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ESA 3 > Urinary System > Flashcards

Urinary System Flashcards

1
Q

What is the predominant cation and anion in the extracellular fluid?

A

cation is sodium and anion is chloride

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2
Q

How do the kidneys affect the intra-cellular composition of ions?

A

By directly affecting the concentration of ions and small molecules in the ECF

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3
Q

How is ultra-filtrate different to plasma?

A

Ultra-fitrate doesn’t contain cells and large organic molecules that are found in plasma

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4
Q

What are the 5 main functions of the urinary system?

A

Control the concentration of substances in the ECF and therefore control the osmolarity of the ECF. Also, to control pH, excrete waste products and control the volume of ECF.
These then impact on blood pressure, cell function and cell size

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5
Q

From what type of mesoderm does the urinary system originate?

A

Intermediate mesoderm

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6
Q

What are the 3 embryological types of kidney systems and how are they different?

A

Pronephros is initial one, in cervical region. Never functions in humans but does involve nephrotomes and develops alongside a duct which runs from cervical region to cloaca.
Next is Mesonephros which develops caudally to pronephros. This is the embryonic kidney. It’s duct is functional but can’t conserve water so can’t concentrate urine. It also sprouts the ureteric bud which drives the development of the final stage.
Metanephros is last one, which starts off as metanephric blastema. This develops into the true kidney. The ureteric bud makes conact with the blastema and eventually develops into calyces and the renal pelvis

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7
Q

Through what developmental error, can there by duplication of the ureter?

A

By complete splitting of the ureteric bud

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8
Q

What are the three parts of the urogenital sinus?

A

Bladder part, pelvic and phallic sections

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9
Q

What are the four parts of the male urethra?

A

pre prostatic, prostatic, membranous and spongy

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10
Q

How many litres, roughly, of ECF are there?

A

About 15 litres

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11
Q

Roughly at which vertebral level, are the kidneys located?

A

T12-L3

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12
Q

Which are the three most common sites of blockage caused by kidney stones?

A

Junction of renal pelvis and ureter
Where ureter crosses pelvic brim
Where ureter enters bladder wall

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13
Q

What are supernumerary renal arteries?

A

Where there’s more than one renal artery going to one kidney

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14
Q

What parts of the nephron are located in the medulla?

A

Loop of Henle and collecting duct

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15
Q

What is the average GFR?

A

Roughly 125 ml/min

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16
Q

What are the two main sections of the renal corpuscle and what are they made up of?

A

Vascular pole - afferent and efferent arterioles and the glomerulus
Urinary pole - Bowman’s capsule

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17
Q

What makes up the filtration barrier of the renal corpuscle?

A

The visceral layer of bowman’s capsule (podocytes) and capillary endothelium (v leaky + fenestrated)

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18
Q

Where in the nephron is lined by simple squamous epithelium?

A

Glomerulus parietal layer and endothelium
Thin descending and ascending limb on loop of Henle
Everywhere else is simple cuboidal

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19
Q

Where in the loop of Henle does active transport not take place?

A

Thin limbs

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20
Q

What makes up the juxtaglomerular apparatus?

A

Macula densa
Juxtaglomerular cells of afferent arteriole
Extraglomerular mesangial cells

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21
Q

Compare the appearance of the collecting duct to the thick ascending limb

A

Both have simple cuboidal but collecting duct lumen is larger and less regular

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22
Q

Describe the path that collecting ducts take through the renal medulla

A

Ducts merge to form larger ducts. First form ducts of bellini, then renal papillae and then exit into calyx

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23
Q

What layers of smooth muscle are there in the urinary bladder?

A

2 Circular layers and 1 longitudinal

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24
Q

How does the diameter of glomerular arterioles contribute to filtration?

A

Diameter of afferent arteriole is always slightly bigger than the efferent arteriole so pressure of blood inside the glomerulus is increased so there’s increased hydrostatic pressure so filtration is promoted

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25
Q

What are the 3 forces involved in plasma filtration?

A

Hydrostatic pressure in cappilary
Hydrostatic pressure in capsule
Osmotic gradient between capillary and tubule

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26
Q

What types of sodium channels are found on apical membranes in different parts of the tubule?

A

PCT - Na-H antiporter and Na-GLucose symporter
Loop of Henle - Na-K-2Cl symporter
Early DCT - Na-Cl symporter
Late DCT and collecting tubule - ENaC

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27
Q

What is the Transport maximum?

