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ESA 3 > Urinary System > Flashcards

Urinary System Flashcards

1
Q

What type of muscle is found in the ureter?

A

Smooth

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2
Q

What makes up the medullary rays found in the pyramids of the renal medulla?

A

Collecting ducts

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3
Q

Which ribs can the kidneys be found by?

A

11 and 12

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4
Q

From anterior to posterior, what structures exit the hilum of the kidney?

A

Renal vein
Renal artery
Ureter

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5
Q

What are the functions of the kidney?

A

Regulation and control of key substances
Excretion
Endocrine (renin, erythropoietin, prostaglandins)
Metabolic (vitamin D activation, insulin, PTH, calcitonin)

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6
Q

If the kidneys fail to control extracellular fluid, what changes can occur?

A

Change in blood pressure
Tissue fluid
Cell function

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7
Q

What is ultrafiltrate in the kidney?

A

Water, ions and small molecules with the same composition as plasma filtered into the nephron.

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8
Q

What are the four parts of the nephron?

A 
Glomerulus
Proximal convoluted tubule
Loop of Henlé
Distal convolute tubule
Collecting duct
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9
Q

What is the general function of the glomerulus?

A

Act as a filter to form the ultrafiltrate

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10
Q

What is the general function of the proximal convoluted tubule?

A 
Major site of absorption
60-70% sodium and water
80-90% potassium
90% bicarbonate
100% glucose and amino acid
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11
Q

What are peritubular capillaries?

A

Capillaries in the kidney which remove reabsorbed materials

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12
Q

What is the main function of the loop of Henlé?

A

Further reabsorption of salts

Creation of osmotic gradient for counter-current multiplication

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13
Q

What is the function of the distal convoluted tubule?

A

Variable reabsorption of electrolytes and water.
Removes sodium and chloride
Active secretion of hydrogen ions

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14
Q

What is the function of the collecting duct?

A

Water reabsorption - variable permeability

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15
Q

Why is the right renal vein short than the left?

A

The left renal vein must pass over the aorta, the right kidney is closer to the inferior vena cava

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16
Q

What artery does the left renal vein pass beneath?

A

Superior mesenteric artery

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17
Q

What can happen if the left renal vein passes under the abdominal aorta?

A

Nephrotic syndrome

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18
Q

What two veins drain into the renal vein on the left, but directly into the inferior vena cava on the right?

A

Suprarenal vein

Gonadal vein

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19
Q

Describe the fat surrounding the kidney

A

Perinephric fat completely surrounds the kidney
Enclosed by extraperitoneal fascia
Layer of paranephric fat posteriorly and posteriolaterally to the kidney on top

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20
Q

What is a polar artery in the kidney?

A

A remnant of the migration of the kidney during development

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21
Q

What joint of the pelvis does the ureter most commonly cross?

A

Sacroiliac joint

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22
Q

What is the first place that the renal pelvis first narrows before the ureter?

A

Pelviuretic junction

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23
Q

What type of muscle is found in the bladder?

A

Smooth

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24
Q

What is the trigone in the bladder?

A

A triangle between the ureteric orifices and the urethral exit which is histologically different from the rest of the bladder and unable to distend

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25
Q

Why can you not palpate a full bladder?

A

It lies below the pubic symphysis

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26
Q

Give the path of blood entering the kidney through the renal artery to the renal vein.

A 
Renal artery
Segmental artery
Interlobular artery
Arcuate artery
Interlobular arteries
Afferent arteriole
Glomerulus
Efferent arteriole
Peritubular capillaries (cortical)/ vasa recta (juxtamedullary)
Interlobular veins
Arcuate vein
Interlobular vein
Renal vein
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27
Q

What are the three kidney systems that develop sequentially, in order?

A

Pronephros
Mesonephros
Metanephros

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28
Q

What is the first kidney system which has renal function in development?

A

Mesonephros

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29
Q

What is the urogenital ridge in development?

A

Region of intermediate mesoderm which becomes the embryonic kidney and gonad. Contains the mesonephros.

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30
Q

What structure in development does the ureteric bud sprout from?

A

Mesonephric duct

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31
Q

What is the function of the ureteric bud in kidney development?

A

Induce undifferentiated mesoderm to form the metanephric blastema

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32
Q

What does the ureteric bud become in the mature renal system?

A

Collecting system.

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33
Q

What is the embryologic origin of accessory renal arteries?

A

As the kidney ascends it creates new blood supplies, sometimes these fail to detach and remain into adulthood.

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34
Q

What is renal agenesis?

A

When the ureteric bud fails to interact with the mesoderm. If unilateral, may remain undetected into adulthood. If bilateral, can be identified in utero by causing low amniotic fluid (oligohydramnios)

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35
Q

What is Wilms’ tumour?

A

A congenital childhood cancer, derived from metanephric blastema cells which have remained in the mature kidney.

Causes a painless, swollen abdomen, occasionally with a large, palpable lump. Other symptoms include a fever and cachexia.

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36
Q

What is an ectopic ureter?

A

When the ureter terminates at a location other than the bladder, such as the urethra or bladder. Causes urinary incontinence as it bypasses sphincter control. Can increase risk of UTIs.

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37
Q

What causes duplication defects?

A

When the ureteric bud splits or two form, causing more than one inductive event.

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38
Q

What is the difference between multicystic renal dysplasia and polycystic kidney disease?

A

Multicystic - congenital atresia of the ureter (narrowing because loss of patency) causing multiple non-communicating cysts to form. Kidney is non functional.

Polycystic - autosomal recessive disease causing abnormal fluid-filled cysts to form in the kidney. Presents early and has good prognosis.

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39
Q

What is the allantois?

A

Part of the gut tube which is continuous with the umbilicus and is used for gas exchange and waste excretion in the placenta.

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40
Q

What are the three parts of the urogenital sinus?

A

Bladder
Pelvic
Phallic

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41
Q

What is the mature derivative of the allantois?

A

Urachus (median umbilical ligament)

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42
Q

What is formed if the urachus remains fully patent?

A

Urachal fistula

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43
Q

What is formed if the urachus remains partially patent with the umbilical end is closed?

A

Urachal cyst

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44
Q

What is the difference in maturation of the mesonephric duct in males and females?

A

Male - becomes ductus deferens. Its connection with the urogenital sinus forms the prostate and prostatic urethra.

Female - regresses

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45
Q

What part of the urogenital sinus forms each segment of the male urethra?

A

Pre-prostatic, prostatic and membranous - pelvic

Spongy - phallic

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46
Q

What is extrophy of the bladder?

A

A congenital anomaly where the urinary bladder protrudes through the abdominal wall

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47
Q

What is hyperspadus?

A

Defect in the fusion of the urethral folds due to androgen insensitivity or not enough produced. The urethra opens on the ventral surface rather than the glans.

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48
Q

What vertebra can the kidneys be found between?

A

T12 to L3

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49
Q

What are the three kidney systems, in sequential order of development?

A

Pronephros
Mesonephros
Metanephros

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50
Q

What is the pronephric duct in kidney development?

A

A duct passing from the cervical region with the pronephros to the cloaca, driving development of the meso- and metanephros

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51
Q

What is the nephrotome?

A

Primitive nephron

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52
Q

What is the urogenital ridge in development?

A

A region of intermediate mesoderm which becomes the embryonic kidney and gonad. Contains the mesonephros.

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53
Q

What primitive kidney has the full function of a developed kidney?

A

Metanephros

Mesonephros can’t conserve water

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54
Q

Where does the ureteric bud sprout from?

A

Mesonephric duct

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55
Q

What is the function of the ureteric bud in kidney development?

A

Induces undifferentiated mesoderm in the caudal region to form a metanephric blastema.
Expands and differentiates into the major and minor calyces.
Drives differentiation of functional nephrons in the blastema

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56
Q

How are accessory renal arteries formed?

