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MD1 Revision > Renal > Flashcards

Renal Flashcards

1
Q

What do the kidneys do?

A 
Make urine
Control blood pressure
Control red cell production
Contribute to vitamin D metabolism
Communicate with CNS
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2
Q

How much plasma does it take to make two litres of urine?

A

200 L

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3
Q

What proportion of the cardiac output goes to the kidneys?

A

20-25%

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4
Q

What are the parts of the nephron?

A 
Bowman's capsule
Proximal tubule
Loop of Henle
Distal tubule
Collecting duct
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5
Q

What are the processes going on in the nephron, and in which order?

A 
Filtration = blood to lumen
Reabsorption = lumen to blood
Secretion = blood to lumen
Excretion = lumen to external environment
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6
Q

What is the epithelium around glomerulus capillaries modified into?

A

Podocytes

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7
Q

What is the Bowman’s space?

A

Plasma enters here before proximal tubule

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8
Q

How do podocytes form part of the filtration barrier?

A

Interdigitate

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9
Q

Through what structure in the podocytes does filtration take place?

A

Podocyte foot processes surround each capillary

Leave slits through which filtration takes place

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10
Q

What maintains capillary oncotic pressure?

A

Albumin

- Loss causes oedema

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11
Q

Define renal blood flow

A

Rate of blood flow through glomerulus

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12
Q

Define renal plasma flow

A

Rate of plasma flow through glomerulus

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13
Q

Define filtration fraction

A

Proportion of plasma filtered by glomerulus

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14
Q

Define GFR?

A

Volume of plasma filtered by glomerulus per unit time

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15
Q

What is the most important force that affects GFR?

A

Hydrostatic pressure in glomerular capillary

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16
Q

What is the hydrostatic pressure in the glomerular capillary?

A

55 mmHg

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17
Q

What happens when the hydrostatic pressure in the glomerular capillaries increases?

A

Damages capillaries > lose nephron > other nephrons have increased blood flow > increase hydrostatic pressure further > damage more nephrons > chronic renal failure

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18
Q

What happens to GFR when the afferent arteriole dilates?

A

Increases

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19
Q

What happens to GFR when the efferent arteriole constricts?

A

Increases

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20
Q

Between which range of mean arterial pressure is GFR maintained, even as mean arterial pressure changes?

A

80-180 mmHg

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21
Q

How is GFR stabilised with variations in mean arterial pressure?

A

Autoregulation

  • Myogenic response
  • Tubuloglomerular feedback
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22
Q

What is the myogenic response?

A

Increase pressure in glomerular capillaries > cells stretch > automatic constriction

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23
Q

What is tubuloglomerular feedback?

A

GFR increases > macula densa picks up too much NaCl in filtrate > afferent arteriole constricts > decrease GFR

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24
Q

What is the effect of the renin-angiotensin-aldosterone system on renal excretion?

A

Angiotensin II
- Increases Na absorption in proximal tubule
- Constricts efferent arteriole
Aldosterone
- Increases Na absorption in collecting ducts

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25
Q

What is the effect of the sympathetic nervous system on renal excretion?

A

Noradrenaline

  • Preferentially binds to afferent arteriole to increase TPR
  • Decreases GFR because of afferent arteriole constriction
  • Increases Na absorption in proximal tubule
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26
Q

How does atrial natriuretic peptide work?

A

If extracellular fluid volume increases > increased venous return > atria stretched > secrete atrial natriuretic peptide > goes to kidney > dilates afferent arteriole > reduces Na reabsorption in collecting duct, inhibits secretion of renin, angiotensin II, and aldosterone > increased Na excretion > increased diuresis

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27
Q

What is the proportion of reabsorption of sodium and water in each part of the nephron?

A 
Proximal tubule
- 70% of Na and water reabsorbed
Loop of Henle
- 20% of Na reabsorbed
- 15% of water reabsorbed > fluid in lumen more dilute
Distal tubule and collecting duct
- 10% of Na reabsorbed
- Area of fine tuning
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28
Q

How is sodium reabsorbed?

A

Active transport

  • Secondary active transport of Na on lumen side
  • Basolateral side covered with Na-K ATPase along all of nephron
    • Driving force of reabsorption of Na
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29
Q

How are anions reabsorbed?

