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ESA 3 > Urinary > Flashcards

Urinary Flashcards

1
Q

Where are the kidneys located?

A

Retroperitoneal, T12-L3, right kidney slightly lower than left due to liver

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2
Q

Describe the path of the ureters.

A

Arise from the renal pelvis and descend in front of psoas major muscle. Cross pelvic brim near burfication of iliac arteries (anterior to common iliac), and underneath the uterine artery/ ductus deferens (water under the bridge). Enter the bladder posteriorly.

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3
Q

Where are common sites for renal stones to form?

A

Uretopelvic junction
Bifurcation of iliac arteries
Where they enter the bladder

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4
Q

Which is longer:
left or right renal vein?
left or right renal artery?

A

Left renal vein is longer (crosses anterior to AA)

Right renal artery is longer (crosses posterior to IVC)

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5
Q

Describe the arterial supply of the kidneys.

A

Renal artery -> segmental artery -> interlobar artery -> arcuate artery -> interlobular artery -> afferent arteriole -> efferent arteriole

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6
Q

How is a high filtration pressure created in the glomerulus?

A

Afferent arteriole has a wider diameter than the efferent arteriole.

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7
Q

How does the PCT appear histologically?

A

Brush border, simple cuboidal epithelium

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8
Q

How does the thin part of the Loop of Henle appear histologically?

A

Simple squamous epithelium with no brush border

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9
Q

How does the thick ascending limb appear histologically?

A

Simple cuboidal epithelium, no brush border

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10
Q

How does the DCT & collecting duct appear histologically?

A

Wider lumen, many mitochondria, no brush border

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11
Q

How is protein movement repelled in ultrafiltration?

A

Basement membrane and podocytes contain negatively charged glycoproteins

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12
Q

What are the 3 forces involved in plasma filtration?

A

Hydrostatic force in glomerular capillary (pushes fluid out into Bowman’s capsule)
Hydrostatic force of fluid in Bowman’s space (to push fluid back into glomerular capillary)
Plasma oncotic force in glomerular capillary pulling fluid in from the Bowman’s space

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13
Q

In auto regulation, what is the myogenic response to maintain GFR during:
increased arterial BP
reduced arterial BP

A

If increased BP, GFR needs to lower so AA constricts

If decreased BP, GFR needs to increase so AA dilates

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14
Q

In tubular glomerular feedback, what is the role of adenosine and prostaglandins?

A

Adenosine reduces GFR if NaCl increased. It will vasoconstrict afferent/ vasodilates efferent arteriole.

Prostaglandins increases GFR if NaCl decreases. It vasodilates afferent arteriole.

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15
Q

Why is reabsorption isotonic in the PCT?

A

As water leaves when solutes are reabsorbed hence no change in osmolarity.

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16
Q

How is Na reabsorbed in the PCT?

A

On apical membrane is cotransported with AA, glucose (or with Na/H anti porter) down its concentration gradient established by Na/K-ATPase on basolateral membrane.

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17
Q

In the PCT, via what channel is Na reabsorbed with glucose?

A

SGLUT on apical membrane. As this is against glucose concentration gradient and 100% of glucose should be rebabsorbed, glucose diffuses back out via basolateral membrane

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18
Q

What is normal GFR approximately?

A

100ml/min

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19
Q

What substances can be used to measure GFR?

A

Inulin (gold standard) or creatinine, as neither are secreted or metabolised by the body so will pass directly into the urine.

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20
Q

What is the equation for clearance?

A

Clearance = (amount in urine x urine flow rate) / plasma concentration

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21
Q

How does a high volume of distribution affect renal clearance?

A

High Vd indicates molecule/ drug is lipophilic so can leave plasma. This reduces the amount available in the plasma for excretion by the kidneys.

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22
Q

How does a low volume of distribution affect renal clearance?

A

Low Vd indicates molecule is hydrophilic so highly confined to plasma, hence more of the drug molecule is available in the plasma for excretion by the kidneys.

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23
Q

How much Na is filtered out of the descending limb of the loop of Henle?

A

None.

Only water moves out here.

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24
Q

If renal artery BP increases, how does this affect Na and H2O transport in the proximal tubule?

A

Reduced activity of Na channels and Na/K-ATPase, so less Na reabsorbed and hence less water reabsorbed. Promotes excretion of Na and H2O so ECF volume decreases to diminish BP rise.

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25
Q

What channels are on the apical membrane of each segment of the nephron to enable Na reabsorption?

A

PCT: Na/glucose or Na/AA or Na/Pi cotransporters or Na/H anti-porter
LoH: NaKCC symporter
Early DCT: NaCl symporter
Late DCT and collecting tubule: ENaC

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26
Q

What channel on the basolateral membrane drives Na reabsorption?

A

Na/K-ATPase

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27
Q

What is the tonicity of filtrate at the hairpin loop?

A

Very hyperosmotic (very concentrated, lots of water reabsorbed in descending limb so this drives solute reabsorption in ascending limb, initially passive in tAL then active in TAL via NaKCC).

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28
Q

How are solutes transported in the TAL?

A

Na/K-ATPase on basolateral sets up conc gradient. Influx of Na, K & Cl on apical membrane. K+ transported back into filtrate via ROMK in order to maintain NaKCC activity. Cl moves into interstitium.
This region uses the most energy in the nephron so is sensitive to hypoxia.

