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J de Zoysa Flashcards

1
Q

What are the roles of the kidney?

A

Elimination of waste products

Control of fluid balance

Regulation of acid-base balance

Production of hormones - epo, vitamin D, aldostrone

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2
Q

Ho do you stage acute kidney injury?

A

Into 3 stages by serum creatinine or urine output. Can be either.

Stage 1: 1.5-1.9x baseline or an increase of >26 umol/L serum creatinine and urine output of <0.5 ml/kg/hr for 6-12 hours.

Stage 2: 2.2.0-2.9 x baseline serum creatinine or <0.5 ml/kg/or >12 hours

Stage 3: 3 x baseline, increase in Cr> 354 umol/L or Renal replacement therapy or <0.3 ml/kg/hr for >24 hours or anuria for >12 hours

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3
Q

What are the types of AKI?

A

Pre-renal
Renal
Post renal

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4
Q

What i the general approach to someone with AKI?

A

Identify those at high risk and optimise their care
Stop all nephrotoxic agents
assess and optimise volume status
Monitor creatinine and urine output.

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5
Q

Who is at risk of AKI?

A 
Chronic kidney disease
Age >75
Heart failure
liver disease
Cardiovasculardisease
Diabees mellitus
Polypharmacy
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6
Q

What meds need to be revised in AKI?

A

at are nephrotoxic, e.g. NSAIDs, gentamicin, anti-hypertve agents.

Meds that are renally excreted, e.g. hypoglycaemic agents

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7
Q

Ho do you assess the volume status of a patient?

A 
Eyes sunken
Dry mucus membranes
Reduced tissue turgor
JVP
Oedema
Heart sounds
Listen t the lungs
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8
Q

What investigations would you do for someone with kidney?

A

Invasive and/ or non-invasive

Streptococcal serology
Viral serology
Bloods
Autoimmune tests

Imaging (ultrasound or CT) to look at structure of kidney and if there is any obstructions.

Renal biopsy - look at nephrons

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9
Q

What is chronic kidney disease AND how is it graded?

Exam

A

Abnormalities of kidney function or structure present for >3 months, with implications for health.

it is classified based on cause, GFR category and albuminuria category.

CKD 1: GFR >90 ml/min
CKD 2: GFR 60- 90 ml/min
CKD 3: GFR 30-60 ml/min
CKD 4: GFR 15-30 ml/min
CKD 5:  GFR <15 ml/min

Albuminuria also applied:
A1: <3 mg/mmol
A2: 3-30 mg/mmol
A3: >30 mg/mmol

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10
Q

How do you measure GFR?

A

1) Clearance of artificially injected substances (inulin) - inject into the blood:
GFR = Vol of urine per time x con inulin in urine/ conc of inulin in the blood.

2) Creatinine clearance - 24 hour creatinine clearance
produced by creatin metaboliscles.

Creatinine clearance (24 hours) = urine creatinine X urine volume / plasma creatinine X time period.

Creatinine clearance depends on muscle mass Ixample, a small child and a body builder may have the same GFR by hugely different creatinine levels.

As kidney functions declines, the amount of kidney excreted in tubules increases and their is decreased muscle mass. This results in an ovresimation of GFR in patients nearing end-stage renal disease. Use a formula to take this into account. These account for gender and race.

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11
Q

What are the risk factors of CKI?

A 
Age
Sex (Men)
Ethnicity (Maori and Pacific islander)
Low income
Obesity
Smoking
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12
Q

What are the main causes of CKD?

A

Diabetic nephropathy
Glomerulonephritis (IgA nephropathy common)
Hypertension
Polycystic kidney disease

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13
Q

Why does CKD progress?

A

Either because of the primary disease or because of the secondary factors that develop. For example, if the cuase of CKD is diabetic nephropathy then you treat the diabetes but also the hypertension (systemic and intraglomerular hypertension), glomerular hypertrophy, calcium and phohatese, dislipidaemia, proteinuria, tubulo-interstitial fibrosis, toxicity of molecules that arent being removed (iron/amonia)

Must focus on both the primary and secondary factors.

95% of patients with CKD will develop hypertension

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14
Q

What do you do to help with hypertension?

A 
Weight  loss
Exercise
Salt restriction
Moderation of alcohol
Stop smoking
Target of 140/80 mmHg or better

Drugs:

1) Induce naturesis (diuretics)
2) Renin: angiotensin (ACEi, Ang II receptor blockers, aldosterone antagonists)
3) SNS blockage - alpha blockers, beta blockers, calcium channel blockers

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15
Q

What is the issue with proteinuria in CKD?

A

It is a prognostic factor. Try to reduce it. Protein restriction.
It causes fibrosis in the nephrons and tubular injury.