A

Renal threshold for glucose = 200mg/ml

Point at which further increases in concentration do not result in increased filtration/excretion

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28
Q

How is clearance calculated?

A

(urine flow rate x amount in urine)/ arterial plasma concentration

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29
Q

What is the reference range for GFR in men and women?

A 
Men = 115-125 ml/min
Women = 90-100ml/min
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30
Q

How is renal plasma flow calculated?

A

Plasma makes up about 55% of renal blood flow. = 0.55 x rbf = 0.55 x 1.1 = 605ml/min

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31
Q

How is filtration fraction calculated?

A

= gfr divided by renal plasma flow

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32
Q

What is the autoregulatory response to decreased BP?

A

Dilation of afferent arteriole to increase hydrostatic pressure in capillary

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33
Q

What is the tubular glomerular feedback response to increased NaCl concentration?

A

GFR needs to decrease so juxtaglomerular apparatus is stimulated to release adenosine to cause vasoconstriction of afferent arteriole

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34
Q

What happens to ECF volume if sodium excretion is less than sodium uptake?

A

Sodium is retained, primarily in ECF so water leaves the nephron which increases ECF volume. There is therefore an increase in blood volume and arterial pressure and there may subsequently be oedema

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35
Q

What channels are there apically in Section 1 of the PCT?

A

Sodium/glucose co transporter
Na/H exchanger
Contransport of sodium with amino acids/ carboxylic acids/ phosphate
also aquaporin channels

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36
Q

What electrolyte transport occurs apically in S2/S3 of PCT?

A

Na/H exchange

paracellular and transcellular chloride transport

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37
Q

What are the driving forces behind water reabsorption of PCT?

A

Oncotic force of peritubular capillary
Osmotic gradient between tubule and interstitium
Hydrostatc force in intersitium

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38
Q

Describe sodium reabsorption in descending limb of loop of Henle

A

Doesn’t absorb sodium but instead has no tight gap junctions so there’s paracellular uptake of water

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39
Q

Describe sodium reabsorption of ascending limb

A

Descending limb concentrated filtrate so there’s reabsorption of sodium through NaKCC2 channel and secretion of potassium via ROMK channel.

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40
Q

Describe sodium reabsorption of DCT

A

Early DCT isn’t very permeable to water to is very diluting. Sodium is reabsorbed via Na/Cl- symporter. There’s also calcium reabsorption

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41
Q

Describe action of principle cells of collecting duct

A

70% of cells in CD are principal cells.
Reabsorb sodium through ENaC but this sets up electrical gradient in lumen for paracellular chloride uptake. Also variable uptake of water through aquaporin 2 channels, sensitive to ADH

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42
Q

What are the four neurohormonal factors that control blood pressure?

A

RAAS
Natriuretic peptide hormone
ADH
sympathetic nervous system

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43
Q

How does the sympathetic nervous system act to increase blood pressure?

A

Acts on alpha1 receptors to cause vasoconstriction of afferent and efferent arterioles to decrease renal blood flow and so GFR. This stimulate reabsorption of sodium via NHE of PCT. Also stimulates renin release
Also acts on beta1 receptors to increase rate and force of heart contraction

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44
Q

How does atrial natriuretic peptide act to control blood pressure?

A

Release from atrial myocytes in response to stretch (increased BP) cause vasodilation of afferent arteriole of glomerulus to increase sodium excretion by increasing GFR

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45
Q

When is renin released?

A

Due to reduced perfusion pressure at baroreceptors in afferent arteriole of kidney.
Also due to reduced NaCl concentration at macula densa. Granular cells of juxtaglomerular apparatus is sympathetically stimulated to release renin

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46
Q

How does renin lead to angiotensin 2 production?

A

Renin cleaves angiotensinogen into angiotensin 1. this is cleaved into angiotensin 2 by ACE

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47
Q

What actions does angiotensin 2 have?

A

Breaks down bradykinin to reduce vasodilation
Acts on vascular smooth muscle to cause vasoconstriction of arterioles
Acts on PCT to increase sodium reabsorption.
Acts of principal cells of collecting duct to stimulate sodium reabsorption via ENaC channels
Stimulates release of noradrenaline
Stimulates release of ADH from hypothalamus

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48
Q

What action does ADH have?