A

Electrochemical gradient drives anion reabsorption

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30
Q

How is water reabsorbed?

A

Moves by osmosis, following solute reabsorption

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31
Q

How are solutes other than sodium and anions reabsorbed?

A

Concentrations increase as fluid volume in lumen decreases

Permeable solutes reabsorbed by diffusion

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32
Q

How is glucose reabsorbed?

A

Na moving down electrochemical gradient using SGLT protein pulls glucose into cell against its concentration gradient
Glucose diffuses out of basolateral side of cells using GLUT protein

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33
Q

Why does glucose appear in the urine in diabetes?

A

Filtration of glucose proportional to plasma concentration
- Higher glucose plasma concentration > more reabsorbed
Tubules have maximum number of transporters > all occupied > not all glucose reabsorbed > glucose in urine

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34
Q

How does the body detect sodium balance?

A

Carotid baroreceptors
Renal arterial pressure receptors
Cardiac atrial baroreceptors

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35
Q

When can renin be released from granular cells in the juxtaglomerular apparatus?

A

Fall in pressure at preglomerular arteriole
Reduction in NaCl delivery to macula densa
Sympathetic nerve activation

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36
Q

What makes up the upper urinary tract?

A

Kidneys

Ureters

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37
Q

What makes up the lower urinary tract?

A

Bladder

Urethra

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38
Q

What is the structure of the kidney?

A 
Cortex
- Outer
- Granular
Medulla
- Inner
- Striated
- Renal pyramids separated by cortical columns
Ureter originates from renal pelvis
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39
Q

What is the blood supply of the kidney?

A

Renal artery and vein enter and leave renal pelvis
Arcuate vessels at boundary between cortex and medulla
Form interlobular and interlobar vesselswH

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40
Q

What makes up the nephron?

A

Renal corpuscle

Tubule > drains into collecting duct

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41
Q

What are the two types of nephrons?

A 
Cortical
- Higher in cortex
- Tubule looks halfway into medulla
- Most common
Juxtamedullary
- Base of cortex
- Tubule loops deep into medulla
- Produces more hyper-osmotic urine
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42
Q

What are the two poles of the renal corpuscle?

A

Vascular pole - arteries come and leave

Urinary pole - filtrate enters tubule

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43
Q

Describe mesangial cells

A

Embedded between capillaries
Type of pericyte
Contractile, impacting on capillary diameter
Involved in phagocytosis

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44
Q

Which cells form the inner layer of Bowman’s capsule?

A

Podocytes

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45
Q

What forms the filtration barrier in the glomerulus?

A

Thick basal lamina

Slit membranes in foot processes of podocytes

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46
Q

Describe the proximal tubule

A 
Thick wall
Simple cuboidal epithelium
Brush border
- Tall microvilli
- Increase surface area
Very folded basement membrane
Many ion pumps and mitochondria
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47
Q

Describe the loop of Henle

A

Descending and ascending limbs
Thin walled part = squamous cells
Ion movement establish hypertonic environment in medulla to further concentrate urine

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48
Q

Describe the distal tubule

A 
Simple cuboidal epithelium
Thinner than proximal tubule
No microvilli
Many ion pumps and more mitochondria than proximal tubule
Further ion reabsorption
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49
Q

What is the macula densa?

A

Each distal tube returns to renal corpuscle that gave rise to it
Passes between afferent and efferent arteriole
Tubule cells become specialised in small region = macula densa
Chemoreceptor function
Monitors filtrate

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50
Q

What do signals from the macula densa cause the juxtaglomerular cells to do?

A

Release renin

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51
Q

Describe the collecting duct

A

Simple cuboidal epithelium becomes more columnar along duct
Large lumen
Impermeable to water, except when stimulated by anti-diuretic hormone

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52
Q

What are the vasa recta?

A

Capillaries from efferent arteriole envelope tubule
Form hairpin loops in medulla among loops of Henle
Crucial for urine concentration

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53
Q

Describe the ureter

A

Simple muscular tube
Conducts urine from kidney to bladder
Regular peristaltic movements regulated by autonomic nerves
Lined by transitional epithelium

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54
Q

Describe the bladder

A

Storage of urine
Lined with transitional epithelium
Smooth muscle contracts during micturition
Controlled b autonomic nervous system, but under healthy adult conditions this regulated voluntarily

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55
Q

Describe the transitional epithelium of the bladder

A

Multilayered, non-permeable epithelium

Outer layers change shape during bladder distension

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56
Q

Describe the urethra

A

Fibromuscular tube innervated by autonomic nerves
Lined first with transitional epithelium then stratified squamous epithelium
Distal urethra surrounded by striated muscle sphincter, controlled by somatic nervous system

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57
Q

Is all of the urinary tract sterile?