A

On ascent of the developing metanephros it develops new arterial supplies which sometimes fail to regress

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57
Q

What is renal agenesis and what causes it?

A

Failure of one or both kidneys to form.

The ureteric bud doesn’t interact with the mesoderm.

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58
Q

Describe Wilm’s tumour.

A

Congenital childhood cancer
Believed to be derived from cells in the metanephric blastema which have remained in the developed kidney
Causes a painless swollen abdomen, fever, cachexia

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59
Q

Describe an ectopic ureter.

A

When the ureter terminates at a location other than the bladder such as urethra or vagina.
Causes incontinence as it bypasses sphincter control.

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60
Q

What causes duplication defects in the kidneys?

A

When the ureteric bud splits or two form, causing more than one inductive event.

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61
Q

What is the difference between multicystic renal dysplasia and polycystic kidney disease?

A

MRD - congenital atresia of the ureter causing multiple non-communicating cysts to form. The kidney is non-functional.

PKD - autosomal recessive disease causing abnormal fluid-filled cysts to grow in the kidney. Presents early and has a poor prognosis.

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62
Q

What is the allantois?

A

Tube attached to the urogenital sinus which is continuous with the umbilicus and is used for gas exchange and waste excretion in the placenta.

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63
Q

What is the adult derivative of the allantois?

A

Urachus (median umbilical ligament)

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64
Q

What are the three parts of the urogenital sinus, from superior to inferior.p?

A

Bladder
Pelvic
Phallic

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65
Q

What part of the urogenital sinus does the mesonephric duct open into?

A

Pelvic region

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66
Q

What is the difference in development of the urogenital sinus and associated structures in males and females?

A

In both, the sinus enlarges and fuses with the ureteric bud junctions to allow drainage into the bladder

In males the mesonephric duct remains and becomes the ductus deferens. The connection with the pelvic urogenital sinus forms the prostate and prostatic urethra. The prostatic, pre-prostatic, and membranous urethra are formed from the pelvic part of the sinus. The spongy urethra is formed from the phallic part of the sinus.

In females the mesonephric ducts regress as there are no testicular androgens to support it. Female urethra is formed from the pelvic sinus

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67
Q

What is extrophy of the bladder?

A

Congenital anomaly where the urinary bladder protrudes through the abdominal wall

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68
Q

Describe hyperspadus.

A

Defect in the fusion if the urethral folds in the male due to androgen insensitivity, or if not enough is produced. The urethra opens on the ventral surface of the penis rather than the glans.

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69
Q

Describe the undifferentiated external genitalia and it’s differing fate in males and females.

A

Undifferentiated - genital tubercle, folds and swelling

Male - genital tubercle elongates and folds fuse to form the spongy urethra.

Females - no fusion so the urethra opens into the vestibule

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70
Q

What duct do tubules in the medulla drain through into the minor calyces?

A

Duct of Bellini

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71
Q

Briefly describe how the renal corpuscle is firmed.

A

The ureteric bud is a blind-ended tube which envelops the glomerulus, creating a double-layered cover.
Visceral layer of the Bowman’s capsule envelops the capillary walls with the basement membrane between them, making up the filtration barrier.
The parietal layer forms a funnel to collect the ultrafiltrate and pass it into the PCT.

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72
Q

What creates the filtration slits in the renal corpuscle?

A

Podocyte’s long processes which interdigitate.

The capillary has a highly fenestrated epithelium.

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73
Q

Where does reabsorption begin in the nephron?

A

Proximal convoluted tubule

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74
Q

Describe the epithelium of the proximal convoluted tubule.

A

Simple cuboidal

Brush border

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75
Q

What are the four areas of the loop of Henlé, from proximal to distal?

A

Pars recta
Thin descending limb
Thin ascending limb
Thick ascending limb

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76
Q

Describe the epithelia of the thick ascending limb of the loop of Henlé.

A

Simple cuboidal

No brush border

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77
Q

Describe the epithelium of the thin limb of the loop of Henlé.

A

Simple squamous

No brush border

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78
Q

Describe the epithelium of the distal convoluted tubule.

A

Simple cuboidal

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79
Q

What are mesangial cells in the juxtaglomerular apparatus?

A

Specialised smooth muscle cells around blood vessels which help to regulate blood flow through the capillaries.

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80
Q

What is the function of juxtaglomerular cells??

A

Synthesis, storage and secretion of renin.

Activated when poorly perfused.

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81
Q

What is the macula densa in the juxtaglomerular apparatus?

A

Specialised cells in the distal convoluted tubule close to the glomerulus.
Sense an increase in sodium chloride concentration and secretes a paracrine vasopressor to decrease glomerular filtration rate.

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82
Q

Where do the renal pyramids empty?

A

Renal papilla.

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83
Q

How do renal stones cause renal colic?

A

They become stuck in the ureter, which spasms as it can’t contract properly.

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84
Q

How many layers of smooth muscle are in the ureter?

A

2

3 in the lower third

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85
Q

How many layers of smooth muscle are there in the bladder?

A

3

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86
Q

What epithelium lines the bladder?

A

Transitional

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87
Q

Describe the difference between cortical and juxtamedullary nephrons

A

Cortical - shorter loop of Henlé, small glomerulus in outer cortex, loose arrangement of peritubular capillaries, high renin, good sympathetic innervation, afferent arteriole has a greater diameter than efferent, disorganised flow

Juxtamedullary - loop of Henlé longer, large glomerulus near medulla, peritubular capillaries in parallel (vasa recta), almost no renin, poor sympathetic innervation, afferent and efferent arterioles have the same diameter, flow of blood opposite to filtrate

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88
Q

What makes up the filtration barrier in the renal corpuscle?

A 
Capillary endothelium
Acellular basement membrane (negative charge to stop proteins passing through)
Podocyte layer (pseudopodia interdigitate to form a slit diaphragm)
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89
Q

In nephrotic syndrome there can be a loss of charge in the basement membrane of the renal corpuscle. What consequences is this likely to have?

A

Albuminurea

Hypoproteinaemia causing generalised oedema

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90
Q

What are the opposing pressures in the renal corpuscle?

A

Hydrostatic pressure of filtration in the capillary (into capsule)

Oncotic pressure between the capillary and tubular lumen, largely by proteins
Hydrostatic pressure of the Bowman’s capsule

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91
Q

Describe the two methods of autoregulation of the pressures in the renal corpuscle to maintain glomerular filtration rate (assuming physiological blood pressure changes)

A

Myogenic response - when the afferent arteriole is stretched due to a higher blood pressure, the smooth muscle contracts. When the opposite happens, the smooth muscle relaxes.

Tubular-glomerular feedback - if renal blood flow increases, the concentration of NaCl in the DCT rises and is detected by the macula densa. This stimulates the JGA to produce adenosine which causes vasoconstriction. If renal blood flow decreases, it is stimulated to produce prostaglandin which causes vasodilation.

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92
Q

What is the function of S-GLUT in the proximal convoluted tubule?

A

Cotransporter for sodium and glucose, moving them against the glucose gradient.
Secondary active transporter.

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93
Q

How is the potassium concentration increase caused by the movement of sodium out of the PCT cells by S-GLUT negated?

A

ROMK channels on the basolateral membrane allows potassium to follow into the interstitium.

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94
Q

What are the consequences of glucose concentrations in the PCT lumen being above the transport maximum for S-GLUT?

A

Glucosuria
Polyuria
Polydipsia

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95
Q

How is H+ secreted into the nephron lumen?

A

Sodium gradient is set up by Na/K ATPase which allows NHE to move H+ into the lumen.

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96
Q

What are the characteristics of the perfect substance used to measure glomerular filtration rate?

A

Freely filtered
Not reabsorbed or secreted
Remains unchanged by filtration

E.g. Inulin

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97
Q

Why is creatinine only used for a quick measure of glomerular filtration rate?

