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PPE - Rhianna > Urinary > Flashcards

Urinary Flashcards

1
Q

Which renal vein is longer? Why?

A

Left because it has to cross over the aorta

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2
Q

Why does the testicular vein drain into the renal vein on the left but not on the right?

A

The left renal vein is longer because it crosses over the aorta.

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3
Q

What spinal levels are the kidneys found at?

A

Left - T11/12

Right - T12/L2

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4
Q

Which kidney is usually lower? Why?

A

Right because it is pushed down by the liver

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5
Q

Which areas make up the parenchyma of the kidney?

A

The cortex and the medulla

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6
Q

Describe the flow of urine as it leaves the collecting ducts.

A

Minor calyx - major calyx - renal pelvis - ureter - bladder - urethra

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7
Q

How can you identify the ureters on an X-ray?

A

Follow the path of the transverse spinous processes

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8
Q

In which operations do the ureters frequently get damaged? Why?

A

Hysterectomy
Because the uterine artery (which has to be cut) travels over the ureter and it is pulsatile so looks slightly arterial

Water under the bridge

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9
Q

Where are the three most common sites for kidney stones?

A

Top - pelvoureteric junction
Middle - as ureter passes over the iliac crest
Bottom - vesicoureteric junction

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10
Q

Describe the type of pain caused by renal stones. Why does it feel like this?

A

Loin to groin in the T11-L2 dermatomes

Colicky because ureter is a pulsatile tube, pushing intermittently against the stone

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11
Q

Where is the perinephric fat?

A

Around the hilum of the kidney. (Where everything else enters)

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12
Q

What is the kidney capsule?

A

Dense fibrous covering which surrounds each kidney.

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13
Q

What is the structure in the kidney that allows filtration to occur?

A

Glomerulus

Glomerular tuft of arterioles inside the Bowman’s capsule

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14
Q

Give three important locations of terminal arteries.

A

Brain, kidney, retina

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15
Q

Which embryological tissue does the urinary system derive from?

A

Intermediate mesoderm

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16
Q

Name the 3 embryological stages of urinary development.

A

Pro nephros
Meso nephros
Meta nephros

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17
Q

What are the two components of the mesonephros and what are their derivatives?

A

Ureteric bud - turns into collecting system and drives metanephros
Mesonephric duct - vas deferens

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18
Q

How does the metanephros develop?

A

Ureteric bud drives development de novo from intermediate mesoderm

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19
Q

What is the cloaca and how is it divided?

A

Where the GI tract and urogenital sinus merge.

It is divided by the growth of the urorectal sinus.

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20
Q

What is the urachus? What is its adult derivative? What happens if it remains patent?

A

Duct that joins urogenital sinus (future bladder) to the umbilicus

Turns into umbilical ligament

If it remains patent, urine leaks from umbilicus

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21
Q

Describe the ascent of the metanephros.

A

Begins in the hindgut and the trunk grows around it, so that it appears to ascend to the level of t11. Renal arteries develop along the ascent.

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22
Q

Why are there often supernumerary renal arteries?

A

Form and reform during the ascent of the kidney.

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23
Q

What causes a horseshoe kidney?

A

Kidneys rotate and fuse during their ascent. The isthmus (fused part) stops it travelling higher than the inferior mesenteric artery.

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24
Q

What causes an ectopic ureter? What complication can be associated with it?

A

2 ureteric buds form - either de novo or by one splitting.

If the ectopic ureter opens inferior to the bladder it can lead to incontinence.

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25
Q

What causes a urorectal fistula? What are the symptoms?

A

Failure of the urorectal sinus to fuse with the perineum.

Faecal contents leak out of urethra and high risk of UTI.

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26
Q

Which type of epithelia are found in the proximal convoluted tubule? State two specialisations.

A

Simple cuboidal

  1. Lots of microvilli to increase surface area for mass reabsorption
  2. Lots of mitochondria to supply the Na/k atpase which sets up the sodium gradient for passive reabsorption
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27
Q

Which type of epithelia are found in the loop of Henle?

A

Simple squamous

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28
Q

Which type of epithelia are found in the distal convoluted tubule?