A

No

Distal urethra has microbiota - often cause of urinary tract infections

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58
Q

What are the most common causes of urinary tract infections?

A

E coli
Proteus
Staphylococcus saprophyticus

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59
Q

Which cause of urinary tract infections is more common in males?

A

Proteus

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60
Q

Which cause of urinary tract infections is more common in sexually active females?

A

S saprophyticus

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61
Q

What are other causes of urinary tract infections, especially in hospital-acquired cases?

A 
Gram negative rods
- Klebsiella
- Enterobacter
- Serratia
- Pseudomonas
Gram positive bactera
- Enterococcus
- Other Staphylococcus
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62
Q

What are viral causes of urinary tract infections?

A 
Don't cause classical urinary tract infection
Usually asymptomatic shedding
- CMV
- Rubella
- Polyomaviruses
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63
Q

What virus may cause haemorrhagic cystitis?

A

Adenovirus

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64
Q

What virus may cause renal disease?

A

Hantavirus

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65
Q

How do bacteria access the urinary tract?

A 
Most infections ascending
- Cause cystitis
- Sometimes cause pyelonephritis
Occasionally via blood; eg:
- Staphylococcus aureus
- Salmonella Typhi
- TB
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66
Q

What are the innate immune defences in the urinary tract?

A

Transitional epithelium
- Resists colonisation by most types of bacteria
- Relatively resistant to bacterial invasion
Some bacteria don’t like to grow in urine
Constant flushing of urine and regular bladder emptying

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67
Q

What host factors affect the pathogenesis of urinary tract infections?

A

Urethra shorter, straighter, and closer to other orifices in perineum in females
Colonisation of distal urethra: more bugs > more likely
Sexual intercourse: pushes bacteria further up urinary tract
No circumcision - infant boys only
Incomplete bladder emptying
- Structural abnormality
- Functional abnormality
Catheterisation

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68
Q

What are some microbial factors that affect the pathogenesis of urinary tract infections?

A 
Adhesins; eg: E coli have
- Type 1 pili
- Pyelonephritis associated pili
Flagella
Polysaccharide capsule
Biofilm formation
Haemolysin
Siderophore production
Urease
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69
Q

How are urinary tract infections diagnosed?

A 
History and physical examination
Imaging
- Not routinely done
- Look for structural and functional abnormalities
Collect appropriate samples
- Before antibiotic treatment
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70
Q

What are the different types of urine samples?

A 
Midstream urine
Catheter sample
Bag sample
- In babies
- Bag over urethra
- Only useful if returns negative result
Suprapubic aspirate
- Insert needle into full bladder via anterior abdominal wall
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71
Q

How much bacteria in a urine sample is considered significant?

A

Midstream urine: >10^5 CFU/mL
Catheter: >10^2 CFU/mL
Suprapubic aspirate: any growth significant

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72
Q

What results on a dipstick analysis of urine are highly suggestive of urinary tract infections?

A

Leukocytes and nitrite

73
Q

What is sterile pyuria?

A 
No growth with white blood cells consistently >10^5/mL
Causes include
- Non-infectious conditions
- Partial treatment
- Difficult to grow bacteria; eg: TB
74
Q

How do you treat uncomplicated cystitis?

A

Alkalinise urine
- Unless using nitrofurantoin because does’t work well under alkaline conditions
Trimethoprmi/nitrofurantoin/cephalexin/co-amoxyclav
3-5 days for women and children
7 days for men
If <2 years old, check for urinary tract abnormality

75
Q

How do you treat pyelonephritis?

A

Trimethoprim/co-amoxyclav/cephalexin
For 10-14 days
Check for urinary tract abnormality
If severe sepsis, use ampicillin/amoxycillin + gentamicin

76
Q

What is asymptomatic bacteriuria?