A

It slightly overestimates GFR as a small amount is secreted.

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98
Q

What is the extracellular prominent ion?

A

Sodium

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99
Q

What is the intracellular prominent ion?

A

Potassium

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100
Q

Describe glomerulotubular balance and its function.

A

67% of the sodium is always reabsorbed.

This blunts sodium excretion as a response to GFR changes which occur despite autoregulation.

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101
Q

What transporters are found in S1 of the proximal convoluted tubule?

A 
NHE
S-GLUT
Na-aa
NaPi
Aquaporin
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102
Q

What transport occurs in S2/3 of the proximal convoluted tubule?

A

NHE
Paracellular Cl- movement
Cl- transporters
Aquaporin

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103
Q

Which limb of the loop of Henlé is impermeable to water?

A

Thick ascending limb

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104
Q

What reabsorption occurs in the thin ascending limb?

A

Passive sodium reabsorption paracellularly

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105
Q

What reabsorption occurs in the thick ascending limb of the loop of Henlé?

A

NKCC2 moves sodium

ROMK on the apical membrane to return potassium to the lumen, maintaining a concentration gradient for NKCC2 to function

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106
Q

Describe the location of membrane proteins on the cells of the distal convoluted tubule for sodium and calcium transport.

A

NCC and a calcium channel on apical membrane

NCX and Na/K ATPase on the basolateral membrane

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107
Q

How do thiazide diuretics work?

A

Inhibit NCC in the distal convoluted tubule

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108
Q

What is the difference in function between principle cells and type B intercalated cells in the late distal convoluted tubule and early collecting duct?

A

Principle - reabsorbs sodium through ENaC. Leak of K+ into the filtrate.

Type B - active reabsorption of chloride

Both have AQP2, under the control of ADH

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109
Q

Describe pressure natriuresis and diuresis

A

When the blood pressure increases over what homeostatic mechanisms can control, it causes a reduction in the number of NHE channels and Na/K ATPase activity in the PCT. This reduces Na+ and therefore water reabsorption.
Will affect the 67% sodium reabsorption.
Causes isoosmotic loss so ECF volume decreases, so the initial rise in blood pressure is diminished.

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110
Q

Describe the short term control of blood pressure.

A

Baroreceptor reflex.
Detects the high pressure side of the system - found in the carotid sinus and aortic arch
Indicate changes to the medulla, which signals to the heart and blood vessels.
For rapid response.

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111
Q

Describe the neurohumeral response in controlling blood pressure.

A

Mid to long term
Alters sodium levels to change plasma volume using the RAAS system, sympathetic nervous system, antidiuretic hormone, and atrial natriuretic peptide.

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112
Q

What cells in the kidney produce renin?

A

Granular cells of the juxtaglomerular apparatus

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113
Q

What stimulates the release of renin?

A

Reduction in delivery of sodium chloride to the macula densa
Reduced perfusion pressure (have baroreceptors)
Beta-1 stimulation

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114
Q

What are the steps in converting angiotensinogen to an active product?

A

Renin converts to angiotensin I (no physiological activity)

ACE converts to AgI to angiotensin II

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115
Q

What are the functions of angiotensin II?

A

Vasoconstriction (release noradrenaline)
Stimulate sodium reabsorption
Release aldosterone
Release antidiuretic hormone

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116
Q

Describe the action of aldosterone.

A

Act on the principal cells of the collecting duct.
Increases expression of ROMK and ENaC to promote sodium and water reabsorption.
Promotes action of basolateral Na/K ATPase which enhances the gradient for sodium movement.

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117
Q

What enzymatic activity does ACE have other than conversion of AgI to AgII?

A

Break down bradykinin

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118
Q

How does sympathetic stimulation affect the kidney?

A

Activates NHE and Na/K ATPase in the proximal convoluted tubule
Increases renin release from granular cells
Constriction of afferent and efferent arterioles

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119
Q

What is the function of antidiuretic hormone?

A

Form concentrated urine by controlling the number of AQP2 channels in the distal nephron.
Promotes sodium reabsorption through NKCC2

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120
Q

What is the function of atrial natriuretic peptide?

A

Control on the low pressure side of the system.
Increases the loss of sodium in the system
Causes vasodilation of the afferent arteriole to reduce GFR, inhibiting sodium reabsorption

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121
Q

What effect do prostaglandins have on the kidney in physiological conditions?

A

Vasodilation, increasing GFR

Reduces sodium absorption

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122
Q

Why should you not give NSAIDs to a person with abnormally reduced GFR?

A

They inhibit cyclooxygenase, stopping the production of prostaglandins which would normally cause vasodilation. This further reduces GFR, leading to kidney failure.

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123
Q

What effects does dopamine have on the kidney?

A

Vasodilation reducing GFR

Inhibits NHE and Na/K ATPase

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124
Q

Give the values for mild hypertension.

A

140/90 to 159/99

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125
Q

Give the values for moderate hypertension.

A

160/100 to 179/109

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126
Q

Give the value for severe hypertension.

A

180/100 upwards.

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127
Q

What is the difference between primary and secondary hypertension?

A

Primary - when the cause is unknown

Secondary - when the cause is known

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128
Q

What is renovascular disease and how does it cause secondary hypertension?

A

Stenosis of a renal artery, reducing perfusion pressure in one kidney. This increases renin production, activating the RAAS. This leads to vasoconstriction and sodium retention in the other kidney, leading to a raised blood pressure.

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129
Q

What is renal parenchymal disease and how can it cause secondary hypertension?

A

Disease of the parenchyme so vasodilator substances are lost, causing inadequate GFR. Sodium and water are therefore retained, causing volume-dependent hypertension.

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130
Q

What is Conn’s syndrome?

A

An adenoma which secretes aldosterone, leading to hypertension and hyperkalaemia.

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131
Q

How can a pheochromocytoma cause secondary hypertension?

A

It secretes catecholamines which act on beta-1 receptors in the kidney, and noradrenaline acts on alpha-1 receptors in blood vessels, to cause vasoconstriction and hypertension.

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132
Q

What conditions can prolonged increased afterload due to increased resistance cause in the CVS?

A

Heart failure
Ischaemia
Myocardial infarction

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133
Q

What conditions can prolonged arterial damage lead to?

A 
Myocardial ischaemia
Myocardial infarction
Cerebrovascular disease (stroke/aneurysm)
Aneurysm
Nephrosclerosis leading to renal failure
Retinopathy
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134
Q

What hormones affect calcium homeostasis?

A

PTH
Calcitonin
Vitamin D

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135
Q

What organ(s) does PTH act on?

A

Bones

Kidney

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136
Q

What organ(s) does calcitriol act on?

A

Bone

Small intestine

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137
Q

Describe the pathway in activation of vitamin D, including where each stage occurs.

A

Vitamin D to 25-vit D (calcidiol) in the liver by 25-hydroxylase.

Calcidiol to calcitriol in the kidneys by 1-alpha hydroxylase

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138
Q

Give one condition in which vitamin D deficiency must be corrected with active vitamin D.

A

Chronic kidney disease

Hypoparathyroidism

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139
Q

What is rickets?

A

Soft and weak bones in children due to a lack of vitamin D and calcium

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140
Q

What is osteomalacia?

A

Softening of the bones in adults due to a deficiency in vitamin D or calcium

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141
Q

Describe the effects of PTH on the bone and kidneys.

A

Bone - stimulates osteoclast activity to release calcium and phosphate.
Also has a lesser stimulatory role in osteoblast activity, but chronically high levels cause bone resorption.

Kidney - increases calcium and magnesium reabsorption.
Decreases phosphate and bicarbonate reabsorption
Stimulates 1-alpha hydroxylase

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142
Q

Give some causes of hypercalcaemia.