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29
Q

Is the tubule fluid at the end of the loop of Henle hypo or hyper osmotic?

A

Hypo osmotic (more dilute compared to plasma)

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30
Q

Which channel do thiazide diuretics act on?

A

NCC (Na Cl channel)

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31
Q

Which channel do amiloride diuretics act on?

A

ENaC channels

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32
Q

How are solutes reabsorbed in the early and late DCT?

A

Early: NCC channel is electroneutral, uptake of Na and Cl
Late: NCC and also ENaC channel which is not electroneutral so drives paracellular Cl uptake

Na leaves by Na/K-ATPase on basolateral membrane throughout DCT

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33
Q

What channels are present in the different cell types of the collecting duct?

A

1) principal cells contain ENaC for Na reabsorption and have ROMK for K+ secretion back into filtrate. Variable water uptake via AQP dependent on ADH
2) Type A-IC secrete acid into filtrate and type B-IC secrete bicarbonate into filtrate

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34
Q

What is the equation for mean arterial blood pressure?

A

BP = CO x TPR

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35
Q

What is the equation for cardiac output?

A

CO = HR x SV

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36
Q

How can blood pressure be controlled acutely?

A

Via the baroreceptor reflex
Nerve endings in the carotid sinus and arch of aorta sensitive to stretch and can change sympathetic output
(Eg increase in BP causes stretch so sympathetic output reduced, hence HR reduced and vessels vasodilated)

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37
Q

Which 4 ways can control blood pressure longer term?

A
  • RAAS
  • Sympathetic nervous system
  • ADH
  • ANP
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38
Q

Where is renin released from?

A

Granular cells of juxtaglomerular apparatus

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39
Q

What stimulates renin release?

A
  1. Reduced NaCl in distal tubule
  2. Reduced perfusion pressure (detected by baroreceptor in afferent arteriole)
  3. Sympathetic stimulation to JGA
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40
Q

How does angiotensin II increase blood pressure?

A
  • stimulates Na reabsorption in kidney
  • vasoconstriction of blood vessels
  • stimulates aldosterone release from adrenal cortex (up regulates ENaC & Na/K-ATPase on principal cells of collecting duct)
  • increases thirst sensation at hypothalamus (so more ADH)
  • increases SNS to release NA
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41
Q

Why is a dry cough a side effect of ACE-inhibitors?

A

ACE breaks down bradykinin which has vasodilator effects.

ACEi means bradykinin would accumulate and this can cause a dry cough.

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42
Q

How does the SNS increase BP?

A
  • vasoconstricton of arterioles
  • decrease GFR so less Na excreted
  • stimulates renin release
  • activates Na/H exchanger and Na/K-ATPase in PCTr
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43
Q

When in ADH release stimulated?

A

Due to increase in plasma osmolarity or severe hypovolaemia

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44
Q

How does ADH increase blood pressure?

A
  • Insertion of aquaporins in DCT

- Stimulates NKCC in TAL for more Na reabsorption

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45
Q

How does ANP act to promote Na excretion?

A

Vasodilates afferent arteriole which increases GFR

Also inhibits Na reabsorption along the nephron

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46
Q

When renal perfusion is compromised, why can administration of NSAIDs further reduce GFR?

A

As NSAIDs inhibit the production of prostaglandins, which act as vasodilators to buffer vasoconstriction from SNS and RAAS.

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47
Q

What values classify stage 1, stage 2 and severe hypertension?

A

Stage 1: 140/90 mmHg
Stage 2: 160/100
Severe: 180 systolic, 110 diastolic

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48
Q

How can renovascular disease lead to secondary hypertension?

A

Renal artery stenosis leads to decreased perfusion pressure. This stimulates renin release and activates the RAAS which will cause vasoconstriction and Na retention, even at the unaffected kidney.

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49
Q

What are some adrenal causes of secondary hypertension?

A
  • Conn’s syndrome (aldosterone secreting adenoma)
  • Cushing’s syndrome (excess cortisol which acts on aldosterone receptors to cause Na & H2O retention)
  • Phaeochromocytoma (tumour of adrenal medulla secretes NA & adrenaline)
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50
Q

How can hypertension be treated?

A

Lifestyle! (Diet, smoking, alcohol, exercise)
If secondary, treat cause.
If primary:
- target RAAS: ACEi, angiotensin II antagonists
- vasodilators: L-type Ca channel blockers, or alpha 1 receptor blockers
- diuretics: thiazides inhibit Na/Cl channel in distal tubule, aldosterone antagonists used but not first line

-beta blockers only used if previous MI etc

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51
Q

What is the approximate intracellular and extracellular concentrations of potassium?

A

Intracellular: 120-150 mmol/L
Extracellular: 3.5-5 mmol/L

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52
Q

How is the resting cell membrane established?

A

NOT Na/K-ATPase
But this does make the gradient for K+ to leave via K+ channels, so the inside becomes more negative (& outside more positive) until it reaches an equilibrium of charge with the outside of the cell = resting membrane potential (approx. -90mV)

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53
Q

How does K+ move between cells and the ECF for control of the internal balance?

