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MBBS - Year 3 > Urology - Abnormal urine > Flashcards

Urology - Abnormal urine Flashcards

1
Q

What is an acid?

A

H+ donor (total dissociation)

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2
Q

What is a base

A

H+ acceptor

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3
Q

What is a weak acid

A

HA ⇌ H ⁺ + A⁻ (partial dissociation)

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4
Q

What is a weak base

A

B + H ⁺ ⇌ BH⁺ (partial dissociation)

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5
Q

What is a buffered solution

A

A solution in which the addition of an acid or base does not affect the pH of the solution

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6
Q

Give Examples of physiological buffers

A

Bicarbonate [HCO₃⁻]
Phosphate [H₂PO₄⁻], [HPO₄2-]
Plasma proteins
Haemoglobin

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7
Q

What is the pH range where life can exist

A

6.8-7.8

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8
Q

What is the normal pH of the body

A

7.3 -7.4

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9
Q

Why is pH so tightly regulated

A

Enzyme dysfunction and denaturation =- DEATH

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10
Q

How is acid and alkali generated in the body

A

Diet (high meat is more acidic) and cellular metabolism (main reason)

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11
Q

What is the Bicarbonate buffer system equation

A

CO2 + H2O ⇌ H2CO3 ⇌ H ⁺ + HCO3-

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12
Q

What happens if you add to a weak acid

A

The conjugate base [A ⁻] of the partially dissociated weak acid [HA] neutralises the acid

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13
Q

What happens if you add a weak base

A

The hydrogen ion [H⁺] from the partially dissociated weak base [BH ⁺ ] neutralises the weak alkali

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14
Q

Where is the bicarbonate buffer system in the body located

A

CO2 + H 2O (lungs - resp)⇌ H 2CO3 ⇌ H ⁺ + HCO 3- (kidneys - metabolic)

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15
Q

What enzyme catalyses CO2 + H 2O ⇌ H 2CO

A

carbonic anhydrase (SLOW reaction)

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16
Q

what causes the reaction in H 2CO3 ⇌ H ⁺ + HCO 3-

A

FAST ionisation reaction

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17
Q

What is the weak acid in the equation CO2 + H 2O ⇌ H 2CO3 ⇌ H ⁺ + HCO 3-

A

H2CO3

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18
Q

What is the conjugate base in the equation CO2 + H 2O ⇌ H 2CO3 ⇌ H ⁺ + HCO 3-

A

HCO3-

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19
Q

Where is CO2 excreted

A

Lungs

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20
Q

Define acidaemia

A

an arterial pH below the normal range (<7.35)

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21
Q

What does a disturbance in bicarbonate primarily

A

Metabolic disorder

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22
Q

What does a disturbance in

A

respiratory disorder

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23
Q

Define alkalaemia

A

an arterial pH above the normal range (>7.45)

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24
Q

Define alkalosis

A

A process that tends to raise the extracellular fluid pH

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25
Q

Define acidosis

A

process that tends to lower the extracellular fluid pH

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26
Q

Why is reclamation of filtered bicarbonate and generation of new bicarbonate needed

A

To neutralise the net endogenous acid production (NEAP) (approx 50-100mmol/day)

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27
Q

How is pH maintained in the kidney

A

NEAP = RNAE

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28
Q

What should RNAE be in a 70kg person

A

70mEq

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29
Q

3 ways to get rid of acid

A

Bicarbonate, lungs, excretion of H+ by kidneys

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30
Q

How does the renal tubular reabsorb bicarbonate an decrease H+

A

reabsorbed an H+ is secreted

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31
Q

What are the 2 things kidneys do to maintain pH

A

Reclamation of bicarbonate
Generate new bicarb

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32
Q

How is HCO3 reabsorbed in early and late segments

A

H+ moves into tubular lumen - forms H2CO3 (conjugate), then separated with an enzyme to CO2 and H2O.
CO2 and H2O diffuses back into cell.
Once again is split into HCO3 and H+ by carbolic anhydrase
The H+ generated is used again to move into the tubular lumen.
1 H+ out 1HCO3 in