A

Malignancy in bone
Ectopic production of PTHrP eg. Squamous cell carcinoma
Primary hyperparathyroidism (usually due to a tumour)
Sarcoidosis/TB/lymphoma (granulomas produce 1,25-vitamin D
Myeloma (produces IL-6 which stimulates osteoclast activity)

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143
Q

What are the symptoms of hypercalcaemia?

A 
Kidney stones
Constipation
Depression
Anorexia
Arrhythmia
Vomiting
Hypertension
Diabetes insipidus
Nephrocalcinosis
Apathy
Drowsiness
Polydipsia and polyuria associated with acute kidney injury
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144
Q

How can hypoparathyroidism cause kidney stones?

A

Lots of calcium is passing through the nephron to be excreted

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145
Q

How can hyperparathyroidism cause kidney stones?

A

The calcium levels in the nephron are above the transport maximum and phosphate is being excreted so they can easily react to form stones.

146
Q

What are the risk factors for renal stones?

A

Increasing age
Previous renal stones
Racial differences (caucasian males highest)

147
Q

What substances can renal stones be made from, aside from calcium?

A

Magnesium
Urate
Cysteine

148
Q

What is the management of renal stones?

A 
Below 5mm passes naturally
Drink plenty of fluid
Pain relief
Shock waves to break up stone
Change diet
149
Q

What effect does water intake greater than excretion have on the plasma osmolarity?

A

Decreases

150
Q

What receptors detect plasma osmolarity and where are they located?

A

Hypothalamic osmoreceptors in the OVLT

151
Q

If there is high osmolarity, what do the hypothalamic osmoreceptors stimulate?

A

Thirst centres

Antidiuretic hormone release

152
Q

What general effect does antidiuretic hormone have on the kidney?

A

Increase aquaporin 2 channels in the collecting duct which increases permeability to urea and water.
Increase function of NKCC2 and potassium secretion

153
Q

What feature of the collecting duct membrane allows tight control of aquaporins by ADH?

A

It has a very high turnover of AQP2 channels on the apical membrane

154
Q

What are the differing effects of ADH on the cortical and medullary collecting ducts?

A

Cortical - increases water reabsorption and potassium secretion

Medullary - increases water and urea reabsorption

155
Q

Why is the cortical collecting duct less able to reabsorb water?

A

The gradient is not as steep

156
Q

Briefly describe diabetes insipidus.

A

Not enough ADH is produced, or an acquired condition where the kidney stops responding.
Can be managed by ADH nasal spray or injections

157
Q

Briefly describe syndrome of inappropriate ADH secretion (SIADH).

A

Too much ADH is produced, causing dilutional hyponatraemia.
Total body fluid increases
Can be caused by faults in the posterior pituitary or ectopic release from tumours

158
Q

What structure maintains the corticopapillary concentration gradient in the kidney?

A

Vasa recta

159
Q

What is the significance of urea being used as an effective osmole in the kidney?

A

ADH can alter its permeability so urea can be recycled from the collecting duct into the thick ascending limb. This causes the osmolarity of the interstitium to rise until ADH levels return to normal.

160
Q

Describe counter-current multiplication.

A

As blood descends towards the interstitium, it mimics the concentration, taking up NaCl.
Water is drawn out of the collecting duct by the vasa recta, but it also takes up salt from the interstitium as it is mimicking the environment.
When it reaches the descending limb, more water is reabsorbed, but as it’s impermeable to salt, the blood is diluted.
The dilutional effect is taken up into the cortex.

161
Q

Give the aortic branches from superior to inferior, starting at the coeliac trunk.

A 
Coeliac trunk
Superior mesenteric
Renal
Gonadal
Inferior mesenteric
162
Q

Give the three layers of tissue surrounding each kidney, from internal to external

A

Renal capsule
Adipose capsule
Renal fascia

163
Q

Where does the ureter narrow?

A

Pelviuretic junction
Where it crosses the bifurcation of the common iliac artery
Entrance to the bladder

164
Q

What distinguishes the ureter from nerves and vessels?

A

Peristalses when touched
Adheres to the peritoneum
Whitish cord

165
Q

What arteries contribute to the ureteric blood supply?

A

Renal
Gonadal
Vesicle
Uterine

166
Q

What muscle do the ureters lie on behind the parietal peritoneum?

A

Psoas major

167
Q

What bony landmark defines the course of the ureter in the abdomen?

A

Tip of the transverse processes

168
Q

What nerve is in close relation to the ureters as they run around the side wall of the pelvis?

A

Obturator nerve

169
Q

What is the relationship between the uterine artery and the ureter in the female?

A

Uterine artery is superior

170
Q

Give some host factors which can contribute to a urinary tract infection.

A

Shorter urethra
Obstruction (pregnancy, stones, tumours, hypertrophy of the prostate)
Incomplete emptying of the bladder due to neurological problems
Ureteric reflux, especially in children

171
Q

Give some symptoms of a lower urinary tract infection.

A

Frequent urination
Dysuria
Low grade fever
Uregncy

172
Q

Give some symptoms of an upper urinary tract infection.

A 
Febrile
Acute polynephritis
Loin pain
Dysuria
Frequency of urination (maybe)
173
Q

In an uncomplicated UTI, how do you diagnose it?

A

Urine dipstick - check for nitrite and leukocyte esterase

174
Q

For a complicated UTI, how do you diagnose it?

A

Urine dipstick

Culture the urine

175
Q

What is a complicated UTI?

A 
One which occurs in:
Men
Children
Women after childbearing age
People with catheters
Pregnant women
176
Q

What things would you check for when screening for a UTI?

A 
Turbid urine
Leukocyte esterase
Nitrite 
Haematuria
Proteinyrea

(Leukocyte esterase is key as more specific for infection)

177
Q

When is urine culture especially important in a suspected urinary tract infection?

A

Children
Males
Complicated infections

178
Q

What can cause urethral syndrome?

A

Low count bactiuria
Vaginal infection or inflammation
Sexually transmitted infections

179
Q

What can cause sterile pyuria?

A 
Antibiotics
Urethritis (gonorrhoea/chlamydia)
Vaginal infection or inflammation
Tuberculosis
Appendicitis
180
Q

How can you treat urinary tract infections?

A

Increase fluid intake
Address underlying disorders
3 day antibiotics if uncomplicated (usually trimethoprim)
7 day antibiotics if complicated
Longer if systemically unwell (co-amoxiclav or gentomicin)

181
Q

What is a diuretic?

A

A substance which promotes diuresis

182
Q

How does aldosterone affect reabsorption in the distal convoluted tubule and collecting duct?

A

ENaC channels on the apical membrane to reabsorb sodium, creating a negative lumen potential.
K+ channels use this to excrete potassium.
Aldosterone increases the expression of both these channels, increasing reabsorption of sodium and excretion of potassium.

183
Q

What diuretics directly block sodium channels?

A

Loop diuretics inhibit NKCC2

Thiazide diuretics inhibit NCC

Potassium sparing diuretics inhibit ENaC

184
Q

How do osmotic diuretics work?

A

They are freely filtered at the glomerulus but aren’t reabsorbed so increase the osmolarity of the tubular fluid, promoting water excretion.

185
Q

What channels are present in the loop of Henlé which aid the movement of sodium and potassium?

A

NKCC2

ROMK

186
Q

What conditions could you use loop diuretics in?

A 
Heart failure (for diuretic effect as well as veno/vasoconstriction
Acute pulmonary oedema
Nephrotic syndrome
Acute hypercalcaemia (with IV fluid)
Renal failure
Liver cirrhosis
187
Q

How do thiazide diuretics work?

A

Bind to the Cl- transporter of NCC

Increase calcium absorption

188
Q

What conditions can you use thiazide diuretics?

A

Chronic hypertension due to vasodilator properties

Not useful in renal failure

189
Q

What are the contraindications for using amiloride or spironolactone diuretics?

A

Renal failure (causes hyperkalaemia)
ACE inhibitors
Potassium suppliments

190
Q

When would you use spironolactone as a treatment?