A

Repeated >10^5 CFU/mL without symptoms
No significance except in pregnancy
Treat with cephalexin/co-amoxyclav/other antibiotic safe in pregnant women

77
Q

How are changes in osmolality detected>

A

Osmoreceptors

  • Anterior hypothalamus
  • Respond to changes in cell size
78
Q

What is the relationship between anti-diuretic hormone and osmolarity?

A

Osmolarity increases > negative water balance > anti-diuretic hormone increases > reabsorb water > concentrated urine

79
Q

When is anti-diuretic hormone released in response to low extracellular fluid?

A

Doesn’t come into play until extracellar fluid really challenged

80
Q

Where is water absorbed along the nephron?

A 
Proximal tubule
- Bulk absorption
Ascending loop of Henle
- Dilution of filtrate
Collecting ducts
- Fine-tuning according to needs
81
Q

What controls the permeability of the collecting ducts to water?

A

Hormones

82
Q

How does anti-diuretic hormone act on the collecting ducts?

A

Anti-diuretic hormone binds to membrane receptor
Receptor activates cAMP
Cell inserts aquaporins in apical membrane
Water absorbed by osmosis into blood

83
Q

What is type II hypersensitivity?

A

Ab-mediated recognition of cell-associated and/or extracellular Ag
Leads to either
- Complement activation, recruitment of inflammatory cells, activation of phagocytes through Fc receptors
- Ab binding elicits abnormal physiological response

84
Q

What type of hypersensitivity are blood transfusion reactions?

A

Type II

85
Q

What do blood transfusion reactions cause?

A

Acute haemolytic reactions

  • Tachycardia
  • Hypotension
  • Chills
  • Haemoglobulinaemia
  • Shock
86
Q

What is Rhesus incompatibility?

A

Rh- mother carrying 1st Rh+ foetus > Rh Ags from developing foetus can enter mother’s blood during delivery > mother produces anti-Rh Abs > if woman becomes pregnant with another Rh+ foetus, her anti-Rh Abs will cross placenta and damage foetal RBCs

87
Q

What is Grave’s disease?

A

Autoimmune B cell makes Abs against TSH receptor > stimulates thyroid hormone production in thyroid gland > thyroid hormones shut down TSH production but have no effect on autoAb production > continues to cause excessive thyroid hormone production

88
Q

What is myasthenia gravis?

A

Ab blocks acetylcholine receptor at neuromuscular junction
- Acetylcholine receptors internalised and degraded
- No Na influx > no muscle contraction
Progressive weakness that follows diurnal pattern

89
Q

What is type III hypersensitivity?

A 
Small Ag:Ab complexes form in circulation > activation of complement > deposition of many C3b on immune complex > complement receptor CR1 on erythrocytes binds immune complexes via bound C3b > in spleen and liver, phagocytic cells remove immune complexes from erythrocyte surface
Removal of complexes affected by
- Ag excess
- Low affinity Ab
- Inefficient complement activation
Can lead to
- Vasculitis
- Glomerulonephritis
- Arthritis
90
Q

How does vasculitis happen in type III hypersensitivity?

A

Formation of Ag-Ab complexes > deposition of immune complexes > complement activation > attraction of inflammatory cells > tissue damaging mediators released > tissue damage > fibrinoid necrosis > vasculitis

91
Q

How does glomerulonephritis happen in type III hypersensitivity?

A 
Immune complex deposition in glomerulus
- Autoimmune
- Post-infection
Produces nephrotic syndrome
- Proteinuria
- Oedema
- Hyperlipidaemia
92
Q

What is the bicarbonate buffer system?

A

HCO3- + H+ > CO2 + H2O

93
Q

What is the role of carbonic anhydrase in the CO2 and bicarbonate buffer system?

A

Catalyses reaction

94
Q

Which buffer systems are the most important for regulating pH?

A

Intracellular Hb

Plasma proteins

95
Q

What is the phosphate buffer system good for regulating?

A

Acute changes in pH

96
Q

How can lungs affect pH?

A

Alter pCO2 through changes in ventilation

97
Q

How can kidneys affect pH?

A

Alter HCO3 by changes in production and excretion

Alter pH by changes in H excretion

98
Q

What abnormal pH syndromes can the lungs cause?

A

Respiratory acidosis

Respiratory alkalosis

99
Q

What abnormal pH syndromes can non-lung organs cause?

