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Kidney Flashcards

1
Q

What is renal blood flow

A

20% of CO

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2
Q

What are proximal tubular cells susceptible to

A

Hypotension and hypoxia

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3
Q

Where is erthropoietin produced

A

Kidneys (px can be anaemic if CKD)

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4
Q

What are the functions of the kidneys

A 
Excretion of electrolytes
Clearance of waste products 
Receptor sites for hormones:
ADH, aldosterone, ANP, PTH
Gluconeogenesis
Production of hormone: renin, vitamin D, erythropoietin, prostaglandins
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5
Q

What are pre-renal causes of AKI

A

Hypoperfusion - anything that causes shock, cardiac output

Renal artery stenosis

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6
Q

What are renal causes of AKI

A

Glomerulonephritis
Diabetes
PKD
Toxins - gentamycin, NSAIDs (reduce prostaglandin production, which reduce renal perfusion)

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7
Q

What are post renal causes of AKI

A

Anything in urinary tract
Takes 2 weeks for damage
Swollen kidney with no urine output is a medical emergency

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8
Q

What are the effects of AKI

A

Fluid overload

Oedema (pulmonary - breathlessness lying flat, pleural effusion, peripheral, sacral, ascites)

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9
Q

What investigations should be undertaken for AKI

A

Chest X-Ray
GFR
ECG for heart failure
Weight change

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10
Q

How is hyperkalameia treated

A

Hyperkalaemia: Treat with calcium gluconate, then insulin (pushes potassium into cells), or calcium resonium for long term treatment. Dialysis.

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11
Q

What are the ECG signs for different hyperkalameia

A

K 5.5-6.5 - Peaked T waves, prolonged PR segment
K 6.5-8 - Loss of P wave, prolonged QRS complex, ST segment elevation, ectopic beats and escape rhythms
K > 8 - Progressive widening of QRS complex, sine wave, VF, asystole, axis deviations, bundle branch block, fascicular blocks

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12
Q

What are signs of metabolic acidosis

A 
Metabolic acidosis: exacerbates potassium issues 
Typical ABGs
pH > 7.3
pCO2 Low
pO2 normal to high
HCO3 low
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13
Q

What is uraemia

A

Retention of metabolic waste products (sulphate, urea, ammonia, creatinine, phosphate)

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14
Q

What are the symptoms of metabolic acidosis

A

breathless, tachypnoeic, nausea, non-specifically unwell

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15
Q

What are the effects of uraemia

A

Pericarditis, pleurisy, encephalopathy

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16
Q

How is AKI diagnosed

A 
Serum creatinine (only rises after losing more than 50% of kidney function) >26.5 in less than 48 hours or rises to 1.5 fold from baseline in the preceding 7 days
Urine output less than 0.5ml/kg/h for 6 hours
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17
Q

What are life threatening complications of AKI

A 
Life threatening pulmonary oedema
Severe metabolic acidosis
Severe hyperkalaemia
Uraemic pericarditis
Uraemic encephalopathy
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18
Q

Where are the insertion sites for dual lumen catheters for RRT

A

Insertion sites:
Internal jugular vein
Femoral vein
Subclavian vein

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19
Q

What is ideal body water composition

A

TBW = 60% ideal
40% intracellular
20% extracellular (15 interstitial fluid and 5 intravascular)

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20
Q

What is thirst stimualated by

A

Increases in plasma osmolality of 1-2% (normally between 280-300)
Decline in plasma volume of 10-15%
Baroreceptor input, angiotensin II

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21
Q

What is ADH and what does it co

A

Binds to V2 receptors on basolateral membrane of principle membrane along distal convoluted tubules and increases AQP2 expression of luminal membrane
Leads to arteriole vasoconstriction

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22
Q

What is ANP

A

Primarily released from atria - in response to volume expansion

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23
Q

What is BNP

A

Released by ventricles - in response to stretch

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24
Q

What do ANP and BNP promote

A

Dilatation of afferent arterioles and constrict the efferent arterioles (higher pressure in glomerulus and increase GF)
Reduce Na reabsorption in the DCT
Inhibit renin secretion
inhibit renal sympathetic tone

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25
Q

What is hyponatremia

A

Na<135 mmol

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26
Q

How does hyponatremia occur

A

Results from intake and subsequent retention of water. Excess of water in relation to Na - impairment in renal water excretion, most often due to an inability to suppress ADH secretion
Depletion of total body Na in excess of concurrent body water losses

27
Q

What are the 3 classifications of hyponatremia

A

Hypovolaemia
Euvolaemia (urine Na >30 mmol/L)
Hypervolaemia

28
Q

What are the causes of hypovalaemic hyponatremia

A 
Extrarenal losses (urine Na<25mmol)
Dermal losses
GI losses
3rd space loss (pancreatitis0
Renal losses (urine Na>30mmol/L)
Diuretic therapy
Cerebral salt wasting
Primary adrenal insufficiency
29
Q

What are the causes of euvolaemic hyponatremia

A 
Water intoxication - primary polydipsia, excess IV hypotonic fluids
Hypothyroidism
Hypopituitarism
Pregnancy 
SIADH
30
Q

What are the causes of hypervolaemia hyponatremia

A 
Urine Na < 25mmol
Congestive cardiac dysfunction
Cirrhosis with ascites
Nephrotic syndrome
Urine Na > 30 mmol/L - chronic kidney disease
31
Q