A

Conn’s syndrome (adrenal hyperplasia or tumour causing primary hyperaldosteronism)
Ascites and oedema due to cirrhosis of the liver
Heart failure (combined with loop diuretics)
Hypertension (combined with another diuretic)

191
Q

When would you use amiloride?

A

In combination with a potassium-losing diuretic

192
Q

What can carbonic anhydrase inhibitors be used as a treatment for?

A

Glaucoma

193
Q

What can osmotic diuretics be used as a treatment for?

A

Treat cerebral oedema

194
Q

How does congestive heart failure cause ECF expansion and oedema?

A

Increased systemic venous pressure increases hydrostatic pressure in the capillaries, causing fluid to move out.

Drop in cardiac output reduces renal perfusion, activating RAAS, causing sodium and fluid retention

195
Q

How does nephrotic syndrome cause ECF expansion and oedema?

A

Glomerular disease increases the permeability to proteins due to loss of the negative charge on the membrane.
This causes hypoalbuminaemia and therefore low oncotic pressure.
There is a reduced circulating volume as water moves out of the capillaries.
RAAS is activated causing sodium and fluid retention

196
Q

How does cirrhosis of the liver cause ECF expansion and oedema?

A

There is reduced albumin synthesis causing a low oncotic pressure, allowing fluid to move into the tissues.
Increased splanchnic venous pressure due to portal hypertension causes ascites.

197
Q

Why can diuretic use (aside from amiloride) cause hypokalaemia?

A

The rate of potassium secretion depends on its concentration gradient and the rate of sodium reabsorption.
As the use of diuretics decreases sodium reabsorption and increases flow rate, potassium excretion is increases.

198
Q

How can you reduce the risk of life-threatening hypokalaemia when giving someone diuretics?

A

Regularly monitor electrolyte levels
Combine potassium sparing diuretics with those that cause loss
Give potassium suppliments

199
Q

Describe the cause and symptoms of hepatic encephalopathy.

A

Advanced liver failure reduces the ability to convert ammonia to urea.
Ammonia builds in the blood, causing neurological symptoms
Confusion, constructional apraxia (can’t draw a 5-pointed star), flapping tremors, coma

200
Q

Give some negative side effects of using diuretics.

A

Hypovolaemia (can affect blood pressure, dehydration)
Hyponatraemia
Increased uric acid levels, precipitating an attack of gout
Glucose intolerance
Increased LDL
Erectile dysfunction
Gynaecomastia (spironolactone)

201
Q

What membrane protein is essential for maintaining the difference in potassium levels in the ECF and ICF?

A

Na/K ATPase

202
Q

How does a fall in extracellular potassium concentration affect the membrane potential?

A

Hyperpolarises

203
Q

How does a rise in extracellular potassium concentration affect the membrane potential?

A

Hypopolarisation

204
Q

What facilitates the movement of potassium out of cells?

A

ROMK

205
Q

What causes increased uptake of potassium into the intracellular fluid?

A

Hormones acting via Na/K ATPase (insulin, aldosterone, catecholamines)
Increased potassium concentration in the ECF
Alkalosis

206
Q

What causes the movement of potassium out of cells?

A 
Exercise
Cell lysis (necrosis)
Reduced ECF osmolarity
Reduced potassium concentration in the ECF 
Acidosis
207
Q

How does skeletal muscle contraction cause a rise in ECF potassium concentration?

A

There is a net increase in potassium during the resting phase of the action potential. The Na/K pump can’t keep up in strenuous exercise.

208
Q

What are some pathological causes of increased potassium concentration in the ECF?

A

Trauma to skeletal muscle causing rhabdomyolysis
Intravascular haemolysis, such as in G6PD deficiency
Chemotherapy causing tumour cell lysis

209
Q

How can diabetic ketoacidosis cause hyperkalaemia?

A

Increased tonicity of the ECF causing water to move in, increasing potassium concentration in the ICF. Potassium then moves down its gradient.

As hydrogen ions move into cells it forces potassium out.

210
Q

Where in the kidney is the majority of potassium reabsorbed?

A

Proximal convoluted tubule and loop of Henlé

211
Q

Where in the kidneys can the reabsorption of potassium be modified and how?

A

Principal cells of the distal convoluted tubule and cortical collecting duct.
ENaC and ROMK on the apical membrane, and Na/K ATPase on the basolateral membrane.
High intracellular potassium concentration and increased sodium reabsorption promotes potassium loss.
Increased ECF potassium concentration stimulates Na/K ATPase and increases the permeability of ROMK. It also promotes aldosterone secretion which increases transcription of Na/K ATPase, ROMK, and ENaC.

212
Q

How does acidosis affect kidney tubules to alter potassium excretion?

A

Inhibits Na/K ATPase and reduces potassium channel permeability

213
Q

How does alkalosis affect the kidneys to alter potassium excretion?

A

Stimulates Na/K ATPase and increases potassium channel permeability

214
Q

What luminal factors in the nephron increase potassium loss?

A

Increased distal tubular flow rate washes away luminal potassium, increasing its loss.

Increased sodium delivery to the distal tubule increases sodium absorption, causing potassium loss.

215
Q

How is potassium actively absorbed by intercalated cells?

A

Proton pump on the apical membrane moves potassium into the cells as it moves hydrogen out, then potassium moves through a channel on the basolateral membrane

216
Q

Increased intake of potassium generally won’t cause hyperkalaemia, except in which circumstances?

A

Renal dysfunction

Inappropriate dosing given by IV

217
Q

What causes reduced renal excretion of potassium?

A

Acute or chronic kidney injury
ACE inhibitors (affects aldosterone)
Potassium sparing diuretics
Addison’s disease (low aldosterone)

218
Q

What ECG changes are seen in hyperkalaemia?

A 
Tall tented T waves
Prolonged PR interval
Depressed ST
No P wave (atrial standstill)
Ventricular fibrillation
Intraventricular block
219
Q

How can you treat hyperkalaemia?

A

IV calcium gluconate to stabilise the membrane potential
Glucose and insulin IV with nebulised salbutamol to shift potassium into the ICF
Dialysis to remove excess potassium (acute or chronic kidney injury)
Treat the underlying cause
Reduce intake

220
Q

What are the causes of hypokalaemia?

A 
Diarrhoea
Bulimia
Vomiting
Diuretics
Osmotic diuresis (diabetes)
Increased aldosterone
Metabolic acidosis
221
Q

What problems can be caused by hyperpolarisation of the membrane in hypokalaemia?

A

Arrhythmias
Paralytic ileus
Muscle weakness
Nephrogenic diabetes insipidus

222
Q

What are the ECG changes in hypokalaemia?

A

Flat T wave then lost
High U wave
Low ST segment

223
Q

How can you treat hypokalaemia?

A

Treat the cause
Replace potassium
Use a potassium sparing diuretic if high aldosterone

224
Q

How can alkalaemia cause free calcium to drop?

A

Causes it to come out of solution

225
Q

What effect does hypocalcaemia have on neuronal excitability?

A

Increases it

226
Q

What is carbon dioxide level in the blood determined by?

A

Respiratory control from chemoceptors.

227
Q

What is the level of bicarbonate determined by?

A

The kidneys

228
Q

What effect does hypoventilation have on pH?

A

Falls

229
Q

What effect does hyperventilation have on pH?

A

Rises

230
Q

What do central chemoceptors detect the change of?

A

Carbon dioxide

231
Q

What do peripheral chemoceptors detect changes in?

A

Carbon dioxide

pH

232
Q

How can the kidneys compensate for respiratory acidosis or acidosis?

A

Alter the rate of excretion of bicarbonate

233
Q

How can respiration compensate for metabolic acidosis?

A

Drop in pH activates peripheral chemoceptors, which stimulate respiratory neurons in the medulla. This increases ventilation to reduce pCO2

234
Q

How can repeated vomiting cause metabolic alkalosis?