A

Inserts aquaporins into apical membrane of principal cells in collecting duct to increase water retention
Stimulates NaK2Cl in thick ascending limb to increase sodium reabsorption

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49
Q

Why are prostaglandins important in blood pressure control?

A

Have vasodilation action and locally act to enhance glomerular filtration and decrease sodium reabsorption. Act as a buffer to excessive vasoconstriction caused by SNS and RAAS

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50
Q

Why are NSAIDs dangerous to give to patients with renal/cardiovascular disease?

A

Inhibit formation of prostaglandins so in renal disease, cause further vasoconstriction so further reduction of GFR and can cause acute renal failure.
Can exacerbate heart failure and hypertension by increasing sodium and so water retention.

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51
Q

What are some adrenal causes of secondary hypertension?

A

Conn’s syndrome - aldosterone secreting adenoma
Cushing’s syndrome
Phaeochromocytoma - tumour of adrenal medulla

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52
Q

How does renovascular disease cause hypertension?

A

Occlusion of renal artery decreases perfusion pressure in that kidney so renin is stimulated to be released from JGA cells causing vasoconstriction and increased sodium reabsorption in other kidney

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53
Q

How can hypertension be treated?

A

ACE inhibitors
Thiazide diuretics - inhibit Na/Cl cotransporter in DCT but can cause hypokalaemia
Beta blockers to decrease heart rate and contractility
vasodilators - alpha1 blockers reduce sympathetic tone
calcium channel blockers reduce entry into smooth muscle cells

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54
Q

What is the steady osmolality of body fluid?

A

275-295 mOsm/kg

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55
Q

Where are changes in osmolarity detected?

A

By osmoreceptors in Organum Vasuloum of the Laminae Terminalis in the hypothalamus

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56
Q

What maintains the concentration gradient set up by the loop of Henle and counter current multiplication?

A

Counter current exchange by Vasa Recta

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57
Q

Where is ADH released from?

A

Posterior pituitary gland

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58
Q

What effects does ADH have on different parts of the nephron?

A

Vasoconstriction of afferent arteriole
Increased Na, K and Cl reabsorption in TAL
Increased water reabsorption in late DCT and CD
Increased K+ secretion in cortical CD
Increased urea reabsorption in Medullary CD

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59
Q

How does ADH increase water reabsorption?

A

Causes insertion of Aquaporin 2 channel on apical membrane, via a GPCR. There are always aquaporin 3 and 4 present so water enters cell and leaves across basolateral membrane. AQP2 is then retrieved by endocytosis in absence of ADH

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60
Q

What happens in SIADH syndrome?

A

Loss of negative feedback of ADH secretion so there’s massive water retention, causing big drop in blood osmolarity and so causes hyponatraemia

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61
Q

In plasma, in what forms does calcium exist?

A

45% as free ionised calcium
45% protein bound (80% of which bound to albumin)
10% complexed to citrates/phosphates etc

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62
Q

How is intestinal absorption of calcium controlled?

A

By vitamin D.

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63
Q

Where in the nephron is calcium reabsorbed?

A

65% in PCT
25% in loop of Henle
10% in DCT

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64
Q

Where is vitamin D produced?

A

D2 is absorbed in the gut and D3 is synthesised in the skin in the presence of UV light

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65
Q

How is vitamin D activated?

A

Hydroxylated in liver to calciferol then it travels to the kidneys where it’s hydroxylated to calcitriol, it’s activa form

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66
Q

What actions do calcitriol and PTH have on calcium?

A

Calcitriol binds to calcium in the gut, increasing its absorption
PTH Increases conversion of calciferol to calcitriol. It also increases reabsorption of calcium from kidney and increases its release from bone and decreases reabsoprtion of phsophate and bicarbonate

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67
Q

What are the main causes of hypercalcaemia?

A

Primary hyperparathyroidism

Hypercalcaemia of malignancy, either haematologcial or non-haematological

68
Q

How is hypercalcaemia managed?

A

Loops diuretics and hydration to increase excretion
Bisphosphonates to inhibit bone breakdown and calcitonin to oppose pTH
Treat underlying condition

69
Q

What factors can lead to renal stone formation?

A

Low urine volume
hypercalcuria
Low urine pH <5.47

70
Q

How are renal stones managed?