What is SIADH

A

Syndrome of inappropriate antidiuretic hormone secretion is characterized by excessive unsuppressible release of antidiuretic hormone (ADH) either from the posterior pituitary gland, or an abnormal non-pituitary source. Unsuppressed ADH causes an unrelenting increase in solute-free water being returned by the tubules of the kidney to the venous circulation

32
Q

What is the treatment for hypovolemia hyponatremia

A

Correct volume depletion e.g. IV 0.9% saline

33
Q

What is the treatment for euvolemia hyponatremia

A

Treat underlying cause, fluid restriction

34
Q

What is the treatment for hypervolemia hyponatremia

A

Treat underlying cause, fluid restriction (vasopressin receptor antagonist)

35
Q

What occurs in the brain in hyponatremia

A

Osmotic gradient between EC and IC fluid within the brain: water moves into cells and raises intracranial pressure due to oedema - neuro symptoms

36
Q

When is agressive therapy for hyponatremia indicated

A

Severe symptoms
Acute hyponatremia
Goal - raise serum Na by 4-6 mmol/L over few hours, no more than 8 mmol/L/day
Hypertonic 3%

37
Q

What is the risk of rapid correction in hyponatremia

A

Risk of central pontine myelinolysis - damage to oligodendrocytes

38
Q

What is hyperatremia

A

Hypernatremia Na > 145mmol/L
From net water loss or hypertonic Na gain
Increase in plasma tonicity pulls water out of cells ,resulting in a decrease in intracellular volume

39
Q

What is severe hyperatremia

A

Na > 145 mmol/L

40
Q

What are the symtpoms of hyperatremia

A

Thirst, anorexia, weakness, stupor, seizures, coma

41
Q

What are the two types of hyperatremia

A

Unreplaced water loss and sodium overload

42
Q

What is unreplaced water loss hyperatremia caused by

A 
Insensible and sweat losses
GI losses
Central diabetes insipidus
Nephrogenic diabetes insipidus
Osmotic diuresis (high glucose)
Poor water intake
43
Q

What is sodium overload hyperatremia caused by

A

Admin of high salt load

Hyperaldosteronism

44
Q

What is the treatment of chronic hyperatremia

A

treat underlying cause, use of hypotonic fluid (5% dextrose), lower Na by maximum of 10 mmol/L day

45
Q

What is the treatment for acute hyperatremia

A

Hypotonic fluid, lower Na by 1-2 mmol/L per hour to restore Na levels within 24 hours. Acute increase in plasma Na can lead to irreversible neuro injury

46
Q

What is hypokalemia

A

Hypokalaemia K<3.5 mmol/L

K enters the body via oral intake or IV, largely stored in the cells, then excreted in the urine

47
Q

What the the 3 caues of hypokalaemia

A

Decreased K intake
Increased K entry into cells
Increased losses - GI/urine

48
Q

What causes increased K entry into cells

A 
Extracellualr pH rise
Increased inslin
Elevated b-adrenergic activity
Hypothermia
Drugs e.g. antipsychotics
49
Q

What causes increased GI losses of K

A

Vomiting
Diarrhoea
Laxative abuse

50
Q

What causes increased urinary losses of K

A

Diuretics
Priamry mineralocorticoid excess
Renal tubular acidosis
Drugs .e.g Amphotericin B

51
Q

What are the ECG changes in hypokalaemia

A 
Flat T waves
U waves
ST depression
PR interval prolonged
Prolonged QT interval
52
Q

What is the treatment for hypokalemia

A

Correct Mg levels
K replacement
If IV maximum 10-20 mmol/hr and cardiac monitoring

53
Q

What is hyperkalemia

54
Q

What are the two causes for hyperkalemia

A

Increased release from cells

Reduced urinary excretion

55
Q

What are the causes of increased K release from cells

A 
Pseduohyperkalemia
Metabolic acidosis
Insulin deficiency
Increased tissue catabolism
Beta blockers
Exercise
Hyperkaelmic periodic paralysis
56
Q

What are reduced urinary excretion causes of hyperkalemia

A

Acute and chronic kidney disease
Reduced aldosterone secretion
Reduced response to aldosterone

57
Q

What are the symptoms of hyperkalemia

A

Paraesthesia
Muscle weakness
Arrhythmias

58
Q

What are the ECG changes of hyperkalemia

A 
any ECG changes are medical emergencies 
Tall peaked T waves
Shortened QT interval
PR interval lengthening
QRS widen
P waves disappear - Sine wave
59
Q

What is the treatment for hyperkalemia

A

IV calcium gluconate - antagonise membrane action of high K
IV insulin with glucose - drive K into cells
Remove K from body: consider loop diuretics
Consider haemodialysis
Other therapies to drive K into cells:
Sodium bicarbonate, beta agonists

60
Q

What are symptoms of hypovolemia

A

GI losses, thirst, lethargy, postural dizziness, reduced urine volume, confusion

61
Q

What are examination findings of hypovolemia

A

pulse is fast and weak, BP postural drop > 20mmHg, loss of skin turgor, sunken eyes, dry mucous membranes

62
Q

What are symptoms of hypervolemia

A

breathlessness, peripheral oedema, weight gain, abdominal bloating, confusion

63
Q

What are examination findings of hypervolemia

A 
Pulse - can be fast, bounding
BP can be high, can be low
Skin turgor generally maintained
Peripheral oedema
JVP can be elevated
Can have ascites

Supporting Life (14 decks)

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