Treat with:
Weight loss
ACEi/AIIRB
Aldosterone antagonists
Statins
Moderate protein restriction
BP <125/70 mmHg
Quit smoking
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16
Q

What happens to phosphate and calcium in CKD?

A

It is increased (deposited) in the kidney. This is also associated with deterioration of disease.

limit phosphate in the diet. Give phosphate binders - calcium carbonate

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17
Q

What else do you need to do for patients with CKD?

A 
Calcium and phosphate maintanence.
Maintain the patients water balance.
Maintain endocrine function: EPO, vitamin D, angiotensin
maintain electrolites.
Maintain electrolyte balance
Maintain acid balance

Patients typically develop metabolic acidosis due to lack of excretion
addition of oral sodium bicarbonate may be required.

Treat the uraemia: seen in CKD 4 and 5.

Uraemia causes loss of appetite, anorexia, nausea, skin itch, cold.

Neurology symptoms: fatigue and lethargy, sleep disturbances, headache, seizures, encephalopathy, peripheral neuropathy, paralysis.

Haematological issues: anaemia (because of reduced EPO), bleeding, platelet dysfunction, infection

Cardiac symptoms: pericarditis, hypertension, heart failure, IHD, cardiomyopathy, CVA, PVD

Depression, anxiey

Due to multiple toxins not excreted.

No single treatment.
Correct the abnormalities - Hb, Calcium/phosphate, other electrolytes, acid/base balance, volume, renal replacement therapy

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18
Q

What is renal replacement therapy?

A

Dialysis - perotoneal, haemodialysis

Renal transplant - cadaveric or living

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19
Q

What is the main difference in electrolytres between ECF and ICF?

A

More K+ in the cell and less Na - maintained by sodium potassium ATPases

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20
Q

What is molarity?

A

The number of Moles per litre of fluid:

1 mole = 6.022x10^23

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21
Q

What is the osmotic concentration?

A

The solute concentration - number of osmols per litre of solution.

Tightly regulated by the balance of salt and water.

Hyperosmolarity is defined as too much cation and too little water

Hyposmolarity is defined as too little cation and to much water.

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22
Q

What is tonicity?

A

It refers to what happens to cells in a solution.

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23
Q

Where is ADH made and secreted, when is it produced and what does it do?

A

Made in the hypothalamus and secreted from the pituitary.

Acts on the distal convoluted tubules and collecting ducts.

There is increased production if BP falls (ANG II) or osmolarity increases (osmoreceptors).

It increases BP and reduces osmolarity

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24
Q

What are the features of aldosterone?

A

Produced in the adrenal glans. Is an mineralocorticoid hormone.

Acts on the distal convoluted tubule and collecting duc.

Increases sodium absorption and potassium excretion.

Stimulated by potassium and angiotensin 2

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25
Q

Where do potasium sparing diuretcs act?

A

On the collecting duct.

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26
Q

What sort of diuiretic is furosemide?

A

A loop diuretic

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27
Q

Where do thiazide diuretcs act?

A

On the distal tubule.

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28
Q

What causes hypernatraemia?

A

Impaired thirst/level of consciousness.
No access.
Burns/diarrhoea/blood loss
Solute diuresis (hyperglycaemia or drugs)

Can be caused by diabetes insipidus where there is a reduction in the production of ADH. -> increased water loss. This elevates the plasma osmolality. The cause can be either central (brain injury) or nephrognic (kidney or acquaporin channel problem)

29
Q

If you are hyperglycaemic what will your urine osmolality?

A

Hypo because the glucose in the urine pulls water with it.

30
Q

What is hyponatraemia?

A

Decreased Na. Caused by too much excretion or too much water.

31
Q

What is pseudohyponatraemia?

A

Low Na in the blood but osmolarity is normal.

True neutopenuia causs the blood osmolality to be low.

Is caused by the movement of water from cells into the blood stream. Can occur with hypoglycaemia (increased osmolarity) or with infusion of mannitol.

32
Q

Also check urine osmolality if suspect Na imbalance.

A

<100 mosm/kg = very very dilute

Too much water

33
Q

What happens to Na levels in volume change?

Not sure about this one.

A

Check the volume stats.
Dehydrated - urine sodium <20 mmol/l
Sodium loss but relatively less than water loss.
- diarrhoea, vomiting
- bowel obstruction
- skin losses - burns, sweating
- urinary losses, diuretics, addisons disease, ketonuria

Can also be caused by hypervoluemia:
Na retention but more water retention
-cirrhosis
Nephrotic syndrome
heart failure
Renal failure

May be euvolaemic:

  • SIADH
  • diuretics
  • fluid replacement
34
Q

What are the features of the syndrome of inapropriate ADH?