A
  • moves into cells by Na/K-ATPase

- moves out of cells by K+ channels

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54
Q

What factors increase K+ uptake by cells? (by Na/K-ATPase)

A
  1. Hormones (insulin, aldosterone & catecholamines)
  2. High ECF [K+]
  3. Alkalosis
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55
Q

What factors promote K+ to move out of cells?

A
  1. Exercise
  2. Cell lysis
  3. Increase in ECF osmolarity (so water leaves & K+ follows)
  4. Decrease in ECF [K+]
  5. Acidosis
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56
Q

Why is IV insulin & dextrose used in hyperkalaemia?

A

Insulin increases activity of Na/K-ATPase, so more K+ into muscle and liver cells

(When high K+ in blood, pancreas release insulin)

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57
Q

How does acidosis and alkalosis affect the internal balance of K+?

A

Acidosis = high ECF H+ so H+ moves into cells and K+ moves out (can lead to hyperkalaemia)

Alkalosis = shift of H+ out of cells so K+ moves in (can lead to hypokalaemia)

not a direct pump, just a reciprocal shift

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58
Q

How can hypo- and hyper-kalaemia affect the ECF [H+]?

A

Hypokalaemia causes K+ to move out, so H+ moves in (can cause acidosis)

Hyperkalaemia causes K+ to move in, so H+ moves out (can

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59
Q

Where in the nephron can K+ be secreted?

A

In the principal cells of the late DCT & collecting duct (no set amount, is controlled dependent on intake)

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60
Q

What is the mechanism for K+ secretion by principal cells?

A

Na/K-ATPase sets up conc. gradient for Na+ to be reabsorbed via ENaC channels on apical membrane. This creates an electrochemical gradient for K+ to move out via K+ channels on apical membrane (as outside is more negatively charged)

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61
Q

What factors affect K+ secretion by principal cells?

A
  • controlled by luminal [K+]
  • acidosis will lower Na/K-ATPase so less secretion, alkalosis will increase secretion
  • aldosterone upregulates
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62
Q

What [K+] indicates hyperkalaemia?

A

> 5 mmol/L

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63
Q

What are some causes of hyperkalaemia?

A
  • Increased intake (rare)
  • Decreased renal excretion (Acute/chronic kidney injury, ACEi, K+ sparing diuretics, low aldosterone state eg Addisons)

Changes in internal balance:

  • Metabolic acidosis
  • Exercise
  • Cell lysis
  • Diabetic ketoacidiosis (no insulin)
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64
Q

What are clinical features of hyperkalaemia?

A

Altered excitability of heart: Arrhythmia, heart block
Paralytic ileus
Acidosis

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65
Q

How would hyperkalaemia show on an ECG?

A

High T waves!

Prolonged PR, depressed ST, possible absent P wave

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66
Q

How can hyperkalaemia be treated short term?

A
  • Calcium gluconate
  • Insulin + glucose to shift K+ into cells (always give glucose with insulin to avoid hypoglycaemia) or nebulised beta agonist eg salbutamol
  • Dialysis to remove excess K+
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67
Q

How can hyperkalaemia be treated long term?

A
  • Treat cause (ie if diabetic KA)
  • Dialysis
  • Oral K+ binding medications
  • Reduce intake
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68
Q

What [K+] represents hypokalaemia?

A

< 3.5 mmol/L

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69
Q

What are some causes of hypokalaemia?

A
  • Excessive loss (bulimia, vomiting, diuretics, diarrhoea, high aldosterone)
  • Problems with internal balance eg metabolic alkalosis
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70
Q

How can hypokalaemia present clinically?

A

Muscle weakness
Paralytic ileus
Heart arrhythmias

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71
Q

How can hypokalaemia present on an ECG?

A

Low T waves
Depressed ST
High U wave

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72
Q

How can hypokalaemia be treated?

A
  • Treat causes
  • Oral/ IV replacement therapy
  • K+ sparing diuretics (can block action of aldosterone on principal cells if due to increased mineralocorticoid activity)
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73
Q

How does hypo- and hyperkalaemia affect the resting membrane potential and thus the excitability of the heart?

A

Hypo: outward flow of K+, RMP more hyperpolarised, more Na channels in active form, heart more excitable

Hyper: less outward K+ flow, RMP more depolarised, more Na channels inactivate, heart less excitable

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74
Q

What ratio is pH dependent on?

A

20 times as much HCO3- compared to CO2

HCO3- determined by kidneys, CO2 determined by respiration

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75
Q

What affect does hypoventilation have on acid base balance?

A

Breathe less CO2 off -> hypercapnia
Increase in CO2 lowers pH -> acidosis

= respiratory acidosis

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76
Q

What affect does hyperventilation have on acid base balance?

A

More CO2 breathed off -> hypocapnia
pH increased -> alkalosis

= respiratory alkalaemia

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77
Q

How is pCO2 controlled?

A

Central chemoceptors detect and can change ventilation rates

Peripheral chemoceptors detect changes in pCO2 and pH of plasma (but have an overall smaller effect)

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78
Q

How can changes in CO2 be compensated?

A

By the kidneys

Erythrocytes produce HCO3- but kidneys controls the concentration in the blood

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79
Q

How is metabolic acidosis caused?