A

Metabolic acidosis

Metabolic alkalosis

100
Q

What are some non-volatile acids produced in the body?

A

Sulphuric and phosphoric acids from proteins and lipids
Lactic acid from anaerobic metabolism
Keto acids from fatty acid metabolism

101
Q

Can non-volatile acids be removed by hyperventilating?

A

No

102
Q

What is the anion gap?

A

Difference between measures cations and anions

In reality, body balanced, but some ions not measured and therefore get gap

103
Q

Which types of acidosis have a high anion gap?

A

Lactic acidosis
Diabetic ketoacidosis
Renal failure

104
Q

How is bicarbonate reabsorbed and acid excreted in the kidney?

A

Na-H antiport secretes H
H in filtrate combines with filtered HCO3 to form CO2
CO2 diffuses into cell and combines with water to form H and HCO3
H secreted again and excreted
HCO3 reabsorbed
Glutamine metabolised to ammonium ion and HCO3
NH4 secreted and excreted
HCO3 reabsorbed

105
Q

How does metabolic acidosis cause hyperkalaemia?

A

H-K exchanger on luminal surface of intercalated type A cells in distal tubule
More H secreted > more K reabsorbed

106
Q

What is transplant rejection characterised by?

A

Specificity

Memory

107
Q

Which immune cell is responsible for graft rejection?

A

T cell

108
Q

Which HLA types are most important for transplants?

A

HLA-A
HLA-B
HLA-DR
Haplotype has to match 6 HLA groups

109
Q

What aspects of the basement membrane of the glomerulus makes it specialised?

A

Type IV collagen
Negatively charged proteoglycans
- Electrostatic repulsion of proteins in blood

110
Q

What is the nephrotic syndrome?

A 
Oedema
- Typically affecting whole body
Proteinuria
Hypoalbuminaemia
Hyperlipidaemia
111
Q

What causes oedema in nephrotic syndrome?

A

Loss of oncotic pressure because of proteinuria

112
Q

What causes nephrotic syndrome, in general terms?

A

Defect in permeability of filter > proteins, especially albumin, escape into urine
Other components follow on from proteinuria

113
Q

Why do proteins normally stay in the glomerulus while the filtrate flows out into the urinary space?

A

Negative charge on circulating proteins and negatively charged proteoglycans in basement membrane repel each other
Physical structure of membrane
Several vital proteins between adjacent podocytes

114
Q

What is inherited nephrotic syndrome (Finnish type)?

A

Nephrotic syndrome caused by inherited defect in nephrin gene

115
Q

What are common causes of nephrotic syndrome?

A 
Diabetes mellitus
- Commonest cause
Some forms of glomerulonephritis
- Minimal change disease
- Membranous glomerulonephritis
Amyloid deposition
Inherited abnormalities in proteins between podocytes
116
Q

How can diabetes cause nephrotic syndrome?

A

Glycosylated proteins lodge in glomerular basement membrane > thickens > becomes leakier > diabetic glomerulonephropathy

117
Q

What is acute renal failure?

A

Acute reduction in glomerular filtration rate (GFR) reflected as reduced creatinine clearance
- Causes increasing serum urea and creatinine

118
Q

What are the three main causes of acute renal failure?

A

Pre-renal = not enough blood perfusing kidney
Renal = problem with machinery itself; eg:
- Glomerular
- Tubular
Post-renal = problems downstream of kidney; eg: prostatic obstruction

119
Q

What are renal causes of acute renal failure?

A 
Acute tubular necrosis
- Most common renal cause
Acute glomerulonephritis
Acute interstitial nephritis
Toxins
120
Q

What is glomerulonephritis?

A

Acute injury to glomerulus, most often immune mediated
Most associated with deposition of immune complexes in glomerulus
- Complement activation
- Formation of membrane attack complexes
Clinical consequences depend on what forms complexes, where they lodge, and how big they are

121
Q

What is acute glomerulonephritis?

A

May be acute, reversible injury; eg: post-Streptococcal glomerulonephritis
May be rapidly progressive
May be slowly progressive to chronic renal failure; eg: some IgA nephropathy
If severe and associated with necrosis of part of capillary tuft, can be associated with clumps of monocytes and epithelial cells = crescents

122
Q

How does IgA nephropathy often present?