A

Inapropriate production in absence of normal stimuli.
Body accumulates too much water. t is stored in cells so the patient doesn’t appear to be overloaded.

urine ismil: not low - usually greater than 150 mosmol/kg

Urine sodium - not low
Plasma osmolality: low

Caused by trauma, such as surgery, chronic lung disease, medications

35
Q

What are the symptoms of hypernatraemia?

A

Depends of speed of development

Slow -> brain adapts, confusion, not quite self

Rapid: cerebal oedema, confusion,seizures, come

36
Q

What are some of the roles of magnesium?

A

Bone formation

It is a co-factor in many enzymatic reactions, including ATP metabolism, muscle contraction and relaxation, release of neurotransmitters
regulation of vascular tone

Cardiac rhythm
Platelet activated thrombosis

Hydration status

37
Q

How is Magnesium homeostasis regulated?

A

Mainly through diet intake. A lot is excreted in the faeces and the rest gets into the blood. Kidneys regulate the amount of magnesium in the system. A lot will go into bone and muscle storage.

Serum Mg is controlled by its excretion in the urine. 60-70% is reabsorbed in the thick ascending limb of the loop of henle

38
Q

How is magnesium absorbed in the nephron?

A

10-20% in the proximal convoluted tubule.
- Magnesium is absorbed through a paracellular (between cells) pathway. It moves with water and Na.

60-70% in the thick ascending limb. Paracellular movement again. Th transport proteins claudin 16 and 19 are important in this movement. Mutations in this pathway lead to stone formation, low serum Mg and Ca and get kidney failure.

10% in the distal convoluted tubule. Active process of Mg excretion.

39
Q

How do you assess magnesium?

A
  • serum Mg (not good measure of total body levels).
  • Red cell Mg
  • 24 hour urine excretion
  • Mg retention test (give load then assess 24 hour urine)
40
Q

What are the symptoms of hypomagnesaemia?

A 
Weakness and fatigue
Fasiculations/cramps
Tetany
Numbness-paresthesia
Seizures
Arrhythmias
41
Q

What are the causes of hypomagnesamia?

A
  • decreased dietary intake
    GI malabsorption
    Endocrine - hyperaldosteronism, DM, SIADH
  • Renal loss - congenital, acquired or drug-induced.

Drug induced include, aminoglycosides, amphotericin B

42
Q

What are the treatment of hypomagnesamia?

A

Oral or IV administration of Mg

43
Q

What can cause hypermagnesaemia?

A

In advanced CKD the compensatory mechanisms start to become inadequate and hypermagnesaemia may develop.
Excessive oral administration of magnesum salts or magnesium containing drugs.
Iatrogenic

44
Q

Where is the majority of K+?

A

Intracellular - maintained by the Na/K pump.

Most of it comes from diet.

45
Q

How is potassium homeostasis maintained?

A

Most taken in via the diet and most excreted via the kidneys.

In CKD then less is excreted via the kidneys and more is excreted via the faeces.

46
Q

What happens to the K+ in hyperglycaemia or DKA?

A

The glucose gets pushed into the cells and the K+ gets pushed out of the cells = hyperkalaemia.

Acidosis can also drive the efflux of K+ and alkalosis wiil drive influx of potassium.

47
Q

How is potassium reabsorbed from the nephron?

A

About 60% from the proximal convoluted tubule
- Na/K ATPase bring K= into the lumen of the nephron but then the K+ is reabsporbed paracellularly.

30% from the thick ascending limb.
- ROMK channel bringing potassium into the lumen and then the Na/K/Cl channel bringing it back into the cell

Variable amount from the collecting ducts.
- regulated by aldosterone, which is produced in response to Ang II in hypotension.

48
Q

What are the symptoms of hypokalaemia?

A

<3.5 mmol/l

  • muscle weakness
  • paralysis
  • cardiac conduction abnormalities
  • cramps
  • constipation
49
Q

How is potassium lost?

A

Renal

  • hyperaldosteronism
  • licorice
  • diuretics
  • renal tubular acidosis

Gut

  • vomiting
  • diarrhoea
  • laxatives
  • ileostomy
50
Q

What are some diuretics that caiuse loose of potassium and where do they act?

A

Mannitol in the proximal convoluted tubule

Frusemide - thick ascending limb

Metollzone - distal concoluted tubule

Spironolactone and amiloride that act on the collecting duct.

51
Q

How do you treat hypokalaemia?

A

Treat the underlying problem/
Use oral for mild losses
Use IV for severe losses.

52
Q

What are the symptoms of hyperkalaemia?