A

Increase in H+ produced by cells reacts with HCO3- to form water and CO2.
Drop in HCO3- causes a decrease in pH = metabolic acidosis

Compensated when peripheral chemoceptors detect change in pH and can increase ventilation to reduce CO2.

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80
Q

How is metabolic alkalosis caused?

A

Increase in HCO3- (eg after repeated vomiting) causes a rise in pH = metabolic alkalosis

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81
Q

Why can metabolic alkalosis only be partially compensated?

A

Compensated by lowering CO2, but ventilation can only be reduced by certain amount otherwise o2 supply would be inadequate

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82
Q

How is HCO3- recovered by the kidneys?

A

In PCT, NHE pumps protons out of cell (driven by Na/K-ATPase on basolateral).
The H+ reacts with HCO3- to form water and CO2. CO2 enters cells to react with water and form H+ and bicarbonate. Bicarbonate cotransported out with Na on basolateral membrane.

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83
Q

How can more HCO3- be produced by the kidneys?

A

Have a high metabolic rate so produce lots of CO2 which react with water to form bicarbonate and H+

Can also make bicarbonate from amino acids:

  • in PCT: glutamine -> alpha ketoglutarate which is broken down to form ammonium (enters urine) & HCO3- (enters ECF)
  • in DCT (alpha intercalated cells): CO2 produced in the cells reacts with water to form H+ and bicarbonate. HCO3- leaves on basolateral side, while H+ is buffed on apical side by (HPO4)2-
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84
Q

What is the anion gap and what should it usually be?

A

Calculated as the difference between (Na+ + K+) and (HCO3- + Cl-)

Should be about 10-15 mmol/L

85
Q

What does an elevated anion gap indicate?

A

Metabolic acidosis

HCO3- replaced by another ion eg lactate/ ketones

86
Q

Why is hypokalaemia a risk after persistent vomiting?

A

Kidneys will stop actively secreting H+ as this would worsen metabolic acidosis.
This means that K+ reabsorption is also stopped (anti porter in intercalated cells)

87
Q

If water intake is less than excretion, how does this affect plasma osmolarity?

A

Osmolarity will increase

88
Q

If water intake is more than excretion, how does this affect plasma osmolarity?

A

Osmolarity will decrease

89
Q

What is normal plasma osmolarity?

A

280-310 mOsm/kg (mmol/L)

90
Q

A problem with water balance will affect what?

A problem with Na balance will affect what?

A

Problems with water balance affects osmolarity

Problems with Na balance affect volume

91
Q

How are changes in plasma osmolarity sensed?

A

By hypothalamic osmoreceptors

92
Q

Which two efferent pathways control plasma osmolarity when stimulated?

A

ADH and thirst

93
Q

When is ADH release from the posterior pituitary stimulated?

A

When increased plasma osmolarity is detected by hypothalamic osmoreceptors

(Decreased osmolarity will inhibit ADH release, negative feedback loop)

94
Q

What stimulates a thirst response?

A

Increased plasma osmolarity (or reduced ECF)

Then drinking stops once sufficient fluid has been consumed

95
Q

Where is ADH produced and released?

A

Produced by neurosecretory cells of the hypothalamus

Secreted from posterior pituitary gland

96
Q

What is diabetes insipidus and how can it be managed?

A

Low plasma ADH levels
Hence inadequate volume of water reabsorbed from collecting ducts so a large volume of urine is produced
Can be managed with ADH injections or ADH nasal spray

97
Q

What is the difference between central diabetes insipidus and nephrogenic diabetes insipidus?

A

Central: due to damaged hypothtalamus or posterior pituitary, eg head injury, tumour, encephalitis, aneurysm

Nephrogenic: acquired insensitivity of kidney to ADH (hypothalamus and PP fine)

98
Q

What is SIADH (syndrome of inappropriate ADH release)?

A

Due to excessive ADH release from posterior pituitary (or another source)

Causes dilutional hyponatraemia (due to excess fluid reabsorption, although plasma osmolarity is fine)

99
Q

How does ADH bring about its actions?

A

Causes insertion of AQP 2 into apical membrane of late DCT and collecting duct, so creates a shuttle for water to transport across as AQP 3 and 4 are in basolateral membranes (but needs a hypertonic interstitium)

100
Q

What is the difference between juxtamedullary and cortisol nephrons?

A

Juxtamedullary have longer loop of Henle, important in production of concentrated urine, have vasa recta

Cortical are more abundant, shorter LoH, have peritubular capillary

101
Q

What is the descending LoH limb permeable and impermeable to?

A

Impermeable to Na

Highly permeable to water due to AQP 1 channel which is always open

102
Q

How does the osmolarity of tubular fluid change as it flows down the descending and then up the ascending limb of the loop of Henle?

A

Descending limb permeable to water and not Na, hence osmolarity of tubular fluid increases at the bottom of the loop

Ascending limb is impermeable to water but permeable to NaCl so becomes hypo-osmotic at top of ascending limb, before entering DCT

103
Q

What is the vertical osmotic gradient?

A

Gradient of increasing osmolarity deeper into the medulla (isotonic at corticomedullary border)

104
Q

How is urea recycled as an effective osmole?