A

Increasing fluid intakes and restricting intake of oxalate, sodium, calcium and animal protein

71
Q

How much HCO3- is filtered by the kidneys each day?

A

4500 mmol

72
Q

What is the average excretion of H+ by the kidneys, per day?

A

50-100mmol

73
Q

What are the effects of alkalaemia?

A

decreased Ca2+ solubility so nerve excitability. If pH is more than 7.45 there’s paresthesia and tetany
Above 7.55 there’s a 45% mortality rate and above 7.65 there’s an 80% mortality rate

74
Q

What are the effects of acidaemia?

A

Increases plasma potassium (hyperkalaemia) by increased activity of H+/K+ exchanger. There’s decreased cardia and skeletal muscle contractility, decreased glycolysis and decreased hepatic function. If pH is less than 7.1 there are severe effects. If it’s lower than 7.0 effects are life-threatening

75
Q

What can cause metabolic acidosis?

A

Tissues producing acid or decreased kidney function meaning decreased HCO3-

76
Q

How can the two different causes of metabolic acidosis be distinguished between?

A

By calculating the anion gap. If there’s decreased kidney function, HCO3- will be replaced by Cl- but if it’s due to acid production then when H+ is produced, there will also be another anion produced.
Do calculation of concentrations of (Na+ + K+) - (Cl- + HCO3-) should be around 10-15 mmol/l
If more than this then HCO3- has been replaced by a different anion and acidosis is due to tissues producing acid, rather than decreased kidney function

77
Q

How can more HCO3- be made by the kidneys?

A

Kidneys are highly metabolically active so produce a lot of CO2 + H20. these react to give H+ + HCO3- the H+ is secreted into lumen and HCO3- enters the ECF
Also, can be made from amino acids. eg glutamin goes to alpha ketoglutarate which breaks down into HCO3- + NH3
HCO3- enters ECF and NH3 reacts with H+ to give ammonium (NH4+) which is excreted in urine

78
Q

How can H+ be excreted in the DCT?

A

By combining with ammonia to give ammonium

By combining with HPO4^2- to give H2PO4-

79
Q

Why does persistent, severe vomiting cause metabolic alkalosis?

A

Increased alkaline tide so increased HCO3- in plasma. Also, there’s decreased volume so kidneys try to take up more Na+ and Cl- so increased action of NHE so more H+ excreted and more HCO3- excreted.
Can be solved by rehydration

80
Q

What are the levels of K+ in the ECF and ICF?

A

ICF - 120-150mmol/l

ECF - 3.5 - 5 mmol/l

81
Q

What are the ECG changes seen in hyperkalaemia?

A

Raised T wave, increased PR interval and depressed ST segment
Then widened QRS complex (atrial standstill)
Eventually ventricular fibrillation

82
Q

What are the ECG changes seen in hypokalaemia?

A

Low T wave and high U wave and depressed AT segment

83
Q

How is K+ handled in different parts of the nephron?

A

67% of K+ is reabsorbed in PCT, irrespective of intake
20% is reabsorbed in TAL, irrespective of intake, driven by Na/K/ATPase and NKCL2
Also some secreted by principle cells of Collecting duct if there are high dietary levels
Intercalated cells of collecting duct reabsorb 10-12% of dietary intake

84
Q

What drives the secretion of K+ from principle cells?

A

Na/K/ATPase sets up gradient of high intracelular K+ and low Na+. Na+ then moves into cell from lumen, down it’s concentration gradient through ENaC. As there’s no accompanying anion, this sets up a negative potential in lumen, which K+ is attracted to so leaves the cell

85
Q

What is meant by external balance of potassium?

A

Balance between GI absoprtion and loss, renal excretion, ECF intake

86
Q

What external balance factors promote secretion of K+ by principal cells?

A

Increased aldosterone, acts by increased protein transcription for ENac and Na+/K+/ATPase channels
Increased ECF K+ concentration as it increases Na+K+ATPase activity
Alkalosis

87
Q

What is meant by internal balance of potassium?

A

Balance between K+ content in ECF and ICF

88
Q

What internal balance factors promote uptake of K+ into ICF?

A

Hormones such as insulin, aldosterone and catecholamines
Alkalosis
Increased ECF potassium concentration

89
Q

What internal balance factors promote shift of K+ into ECF?