A

Haematuria

Without acute renal failure

123
Q

How do glomeruli react to immune complex-mediated injury?

A 
Glomerular cells proliferate
- Mesangial
- Endothelial
- Podoctyes
Inflammatory cells infiltrate
- Neutrophils
- Lymphocytes
- Monocytes
Basement membrane proliferates
- New layers form
- Spikes/protrusions on epithelial surface
124
Q

What is the difference between diffuse and focal glomerulonephritis?

A 
Diffuse = every glomerulus abnormal
Focal = some glomeruli abnormal
125
Q

What is the difference between global and segmental glomerulonephritis?

A 
Global = all/most of glomerulus involved
Segmental = part of glomerulus involved
126
Q

Describe glomerulonephritis in systemic lupus erythematosis (SLE)

A

Kidney targeted in SLE
Common in young women
Kidney has massively high immune complex load
Can see immune complex depositing as clotted protein in lumen
Often leads to immune mediated glomerular injury

127
Q

What does IgA nephropathy look like under the electron microscope?

A

Dark deposits of abundant immune complexes in mesangium

128
Q

What does membranous nephropathy look like under the electron microscope?

A

Dark deposits of abundant immune complexes along outer aspect of basement membrane

129
Q

What is crescent formation in glomerular injury?

A

Seen generally in severe cases of acute renal failure
Crescent made of exuded
- Fibrin
- Monocytes
- Podocytes
Not specific to any form of glomerulonephritis
Response to severe injury with necrosis of segment of glomerulus

130
Q

How can injury to the glomerulus progress?

A

Segments of glomerulus destroyed = necrotising lesions >
Segments of glomerulus scar and contract = sclerosing lesions >
Entire glomerulus may become sclerotic ball without patent capillaries

131
Q

What is the progression of glomerular disease?

A

Varies in different conditions
Some resolve completely; eg: acute post-infectious glomerulonephritis
- Can still progress to chronic renal failure if glomerular injury severe enough
Others associated with continuing stimulus and progress
- Lupus nephritis
- HIV nephropathy
Some progress with continuing deposition of immune complexes > chronic renal failure
- IgA nephropathy

132
Q

What is the progression of damage to the glomerulus in diabetic nephropathy?

A

Early: protein leakage and nephrotic syndrome
Later: damage accumulates > major cause of chronic renal failure

133
Q

What is the interstitium in the nephron?

A 
Connective tissue in which lie
- Glomeruli
- Tubules
- Blood vessels
Very inconspicuous in normal kidney
More visible in various diseases
- Can swell acutely due to oedema
- Can become expanded and fibrotic due to interstitial fibrosis
134
Q

What are the most important causes of tubulointerstitial injury?

A

Ischaemic injury of tubular epithelial cells > acute tubular necrosis
Infection of tubules and interstitium = acute pyelonephritis
Acute/chronic tubulointerstitial nephritis

135
Q

What is acute tubular necrosis?

A

Most common renal cause of acture renal failure
Acute injury to tubular epithelial cells
Usually due to ischaemia
- As blood supply falls tubular epithelium dies before other parts
Epithelial cells degenerate and detach from tubular basement membrane
GFR falls
Electrolyte balance fails
Urea and creatinine accumulate in blood

136
Q

Is acute tubular necrosis reversible?

A

Yes, if patient support; eg: with dialysis for few weeks
Regeneration and complete recovery in weeks
Often associated with diuresis

137
Q

What is the difference between hypoperfusion and ischaemic acute tubular necrosis?

A

Hypoperfusion = renal perfusion falls sufficiently > GFR falls, but tubular epithelium survives - pre-renal cause of acute renal failure
Acute tubular necrosis = hypoperfusion severe and protracted enough to cause necrosis of tubular epithelium

138
Q

What is toxic acute tubular necrosis?

A 
Similar appearance and outcome to ischaemic acute tubular necrosis
Toxins affecting tubular epithelium
- Heavy metals
- Some antibiotics
- Some cancer chemotherapy drugs
139
Q

What is acute interstitial nephritis?

A

Presents as acute renal failure, sometimes with blood/protein in urine
Interstitium and tubules infiltrated by inflammatory cells, often with many eosinophils
Fever, maybe rash
Very often because of drug allergy

140
Q

What is pyelonephritis?