A

As its concentration increases in more distal parts of the nephron, more urea flows into interstitium and is recirculated (water follows it out of CCD and then urea flows back into the loop)

105
Q

What maintains the concentration gradient established by the loop of Henle, by acting as a counter current exchanger?

A

Vasa recta, as the flow in the vasa recta is in the opposite direction (descending limb of vasa recta sits next to ascending limb of LoH)

(Vasa recta needed as the osmotic gradient created would not last long if the osmoles were washed out of the interstitium)
* but vasa recta have no facility for active transport *

106
Q

How does water flow into the ascending limb of vasa recta?

A

As the ascending limb of the vasa recta sits next to the descending limb of the LoH, lots of water leaves the descending limb and moves into the ascending limb of the vasa recta

So, water laden blood in the vasa recta is taken up out of medulla to cortex

107
Q

What happens in the descending vasa recta?

A

NaCl flows out of the ascending loop of Henle and diffuses into the vasa recta, so blood at the tip of the hairpin loop in the vasa recta increases in osmolarity.

108
Q

What basic principle do diuretics work by?

A

Block Na and water reabsorption so promote diuresis

109
Q

What is an example of a loop diuretic?

A

Furosemide

Loop diuretics are very potent diuretics

110
Q

Where do thiazides act?

A

DCT (NaCl channels)

Thiazides are less potent than loop diuretics

111
Q

What is an example of a potassium sparing diuretic and what channel does it act on?

A

Amiloride, blocks ENaC channel

112
Q

What is an example of an aldosterone antagonist?

A

Spironolactone

113
Q

What channel do loop diuretics act on?

A

Block NaKCC cotransporters

114
Q

What conditions can loop diuretics treat?

A

Heart failure
Pulmonary oedema
Fluid retention and oedema due to renal failure, cirrhosis, nephrotic syndrome
Hypercalcaemia (as it impairs calcium absorption in LoH so increases renal excretion of Ca)

115
Q

How do thiazides affect Ca absorption?

A

Work on NaCl channel in DCT

Blocking Na absorption here increases Ca absorption (so reduces its loss in urine)

116
Q

What are thiazides widely used for?

A

Hypertension

as they’re less potent than loop diuretics

117
Q

What are the two sub groups of potassium sparing diuretics?

A
  • ENaC channel inhibitors

- Aldosterone antagonists

118
Q

What can be a side effect of potassium sparing diuretics, especially if used with ACEi or K+ supplements?

A

Hyperkalaemia

(ACEi as less aldosterone, so less Na reabsorption and less K+ secretion)

(So usually use ENaC inhibitors with loop diuretics/ thiazides to minimise K+ loss)

119
Q

What is the best drug to treat hypertension due to Conn’s syndrome (primary hyperaldosteronism)?

A

Aldosterone antagonists

120
Q

What diuretics can cause:
Hyperkalaemia
And hypokalaemia?

A

Hyperkalaemia can be caused by potassium sparing diuretics or aldosterone antagonists

Hypokalaemia can be caused by thiazides and loop diuretics

121
Q

Since diuretics can cause hyper and hypo- kalaemia, how can this be overcome?

A
  • use a combination of a loop or thiazide alongside a K sparing antagonist
  • use a loop or thiazide with K+ supplements

(Avoid using K+ supplements with a K+ sparing diuretic though!!)

122
Q

How does glomerular disease cause peripheral oedema?

A

Increase in GBM permeability to protein so more protein lost in urine -> low plasma albumin -> reduced oncotic pressure -> draws fluid in

123
Q

What are some adverse affects of diuretics?

A
  • potassium problems
  • hypovolaemia
  • hyponatraemia
  • other specific problems (eg thiazides can cause erectile dysfunction)
124
Q

What are renal stones made of?

A
  • Majority calcium stones (calcium oxalate with calcium phosphate, or calcium phosphate alone, uric acid stones, struvite stones = infection stones)
  • other types eg cysteine stones, drug stones
125
Q

Why do renal stones form?

A
  • if solvent contains more solute
  • decrease in water content
  • increase in mineral content
  • change in urine pH (so decrease in solubility of solute in urine)
126
Q

Alkaline urine favours the formation of which stones?

A

Calcium phosphate stones

127
Q

Acidic urine favours the formation of which stones?

A

Uric acid stones and calcium oxalate stones

128
Q

What are Randall’s plaque?

A

How calcium oxalate stones form, with a core of calcium phosphate that is surrounded by calcium oxalate

129
Q

How does PTH increase serum Ca levels?

A
  • stimulates osteoclasts
  • stimulates Ca reabsorption from intestines
  • stimulates renal Ca reabsorption
  • stimulate calcitriol formation
  • increases phosphate excretion
130
Q

How does vitamin D increase serum Ca?

A

Increase absorption from gut

Increase reabsorption from bone

131
Q

What is calcitonin?

A

Hormone from C cells of thyroid to lower serum Ca
Inhibits osteoclasts
Increases renal excretion

132
Q

Which renal stone is radiolucent (cannot be seen on x Ray)?

A

Uric acid stones

133
Q

What are struvite stones?

A

Infection stones more common in women

Often form a stag horn calculus (cast of the collecting system)

134
Q

What are some causes of Hypercalcaemia?