A

Low ECF K+ concentration
Exercise in recovery phase of action potential
Cell lysis such as in crush injury (rhabdomyolysis), intravascular haemolysis such as in incompatible blood transfusion or cell lysis in chemotherapy
Plasma tonicity - increased ECF osmolarity draws water out of cells. This increases ICF K+ concentration so it moves out down its concentration gradient

90
Q

What are are the common external balance causes of hyperkalaemia?

A

Increased uptake with decreased renal function

Inadequate renal function due to kidney injury or reduced aldosterone (ACEi, K+ sparing diuretics)

91
Q

What are the common internal balance causes of hyperkalaemia?

A 
Diabetic ketoacidosis (no insulin decreased K+ uptake)
Metabolic acidosis
Cell lysis
92
Q

What is the common external balance cause of hypokalaemia?

A

Excessive loss ie in diarrhoea/vomiting or due to diuretics/high aldosterone levels

93
Q

What’s the common internal balance cause of hypokalaemia?

A

Metabolic alkalosis

94
Q

How should hyperkalaemia be treated?

A

Initially with IV calcium gluconate to decrease its effect on the heart and IV insulin with glucose to promote uptake. Also nebulised beta agonists eg salbutamol.
Depending on severity, maybe dialysis to remove excess

95
Q

How should hypokalaemia be treated?

A

Treat cause
IV or oral K+ replacement
K+ sparing diuretics if due to aldosterone

96
Q

How does COPD lead to type 1 respiratory failure?

A

There’s airway narrowing so increased resistance to ventilation. Therefore there’s a ventialtion perfusion mismatch. Resp rate increases but as there’s decreased elasticity, there’s decreased recoil and it’s harder to force air out. Decreased ventilation means there’s decreased pO2 but pCO2 is still normal

97
Q

How does COPD lead to type 2 respiratory failure?

A

Low pO2 of type 1 resp failure increases respiratory drive. Eventually, ventilation decreases so much that pCO2 is affected and is now main respiratory drive

98
Q

What is shown in spirometry of a patient with COPD?

A 
Reduced FEV1:FVC
If over 80%, mild COPD
If between 50 and 79%, it's moderated
If between 30 and 49% it's severe
and if it's lower than 30, it's very severe
99
Q

How is COPD managed?

A

No cure, only aims to improve health status, mobility, symptoms and number of exacerbations. First advice is to stop smoking as it reduces rate of deterioration.
Can be given steroid/beta agonist inhalers for frequent exacerbations
Activity programmes also used as they improve MRC score

100
Q

What is an exacerbation of COPD?

A

Classed as increase wheeze and dyspnoea also increased sputum and worsening chest tightness and fluid retention

101
Q

How are COPD exacerbations treated?

A

Bronchodilators, antibiotics if indicated by sputum, corticosteroids, oxygen and assisted ventilation

102
Q

What are the common types of normal flora of the respiratory tract?

A 
Viridans streptococci
Neisseria
Anaerobes
Candida
Streptococcus pneumoniae
Streptococcus pyogenes
Haemophilus influenzae
Psuedomonas
E coli
103
Q

What are the specific immune defences in respiratory tract, protecting it from infection?

A

Muco-ciliary clearance mechanism
Coughing and sneezing reflexes
Mucosa - lymphoid follicles in pharynx and tonsils. Mucosa secrete IgA and IgG. Macrophages in alveoli

104
Q

What is hospital acquired pneumonia?

A

Pneumonia that develops at least 48 hours after admission, with no previous signs on admission.

105
Q

What are the organisms that most commonly cause hospital acquired pneumonia?

A

Enteric gram negatives
Pseudomonas
Anaerobes
Staph. aureus

106
Q

What are the most common symptoms of pneumonia?

A 
Malaise
Fever
Productive cough with either clear/purulent or rust coloured sputum
Dyspnoea
Pleuritic chest pain
107
Q

What chest signs are found in pneumonia?

A 
Bronchial breath sounds
crackles
wheeze
dullness on percussion
Increased vocal resonance
108
Q

How is the severity of pneumonia assessed?

A

CURB 65
C - confusion with AMT 7
R - Resp rate over 30
B - Blood pressure 3 signs - consider ITU referral

109
Q

In an immunocompromised host, what oppurtunistic pathogens can cause pneumonia?