A

Simple cuboidal.

Few microvilli and few mitochondria

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29
Q

Where are transitional epithelia found?

A

Minor calyx down to the superior urethra.

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30
Q

What are the four parts of the urethra and the type of epithelia found there?

A

Pre prostatic - transitional
Prostatic - transitional
Membranous - Pseudostratified columnar
Spongy - stratified squamous

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31
Q

What two factors influence whether a particle is filtered at the glomerulus?

A

Size - only small get through the endothelial wall and the filtration slits in the podocytes

Charge - negative are repelled by glycoprotein basement membrane so positive get through more easily

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32
Q

What are the three layers a that separate the blood from the ultra filtrate at the Bowman’s capsule?

A

Fenestrated endothelial
Glycoprotein basement membrane
Podocytes with filtration slits

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33
Q

In the glomerulus, is the afferent or efferent arteriole wider? Why?

A

Afferent to produce a hydrostatic pressure that forces some of the blood to be filtered.

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34
Q

What are the three pressures acting on the blood at the glomerulus?

A

Hydrostatic into the filtrate - from the different diameters of the afferent and efferent arterioles

Hydrostatic back pressure of the filtrate

Oncotic draw of the concentrated proteins in the plasma.

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35
Q

By which two mechanisms does the glomerulus auto regulate the filtration rate?

A

Myogenic regulation

Tubuloglomerular feedback

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36
Q

If the pressure in the afferent arteriole to the glomerulus increases, how will the myogenic auto regulation respond?

A

Increase in pressure risks an increase in GFR.

Smooth muscle senses the stretch and contracts to prevent extra blood reaching the glomerulus.

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37
Q

If the pressure in the afferent arteriole to the glomerulus decreases, how will the myogenic auto regulation respond?

A

Decrease in pressure risks an decrease in GFR.

Smooth muscle senses the relaxation and dilates to allow extra blood to reach the glomerulus.

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38
Q

If the pressure in the afferent arteriole to the glomerulus increases, how will the tubular glomerular auto regulation respond?

A

There is a brief increase in GFR. More NaCl reaches the distal tubule.
This is sensed by the macula dense cells and the juxtamedullary apparatus releases adenosine to vasoconstrict the afferent arteriole and stop the increase in GFR.

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39
Q

If the pressure in the afferent arteriole to the glomerulus decreases, how will the tubuloglomerular auto regulation respond?

A

There is a brief decrease in GFR. Less NaCl reaches the distal tubule. This is sensed by the macula densa cells and the juxtamedullary apparatus release prostaglandins to vasodilate the afferent arteriole and increase the GFR back to normal.

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40
Q

Why does the distal tubule travel up to the glomerulus and nestle between the afferent and efferent arterioles?

A

So that it can communicate with the juxtamedullary apparatus and regulate the filtration rate based on how much NaCl it senses.

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41
Q

What is glomerular filtration rate? What is a normal rate?

A

Rate of kidney function

Should be over 90 ml/min

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42
Q

How do we calculate GFR? Why is it a slight overestimate?

A

Clearance of creatinine.

Creatinine is slightly secreted into the tubule so it appears that clearance is greater than it is.

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43
Q

What are the ideal characteristics of a substance we could use to calculate GFR?

A
  1. Freely filtered
  2. Not re absorbed
  3. Not secreted
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44
Q

What is creatinine? What type of person would have higher natural levels?

A

Product of muscle breakdown

Muscular, young, male

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45
Q

By what process does the kidney control blood volume?

A

Reabsorption of Na

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46
Q

Where does bulk Na reabsorption occur? How much of the total is reabsorbed?

A

Proximal convoluted tubule

67%

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47
Q

Which Na transporters are present in the PCT?

A

Early - Na glucose

Later - Na H

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48
Q

Which Na transporters are present in the Descending limb of the loop of Henle?

A

None. Just loose junctions and aquaporins for water to set up gradient for the ascending limb.

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49
Q

Which Na transporters are present in the thin ascending limb of the loop of Henle?

A

Just the Na k atpase.