A
  • increased PTH (due to parathyroid hyperplasia, tumour, or PTHrp from malignancy)
  • destruction of bone tissue (primary bone marrow tumour, bone metastises, Paget’s disease, immobilisation)
  • other: eg thiazides, excessive vitamin D intake
135
Q

How does Hypercalcaemia present?

A

Opposite of hypo!! (=tetany)

  • renal stones
  • moans (depression, lethargy)
  • painful bones (fractures)
  • groans (gallstones, abdominal pain, constipation, peptic ulcers)
136
Q

Which dermatomal level does renal colic distribute in?

A

L1

137
Q

What is renal colic?

A

Excruciating bouts of pain lasting 20-60 minutes due to peristaltic contractions when ureter attempts to expel the stone

138
Q

How do renal stones present?

A
  • mostly asymptomatic
  • renal colic
  • dull ache pain in loins if stones in kidney
  • UTIs recurrently
  • haematuria
  • urine outflow obstruction
139
Q

How can renal stones be investigated?

A
  • mixed stream urine
  • catch stones in sieve and analyse
  • abdominal x Ray (but can’t see uric acid stones)
  • CT (can see all stones)
  • analyse serum (U&Es etc)
140
Q

What are some complications that can occur from renal stones?

A
  • acute pylonephritis
  • necrosis of renal parenchyma
  • urinary obstruction causing kidneys to swell
  • ulceration through wall of collecting system
141
Q

How can urinary stones be treated?

A
  • analgesia
  • bed rest
  • warmth to site of pain
  • ESWL (high intense pulses of energy to fragment the stone so it can be passed)
  • ureteroscopy
  • cut through skin into kidney and remove stone
142
Q

How can renal stones be prevented?

A
  • drink more water!!
  • thiazides to lower urine calcium
  • potassium citrate to alkalinise urine (reduce calcium oxalate, uric acid and cysteine stones BUT may induce calcium phosphate stones)
143
Q

How do the symptoms differ between a lower UTI and an upper UTI?

A

Lower UTI = cystitis
-frequency, urgency, burning sensation, dysuria

Upper UTI = acute pyelonephritis
-fever, loin pain, also +/- frequency, urgency

144
Q

What is the difference between uncomplicated and complicated UTI?

A

Uncomplicated is by a usual organism (ie coliform) in someone with a normal urinary tract and normal urinary function.

Complicated is usually in males and children, or by a virulent organism (eg Staph aureus), or in someone with an abnormal urinary tract (eg catheter) or with impaired renal function or impaired host defences (eg poorly controlled diabetes)

145
Q

How is a suspected UTI investigated?

A
  • no need to culture if uncomplicated!

- culture if complicated, ie pregnant, male, child,

146
Q

How is a urine specimen collect?

A
  • mid stream urine specimen is more representative or urine in the bladder
  • may get false positive from collection bags due to bacteria on skin
  • transport at 4C with boric acid to preserve
147
Q

What does dipstick testing look for in the urine?

A
  • turbidity (turbid indicates infection)
  • nitrites (some bacteria have enzymes that reduce nitrates to nitrites)
  • leukocyte esterase
  • proteinuria
  • haematuria
  • dipstick cannot diagnose eg as older patients or catheterised patients may have bacteria anyway so must culture for complicated cases *
148
Q

How are UTIs treated?

A
  • drink more water!!
  • uncomplicated: 3 day course
  • complicated lower UTI: 5-7 days course
  • address underlying disorders eg enlarged prostate, diabetes
149
Q

What antibiotics can and cannot be used for UTIs?

A

Cannot use amoxicillin at 50% of isolates are resistant!!

Use trimethoprim or nitrofurantoin

150
Q

How would pyelonephritis be treated?

A 
14 day course
Not nitrofurantoin!
Use Co-amoxiclav
Ciprofloxacin effective as 7 day
Possibly IV
151
Q

When would prophylaxis for UTIs be considered?

A

If 3+ infection in a year and no underlying condition

Use singly nightly dose of trimethoprim or nitrofurantoin

152
Q

What are the layers of the detrusor muscle?

A

Transitional epithelium
Inner longitudinal muscle layer
Middle circular muscle layer
Outer longitudinal muscle layer

153
Q

What is the innervation of the detrusor muscle?

A

Parasympathetic:

  • pelvic nerve S2,3,4
  • contracts
  • ACh to M3 receptors

Sympathetic:

  • hypogastric nerve T10-L2
  • relaxes
  • NA to beta 3 receptors
154
Q

What is the innervation of the internal urethral sphincter?

A

Sympathetic

  • hypogastric nerve T10-L2
  • contraction
  • NA to alpha 1 receptors
155
Q

What is the innervation of the external urethral sphincter?

A

Somatic motor

  • pudendal nerve S2,3,4
  • ACh to nicotinic receptor
  • contraction
156
Q

What is the normal voiding reflex?

A

Bladder feels full at about 400ml
Brain Micturition centre send signal to spinal Micturition centre which activates parasympathetic stimulation
Signal to bladder via pelvic nerve to contract detrusor muscle and increase intravascular pressure
Cerebral cortex makes decision to urinate and reduce somatic stimulation to the external urethral sphincter so it relaxes, and urine can be expelled

157
Q

How is urine stored in the bladder?