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33
Q

how does urinary phosphate (Pi) buffers generate new bicarbonate

A

Acidosis stimulates excretion of urinary Pi
buffers as titratable acid

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34
Q

How does synthesis of NH4+ from NH3 generate new bicarb

A

Acidosis stimulates renal ammoniagenesis
from glutamine

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35
Q

What is the pH range of urine

A

4.5- 8.0

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36
Q

What is the concentration of free H+ in urine at pH 4

A

0.1mmol/L

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37
Q

What would happen if no bufferes were used in urine to eliminate 70mmol of H+

A

you would excrete 700L of urine a day

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38
Q

What are the 2 buffer systems

A

Phosphate buffer system
Ammonia buffer system

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39
Q

What is the phosphate buffer system

A

NaPO4- binds to the secreted H+ creating NaH2PO4 which is excreted in urine

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40
Q

What is the ammonia buffer system

A

making NH4- and Cl-, the amonium chloride is excreted.

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41
Q

How does the amonia buffer system generate bicarb

A

Glutamine is broken down in the cell to 2NH+4 and 2HCO3. Ammonia is actively transported into the lumen and excreted and sodium (Na+ is actively reabsorbed). Bicarb is generated

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42
Q

What would happen to urinary HCO 3- excretion if a drug that inhibits
carbonic anhydrase is administered?

A
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43
Q

What is the urine anion gap

A

(Urine sodium + urine potassium)- urine chloride

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44
Q

What happens if there is more chloride than cations

A

Negative UAG - it indicated another cation is being excreted (NR4+)

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45
Q

what is increase renal amonium excretion the correct response of

A

metabolic acidosis. Tubular function is intact

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46
Q

What are clinical examples of respiratory acidosis

A

Emphysema, hypoventilation

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47
Q

What are clinical examples of metabolic acidosis

A

Lactic acidosis, renal failure, ketoacidosis, renal tubular acidosis

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48
Q

What are clinical examples of respiratory alkalosis

A

Congestive cardiac failure, raised intracranial pressure, hyperventilation

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49
Q

What are examples of metabolic alkalosis

A

Vomiting, diuretics, Cohns syndrome

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50
Q

What is the equation for RNAE

A

RNAE = [(U NH4x V)] + (U TA x V)] – (U HCO3_ x V)

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51
Q

What is the Henderson-hasselbach equation

A

pH = pKₐ + log([A⁻]/[HA])
One way to determine the pH of a buffer is by using the Henderson–Hasselbalch equation. In this equation, [HA] and [A⁻] refer to the equilibrium concentrations of the conjugate acid–base pair used to create the buffer solution.

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52
Q

What is the structure of the glomerula

A

Learn image

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53
Q

What is the purpose of a nephrone

A

To be a sieve to form a filtrate

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54
Q

What allows filtrate to form

A

Fee started capilary

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55
Q

What does the glomerular filtration barrier look like (what layers form or)

A
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56
Q

Where does the filtrate form

A

Bowman’s space

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57
Q

Define focal

A

Affecting only some glomeruli

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58
Q

Define diffuse

A

Affecting all glomeruli

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59
Q

Define segmental

A

Affecting only part of glomeruluS

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60
Q

Define global

A

Affecting whole glomerulus

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61
Q

Define proliferation

A

Increase in number of cells

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62
Q

Define expansion

A

Increase in intercellular matrix

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63
Q

Define crescent

A

Proliferation of cells within Bowman’s space

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64
Q

What are the 4 immunological mechanisms underlying glomerulonephritis

A

Intrinsic
Planted
Circulating
Non-specific deposition

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65
Q

What is intrinsic immunological mechanism of GN

A

Antibody binding to intrinsic glomerular antigens
- eg Goodpasture’s Disease

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66
Q

What is planted immunological mechanism of GN

A

Antibody binding to “planted” glomerular antigens
- eg post-Streptococcal glomerulonephritis

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67
Q

What is circulating complexes immunological mechanism of GN

A

Deposition of circulating antigen-antibody complexes
- eg lupus nephritis

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68
Q

What is the non-specific deposition mechanism of GN

A

The heavy chain is non-specific and is ‘sticky’ binding
-eg IgA nephropathy

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69
Q

What is the vascular mechanism of GN

A

Pauci-immune” capillary inflammation (eg systemic vasculitis) - granulomatitis with polyangitis - inflammation leading to ischaemia and damage
Pauci - means poor

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70
Q

What are some of the indications for renal biopsy

A

Nephrotic syndrome (adults)
Renal dysfunction of unknown cause (particularly acute)
To guide treatment or assess prognosis where diagnosis known
Dysfunction of transplant kidney - rejection
(Haematuria)
(Proteinuria)