Na moves passively out here due to the gradient set up in the descending limb.

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50
Q

Which Na transporters are present in the thick ascending limb of the loop of Henle?

A

Nak2cl

And ROMk to leak k and keep the Nak2cl functioning.

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51
Q

Which Na transporters are present in the DCT and collecting duct?

A

ENaC and associated k channel

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52
Q

Which part of the nephron is most sensitive to hypoxia?

A

Thick ascending limb because the nak2cl uses most atp.

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53
Q

Why is 67% of the Na always absorbed at the pct and not a fixed amount? What is this mechanism called?

A

Keeps the Na that travels through the rest of the nephron more constant than if a fixed amount was absorbed.

Glomerulotubular balance.

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54
Q

How is osmolarity and electro neutrality maintained through the pct?

A

As Na is removed, opposing ions eg cl and urea are left behind and make up a greater proportion of the filtrate. So elctroneutrality of ions is maintained. These also attract a similar level of water as the Na.

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55
Q

What 3 factors can increase renin release?

A
  1. Decreased NaCl in distal tubule detected by macula densa cells
  2. Decreased perfusion in afferent arteriole
  3. Increased sympathetic stimulation
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56
Q

Where is renin released?

A

Granular cells in Juxtaglomerular apparatus

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57
Q

What is the action of renin?

A

Angiotensinogen - angiotensin 2

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58
Q

What is the action of angiotensin converting enzyme? (ACE)

A

Angiotensin 1 - 2

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59
Q

Give 4 actions of angiotensin 2.

A

Increased sympathetic stimulation
Vasoconstrict
Increased Na/H action in the pct (increased Na absorption)
Aldosterone release from adrenal cortex

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60
Q

What is the main action of aldosterone?

A

Increase ENaC action and associated k channel in the DCT. Increased reabsorption of Na.

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61
Q

What are 3 actions of anti diuretic hormone?

A

Increased action of nak2cl channel in thick ascending limb of loop of Henle. Therefore increased reabsorption of Na.

Up regulation of aquaporin 2 channels

Increase urea reabsorption

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62
Q

What stimulates thirst and release of adh?

A

Osmoreceptors sense low osmolarity in hypothalamus - posterior pituitary

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63
Q

How do beta blockers inhibit raas?

A

Decreased sympathetic stimulation.

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64
Q

Give 3 substances which decrease blood volume via the kidney?

A

Natriuretic peptides
Prostaglandins
Dopamine

65
Q

Why are NSAIDs not given in renal failure?

A

Renal failure - decreased GFR so filtrate sits in the kidney for longer.
Prostaglandins normally help to decrease Na reabsorption and vasodilate so would act as a buffer for a while.
But NSAIDs block prostaglandin formation so would lead to too much vasoconstriction and too much Na reabsorption and further decrease GFR.

66
Q

Give 3 causes of secondary hypertension which act by increasing renin production.

A
  1. Increased sympathetic drive - Horner’s, phaechromocytoma
  2. Decreased perfusion to nephron - renal artery occlusion
  3. Decreased NaCl in DCT - renal failure (low GFR)
67
Q

Give 2 causes of secondary hypertension which act by increasing influence of aldosterone.

A
  1. Conn’s disease - Aldosterone secreting tumour

2. Cushing’s - corticosteroids at high levels act on mineralocorticoid receptors (aldosterone is a mineralocorticoid)

68
Q

What determines plasma osmolarity?

A

Relative Na and h20 which is modulated by the movement of water

69
Q

Is a solution with high osmolarity salty or watery?

A

Salty

70
Q

Is a solution with low osmolarity salty or watery?

A

Watery

71
Q

How does is plasma osmolarity detected? What is the response if it gets too high?

A

Osmoreceptors in the ovlt of the hypothalamus

If it gets too high (salty)
Increase ADH
Increase thirst sensation and desire for salty food.

72
Q

How does adh upregulate the aquaporin 2 channels? How does it affect the aquaporin 3 and 4 channels?

A

Gs receptor - cAMP - insert aquaporin 2 on the apical membrane

Aquaporin 3 and 4 are always present on the baseplate real membrane so no effect by adh .