A

Bladder has folds so can fill with urine with little change in its pressure
At 400 ml stretch receptors signal to brain to void, but sympathetic activation via the hypogastric nerve causes the detrusor muscle to relax, and the internal urethral sphincter to contract
Cerebral cortex makes the the conscious decision not to urinate, and increases somatic stimulation to the external urethral sphincter so it contracts

158
Q

What are the types of urinary incontinence?

A

Stress UI (involuntary leakage on exertion/ cough/ sneeze)

Urgency UI (involuntary leakage accompanied with urgency)

Mixed UI

159
Q

What are some risk factors for urinary incontinence?

A 
Age
Childbirth
Pelvic prolapse
Obesity
Co-morbidities
Menopause
Family predisposition
160
Q

How can general urinary incontinence be managed?

A
  • lifestyle interventions (fluid intake, smoking, obesity, less caffeine, fixed voiding schedule)
  • contained devices (sheath device, incontinence pads)
161
Q

How can SUI be managed?

A
  • pelvic floor training
  • Duloxetine drug
  • surgery (females: vaginal tapes, intramural bulking agents, sling procedures)
    (males: artificial urinary sphincter is gold standard)
162
Q

How can UUI be managed?

A
  • voiding schedule
  • botulinum toxin (inhibit ACh release so it cannot act on M3 receptors at detrusor so prevents contraction by pelvic nerve )
  • anticholinergics (act on M2 and M3 receptors)
  • beta 3 adrenoceptor agonists
163
Q

What is minimal change glomerulonephritis?

A 
Minimal change visible, can only see damage to podocytes with electron microscopy
Mainly in childhood
Heavy proteinuria/ nephrotic syndrome
Responsive to steroids
Low progression to renal failure
164
Q

What is FSGS?

A 
= focal segmental glomerular sclerosis 
Nephrotic 
Adults
Less responsive to steroids
Circulating factor damages podocytes (transplants)
Can progress to renal failure
165
Q

What is the commonest cause of nephrotic syndrome in adults?

A

Membranous glomerulonephritis

Immune complex subepithelial deposits

166
Q

Which is the commonest glomerulonephropathy causing haematuria?

A

IgA nephropathy
Relationship with mucosal infections (as IgA is activated so can deposit in nephron)
Often progresses to renal failure

167
Q

What are examples of hereditary nephropathies?

A

-Thin GBM Nephropathy
thin GBM
isolated haematuria

-Alport syndrome
x linked 
abnormal collagen IV
abnormal BM
associated with deafness
168
Q

What is the difference between proteinuria and nephrotic syndrome?

A

Proteinuria is excess serum proteins in urine (<3.5g in 24hours) usually due to podocyte damage causing widening of the fenestration slits so protein leaks out.

Proteinuria is a less severe nephrotic syndrome.
Nephrotic syndrome is >3.5g of protein in urine over 24 hours which reduces oncotic pressure in the blood so leads to generalised oedema.

169
Q

What is Goodpastures syndrome?

A

Acute onset of severe nephritic syndrome
Autoimmune
Auto antibody to collagen IV in BM but only affects kidney
Haematuria
Treatable by immunosuppression and plasmaphoresis

170
Q

What is vasculitis?

A

Autoimmune inflammation of blood vessels
Affects kidney as it is highly vascularised
No immune complex but associated with ANCA

171
Q

What are some risk factors for prostate cancer?

A
  • increasing age
  • family history (BRCA2 gene mutation)
  • race (black > white > Asian)
172
Q

How can suspected prostate cancer be investigated?

A

Digital rectal examination
Serum PSA (prostate specific antigen)
Ultrasound guided biopsy of prostate
MRI/ bone scan for metastises

173
Q

How can prostate cancer be treated?

A 
Surveillance 
Robotic prostatectomy 
Chemotherapy 
Radiotherapy
Hormones
174
Q

What is the most common type of bladder cancer?

A

Transitional cell carcinoma

175
Q

What are some risk factors for bladder cancer?

A

Smoking
Occupational exposures (hydrocarbons, rubber, plastic, paint etc)
Schistosomiasis

176
Q

What is a common symptom of bladder cancer, renal cancer and prostate cancer?

A

Haematuria

177
Q

How can renal cell carcinoma be treated?

A

Nephrectomy (removal of kidney, adrenal, upper ureter and surrounding fat)

178
Q

How can bladder cancer be treated?

A

Cystectomy (remove bladder and womb)
Radiotherapy
Chemotherapy

179
Q

What is the difference between AP and PA projection of a CXR?

A

Usually do PA, patient standing and x Ray source from behind

Do AP if patient too unwell to stand
Will show scapulas more prominently and heart will appear larger

180
Q

How many anterior ribs and how many posterior ribs should be visible on a CXR?

A

5-7 anterior

8-10 posterior

181
Q

What is the DR ABCDE approach when analysing a CXR?

A 
D= demographics (name, age, PA/AP)
R= RIPE (rotation, inspiration, picture, exposure)
A= airways
B= breathing
C= circulation
D= diaphragm 
E= everything else
182
Q

What is the cardio thoracic ratio?