A 
Can be normal pathogen that's particularly virulent or an oppurtunistic pathogen:
Cytomegalovirus
Pneumocystis jiroveci
Candida
Aspergillus
Mycobacterium
Cryptosporidia
Toxoplasma
110
Q

What antimicrobials are given in pneumonia?

A

If hosptial acquired, more likely to be gram -ve so IV co-amoxiclav
If community, most common is pneumococcal so give a penicilli.

111
Q

What are some host factors that promote development of a UTI?

A

Shorter urethra, ie in females
Obstruction
Neurological problems leading to residual urine
Ureteric reflex problems

112
Q

What are some bacterial factors that promote the development of a UTI?

A

Faecal flora colonising the perineum
Adhesion by fimbriae and adhesins
K antigens that allow formation of polysaccharide capsule, protecting bacteria against host defences
Haemolysins that cause damage to membranes of urinary tract
Urease, produced by some bacteria that forms ammonia for a favourable environment for survival

113
Q

When might white cells be present in urine but without bacterial growth?

A 
Appendicitis
Previous antibiotic use
Urethritis caused by STI
Vaginal infection or inflammation
Tuberculosis
Chemical inflammation
114
Q

What are the 3 most common causative agents of UTIs?

A

Coliforms such as E coli
Coagulase negative staphylococcus
Proteus

115
Q

How is an uncomplicated UTI treated?

A

Increased fluid intake

3 day course of trimethoprim or nitrofurantoin

116
Q

How is treatment of complicated UTI different to that of an uncomplicated one?

A

Increase antibiotic course from 3 to 5 days.
Follow up with culture to check infection has cleared
Can also use cephalexin as well as trimethoprim and nitrofurantoin

117
Q

How is pyelonephritis treated?

A

14 day course of systemic, broad spectrum antibiotic such as co-amoxiclav or ciprofloxacin

118
Q

What are the symptoms of bacterial cystits?

A 
Dysuria
Frequency
Haematuria
Urgency 
\+/- low grade fever
119
Q

What action to loop diuretics have on the nephron?

A

Block Na-K-2Cl in the loop of Henle so decreased Na and K reabsorption.

120
Q

What action do Thiazide duretics have on the nephron?

A

Block Na-Cl symporter in early DCT so also increases calcium reabsorption.

121
Q

What action do Potassium sparing/aldosterone antagonists have on the nephron?

A

Block aldosterone receptors in late DCT and early collecting duct so decreased transcription of ENac and Na/K/ATPase channels so decreased Sodium reabsoprtion and so decreased K excretion

122
Q

What diseases cause diuresis?

A

Diabetes mellitus
Nephrogenic and cranial diabetes insipidus
Psychogenic polydipsia

123
Q

What adverse effects can arise from diuretic use?

A 
Hypo- and Hyperkalaemia
Hyponatraemia
Hypovolaemia
Increased risk of gout attacks
Glucose intolerance
Increased LDL levels
Erectile dysfunction with thiazides
124
Q

What stimulates urination?

A

Afferent fibres in detrusor muscle sense when bladder is filled with roughly 400mls. These travel through S2-S4 to micturition centre in cerebral cortex. This increases parasympathetic stimulation through pelvic nerve (S2-S4) which releases ACh to contract detrusor muscle. Micturition centre and Pons make conscious decision to urinate which transmits through somatic pudendal nerve to external urethral sphincter to relax - urination

125
Q

What occurs in the continence phase of urination?

A

When bladder is filling, continence centres make conscious decision to retain urine so send signals via pudendal nerve to contract external urethral sphincter. Sympathetic nervous system also transmits via hypogastric nerve (T10-L2) so relax detrusor muscle and contract internal urethral sphincter

126
Q

What is the stress-relaxation phenomenon of the bladder?

A

Bladder walls have many rugae so when bladder distends, these folds disappear but intra-vesicular pressure remains the same

127
Q

What are the 4 main types of urinary incontinence?

A

Stress
Urgency
Mixed
Overflow

128
Q

How is urinary incontinence managed conservatively?

A 
Modified fluid intake
Weight loss
Cessation of smoking
Avoid constipation
Decreased caffeine intake
Timed voiding with fixed schedule
129
Q

How can stress urinary incontinence be surgically managed?