A

More hydrogen ions are being produced to replace that lost from the stomach. Bicarbonate is being produced and taken into the plasma.

235
Q

Describe how bicarbonate is reabsorbed in the proximal convoluted tubule.

A

Bicarbonate and hydrogen ions are converted to carbon dioxide and water in the lumen.
Carbon dioxide and water diffuses into the tubular cells, then dissociates to hydrogen and bicarbonate.
NHE moves hydrogen back into the lumen and sodium into the cell. Na/H ATPase also moves sodium out and hydrogen in on the basolateral membrane. Na-HCO3- cotransporter on the basolateral membrane moves bicarbonate out into the ECF.

236
Q

Where is carbonic anhydrase found in the proximal convoluted tubule?

A

On the brush border

237
Q

How is ammonium and bicarbonate produced in the kidney?

A

Glutamine broken down to alpha-ketoglutarate and NH4+

Alpha-ketoglutarate broken down further to 2HCO3-

238
Q

How are hydrogen ions secreted in the distal convoluted tubule?

A

Using a proton pump

239
Q

Why does hydrogen ion secretion in the distal convoluted tubule not significantly reduce pH?

A

H+ is buffered by NH3+ and filtered HPO4+.

240
Q

How does low pH affect the amount of H+ secreted

A

Enhances NHE activity
Enhances proton pump
Enhances ammonium production in the proximal convoluted tubule through the breakdown of glutamine
Increased capacity to export HCO3- from the tubular cells to the ECF
This all increases the buffering capacity of the urine as well as increasing alkalinity of the ECF

241
Q

Give an example of a condition which can cause metabolic acidosis

A

Diabetic ketoacidosis

Lactic acid production in profound shock

242
Q

Describe what is meant by the anion gap

A

The main cations in the plasma are Na+ and K+, and the main anions are Cl- and HCO3-, so these are the ones which are measured.
A normal anion gap is very small (this is only in the measured amounts, there is no actual gap)
If other anions replace HCO3-, such as ketones, the anion gap will increase.

243
Q

Why is persistent vomiting more likely to cause metabolic alkalosis if there is also volume depletion?

A

The capacity to lose bicarbonate is reduced due tot he high rate of sodium recovery.
Recovering sodium favours hydrogen excretion, and therefore HCO3- recovery, as it utilises NHE

244
Q

What effect does hyperkalaemia have on the acidity of the blood?

A

It can cause metabolic acidosis

245
Q

What are the nerve roots of neurons in control of the storage phase of bladder control?

A

T10 to L2

246
Q

What nerve roots are in control of the voiding phase of bladder control?

A

S2-4

247
Q

What are the functional divisions of the bladder?

A

Body - temporary store of urine
Trigone - sensory
Neck - connects bladder to urethra

248
Q

What is the significance of the bladder being a midline structure?

A

Has bilateral innervation

249
Q

What are the three muscular components in control of micturition?

A

Detrusor urinae muscle
Internal urethral sphincter (physiological)
External urethral sphincter (anatomical)

250
Q

What are the layers of the detrusor muscle?

A

Inner longitudinal
Middle circular
Outer longitudinal

251
Q

Why is it important for the muscles in the bladder to be in every direction?

A

Confers strength irrespective of the direction of expansion

252
Q

What is the difference between internal and external urethral sphincters?

A

Internal - passive valve, physiological sphincter, smooth muscle

External - voluntary control, anatomical sphincter, skeletal muscle

253
Q

Where can the bladder be found?

A

In the true pelvis behind the pubic symphysis

254
Q

What parasympathetic receptors are found in the bladder, and what nerve stimulates them?

A

M3

Pelvic nerve

255
Q

What sympathetic receptors are found in the bladder, and what nerve stimulates them?

A

Beta 3
Alpha 1
Hypogastric nerve

256
Q

What is detrusor-sphincter dyssenergia?

A

When the bladder and sphincter no longer coordinate their relaxation and contraction

257
Q

What parts of the urinary system work together in the continence phase to pass urine into the bladder and store it?

A 
Ureters
Urinary bladder
Bladder neck
Urethra
External urethral sphincter
258
Q

What is the normal capacity of the bladder?

A

300-1000ml

259
Q

What is the communication pathway from the brain to allow micturition?

A

Cerebral cortex
L-region of the pontine continence centre
Sympathetic nuclei in spinal cord
Detrusor muscle and external urethral sphincter motor neurons in the sacral cord

260
Q

What does the sympathetic output from the pons cause in the urinary system?

A

Silence activity of detrusor muscle
Relax detrusor muscle
Increase urethral sphincter pressure
Storage of urine

261
Q

Where do the T10-12 and L1-2 nerves terminate in bladder control?

A

T10-12 inferior mesenteric ganglion

L1-2 hypogastric plexus

262
Q

Where is the somatic outflow for bladder control?

A

Onuf’s nucleus on the ventral horn

S2-4

263
Q

Describe the stress-relaxation phenomenon.

A

Rugae flatten as the bladder fills and stress on the bladder reduces, causing pressure to stay the same.

264
Q

What is the effect of bilateral lesions of the pontine centres in bladder control?

A 
Unable to store urine
Reduced bladder capacity
Excessive detrusor activity
Relax urethra
Premature voiding
Leaking
265
Q

What is the effect of micturition centres that causes voiding of the bladder?

A

Strong contraction of detrusor muscles
Increased pressure
Relax internal urethral sphincter
Voluntary relaxation of external sphincter

266
Q

Give the communication pathway from the brain to allow micturition.

A 
Cerebral cortex (Brodmann's areas)
Pons (M-region, Barrington's nucleus)
Sacral levels of parasympathetic outflow
Detrusor muscle
External urethral sphincter
267
Q

What do the axons of the parasympathetic innervation of the bladder pass through?

A

Nervi erigentes

268
Q

What are the risk factors for prostate cancer?

A

Increasing age
Family history (BRCA 2)
Black>white>asian

269
Q

What are the problems with screening for prostate cancer?

A

Overdiagnosis (increases with benign, infection, inflammation)
Overtreatment
Quality of life (comorbidities of established treatment)
Cost effectiveness

270
Q

What is the presentation of prostate cancer?

A

Asymptomatic
Urinary symptoms (noctiuria, difficulty passing)
Bone pain if metastatic
Haematuria is uncommon

271
Q

How do you diagnose prostate cancer?

A

Digital rectal exam with a serum PSA.

Ultrasound guided biopsy

272
Q

What is acute kidney injury?

A

An abrupt decline in actual GFR.

Upsets the ECF volume, acid-base waste removal, and electrolyte balance. Nitrogenous waste products accumulate.

273
Q

The serum levels of what substance are used to detect acute kidney injury?

A

Creatinine

274
Q

Give some pre-renal causes of acute kidney injury.

A

Cirrhosis of the liver
Heart failure
Haemorrhage
Volume depletion e.g. diuretics paired with vomiting and diarrhoea

275
Q

Give some renal causes of acute kidney injury.

A 
Intrarenal vascular
Glomerulonephritis
Ischaemic ATN
Toxic ATN
Interstitial disease
Intrarenal obstruction
276
Q

Give a brief description of the initial changes to the kidney in prerenal AKI.

A

Actual GFR reduced due to decreased renal flow
No cell damage
High aldosterone and ADH

277
Q

How do NSAIDs and ACEi affect GFR?

A

NSAIDs stop prostaglandin production, preventing vasodilation of the afferent arteriole.
ACEi stop vasoconstriction of the efferent arteriole
They both reduce GFR and prevent autoregulation

278
Q

What can cause impaired autoregulation in the kidney?

A 
Preglomerular vasoconstriction:
Sepsis
Hypercalcaemia
Hepatorenal syndrome
NSAIDs

Post glomerular vasodilation:
ACEi
A2R inhibitors

279
Q

Describe acute tubular necrosis.