A

Measure widest part of heart and the ribs laterally. If over 50
% then the heart is enlarged.

183
Q

What does air below the right side of the diaphragm indicate?

A

Bowel perforation

184
Q

How would COPD appear on a CXR?

A

Hyperinflated lungs
Blunting of costophrenic angles
Flattened hemidiaphragms

185
Q

When may the trachea deviate?

A
  • lobe collapse (towards affected lung)
  • pneumonectomy (towards affected lung)
  • massive pleural effusion (away from affected lung)
  • tension pneumothorax (away from affected lung)
186
Q

When would percussion be hyper resonant and when would it be dull?

A

Dull over solids eg organs and ‘stony dull’ over fluid ie pleural effusion

Hyper resonant over hollow structures ie pneumothorax

187
Q

What is the endocrine function of the kidney?

A

Renin
Erythropoietin
Activated vitamin D

188
Q

What are some signs and symptoms of kidney disease?

A 
Often asymptomatic
Signs often relate to reduced function eg...
-Hyperkalaemia 
-Na overload -> H2O overload -> oedema/ hypertension
-Acidosis
-Proteinuria
-Haematuria
-Glycosuria
-More frequent urination

Hormonal function reduced:

  • anaemia (less erythropoietin)
  • hypertension (more renin)
  • metabolic bone disease (less vitamin D activated)
189
Q

What is the most common cause of macroscopic Haematuria?

A

IgA nephropathy

190
Q

What is the classic triad of findings in nephrotic syndrome?

A
  • proteinuria >3.5g/24 hours
  • hypoalbuminaemia
  • oedema

(Diagnose with renal biopsy)

191
Q

What are causes of nephrotic syndrome?

A
  • Minimal change
  • Focal segmental glomerulonephritis
  • Membranous glomerulonephritis
192
Q

Why can nephrotic syndrome present with xanthelasma?

A

High plasma lipid levels due to increased excretion of lipoproteins
Also increased liver synthesis of lipids due to hypoalbuminaemia

193
Q

How can nephrotic syndrome clinically present?

A
  • oedema
  • muehrckes bands on nails (Unknown pathogenesis)
  • xanthelasma
  • fat bodies in urine
  • increased DVT risk
194
Q

What is the most common nephritic syndrome?

A

Post-streptococcal glomerulonephritis (IgA nephropathy)

195
Q

What are some difference between nephrotic and nephritic syndrome?

A

Nephrotic syndrome is more gradual, associated with more proteinuria, less Haematuria, more oedema, low albumin

Nephritic syndrome has a faster onset, associated more with Haematuria, raised blood pressure

196
Q

What is an acute kidney injury?

A

Reduction in actual GFR
(hence increase in nitrogenous waste products, upset of ECF volume, electrolyte balance and acid base disturbance)

increase in serum creatinine!!

197
Q

What are causes of AKI?

A
  • pre-renal: volume depletion, heart failure, obstruction
  • renal: renal artery occlusion/ glomerular disease, ischaemic acute tubular necrosis, toxic acute tubular necrosis
  • post-renal: urinary tract obstruction eg cancers, prostatic hyperplasia
198
Q

How does the kidney respond to pre renal AKI when actual GFR is reduced due to reduced renal blood flow?

A

Auto regulation

Reduce afferent arteriole tone and increase efferent arteriole tone

199
Q

How may NSAIDs and ACEi/AII antagonists affect renal auto regulation?

A

NSAIDS reduce prostaglandins so less vasodilation of afferent arteriole

ACEi mean less angiotensin II to vasoconstrict efferent arteriole

200
Q

What are some causes of pre renal AKI?

A

-Reduced ECF:
Blood loss, heart failure, systemic vasodilation (eg due to cirrhosis/ sepsis/ anaphylaxis)

-Impaired renal auto regulation:
NSAIDs, ACEi, sepsis

201
Q

What is ATN and what can it be caused by?

A

Acute tubular necrosis due to…

  • ischaemia
  • nephrotoxins
  • sepsis

ATN is not usually necrosis but damaged cells that can’t reabsorb water or salts or expel excess water

202
Q

What are examples of nephrotoxins?

A

Endogenous (eg myoglobin released due to muscle necrosis from rhabdomyolysis)

Exogenous (drugs eg ACEi, NSAIDs, aminoglycosides, poisons, x Ray contrast)

203
Q

What determines creatinine concentration?

A
  • renal function

- muscle mass (age, sex, race)

204
Q

When is eGFR not useful?

A
  • only in adults, not children
  • needs to be corrected for black patients
  • not useful for AKI, only CKD
205
Q

What are some consequences of CKD?

A
  • acidosis (treat with oral NaHCO3)
  • anaemia (less erythropoietin produced, can treat with SC erythropoietin injections)
  • metabolic bone disease (less active vit D -> osteomalacia, also increase in phosphate causes drop in Ca so PTH increases)
206
Q

At what eGFR level is dialysis required?

A

Usually 8-10 ml/min

207
Q

What are the options for renal replacement therapy?

A
  • haemodialysis
  • peritoneal dialysis
  • kidney transplant (best for survival)
208
Q

Which arteriole has the juxtaglomerular cells on?

A

Afferent arteriole

ESA 3 (6 decks)

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