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71
Q

What are complications of renal biopsy

A

Pain
Bleeding - macroscopic haematuria (5%)
- blood transfusion (0.5%)
- embolisation 1 in 1000
- nephrectomy 1 in 2000
- death

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72
Q

What are key contraindications for renal biopsy

A

Abnormal clotting / thrombocytopenia
Drugs (aspirin , clopidogrel, warfarin, DOACs etc)
Uncontrolled hypertension (eg >170/100)
Single kidney
Hydronephrosis - obstruction to outflow
Urinary tract infection

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73
Q

What 3 ways would you use to interpret renal biopsy

A

Light microscope
Immunostaning
Electron microscopy

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74
Q

What would you see for light microscopy

A

Basic morphology / cellular infiltrate

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75
Q

What stain would you use on a renal biopsy in light microscopy

A

Special stains – eg silver highlights collagen

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76
Q

What would you be looking at/for in immunostaining

A

Immunoglobulin or complement components

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77
Q

What would you be looking at/for in electron microscopy

A

Ultrastructural detail, including immune deposits

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78
Q

What are some presentations of renal disease

A

Haematuria
Proteinuria
Hypertension
Nephrotic syndrome
Nephritic syndrome
Acute kidney injury
Chronic kidney disease

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79
Q

Diagnose and what are the features of the disease
45 year old man with frothy urine, generalised oedema Urine dipstick 4+ protein Investigations:
- Urine protein excretion 5g/24hrs
- Albumin 22

A

Nephrotic syndrome
Proteinuria Hypoalbuminaemia Oedema

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80
Q

What is the most common cause of nephrotic syndrome in children (>75%)

A

minimal change disease

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81
Q

What would you expect to see on a light microscope biopsy of minimal change disease

A

Would be normal

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82
Q

What would you expect to see on an electron microscope biopsy of minimal change disease

A

fusion of podocyte foot processes (non- specific result of proteinuria)

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83
Q

What is the causes of MCD

A

IDIOPATHIC
Drugs - NSAIDS
Lymphoma

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84
Q

How do you treat MCD

A

Steroids
May relapse later and need more immunosuppression

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85
Q

What does FSGS stand for

A

Focal Segmental Glomerulosclerosis

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86
Q

How does FSGS present

A

Presents with nephrotic sydrome ± renal impairment Patchy (focal) involvement of kidney: may miss on biopsy

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87
Q

What would you see on immunoflourescence

A

Segmental sclerotic lesions with C3 and IgM deposition

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88
Q

How to treat FSGS

A

Not as responsive to steroids than MCD. Need very high dose
May get renal failure
May need transplant

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89
Q

What are the primary and secondary causes of FSGS

A

Obesity - IV heroin use - HIV - Drugs (eg pamidronate)

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90
Q

What is the most common cause of nephrotic syndrome in adults

A

MN membranous nephropathy

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91
Q

What would you see on histology for MN

A

spikes” on basement membranes, IgG deposition

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92
Q

What is MN associated with

A

Malignancy → careful history, consider investigation Drugs (eg gold, penicillamine, captopril) - Infections (eg hepatitis, malaria)

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93
Q

What will occur if you don’t treat (rule of 1/3)

A
  • 1/3 improve spontaneously - 1/3 remain the same - 1/3 develop progressive disease
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94
Q

How to treat MN

A

Immunosuppression
If use steroids its in association with other immunosuppression (e.g. retuximab)

95
Q

How does Mesangiocapillary Glomerulonephritis (aka Membranoproliferative GN) present

A

several ways, including nephrotic or nephritic syndromes Mesangial proliferation (often “lobular”)

96
Q

For MGN how would it appear in histology

A

Thickened capillary walls, “double contouring” of basement membrane Positive immunofluorescence (eg C3)

97
Q

What is MGN associated with

A

Infections (eg hepatitis, malaria, endocarditis, shunt nephritis) - Cryoglobulinaemia - Malignancy

Can occur post transplant

98
Q

How does diabetic nephropathy present

A

microvascular complications (eg retinopathy, peripheral neuropathy)
low level proteinuria – “microalbuminuria” Proteinuria then becomes heavier (± nephrotic syndrome)
Progressive decline in GFR (often supranormal early in disease)