A 
Intramural bulking agents
Fascial sling to support urethra
Low tension vaginal tapes
Open retropubic suspension to correct anatomical position of urethra
in males:
Male sling
Artificial urinary sphincter
130
Q

How can Urge urinary incontinence be pharmacologically managed?

A

Antichlinergics

Botox

131
Q

How can urge urinary incontinence be managed surgically?

A

Sacral nerve neuromodulation
Autoaugmentation to increase functional capacity and decrease pressure
Augmentation cystoplasty
Ileal conduit

132
Q

Where are the main sites of glomerular injury?

A

Subepithelial (podocytes)
Within GBM
Mesangial/paramesangial
Subendothelial

133
Q

What is nephrotic syndrome?

A

More than 3.5 grams of protein lost in urine per day (torrential) most often due to podocyte injury. There’s normally generalised oedema due to decrease in oncotic pressure

134
Q

What are the 3 main primary causes of nephrotic syndrome?

A 
Minimal change glomerulonephritis (in children. flatted foot processes)
Focal segmental glomerulosclerosis (circulating factor. Scarring of podocytes)
Membranous glomerulonephritis ( IgG immune deposits at podocytes)
135
Q

What’s a secondary cause of nephrotic syndrome?

A

Diabetes mellitus (microvascular damage in glomerulus and scarring of basement membrane)

136
Q

What are 2 inherited causes of nephritic syndrome?

A 
Alport syndrome (x - linked) associated with deafness and type 4 collagen in GBM so GBM is thickened and split
Thin glomerular basement membrane syndrome which is benign with isolated haematuria
137
Q

What are 3 non-inherited causes of nephritic syndrome?

A

IgA nephropathy - IgA deposits in mesangium so mesangial proliferation and scarring. Associated with mucosal infections.
Vasculitis - ANCA causes vessel inflammation and glomerulus gets blocked with thrombi. Neutrophils are hyperactivated and so attack endothelium. Causes segmental necrosis and cresents
Goodpasture syndrome - IgG deposits abnormally due to autoantibody against Type 4 collagen in GBM (as well as in pulmonary basement membrane so associated with pulmonary haemorrhage)
Extremely rapidly progressing with hypertension haematuria and general feeling of unwell

138
Q

What’s the difference between focal and diffuse glomerular damage?

A

Focal - affects less than 50% of glomeruli

Diffuse affects more than 50% of glomeruli

139
Q

What is meant by glomerulosclerosis and glomerulonephritis?

A

Glomerulosclerosis is collapse of capillary and scarrin

Glomerulonephritis is inflammation in glomerular tuft

140
Q

How is prostate cancer treated?

A

If localised, with surveillance at first and potentially radiotherapy or a radical prostatectomy
If locally advanced, surveillance and maybe hormones and/or radiotherapy
If metastasised then surgical castration or medical castration where LHRH agonists are given to decrease testosterone. Palliative treatment includes single dose radiotherapy, bisposphonates and chemotherapy

141
Q

What are the symptoms or renal cell carcinoma?

A

Haematuria
Loin pain
Swelling
Hypertension

142
Q

What are some common sites of metastases in renal cell carcinoma?

A

Right atrium
Lymph nodes
Subcapsular fat

143
Q

How can renal cell carcinoma be treated?

A

Surveillance
radical or partial nephrectomy
Removal of kidney, adrenal gland, fat and upper ureter

144
Q

How is upper tract transitional cell carcinoma investigated?

A

Ultrasound
CT urogram
Retrograde pyelogram
Uretoscopy

145
Q

How is bladder carcinoma treated?

A

If low risk and non muscle invasive then consider intravesical chemotherapy
If higher risk and non muscle invasive, give intravesical chemotherapy
If muscle invasive, give neoadjuvant chemotherapy and a radical cystectomy or radiotherapy

146
Q

How does upper tract transitional cell carcinoma present?

A

Haematuria and flank pain

147
Q

How does bladder carcinoma present?

A

haematuria
frequency
dysuria

148
Q

What is oliguria?

A

Abnormally low urine production. Defined as less than 500ml a day or less than 20ml an hour.

149
Q

What is the pre-renal cause of AKI?

A

Reduced renal perfusion. May be due to reduced effective extracellular fluid volume or impaired renal autoregulation.

150
Q

What are some post-renal causes of AKI?