A

Bacterial infection of kidney affects
- Parenchyma of kidney
- Calyces and renal pelvis fill with pus
Acute/chronic
Can occur with/without obstruction to urine flow
Organisms ascend from lower urinary tract to reach kidney

141
Q

Describe acute pyelonephritis

A 
Typically
- Acute onset
- Fever
- Chills
- Lumbar tenderness and pain
- Discomfort with urinating and frequency
Renal function usually preserved
Hypertension not component
Urine contains organisms and white blood cells
142
Q

What are the common organisms causing acute pyelonephritis?

A

Commonly Gram negative bacteria

  • E coli
  • Klebsiella
  • Proteus
  • Pseudomonash
143
Q

Describe chronic pyelonephritis

A

Can cause obstruction/be non-obstructive
Interstitial scarring
Tubular atrophy
Depressed saddle-shaped scars on renal surface

144
Q

What is reflux nephropathy?

A

Renal damage due to back flow of urine from lower tract

145
Q

What is end stage kidney disease?

A

Kidneys no longer able to perform their tasks, particularly maintenance of urea and creatinine levels in blood
Without treatment:
- Worsening uraemia
- Death

146
Q

What does end stage kidney disease look like macroscopically?

A

Shrunken
Pitted
Scarred

147
Q

What is chronic renal failure?

A 
Insufficient GFR to
- Eliminate metabolic wastes
- Maintain water and solute homeostasis
A little proteinuria
Irreversible
Develops over months-years
Often accompanying hypertension
148
Q

What is the urine flow in acute renal failure?

A

Less than 500 mL/day

149
Q

How is GFR assessed?

A

Creatinine clearance = urine concentration x urine volume in 24 hours / plasma concentration = GFR

150
Q

What are the symptoms of acute renal failure?

A

Oliguria
Anuria rarely
GFR falls acutely - hours to days
Can be asymptomatic - easily missed

151
Q

What are the pre-renal causes of acute renal failure?

A 
Systemic perfusion pressure <70 mmHg
Glomerular hydrostatic pressure <45 mmHg
Causes
- Shock
- Sepsis
- Haemolysis
- Rhabdomyolysis
152
Q

What can be seen with acute tubular necrosis?

A

Oliguria
+/- acidosis
Hyperkalaemia

153
Q

What are the post-renal causes of acute renal failure?

A 
Outlet obstruction
Can be
- Ureteric
- Cystic
- Urethral
Stones
Clots
Fibrosis
Tumours
154
Q

What does chronic renal failure lead to?

A

End stage kidney disease

155
Q

What happens to the remaining nephrons in chronic renal failure?

A

Remaining nephrons hypertrophy > glomerular hyperfiltration > tubules can’t keep up with extra filtration

  • Loss of functional reserve
  • Glomerular hypertension
  • Further damage and glomerulosclerosis
156
Q

What is uraemia?

A 
Accumulation of uremic toxins
Mostly urea
Symptomatic with <30% normal renal function
- Fatigue
- Loss of appetite
- Skin pigmentation
157
Q

What are the common causes of chronic renal failure?

A

Diabetes
Hypertension
Chronic glomerulonephritis
Cystic disease

158
Q

What are the salt and water imbalances in chronic renal failure?

A 
Predominantly glomerular disease
- Na retention > hypertension
Predominantly tubular disease
- Na wasting > hypotension
- Impaired concentrating ability > polyuria
159
Q

What are potassium levels in chronic renal failure?

A

Tend to rise, especially late stage

160
Q

What is the pH in chronic renal failure?

A

Falls because

  • H accumulates
  • Failure to excrete non-volatile acids
161
Q

What are calcium and phosphate levels in chronic renal failure?

A

Reduced phosphate excretion due to low GFR > rise in blood phosphate levels > reciprocal reduction in blood Ca levels to stop precipitation

162
Q

How does chronic renal failure lead to high parathyroid hormone levels?

A

Reduced renal mass > reduced vitamin D activation > parathyroid hormone released to compensate

163
Q

What is primary hypertension?

A 
Also called idiopathic/essential
Small changes in 
- Renal Na homeostasis
- Vessel wall tone/structure
Due to 
- Genetic polymorphisms
- Environmental factors
Diagnosis of exclusion
No specific thing causing hypertension
164
Q

In what proportion of hypertension is the cause unknown?