73
Q

If osmolarity is normal but volume falls, what happens to ADH?

A

Volume trumps osmolarity eg in shock because good tissue effusion is the most important thing.
So even if osmolarity is normal, when volume falls dramatically, adh is released more readily.

74
Q

What is the pathophysiology of diabetes insipidus?

A

Decreased effect of ADH.
Either decreased production from p pituitary or insensitivity.
Leads to polyuria and polydipsia.
Long term risk of Hypokalaemia

75
Q

What is the pathophysiology of SIADH?

A

Excessive adh production from the p pituitary or from an adh secreting tumour.
Leads to retention of water and dilutional hyponatraemia

76
Q

Why is the corticopapillary osmotic gradient necessary?

A

Inserting aquaporin channels is not enough to make water be reabsorbed. Needs an osmotic gradient to move along.

77
Q

What process generates the corticopapillary osmotic gradient?

A

Counter current multiplication -

Ascending limb loh is impermeable to water
1. Nak2cl - pumps out salt - salty interstitial and dilute urine
2. ADH causes urea to move into interstitium but it is salty so it moves into loh. Water can’t follow.
3. Loh full of urea - salty. But most salty bit is before nak2cl. =gradient
So the deep area becomes full of urea and top bit is dilute.
This repeats and the effect is multiplied.

78
Q

What process maintains the corticopapillary osmotic gradient?

A

Counter current exchange

Vasa recta flows opposite to filtrate
So it enters at the least concentrated section. It takes up salts following the gradient so that by the time it gets deep into the cortex it is isoosmotic with the filtrate and doesn’t wash away the gradient.

79
Q

How does the lung compensate for metabolic acidosis/alkalosis?

A

Detects pH at the peripheral receptors.
Acidosis - increases ventilation to blow off O2
Alkalosis - decreases ventilation (to a point until O2 drops)

80
Q

How does the kidney compensate for respiratory alkalosis?

A

PH in tubular cells tips kidney towards less recovery of HCO3.
By decreasing action of Na/H anti porter and therefore hco3/Na symporter.

81
Q

How does the kidney compensate for respiratory acidosis? 3 ways)

A

Increased recovery and production of hco3

Recovery - increases Na/h and therefore hco3/Na
Production - 1. increases ammonium production 2. Increases action of h atpase to excrete more h and to shift the carbonic anhydrase reaction towards hco3 production.

82
Q

What is the anion gap?

A

Normally we only measure k, Na, cl and hco3. There is usually 5-10mmol difference between the cations and the anions. But if the anions are even less there is an anion gap. This indicates that there is an alternative production of anions from acids other than co2. For example lactate or ketones. Strong indication of metabolic acidosis.

83
Q

What is the relationship between metabolic ph and potassium levels?

A

Metabolic Acidosis - Hyperkalaemia
(And Hyperkalaemia - metabolic acidosis)

Metabolic alkalosis - Hypokalaemia
(And Hypokalaemia - metabolic alkalosis)

Via k/h pump in the intercalated cells of the DCT.

84
Q

How does the lung compensate for metabolic acidosis/alkalosis?

A

Detects pH at the peripheral receptors.
Acidosis - increases ventilation to blow off O2
Alkalosis - decreases ventilation (to a point until O2 drops)

85
Q

How does the kidney compensate for respiratory alkalosis?

A

PH in tubular cells tips kidney towards less recovery of HCO3.
By decreasing action of Na/H anti porter and therefore hco3/Na symporter.

86
Q

How does the kidney compensate for respiratory alkalosis? (3 ways)

A

Increased recovery and production of hco3

Recovery - increases Na/h and therefore hco3/Na
Production - 1. increases ammonium production 2. Increases action of h atpase to excrete more h and to shift the carbonic anhydrase reaction towards hco3 production.

87
Q

What is the anion gap?

A

Normally we only measure k, Na, cl and hco3. There is usually 5-10mmol difference between the cations and the anions. But if the anions are even less there is an anion gap. This indicates that there is an alternative production of anions from acids other than co2. For example lactate or ketones. Strong indication of metabolic acidosis.