A

Due to obstruction of urine outflow, distal to the renal pelvis. If in pelvis or ureter, needs to be bilateral or for other kidney to be non-functioning.
Cause can be from within the lumen, e.g. clot, calculi, tumour, papillary necrosis
Can be from within wall eg ureteric stricture or congential problem but these normally cause CKD (eg neurogenic bladder)
Can be due to external pressure, eg AAA, malignancy, diverticulitis, prostatic hypertrophy

151
Q

What are some intrinsic causes of AKI?

A

Acute tubular necrosis due to acute ishaemia or due to nephrotoxins.
Glomerular arteriolar disease, often due to immune acute glomerulonephritis
Acute tubular nephritis - inflammation of interstitium due to toxins or infection

152
Q

What are some nephrotoxins?

A

Can be endogenous eg bilirubin, urate of myoglobin from rhabdomyolysis
or exogenous eg drugs such as NSAIDs or ACE inhibitors, CT contrast or antifreeze and weedkiller

153
Q

How is AKI treated?

A

If pre-renal cause, correct volume problem to restore perfusion
If intrinsic acute tubular necrosis, treatment is supportive so avoid further nephrotoxins and maintain perfusion
If post-renal, reestablish flow with urological intervention

154
Q

When is dialysis indicated for AKI?

A

If there’s hypercalcaemia, uraemic symptoms, volume overload, metabolic acidosis, pericardial rub, presence of dialyzable nephrotoxin

155
Q

How can microscopy be used to investigate AKI?

A

If hyaline casts, may be pre-renal cause although they can be present normally
If muddy brown casts, may be acute tubular necrosis
If red blood cells cast, may be Rapidly Progressive glomerulonephritis

156
Q

How is fractional Na excretion used to evaluate Acute Tubular Necrosis?

A

(Urine Na x Plasma creatinine) / (Plasma Na x urine creatinine) x 100
If less than 1, pre-renal AKI
If more than 1, ATN

157
Q

What are some differential diagnoses and what other signs can help confirm diagnosis of glomerular disease?

A 
Polycystic kidney disease
Renal stones
Renal tumour
Arteriovenous malformation
Glomerular disease

If there’s also proteinuria and/or hypertension, more likely to be a glomerular problem

158
Q

What type of macroscopic haematuria is found in glomerular disease?

A

Episodic brown smokey urine with out blood clots

159
Q

What kind of infection can cause nephritic syndrome in children?

A

Streptococcal infection such as impetigo or pharyngitis causing post-streptococcal glomerulonephritis

160
Q

What are some symptoms of chronic kidney disease?

A 
Breathlessness
Lethargy/tiredness
itching
Nausea/vomiting
Sleep reversal
Nocturia
Restless legs 
Aches and pains
161
Q

What can chronic kidney disease be caused by?

A 
Immune system
Infection
Vascula problems
Hypertension
Genetic
Obstruction
Systemic disease
Unknown cause
162
Q

What changes are seen in chronic kidney disease?

A

Functioning renal tissue is replaced by extracellular matrix and there’s glomerulosclerosis and tubular interstitial fibrosis. Progressive loss of excretory and hormonal functions

163
Q

What effect can CKD have on haemopoiesis?

A

Kidneys secrete erythropoietin so when damaged erythropoietin levels fall, there’s decreased red blood cell formation and survival so there are symptoms of anaemia

164
Q

How can serum creatinine levels be used to assess GFR?

A

Calculate eGFR using serum creatinine, age and ethnicity

= 186 x ([serum creatinine] x 88.4) ^-1.154 x age ^-0.203 x 0.742 if female x 1.21 if black

165
Q

What are the differences between acute and chronic transplant rejection?

A

Acute rejection happens within 6 months. There’s increased serum creatinine levels and fever and pain at graft. There’s immune cell infiltrate and tubular damage but responds to further immunosuppression
Chronic rejection happens over 6 months after transplant. There’s progressively increasing creatinine levels and proteinuria. There are vascular changes, fibrosis and tubular atrophy. Doesn’t respond to further immunosuppression

166
Q

How often must haemodialysis be carried out?

A

3 times a week, 4 hours at a time

167
Q

How can the cause of CKD be assessed?

A

Auto-antibody screen
Measure levels of complement, ANCA and CRP
Carry out imaging

ESA 3 (5 decks)

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