A 
Fatigue or weakness
Paraesthesia
Nausia or vomiting
Dyspnoea
Palpitations

Causes arrhythmias - peak T waves, prolonging of the P interval and widening of the qrs. Can develop of VF and cardiac arrest.

53
Q

What is pseudohyperkalaemia?

A

Only in lab tests, if the blood samples are left standing for too long the cells can break down releasing the K+.

54
Q

What are the causes of hyperkalaemia?

A

Increased intake.

Disruption of cell intake

  • beta blockers
  • acidosis
  • rhabdomyalsis

Decreased excretion

  • renal failure
  • hypoaldosteronism
  • ACEi/ARB
  • other drugs

Addison’s disease - decreased production of aldosterone and cortisol - low blood pressure, high potassium - causes lethargy and weakness - hyperpigmentation

55
Q

What is the treatment of hyperkalaemia?

A 
Stabilize the action potentials - can do this with IV calcium (lasts 30 minutes)
Push K into cells
reduce K absorption
Increase elimination
Fix underlying problem.
Beta agonists (salbutamol)
- this will push K intracellularly. (lasts several hours)

Insulin will also push K intracellularly - also need to give with dexterose.

Treat the acidosis - oral bicarbonate.

Reduce K absorption through GI. By giving Ca/K exchangers.

Increase elimination - K+ losing diuretic or dialysis

56
Q

What is chronic kidney disease mineral and bone disorder?

A

The kidney retains phosphate. Low calcium causing hyperparathyroidism.

The low calcium is caused by impaired vitamin D metabolism in the kidney, which is required for Ca and Mg intestinal absorption.

Need to reduce dietary phosphate.
Phosphate binders (calcium carboxylase)
Review medications that may contribute to the hyperkalaemia - such as ACEi and ARB

Restrict dietary potassium

57
Q

What is haemodialysis?

A

Blood removed put through a machine and cleaned and then put back in.

4-5 hours 3 x per week.

Peritoneal dialysis is another option

58
Q

What is nephrotic syndrome?

A

Nephrotic syndrome
- high proteinuria - caused by damage to the basement membrane of the bowmans capsule. No RBCs because the blood vessels are intact.

Causes the serum albumin to be low causing oedema.

59
Q

What is nephritic syndrome?

A

Damage to the blood vessels causing an increase of protein and blood in the urine. Causes hypertension and peripheral oedema.

60
Q

What is rapidly progressing glomerulonephritis?

A

Rapidly deteriorating renal function and crescents on biopsy.

Can be caused by an Ab that targets the basement membrane or an immune complex

61
Q

What are cresents in the glomerulus?

A

They are a sign of glomerulonephritis.

It is a non-specific response to injury of the capillary wall. Physcial gaps appear in the filtration barrier (endothelium, basement membrane and podocyte barrier). This allws RBCs, WBCs and plasma proteins to enter into the bowmans space.
The contents of bowmans space can enter the interstitium, contributing to periglomerular inflammation.

This causes the proliferation of cells in the bowmans space that can cause fibrosis.

The creasents can be cellular or fibrotic. Fibrotic is not reversible.

The degree of cresent formation is associated with the degree of glomerulonephritis.

62
Q

What is Goodpasture’s disease?

A

Autoantibody against a type of collagen that is found in both the glomerulous and in the lungs.
It causes haemoptysis and haematuria glomerulonephritis.

Treat with prednisone, cyclophosphamide and give plasma exchange (remove plasma and replace). Dialysis

63
Q

What are the 5 key m ages about hypertesnion?

A

1) it is common
2) it is the major cause of morbidity and mortality
3) salt restriction is important
4) long-acting diuretics are the cornerstone of therapy
5) treat using complementary multi-drug therapy and lifestyle changes.

64
Q

How do you treat modest hypertension?

A

With monotherapy.

Age <55 years then ACEi
>55 years = diuretics

Social advice

Optimise drug dose - most patients need multiple drugs

65
Q

What is resistant hypertension?

A

When the blood pressure is not at target levels despite optimal dose of three complimentary drugs, one of which is a diuretic.

Usually caused by suboptimal doses, or non-complementary drugs, non-compliance, competing drugs (NSAIDS, sodium), white coat hypertension or secondary HT

Secondary causes - endocrine or renal

66
Q

What is chronic kidney disease determined by?

A

The cause, GFR and albuminuria

67
Q

What is end stage kidney disease?

A

End stage renal failure is insufficient kidney function to keep patients feeling well.

68
Q

What is glomerulonephritis?

A

Acute inflammation of the kidney, typically caused by an immune response

Can present as nephrotic syndrome, nephritic syndrome, rapidly progressing GN, asymptomatic urine abnormalities, AKI or CKD

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