88
Q

What is the relationship between metabolic ph and potassium levels?

A

Metabolic Acidosis - Hyperkalaemia
(And Hyperkalaemia - metabolic acidosis)

Metabolic alkalosis - Hypokalaemia
(And Hypokalaemia - metabolic alkalosis)

Via k/h pump in the intercalated cells of the DCT.

89
Q

Give five host factors that raise the risk of UTI.

A 
Female
Pregnant
Enlarged prostate
Ureteric reflux - children
Renal calculi
90
Q

Give 3 bacterial factors that make them good at infecting the urinary tract.

A

Fimbriae
Haemolysins - break down blood cells
Urease - break down urea to make it more alkali

91
Q

Which are the two most common bacteria causing UTI? Why?

A

E. coli
Enterococcus faecalis

Proximity of gut outflow to urinary tract

92
Q

What is the classic presentation of a UTI?

A

Polyuria with urgency
Dysuria
Suprapubic pain

93
Q

Which two symptoms might make you consider a UTI is pyelonephritis?

A

Fever

Loin pain

94
Q

Which patients are more likely to have an asymptomatic UTI? Why is this significant?

A

Pregnant

Foetus at risk of premature delivery and stunted growth

95
Q

What characteristics make a UTI complicated?

A 
Pregnant
Male
Paediatric
Treatment failure
Suspected pyelonephritis
96
Q

What test would you carry out in a suspected UTI? What result would indicate a positive result?

A

Midstream dipstick

Presence of leukocyte esterase and nitrite
Alkali
Visual turbidity (opaque)

97
Q

How would you treat an uncomplicated UTI?

A

Trimethoprim 3 days

Or nitrofurantoin 3 days

98
Q

What is the neural control of bladder filling?

A

Sympathetic (hypo gastric nerve) t10-l2
Inhibits detrusor via b3 receptors to relax smooth muscle
Excites internal urethral sphincter via alpha 1 receptors to prevent leak

99
Q

What is the autonomic control of micturition?

A

Parasympathetic (pelvic nerve) s2-4
Excites detrusor via m3 receptors to squeeze
Inhibits internal urethral sphincter to relax and release

100
Q

What is the somatic control of micturition?

A 
Pudendal nerve (s2-4) excites external urethral sphincter at rest
Inhibits during voiding
101
Q

What are the key differences between the internal and external urethral sphincters?

A

Internal -

  1. physiological sphincter of smooth muscle
  2. Autonomic control

External -

  1. Anatomical sphincter of skeletal muscle
  2. Somatic control
102
Q

Describe the histological structure of the detrusor muscle. Why is this significant?

A

Smooth muscle in many directions. Confers strength when stretching in any direction.

103
Q

What is stress incontinence? Give a common cause?

A

Incontinent when coughing or sneezing

Pelvic floor weakness

104
Q

What is urge incontinence? What are some common causes?

A

High intraabdominal pressure - ovarian cyst, pregnant, prolapse

Upper motor neuron lesion - increased detrusor tone and detrusor-sphincter dyssynergia

105
Q

What is overflow incontinence? What is a common cause?

A

Constant leak, often worse at night.

Lower motor neuron lesion - decreased tone of detrusor leading to overfilling.

106
Q

What is acute injury? What are the main diagnostic criteria?

A 
An actual (not the value on the blood test) decrease in GFR. 
Measured by raised creatinine and decreased urine output.
(Also some decrease in GFR)
107
Q

What causes pre renal AKI? Give 5 pre renal causes of AKI.

A

Decreased perfusion of the kidney

  1. Hypovolaemia
  2. Sepsis
  3. Heart failure
  4. Cirrhosis
  5. Drugs - NSAIDs (lack of prostaglandin relaxing afferent) and ACE (lack of angiotensin constricting efferent)
108
Q

How does the kidney compensate for pre renal AKI? At what point does this become overwhelmed?