99
Q

What would histology show in diabetic nephropathy

A

Kimmelstiel-Wilson lesions (nodular glomerulosclerosis)

Darker purple spoons on image

100
Q

How does amyloidosis present

A

heavy proteinuria ± nephrotic syndrome ± renal failure

101
Q

What is amyloidosis

A

Deposition of amyloid within multiple organs, including kidneys
AL – light chain deposition (eg myeloma)
AA – chronic inflammation (eg infection, connective tissue disorders)

102
Q

What stain would you use for amyloidosis

A

Stains with congo red (apple green birefringence under polarized light)

103
Q

What would you expect to see in electron microscopy of amyloidosis

A

Fibrils

104
Q

What are the common causes of nephrotic syndrome according to age

A
105
Q

Diagnose
24 year old man presents with macroscopic haematuria Had developed a sore throat the previous day General examination and blood pressure normal Settled spontaneously, but persistent microscopic haematuria 4 weeks later

A

IgA Nephropathy (Berger’s Disease)

106
Q

What is the most common cause of glomerulonephristis

A

IgA nephropathy

107
Q

What is burgers disease

A

Deposition of circulating IgA within mesangium leading to expansion of mesangial matrix and mesangial cell proliferation

108
Q

How does burgers disease present

A

Asymptomatic microscopic haematuria
- Episodic macroscopic haematuria (eg exercise, respiratory tract infection)
- Progressive renal impairment, end stage renal failure

109
Q

What are other associations with burgers disease

A

Liver disease
Henloch-schonlein purpurin (abdo and joint pain, skin rash)

110
Q

Diagnose and state likely presentation
30 year old man presents feeling unwell Sore throat 2 weeks ago Ankle swelling and dark urine for the last few days
Urine dipstick positive for blood
BP 160/100
Creatinine 170

A

NEPHRITIC” PATTERN
Hypertension Haematuria Renal impairment

111
Q

What is post infectious glomerulonephritis

A

2-3 weeks after Group A Streptococcal infection (throat, skin)
Damage due to post immune responce

112
Q

How does post infectious glomerulonephritis present

A

Nephrotic illness

113
Q

What would immunology show for PIG

A

Often low C3, normal C4 (alternate complement pathway activation) ?Antibody binding to planted Streptococcal antigens

114
Q

What would you see on biopsy

A

neutrophil infiltration, mesangial and epithelial cell, proliferation, IgG and C3 deposition, subepithelial deposits

115
Q

How do you treat PIG?

A

supportive case only

116
Q

What systemic vascular most commonly affects kidneys

A

Wegener’s granulomatosis (GPA), microscopic polyangiitis (MPA)

117
Q

How does vascular is cause glomerulonephritis

A

Inflammation of blood vessels leading to multiorgan involvement

118
Q

What would vasculitis show on biopsy

A

Focal necrotising glomerulonephritis ± crescents on biopsy, but pauci-immune

119
Q

How do you treat vascular glomerulonephritis

A

immunosuppression +/- plasma exchange

120
Q

What is the clinical presentation of cresent nephritis

A

nephritic illness with rapidly deteriorating renal function

121
Q

What is crescent nephritis

A

Rapidly progressive glomerulonephritis

122
Q

What would renal biopsy show for crescent nephritis

A

shows acute inflammatory process with crescent formation – cellular proliferation in Bowman’s space

123
Q

What is the WHO classification of lupus nephritis

A

I: Normal glomeruli (including minimal change) II: Mesangial disease
III: Focal proliferation (<50%)
IV: Diffuse proliferation (>50%)
V: Membranous nephropathy
VI: Advanced sclerosis

124
Q

What MUST you do if you suspect lupus nephritis

A

Renal biopsy

125
Q

What urine tests can be done for patients with glomerular disease

A

Dipstick (blood, protein, leucocytes, nitrites)
Microscopy (cells, casts, crystals)
Culture
Protein quantification

126
Q

What blood tests can be done for patients with glomerular disease

A

Haematology (FBC, ESR, coagulation, blood film) - Biochemistry (U&E, LFT, Ca, PO4, CRP)
Immunology: autoantibodies (ANA, ANCA, anti-GBM etc), serum immunoglobulins and electrophoresis serum free light chains, cryoglobulins, complement levels
Microbiology:blood cultures, serology (eg hepatitis B/C, HIV, ASO titre)

127
Q

What imaging can be done for patients with glomerular disease

A

Chest radiograph
Renal ultrasound
Other (eg CT, MRI, angiography, nuclear medicine)

128
Q

define proteinuria

A

Excessive protein in the urine
Normal urine protein <150mg/day (usually 40-80 mg/day)

129
Q

how does proteinuria present?

