what does angiotensin II bind to?

A

it binds to 1 of 2 G-protein coupled receptors; the AT1 and AT2 receptors (most actions occur via the AT1 receptor)

41
Q

affect of angiotensin II on: arterioles

A

vasoconstriction

42
Q

affect of angiotensin II on: kidney

A

stimulates Na+ reabsorption

43
Q

affect of angiotensin II on: sympathetic nervous system

A

increased release of NA

44
Q

affect of angiotensin II on: adrenal cortex

A

stimulates release of aldosterone

45
Q

affect of angiotensin II on: hypothalamus

A

increases thirst sensation and stimulates anti-diuretic hormone (ADH) release

46
Q

what are the cardiovascular effects of angiotensin II?

A

• acts on AT1 receptors found in the endothelium of arteries throughout the circulation to cause vasoconstriction
• this signalling occurs via a Gq protein, to activate phospholipase C and subsequently increase intracellular calcium
• the net effect of this is an increase in total peripheral resistance and therefore BP

47
Q

what are the neural effects of angiotensin II?

A

• acts at the hypothalamus to stimulate the sensation of thirst, resulting in an increase in fluid composition
• this helps to raise the circulating volume and in turn BP
• also increases the secretion of ADH from the posterior pituitary gland — resulting in the production of more concentrated urine to reduce the loss of fluid from urination
• stimulates the SNS to increase the release of NA resulting in an increase in cardiac output, vasoconstriction of arterioles, release of renin

48
Q

what effect does angiotensin II have on the renal artery and afferent arteriole and how?

A
  • vasoconstriction
  • voltage-gated Ca++ channels open and allow an influx of Ca++
49
Q

what effect does angiotensin II have on the efferent arteriole and how?

A
  • vasoconstriction — greater than the afferent arteriole
  • activation of AT1 receptor
50
Q

what effect does angiotensin II have on mesangial cells and how?

A
  • contraction, leading to a decreased filtration area
  • activation of Gq receptors and opening of voltage-gated Ca++ channels
51
Q

what effect does angiotensin II have on the PCT and how?

A
  • increased Na+ reabsorption
  • increased Na+/H+ antiporter activity and adjustment of the starling forces in the peritubular capillaries to increase paracellular reabsorption
52
Q

angiotensin II is also an important factor in _______________, which helps to maintain a stable glomerular filtration rate. the local release of ___________, which results in a preferential vasodilation to the afferent arteriole in the glomerulus, is also vital to this process.

A
  • tubuloglomerular feedback
  • prostaglandins
53
Q

where is aldosterone released from?

A

zona glomerulosa of the adrenal cortex

54
Q

what does aldosterone do?

A

acts on the principal cells of the collecting ducts by increasing the expression of apical epithelial Na+ channels (ENaC) to reabsorb urinary sodium. the activity of the basolateral NaK ATPase is increased

• this causes the additional Na+ reabsorbed through ENaC to be pumped int the blood by NaK pump. in exchange, K+ is moved from the blood into the principal cell of the nephron, this K+ then exits the cell into the renal tubule to be excreted in urine
• as a result, aldosterone causes reduced levels of K+ in blood

55
Q

what is the overall affect of the RAAS system?

A

causes water and salt retention. effective circulating volume increases. perfusion of the JGA increases

56
Q

what is ramipril?

A

ACE inhibitor

57
Q

what do ACE inhibitors do and when are they used?

A
  • used in the treatment of hypertension and HF
  • inhibit the action of ACE and so reduce the levels of angiotensin II — reduces the activity of RAAS
  • decreased arteriolar resistance
  • decreased arteriolar vasoconstriction
  • decreased cardiac output
  • reduced K+ excretion in the kidneys

these actions help to looser BP in HT patients and also help to improve outcomes in conditions such as HF

58
Q

what are typical SEs of ACEI?

A
  • dry cough
  • hyperkalaemia
  • headache
  • dizziness
  • fatigue
  • renal impairment
  • rarely angioedema
59
Q

what are the 2 most important prognostic factors in chronic kidney disease?

A

hypertension and proteinuria

60
Q

what are 3 the main hormones made by the kidneys?