A

Tries to increase prostaglandins - increases relaxation of afferent
Tries to increase angiotensin via tubuloglomerular feedback - increases constriction of efferent

Compensation is overwhelmed when mean arterial pressure goes below 80mmHg

109
Q

Which type of AKI responds well to fluid?

A

Pre renal (before it descends into acute tubular necrosis)

110
Q

What are 3 main causes of acute tubular necrosis?

A
  1. Pre renal AKI that is not treated with fluid
  2. Ischaemia (renal artery stenosis)
  3. Nephrotoxins
111
Q

Which area of the tubule is mostly affected by acute tubular necrosis?

A

Proximal convoluted tubule

Because it has a high demand for O2

112
Q

What would you find in a urine dipstick in a case of acute tubular necrosis?

A

High specific gravity (lots dissolved in it)
Low osmolarity
High Na (PCT heavily affected)

113
Q

What would you find in a urine dipstick in a case of glomerulonephritis?

A

Blood and protein - damage is close to artery.

114
Q

What would you find in a urine dipstick in a case of acute pyelonephritis?

A

Can be normal because the damage is interstitial

Some inflammatory cells and nitrites indicate infection.

115
Q

What would you find in a urine dipstick in a case of pre renal AKI?

A

Difficulty passing any urine
Slight increase in specific gravity and decrease in osmolarity. Some increase in sodium.
Anything drastic could indicate that it has deteriorated into acute tubular necrosis.

116
Q

What would you find in a urine dipstick in a case of post renal AKI?

A

Anuria

117
Q

Give 3 endogenous Nephrotoxins?

A

Myoglobin (eg rhabdomyelysis)
Bilirubin (eg in cirrhosis)
Urate (eg gout)

118
Q

Give 3 nephrotoxic drugs.

A

Ace inhibitors
NSAIDs
Gentamicin

119
Q

Give a nephrotoxic substance present in sepsis.

A

Endotoxins eg E Coli.

120
Q

What is the main cause of post renal AKI? Can you give some specific examples?

A

Obstruction- renal stones (must block both kidneys), post TB strictures, prostate enlargement, tumour, blocked catheter

121
Q

What is the most important life threatening symptom of AKI? How should it be treated?

A

Hyperkalaemia leading to a sine wave ecg.

Give ca gluconate to prevent sudden cardiac arrest.

122
Q

What are the indications for dialysis?

A
  1. Intractable Hyperkalaemia
  2. Intractable fluid overload
  3. Metabolic acidosis
  4. Dialysable Nephrotoxins eg aspirin OD
  5. eGFR of 8-10
  6. Uraemic symptoms
123
Q

What is a normal GFR?

A

About 100 (90-120)

124
Q

At what GFR does mortality start to increase in ckd?

A

75

125
Q

What are uraemic symptoms? What do they indicate?

A

Nausea and vomiting
Weight loss
Pruritis (itching)

In someone with ckd it is an indication to start dialysis.

126
Q

Give some risk factors for ckd.

A 
Advancing age
South Asian ethnicity
Diabetes
Hypertension
Is harming heart disease
127
Q

What are the 3 most common causes of ckd?

A
  1. Hypertension and vascular damage
  2. Diabetes
  3. Ischaemic heart disease

(Idiopathic is most common)

128
Q

Give some paediatric causes of ckd.

A

IgA nephropathy

Polycystic kidney disease

129
Q

Give some complications of ckd.

A

Ischaemic heart disease
Renal anaemia
Metabolic bone disease
Metabolic acidosis

130
Q

Why does Ischaemic heart disease arise from ckd? How would you prevent it?

A

Vascular damage
Statin for lipid levels
ACE for blood pressure

131
Q

Why does renal anaemia arise from ckd? How would you treat it?

A

Decreased production of erythropoietin

IV erythropoietin

132
Q

How does metabolic acidosis arise from ckd? How would you prevent it?

A

Kidney can’t reabsorb as much hco3 as it should

Oral NaHCO3

133
Q

How does metabolic bone disease arise from ckd? How would you treat it?

A

Decrease in active vitamin d decreases ca
Kidney can’t excrete phosphate so it binds to ca and leaves less free ca

Low ca
High PTH

Osteoporosis etc

Treat with active vitamin d

134
Q

In kidney disease, when should ACE be used?