A

Asymptomatic and incidental detection on urine dipstick
Heavy proteinuria —> peripheral oedema, frothy urine

130
Q

What are the 6 mechanisms of Proteinuria
GTOPPP

A
  • Glomerular
  • Tubular
  • Overflow
  • Post-renal
  • Physiological or Benign
  • Pathological
131
Q

what is benign proteinuria (primary and secondary cause)

A

Orthostatic proteinuria – children and adolescents. Usually <3.5g/day
Transient proteinuria secondary to fever, heavy exercise, vasopressor, intravenous albumin. Usually <1g/day

132
Q

what is pathological glomerular proteinuria

A

Disruption of the filtration barrier
Can be associated with microscopic haematuria - Usually >1g/day

133
Q

Give some examples of primary causes of glomerulonephritis

A

Minimal change disease
Primary Focal Segmental glomerulosclerosis
Idiopathic membranous nephropathy
IgA nephropathy
Idiopathic membranoproliferative glomerulonephritis (MPGN)

134
Q

Give some examples of secondary causes of glomerulonephritis

A

Diabetes Mellitus
Systemic Amyloidosis
Secondary Focal Segmental glomerulosclerosis eg: Obesity, Hypertension, HIV infection
Autoimmune disease – eg: SLE
Secondary membranous nephropathy eg: cancer, drugs
MPGN – Hepatitis B or C

135
Q

Define glomerulonephritis

A

Glomerulonephritis is damage to your glomeruli, tiny filters inside your kidneys.

136
Q

What is tubular proteinuria

A

Usually < 1-2 g/day
Low molecular weight proteins are filtered at the glomerulus and reabsorbed by proximal tubules
Tubulo-interstitial nephritis:

137
Q

What are the 3 causes of tubulo-interstitial nephritis. Give examples for each

A

Drugs - eg: Antibiotics, NSAIDs, PPIs
Autoimmune disease - eg: Crohn’s disease, Sarcoidosis, Sjogren’s disease
Infections - eg: Tuberculosis, CMV infection, Leptospirosis

138
Q

What is overflow proteinuria

A

Excess production of low molecular weight proteins exceeds resorptive capacity of tubules

139
Q

What are 3 examples of overflow proteinuria and the excess proteins they produce

A

Myeloma (free light chains)
Rhabdomyolysis (myoglobin)
Haemolysis (haemoglobin)

140
Q

what is post-renal proteinuria

A

Inflammation or lower urinary tract – infection, stones

141
Q

what are the 3 key clinical features of nephrotic syndrome

A

Hypoalbuminaemia – serum albumin < 3g/dL
Oedema
Hyperlipidemia

142
Q

what are the 3 key clinical things that will occur if nephrotic syndrome is left untreated

A

Infection
Thrombosis
Established renal failure
- High mortality

143
Q

True of False:
Nephrotic syndrome is always caused by glomerular disease

A

True

144
Q

What are the general management and treatments for nephrotic syndrome

A

Low sodium diet and fluid restriction
Diuretics
Renin Angiotensin Aldosterone Inhibition and BP control
- Angiotensin constricts efferent arteriole and increases GFR
- Inhibition of angiotensin dilates efferent arteriole and decreases GFR – decreasing proteinuria
Statin
Anticoagulation

145
Q

How does Minimal Change disease look on a microscope and how is it treated

A

Normal glomerulus on light microscopy
90% of NS in children
Steroid responsive
Uncommonly associated with renal impairment

146
Q

What is Focal Segmental Glomerulosclerosis what are some of the primary and secondary causes

A

Focal (<50% glomeruli), Segmental (part of the glomerulus)
Primary or Idiopathic – Steroid and immunosuppression
Secondary – Obesity, Hypertension, HIV infection, Bisphosphonates

147
Q

what is mebranous nephropathy and give primary and secondary causes

A
  • ~30% of nondiabetic adult NS
  • Glomerular basement membrane immune deposits
  • Primary or Idiopathic – Anti PLA2R – Immunosuppression
  • Secondary – hepatitis, malignancy, autoimmune, drugs
148
Q