A

90-95%

165
Q

What is secondary hypertension?

A 
Hypertension secondary to underlying cause
Kidney disease
- Most common
- Renal artery stenosis
- Chronic kidney disease
Endocrine
- Adrenal tumoours
   - Conn's disease
   - Cushing's disease
   - Pheochromocytoma
Congenital/other
- Coarctation of aorta = congenital narrowing of aorta
- Obstructive sleep apnoea
- Oral contraceptive pill
- Pregnancy
- Increased intracranial pressure
- Hypercalcaemia
166
Q

What are the indications to treat primary hypertension?

A 
Increased cardiovascular risk
- Consider patient's overall cardiovascular risk
Diabetes
Cardiovascular complications
- Left ventricular hypertrophy
- Abdominal aortic aneurysm
- Ischaemic heart disease
- Ischaemic stroke
- Thrombo-embolism/infarction of other organs
- Arteriosclerosis
- Arteriolosclerosis
Target organ damage
- Due to arteriosclerosis and arteriolosclerosis
- Retina
- Kidney
- Brain
167
Q

What are the sequelae of arteriosclerosis?

A

Arteries lose elasticity and may become narrowed
Too much collagen in intima with wear and tear
Impairs artery’s role in controlling blood pressure
Can impair blood supply to downstream issues

168
Q

What is the pathophysiology of hyaline arteriolosclerosis?

A

Blood pressure too high > stresses smooth muscle cells > produce too much matrix > proteins from blood can leak across damaged endothelium

169
Q

What are the sequelae of hyaline arteriolosclerosis?

A

Poor blood supply to tissues

Possibly microaneurysms and haemorrhage

170
Q

What are the early changes in hypertensive retinopathy?

A

Arterioles constrict
- Autoregulation to decrease local blood flow
Arterioles cause venules to taper where they cross = AV nipping

171
Q

What are the late changes in hypertensive retinopathy?

A 
Arteriolar wall thickens = hyaline arteriolosclerosis - becomes visible
Retinal damage
- Small haemorrhages
   - Flame = superficial
   - Dot = deep
- Small infarcts
   - Cotton wool spots = infarcts in retinal axons with disrupted axoplasmic transport
- Embolus - large pale area of infarct
172
Q

Describe benign nephrosclerosis

A 
Vascular changes - come 1st
- Damage through chronic ischaemia
- Arteriosclerosis
- Hyaline arteriolosclerosis
Glomerular changes
- Glomerular sclerosis
Tubular changes
- Atrophy
Interstitial changes
- Fibrosis
- Mononuclear infiltrate
As part of normal ageing
Accelerated with hypertension
Slow progressive loss of kidney function
- Mild proteinuria
173
Q

Describe hyaline arteriolosclerosis in the basal ganglia

A 
Holes after infart
Tiny infarcts = lacunar infarcts
Haemorrhage
Thromboembolic stroke
Multiple strokes can result in cognitive impairment - form of dementia = vascular dementia
174
Q

What is malignant hypertension?

A

Rapidly rising blood pressure
Systolic >200 mmHg
Diastolic >120 mmHg

175
Q

What does malignant hypertension cause?

A 
All effects of benign hypertension AND
Hyperplastic arteriolosclerosis
Fibrinoid necrosis - necrotising arteriolitis
Resulting in 2 specific diagnoses
- Hypertensive encephalopathy
- Malignant nephrosclerosis
176
Q

What is hyperplastic arteriolosclerosis?

A 
In small arteries/arterioles
Proliferation of smooth muscle cells
Deposition of basement membrane-like material causing sclerosis
Reduced lumen
Onion skinning
177
Q

What is necrotising arteriolitis?

A

In small arteries/arterioles
Necrosis of vessel wall, with fibrin and fibrinogen deposited
Can result in haemorrhage and thrombi

178
Q

What is hypertensive encephalopathy?

A 
Small infarctions
Haemorrhages > vasogenic oedema
Increased intracranial pressure
Presenting as
- Headaches
- Nausea
- Vomiting
- Seizures
- Loss of consciousness
179
Q

What is malignant nephrosclerosis?

A

Rapidly progressing renal failure

MD1 Revision (9 decks)

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