A

Cells of the proximal convoluted tubule are damaged so they can’t reabsorb salt/water properly, or expel an overload of water.
Caused by ischaemia, nephrotoxins, and sepsis.

280
Q

Give some examples of endogenous nephrotoxins.

A

Myoglobin
Bilirubin
Urate

281
Q

Give some examples of exogenous nephrotoxins.

A 
Endotoxins
Contrast
ACEi
Gentomycin
NSAIDs
Weed killer
Antifreeze
282
Q

What causes acute tubulo-interstitial nephritis?

A

Infection - acute pyelonephritis

Toxins - penicillins, PPI, NSAIDs

283
Q

Why must both kidneys be affected to cause post-renal acute kidney injury?

A

One kidney can function on its own

284
Q

Give some causes of post-renal acute kidney injury.

A

Stones, blood clots, tumours in the lumen
In the wall - congenital megaureter, strictures post-TB
Outside - enlarged prostate, aortic aneurysm, ureter ligation, tumours (uterus/cervix)

285
Q

What changes in blood biochemistry are you likely to see with AKI?

A

High urea and creatinine

May have hyperkalaemia, hyponatraemia, hypocalcaemia, hyperphosphataemia

286
Q

What would you notice on examination that would suggest that your patient is volume-depleted?

A 
Cool periphery
High pulse
Low blood pressure, postural hypotension (relative)
Low JVP
Low skin turgor
287
Q

What would you notice on examination that would suggest that your patient is volume-overloaded?

A

Gallop rhythm
May have blood pressure change (relative)
Raised JVP
Pulmonary and peripheral oedema

288
Q

What would you notice on examination that would suggest that your patient has a severe infection?

A 
Pyrexia
Rigor
Vasodilation, warm periphery
Bounding pulse 
Rapid capillary refill
Hypotension
289
Q

What would you expect to see in a patient with a urinary tract obstruction?

A 
Anuria
Single functioning kidney
Loin or suprapubic pain
Palpable bladder
Pelvic/abdominal mass
Enlarged prostate
History of stones, prostatism, pelvic/abdominal surgery
290
Q

What do you look for on a urine dipstick when suspecting AKI?

A

Haematuria
Proteinuria
Leukocytes (suggest inflammation)
Not seen in pre-renal.

291
Q

What investigations can you use in acute kidney injury and when would you use them?

A

Urine dipstick - all
Urine culture - suspected infection
Ultrasound - obstruction or unclear cause
CXR - look for fluid overload/infection
Biopsy - if AKI not improving or intrinsic cause

292
Q

What can you do to prevent AKI?

A

Identify and monitor at-risk patients
Ensure they are sufficiently hydrated
Avoid nephrotoxins
Detect early and identify the cause

293
Q

What are the risk factors for AKI?

A 
Age
CKD
Heart/liver disease
Diabetes mellitus
Previous AKI
Dehydration or volume depletion
Sepsis
Critical illness
Burn or trauma
Cardiac surgery
Emergencies
Nephrotoxins
Radio-iodinated contrast within a week
294
Q

What is the management for volume overload in acute kidney injury?

A

Restrict dietary sodium and water

295
Q

What is the management for hyperkalaemia in acute kidney injury?

A 
Give calcium gluconate
Restrict dietary potassium
Stop potassium sparing diuretics
Dextrose and insulin (drives potassium into cells)
Sodium bicarbonate (if bicarb low) 
Beta-2 agonist
Exchange resin
296
Q

What is the management for acidosis in acute kidney injury?

A

Restrict dietary protein

Sodium bicarbonate

297
Q

When would you suggest dialysis for a patient with acute kidney injury?

A

Hyperkalaemia refractory to treatment
Metabolic acidosis if sodium bicarbonate inappropriate
Best way to remove a nephrotoxin e.g. aspirin overdose/ethylene glycol
Fluid overload refractory to diuretics

298
Q

What are the symptoms of uraemia?

A

Low conciousness
Pericarditis
Intractable nausea and vomiting

299
Q

What problems can deranged excretion in the kidney cause?

A 
Hyperkalaemia
Sodium overload with water overload (peripheral/pulmonary oedema, hypertension)
Acidosis (acidotic breathing)
Lethargy and fatigue
Uraemic syndrome (late)
300
Q

What problems can impaired tubular function in the kidney cause?

A

Inability to concentrate urine (increased frequency, noctiuria)
Contributes to acidosis
Glycosuria with normal blood glucose (low Tm)

301
Q

In what patients should you screen for kidney disease?

A 
Hypertension
Heart disease
Diabetes
Urinary tract obstruction
Systemic disease (SLE/myeloma/other immune)
302
Q

What problems can be caused if there are hormonal changes in kidney disease?

A

Metabolic bone disease - vitamin D not activated
Anaemia - reduced erythropoietin
Hypertension - increased stimulation of renin release

303
Q

What can cause microscopic haematuria?

A 
Urinary infection
Polycystic kidneys
Renal stones
Renal/bladder tumours
Arteriovenous malformations
Kidney/glomerular disease
304
Q

In glomerulonephritis, what would you expect to see in the urine microscopically?

A

Dysmorphic red cells

Red cell casts

305
Q

What problems will a patient with proteinuria have?

A

Frothy urine
Oedema - reduced oncotic pressure
Frequent infection - reduced immunoglobin
High thromboembolic risk - imbalanced regulators of the coagulation cascade

306
Q

What is the classic ‘triad’ seen in nephrotic syndrome?

A

Proteinuria
Hypoalbuminaemia
Oedema
Hyperlipidaemia

307
Q

What is nephrotic syndrome?

A

Focal segmented glomerulosclerosis, affecting the podocytes so effective filtration is lost. Protein is able to filter into the urine, but not red blood cells

308
Q

What is the clinical presentation of nephrotic syndrome?

A 
Oedema of the legs and fact
Blisters
Muehrcke's bands
Xanthelasma
Fat bodies in urine
Deep vein thrombosis 
Proteinuria
309
Q

What is nephritic syndrome?

A

Thin glomerular basement membrane and small pores in the podocytes, allowing protein and red blood cells to pass into urine.

310
Q

What is the clinical presentation of nephritic syndrome?

A 
Rapid onset
Oliguria
Hypertension
Oedema
Haematuria
Normal serum albumin
High creatinine
Proteinuria
311
Q

What are the symptoms of uraemic syndrome in advanced chronic kidney disease?

A 
Tiredness and lethargy
Nausea and vomiting
Breathlessness
Aches and pains
Sleep reversal
Noctiuria
Restless legs
Pruritis
Chest pain
Seizures
Coma
Pale
312
Q

What are the symptoms of end-stage renal failure?

A 
Overwhelming fatigue
Difficulty concentrating
Feelings of guilt
Symptoms of volume overload (oedema, dyspnoea)
Cramps
Nausea
Vomiting
Pruritis
Sexual dysfunction
Increased infection
313
Q

Why should you treat electrolyte and acid-be disturbances when they are asymptomatic in end stage renal disease?

A

They can worsen bone disease and cause muscle wasting.

314
Q

What causes anaemia in end stage renal failure or chronic kidney disease?

A

Reduced erythropoietin
Increased risk of bleeding
Shortened RBC survival
Iron deficiency

315
Q

What are the symptoms of uraemic syndrome?

A

Nausea
Vomiting
Pruritis

316
Q

What causes uraemic syndrome in chronic kidney disease?

A

Accumulation of waste products

317
Q

Why might patients need the dose of their medication altered with chronic kidney disease?

A

Reduced metabolism or elimination

Altered sensitivity

318
Q

Briefly describe haemodialysis.

A

Filtering the blood externally using a semipermeable membrane and a counter-current with diasylate.
Needs to be done for 4 hours, 3 days a week.

319
Q

What are the advantages of haemodialysis?