What is diabetic nephropathy what does it look like under a microscope and how is it treated

A
  • Type 1 or Type 2 DM
  • Progressive CKD and ERF
  • Glycaemic control, BP control and RAAS inhibition
  • Glomerulosclerosis – Kimmelstein Wilson nodules
149
Q

what is amyloidosis

A
  • Extracellular deposition of beta sheet fibrils
  • Systemic disorder
150
Q

what are the 2 types of amyloidosis

A
  • AL Amyloid – Ig light chains
  • AA Amyloid – Amyloid A. Chronic Inflammation.
151
Q

label the renal corpuscle

A
152
Q

label the ultrafiltration barrier

A
153
Q

what cahrge is the ultrafiltration barrier

A

-ve
therefore -ve charged albumin is not filtered even though it would fit.

154
Q

what is hydrostatic pressure

A

o Force a fluid exerts on the walls of its compartment (capillaries and bowmans capsule) – pushing out
o Main force – glomerulus forcing fluid out of glomerulus

155
Q

what is oncotic pressure

A

pressure exerted by plasma proteins on the wall of the compartment – sucking in

156
Q

what is the equation to calculate Net Filtration Pressure (NFP)

A

Net Filtration Pressure (NFP) (10mmHg) = HPg (55mmHg) – HPbc (15mmHg) – OPgcp (30mmHg)
HP glomerulus opposed by HP bowman’s capsule and OP glomerular capillary protein
-Ignore OP bowman’s capsule as not enough protein present

157
Q

what is the GFR

A

Glomerular Filtration Rate (GFR) is the total amount of filtrate formed by all the renal corpuscles by both kidneys per minute
- Indication of kidney impairment
- Takes into account NFP, surface area available, and permeability of glomeruli
GFR = (surface area + permeability) x NFP
GFR – Kf x NFP

158
Q

Which of the following would cause the greatest decrease in GFR in a person with
otherwise normal kidneys?
- Decrease in renal arterial pressure from 100 to 80 mm Hg
- 50% increase in proximal tubular sodium reabsorption
- 50% decrease in afferent arteriolar resistance
- 50% decrease in efferent arteriolar resistance
- 5 mm Hg decrease in Bowman’s capsule pressure

A

50% decrease in afferent arteriolar resistance
A 50% decrease in efferent arteriolar resistance would cause a substantial decrease in GFR.
A decrease in renal arterial pressure from 100-80 mm Hg in a normal kidney would only
cause a slight reduction in GFR because of autoregulation. The other options would tend to
increase GFR.

159
Q

Fill in the gap
Net contribution by the kidneys to whole-body glucose production is minimal
(<10%) except under conditions of ___________, when they can contribute
up to 30% to 40%.

A

Net contribution by the kidneys to whole-body glucose production is minimal
(<10%) except under conditions of PROLONGED FASTING, when they can contribute
up to 30% to 40%.

160
Q

Which of the following, compared with normal, might you expect to find 3 weeks
after a patient ingested a toxin that caused sustained impairment of proximal tubular
NaCl reabsorption? Assuming no change in diet or ingestion of electrolytes.
- No change in GFR, no change in afferent arteriolar resistance
- Decreased GFR, increased afferent arteriolar resistance
- Increased GFR, increased afferent arteriolar resistance
- Increased GFR, decrease afferent arteriolar resistance

A

Decreased GFR, increased afferent arteriolar resistance
Impairment of proximal tubular NaCl reabsorption would increase NaCl delivery to the
macular densa, which in turn would cause a tubuloglomerular feedback-mediated increase in afferent arteriolar resistance. The increased afferent arteriolar resistance would decrease GFR.

161
Q

Which mediator acts to selectively modulate the sympathetic vasoconstrictive
effects on the afferent arterioles to prevent sustained damage
- Brain natriuretic peptide
- Prostaglandin
- Angiotensin II

A

prostaglandin

162
Q

Fill in the gap with INCREASE or DECREASE
A selective decrease in efferent arteriolar resistance would ______ glomerular
hydrostatic pressure, ______ GFR, and ______ renal blood flow

A

A selective decrease in efferent arteriolar resistance would decrease glomerular
hydrostatic pressure, decrease GFR, and increase renal blood flow
- Add increase or decrease

163
Q

What are the 2 renal circulation capillary beds called

A

glomerular and peritubular capillaries

164
Q

what separated these 2 capillary beds

A

the efferent arteriole

165
Q

what is the renal pelvis

A

a large and wider cavity where the urine collects before the tube narrows into the ureter.