A

vitamin D, erythropoietin and renin

61
Q

diabetic nephropathy:

the early stages cause an elevated _____ with enlarged kidneys but the principal feature of diabetic nephropathy is _________. This develops insidiously, starting as intermittent microalbuminuria before progressing to constant proteinuria and occasionally_____________ (= loss of protien eg. proteinurea, hyperalbuminurea)

A
  • GFR
  • proteinuria
  • nephrotic syndrome
62
Q

what is the leading cause of end stage renal failure in the developed world?

A

diabetic nephropathy

63
Q

albuminuria persistency means increased risk of developing what?

A

heart attack

64
Q

what are the 5 stages of injury in diabetic nephropathy?

A
  1. hyperfiltration
  2. microalbuminuria
  3. macroalbuminuria
  4. proteinuria
  5. declining renal function
65
Q

describe the pathology of nephropathy

A
  1. hyperglycaemia causes glycosylation of glomerular proteins
  2. thickening of glomerular basement membrane
  3. mesangial expansion
  4. nodular sclerosis
  5. advanced renal sclerosis
66
Q

what are areas of nodular glomerulosclerosis referred to as?

A

Kimmelstiel-Wilson lesions

67
Q

how is diabetic nephropathy treated?

A

aims of treatment = glycaemic control, BP control (these drugs help delay the progression of kidney diseases by blocking RAAS) — ACEI, ARBs (losartan), Renin-inhibitors (aliskiren) — delay progression because they lower BP which lowers the GFR

secondary treatments = lipid lowering, reduce other CV risks

68
Q

peritoneal dialysis vs haemodialysis

A
69
Q

sepsis treatment

A

• antibiotics
• fluid added to veins
• vasopressors — narrow blood vessels and help increase BP
• may need surgery to remove infected tissue

70
Q

hyperkalaemia treatment

A

• IV calcium to ameliorate cardiac toxicity
• identify and remove sources of K+ i taken
• enhance K+ uptake by cells to decrease the serum conc — IV glucose and insulin infusions
• IV insulin can cause hypoglycaemia - patients with acute kidney injury and chronic kidney disease are especially susceptible - sufficient dextrose in the treatment regimen can minimise the risk
• correct metabolic acidosis with sodium bicarbonate
• increase K+ excretion from the body — IV saline accompanied by a loop diuretic such as furosemide
• emergency dialysis for those with potentially lethal hyperkalaemia

71
Q

what is pyelonephritis?

A

kidney infection

• usually starts in bladder and moves upstream to one or both kidneys
• the usual organisms are the same for lower UTI = Escherichia coli, Klebsiella spp, Proteus spp, Enterococcus spp
• repeated attacks of acute pyelonephritis can lead to chronic pyelonephritis, which involes destruction and scarring of renal tissue due to repeated inflammation

72
Q

symptoms of pyelonephritis

A

> unilateral or bilateral loin pain, suprapubic pain or back pain
fever
malaise/nausea/vomiting/anorexia/diarrhoea can occur
may or may not be lower UTI symptoms with frequency, dysuria, gross haematuria or hesitancy
pain on firm palpation of one or both kidneys

73
Q
A
74
Q

if you have a GFR over 60, and no albumin…..

A

you do NOT have ckd

75
Q

what type of anaemia can you get in ckd and why?

A

normocytic — due to decrease in erythropoietin production

76
Q

what gives you a metabolic acidosis?

A

sepsis

77
Q

which diuretics cause metabolic alkalosis/acidosis as an adverse side effect?

A

thiazide and loop —> metabolic alkalosis

K+ sparing —> metabolic acidosis

78
Q

what type of diuretic can cause hyperglycaemia in diabetes as an unwanted side effect?

A

thiazide

79
Q

what drug type reduce diuretic efficacy? how?

A

NSAIDs — by inhibiting prostaglandin synthesis

80
Q

what can corticosteroids enhance when using thiazide or loop diuretics?

A

hypokalaemia

81
Q

what can ACE inhibitors potentiate when using K+ sparing diuretics?

A

hyperkalaemia

82
Q

what kind of diuretics cause gynecomastia and gastric problems (inc peptic ulcers)?

A

K+ sparing

83
Q

why do K+ sparing diuretics cause gynacomastia?

A

aldosterone antagonism

PBL SEM 4 (50 decks)

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