A

Less responsibility

Days off

320
Q

What are the disadvantages of haemodialysis?

A

Travel and waiting times
Tied to dialysis time
Restriction on fluid and food intake

321
Q

What are the different methods of haemodialysis?

A

Create an arterovenous fistula to engorge the vein, making it easier to insert a cannula multiple times a week.

Dialysis catheter placed directly into the subclavian vein.

322
Q

What are the contraindications for haemodialysis?

A

Failed vascular access
Heart failure - dialysis can cause destabilisation
Coagulopathy

323
Q

What are some complications of haemodialysis?

A

Infection
Thrombosis due to the lines or AV fistula
Venous stenosis
Bleeding
Access failure
Steal syndrome - causes an ischaemic hand
CVS instability

324
Q

Briefly describe peritoneal dialysis.

A

The peritoneal cavity is filled with diasylate fluid through a tube into the abdomen with a one-way valve. After a time, it is drained out with waste products. The peritoneum acts as a filter.
Can be done 4-5 times a day, or overnight.

325
Q

What are the advantages of peritoneal dialysis?

A 
Self-sufficient
Less food and fluid restriction
Easy to travel
Initially renal function is preserved
Take fewer tablets
326
Q

What are the disadvantages of peritoneal dialysis?

A

Frequent changes

Responsibility

327
Q

What are the contraindications in peritoneal dialysis?

A

Failure of the peritoneal membrane
Adhesions
Hernia
Stoma
Patient or carer unable to connect and disconnect the machine
Obese/large muscle mass (proportionally smaller peritoneum)

328
Q

What are some potential complications of peritoneal dialysis?

A 
Peritonitis
Exit or tunnel site infection
Ultrafiltration failure
Leaks (scrotal or diaphragmatic)
Develop herniae
329
Q

What are the benefits of home or nocturnal dialysis?

A

Allows more dialysis hours
Better toxin clearance
Patient feels better
Need fewer medication

330
Q

What are the three types of kidney transplant, and which is best?

A

Live donor - best
Deceased after brain death
Deceased after circulatory failure

331
Q

What are the advantages of kidney transplant?

A

Reduced morbidity and mortality

Greater quality of life

332
Q

What are the disadvantages of kidney transplants?

A

Perioperative risks
Malignancy risk
Infection risk

333
Q

How are kidneys matched from donor to recipient?

A

Tissue type - HLA and ABO

Number of points they have (length of time on the register, age)

334
Q

What are the symptoms that an elderly person may have if they have end of life care for end-stage renal failure?

A 
Pain (bone, neuropathy, MSK)
Constipation
Fatigue
Pruritis
Cramps
Restless legs
Sleep disturbance
Nausea
Loss of appetite
335
Q

What is chronic kidney disease?

A

Irreversible and sometimes progressive loss of renal function over months to years. Normal parenchymal tissue is replaced by fibrosis and ECM.

336
Q

Who is most at risk for chronic kidney disease?

A

Elderly
Ethnic minorities
Socially disadvantaged

337
Q

What is the aetiology behind chronic kidney disease?

A 
Glomerulonephritis
Pyelonephritis
Alport's syndrome
Polycystic kidney disease
Obstruction
Reflux causing nephropathy
Diabetes mellitus
Myeloma
Hypertension
Unknown
338
Q

How can you reduce the rate of disease progression in patients with chronic kidney disease?

A

Managing predisposing comorbidities such as hypertension and diabetes

339
Q

What simple bedside test can you do which helps to predict development of end-stage renal failure in a patient with chronic kidney failure?

A

Urine dipstick - proteinuria

340
Q

What is the best way to measure renal function, and how is it usually done?

A

Glomerular filtration rate.

Take serum creatinine and use it to calculate eGFR

341
Q

What determines creatinine concentration?

A

Kidney function

Muscle mass - age, sex, race

342
Q

What are some downsides of using eGFR as a measure of kidney function?

A

It is only useful in adults
Must be corrected for black patients
Only defines chronic kidney disease, not acute kidney injury

343
Q

What investigations should you do with suspected chromic kidney disease?

A 
Autoantibody screen
Look for complement/immunoglobin/CRP
Ultrasound (for size and hydronephros)
CT
MRI
344
Q

What are some complications associated with late stage chronic kidney disease?

A

Acidosis - affects muscle, bone, renal function progression

Anaemia

Mineral and bone disorders - calcium, phosphorus, PTH, vitamin D metabolism, bone turnover and strength, vascular/soft tissue calcification

345
Q

Describe how low GFR can lead to high PTH, and how this affects bone.

A

Low GFR causes phosphate to rise, which is normally excreted. This causes calcium to drop as more calcium phosphate is formed. Hypocalcaemia then stimulates PTH production.
The low GFR also reduces active vitamin D, which also causes hypocalcaemia.

It can lead to osteitis fibrosa cystica.

346
Q

Describe osteitis fibrosa cystica.

A

Inflammation of the bone causing enlargement, tenderness and a dull aching pain.
Caused by high PTH

347
Q

What is renal osteodystrophy?

A

Bone changes due to chronic kidney disease.

Sclerosis at the end plates of vertebrae and erosion at the tips of terminal phalanges.

348
Q

What are the modifiable risks for chronic kidney failure?

A 
Lifestyle (smoking, obesity, lack of exercise)
Diabetic control
Blood pressure control
ACEi/ARBs in proteinuria
Lipid lowering
349
Q

What are the indications for dialysis?

A 
Uraemic syndrome 
Uncontrollable acidosis
Pericarditis
Fluid overload
Hyperkalaemia
350
Q

What nerve acts via M3 receptors at the bladder?

A

Pelvic nerve

351
Q

What nerve acts via adrenoceptors at the bladder and urethra?

A

Hypogastric nerve

352
Q

What nerve acts via nicotinic receptors on the external urethral sphincter?

A

Pudenal nerve

353
Q

Describe the characteristics of a lower motor neuron lesion to the bladder.

A

Low detrusor pressure
Chronic retention with/without outflow incontinence
Reduced perianal sensation and lax anal tone
Distended abdomen as the bladder is large

354
Q

Describe the characteristics of an upper motor neuron lesion to the bladder.

A

High pressure detrusor contraction
Detrusor-sphincter dyssynergia
Hydronephrosis, hydroureters due to back pressure, thick detrusor muscle

355
Q

Describe stress urinary incontinence

A

Involuntary leak on effort, exertion, cough, and sneeze. Common after childbirth.

356
Q

Describe urge urinary incontinence

A

Urgency with involuntary leak

357
Q

Describe overflow incontinence

A

Not always associated with pain
Acontractile bladder
Often have noctiuria

358
Q

Describe the symptoms of an overactive bladder.

A

Urgency
Frequency
Noctiuria

359
Q

What are the risk factors for incontinence?

A 
Age
Pregnancy
Childbirth
Prolapse of the uterus/vagina
Pelvic surgery
Obesity
Cognitive impairment
High intraabdominal pressure
UTIs
Drugs
Menopause
Race
Genetics
Anatomical or neurological abnormalities
360
Q

Describe the sequence for neural detection of bladder filling.

A

Mechanoreceptors in the bladder wall detect filling, sending the information via sacral parasympathetic fibres to the spinal cord. The spinal centres the relay bladder fullness information to the thalamic micturition centres, which then send it on to the cerebral cortex.

361
Q

What nerve is responsible for contraction of the detrusor muscle of the bladder, and what is its segmental origin?

A

Pelvic parasympathetic

S2-4

362
Q

Describe what happens in the bladder during micturition.

A

Pontine micturition excitatory centre activates S2-4 to contract the detrusor muscle.
The internal urethral sphincter is relaxed by inhibition of its sympathetic drive
The external urethral sphincter is relaxed by cortical micturition centres by acting on S2-4 bladder motor neurons.

ESA 3 (5 decks)

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