166
Q

what is the renal blood flow in order from the aorta to the vena cava

A
167
Q

what % of cardiac output does the kidney recieve

A

20%

168
Q

what is the normal volume and concentraton of urine

A

1.5L of water is excreted daily with 600miliomoles of solute

169
Q

how much blood evers the glomerulus’s every minute

A

1L/min

170
Q

what are the 6 functions of the kisneys (VCpMEE)

A

Volume, Concentration, pH, Metabolic, Excretory and Endocrine

171
Q

What role do the kidneys have in maintaining volume

A

BLOOD PRESSURE
Kidney are key to maintain blood volume
Directed by excretion or retention
Blood volume mediates blood pressure
BP = amount of blood + size of blood vessel

172
Q

what are the key ions that need to be regulated to maintain correct concentrations in the urine and blood
(SPCMHBC)

A

o Sodium
o Potassium
o Chloride
o Magnesium
o Hydrogen
o Bicarbonate
o Calcium

173
Q

how does the kidney regulate pH

A

Regulation of acid/base balance
Modulation of hydrogen and bicarbonate (respiratory/metabolic acidosis/alkalosis)

174
Q

what role does the kidneys have in maintaining metabolism

A

Kidneys produce glucose through glucogenesis
Glucose production is minimal (~<10%) except under prolonged fasting (30-40%).

175
Q

What roles does the kidney have in excretion

A

peeing :)
urea, creatinine, water soluble drugs and toxins

176
Q

what 4 ways do the kidneys have a role in endocrine maintenance and production

A
  1. Renin production – linked back with regulation of blood volume
  2. RAAS 1 of 4 pathways to correct low volume
  3. EPO – new RBC production
  4. Vitamin D – controls calcium and phosphorus metabolism
177
Q

true or false
Blood flow is linked to rate of renal filtration and excretion.

A

true

178
Q

true or false
it is vital local renal blood flow is autoregulated to prevent damage

A

true

179
Q

how is bp maintained across the kidneys

A

dilation and constriction of the afferent and efferent arterioles

180
Q

what are the 2 key vasoconstrictors

A

sympathetic nerves and RAAS (ANGII)

181
Q

what are the 2 key vasodilators

A

prostaglandins and natriuretic peptides (ANP, BNP)

182
Q

how do the sympathetic nerves cause vasoconstriction

A
  • Sympathetic tone increases as part of flight-flight response or low extracellular volume
  • Sympathetic nerve terminals release norepinephrine into the interstitial space
  • At high levels of nerve stimulation, BOTH afferent and efferent arteriolar resistances rise (constrict), thus generally decreasing both RBF and GFR
    o ALL above prevent fluid loss and maintain BP for response (fight or flight)
183
Q

what effect does RAAS have on blood flow and how does it work

A

RAAS – Increased Efferent
* Angiotensin II – response to low extracellular volume
* Multiple actions depending on conc.:
* Constricts efferent and afferent arterioles
* Works with PROSTAGLANDINS to constrict efferent more than afferent – maintaining GFR with reduced renal perfusion. Maintaining fluid in capillaries

183
Q

what effect does prostaglandins have and how does it work at changing bp

A
  • Dampen renal vasoconstrictor effects of sympathetic nerves or angiotensin II – particular the afferent arteriole
  • Prevents severe vasoconstriction and renal ischaemia
183
Q

what effect do natriuretic peptides have on bp control and how des it work

A
  • ANP and BNP released from heart from increased pressure and circulating volume
  • Act mainly on afferent arteriole – increases renal blood flow and GFR
  • ANP – inhibits secretion of renin – lowering ANG II
184
Q

what 2 factors need to be controlled to maintain stable renal blood flow

A

renal blood flow and mean arterial pressure

185
Q

what is the stable blood flow in mmHg

A

60-160mmHg

186
Q

what are the 2 mechanisms for maintaining a stable blood flow

A

myogenic response and tubuloglomerular feedback mechanism

187
Q

explain the myogenic response

A
  • Can constrict in response to pressure – prevents overstretching – increasing vascular resistance – helps prevent excessive increase in renal blood flow and GFR when BP rises
188
Q