A

Angiotensin constricts efferent arteriole. Ace dilates efferent arteriole

AKI - ace is toxic because it further lowers GFR
CKD - ace is protective, especially in proteinuria because less starling forces less protein out. Also rests the kidney.

135
Q

In kidney disease when should NSAIDs be used?

A

Prostaglandins relax afferent arteriole. NSAIDs constrict afferent arteriole.

Further decrease GFR in both AKI and CKD.
Toxic!!

136
Q

Where would a transplanted kidney be plumbed in?

A

Iliac artery

137
Q

Why do people on dialysis still accumulate morbidity?

A

Because it can only improve GFR slightly to about 15.

138
Q

What are the two types of dialysis?

A

Haemolytic

Peritoneal

139
Q

Give 2 advantages and 5 disadvantages of haemolytic dialysis.

A
  1. Less responsibility
  2. Days off
  3. Travel time and lack of flexibility
  4. Severe fatigue
  5. Risk of loss of consciousness or exsanguination
  6. Food and fluid restriction
  7. AV fistula required
140
Q

Give 3 advantages and 5 disadvantages of peritoneal dialysis.

A
  1. Independence
  2. Flexibility
  3. Less food and fluid restrictions
  4. Frequent peritonitis
  5. Leaks
  6. Hernia
  7. Need to be capable and dexterous
  8. Frequent bag changes.
141
Q

Give four key symptoms of nephrotic syndromes.

A
  1. Proteinuria (O)
  2. Hypoalbumenaemia (loss through podocytes damage)
  3. Oedema (decrease oncotic draw)
  4. Hyperlipidaemia (liver up regulation to produce more albumen)
142
Q

Give 3 key symptoms of nephritic syndromes.

A
  1. Haematuria with red cell casts
  2. Hypertension
  3. Low urine output
143
Q

What is the likely site of damage in nephrotic syndrome?

A

Podocytes leading to leaking of protein…

144
Q

What is the likely site of damage in nephritic syndrome?

A

Endothelium leading to blood loss, clotting, low perfusion and AKI

145
Q

Give 3 causes of nephrotic syndrome

A
  1. Minimal change glomerulonephritis/focal segmental glomerulosclerosis (kids/adults)
  2. Membranous glomerulonephritis (common)
  3. Diabetes
146
Q

How does diabetes cause nephrotic syndrome

A

Microvascular damage leading to mesangial sclerosis (inflammatory thickening of bm and damage to podocytes)

147
Q

Give 3 causes of nephritic syndrome.

A

IgA nephropathy
Good pastures
Wegeners granulomatosis

148
Q

What is a normal urine output and what would be considered to be Anuria?

A

500ml to 3 L

Anuria is less than 50ml

149
Q

What is a normal range for serum HCO3?

A

22-29

150
Q

What is a normal range for serum Na?

A

133-146

151
Q

What is a normal range for serum K?

A

3.5-5.3

152
Q

What is a normal range for serum creatinine?

A

60-120

153
Q

What is the difference between ionised Ca and total serum Ca? Give their normal ranges.

A

Ionised is free ca, total includes albumen bound.
Need to look at ionised only or adjusted total because otherwise it might be confounded by a low albumen.

Ionised - 1.1-1.4
Total - 2.2-2.6

154
Q

What type of vitamin d is reported in a lab result?

A

Calcidiol

This is the type that has been conjugated by the liver but has not been activated by the kidney.
It is the type that is usually given as a supplement

155
Q

Which type of vitamin D is usually given as a supplement? Why? When would this be inappropriate?

A

Calcidiol. Yet to be activated by kidney.

Inappropriate in CKD so give calcitriol (activated). But this is powerful so minimise use.

156
Q

What is a normal range for serum pH?

A

7.35-7.45

157
Q

What is a normal range for serum glucose?

A

3.3-6

But under 11 is acceptable for a random non fasting.

158
Q

What is the ideal hba1c to aim for?

A

Less than 6.5%

PPE - Rhianna (7 decks)

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