Explain the tubuloglomerular feedback mechanism

A
  • Increase arterial pressure increases filtration and ultimately Na+ and Cl- in proximal tubule.
  • Sensed by macula densa cells of the JGA
  • Macula densa cell to release paracrine agents which triggers contraction of nearby vascular smooth-muscle cells in afferent arteriole
  • Increased afferent arteriolar resistance decreases GFR, counteracting the initial increase in GFR
189
Q

what is autoimmunity

A

when your immune system thinks your body is a pathogen

190
Q

What is type 1 hupersensitivity

A

Immediate hypersensitivity - Allergy NOT autoimmunity
* IgE secreted by B cells into blood and bind IgE receptors on mast cells and eosinophils
* IgE bound to antigen causes histamine release from mast cells to open ‘holes’ in a parasite for the rest of the immune system to recognise.
* IgE is important for allergies e.g. asthma

191
Q

what is anaphylaxis

A

potentially fatal shock response where large amounts of histamine is released narrowing the airways and reducing blood pressure through vasodilation.

192
Q

what is autoimmunity anti-body mediated type 2 reaction

A

cell bound antigen
* Antibodies (IgG, IgM bind self-antigen on tissue. Fc domains activate complement and recruit NK calls, macrophages, neutrophils etc leading to tissue damage and inflammation

193
Q

Give some examples of diseases the self antigen and the target for type 2 reactions

A
194
Q

what is the self antigen and target for goodpastures disease, pemphigus vulgaris and graves disease

A

Good pastures disease - collagen type IV - kidney, lungs
pemphigus vulgaris - cadhedrin - skin rash
graves disease- thyroid stimulating hormone - hyperthyroidism

195
Q

specifically how is graves disease type II

A

Antibodies bind thyroid stimulating (THS) hormone receptors stimulate thyroxine release. Hyperthyroidism

196
Q

specifically how is hashimotos disease type II

A

Antibody binds to thyroid stimulating hormone (TSH) receptors. antibodies damage the thyroid - hypothyroidism

197
Q

specifically how is antiglomerular basement membrane disease type II

A

Autoantibodies bind collagen in the glomerulus basement membrane
Often follows damage to the lungs (smoking) which reveals cryptic antigens

198
Q

specifically how is goodpastures syndrome type II

A

autoantibodies to collagen in the kidneys and lungs

199
Q

what is Autoimmunity Antibody-mediated Type III

A

Immune Complex Disease
* Antibodies bind soluble self-antigen and form immune complexes.
* Immune complexes get stuck in small blood vessels
* Fc domains activate complement recruiting NK cells, neutrophils etc leading to inflammation and damage.
* IgA is made by B cells in response to infection of mucosal surfaces.
* IgA binds and IgA receptor and is secreted across epithelial cells to protect mucosal surfaces

200
Q

what are some examples with their self antigen and target for type 3

A
201
Q

How is SLE type 3

A

Antibodies against DNA form immune complexes that deposit in small blood vessels. The complexes bind complement, induce recruitment of neutrophils leading to inflammation

202
Q

How is Post-steptococcal glomerulonephritis type 3

A
203
Q

how is glomerulonephritis type 3

A
204
Q

what causes IgA nephropathy

A

infection - frequent coughs and colds
IgA is recognised by autoantibodies and incorportaed into immune complexes that lodge in the glomerulus - mesangial deposits of IgA in biopsy of glomerulus

205
Q

The is Tcell mediated damage Type 4

A

Delayed Type
* Cell mediated type 4 hypersensitivity
* Activated autoreactive cytotoxic T cells that are not destroyed in the thymus release cytotoxic cytokines (TNF) and perforins - kill cells
* Cell mediated type IV hypersensitivity does not involve antibodies

206
Q

what are some examples of type 4 reactions with the self antigen and target

A
207
Q

why is typ4 called the delayed type

A
208
Q

how is type 1 diabetes a type 4 reaction

A

cytotoxic t cells recognising islet cells proteins contribute to type 1 diabetes
activated cytotoxic t cells release perforins and kill islet cells

209
Q

what is genetic autoantibody formation

A

antibodies recognise HLA
self reactive T cells are released from the thymus.
they can also be stimulated by cytokines during infections

210
Q

give some examples of different conditions and the HLA target

A
211
Q

how does autoimmunity occur after infection

A

cytokines generated during infection can stimulate low numbers of self-reactive T cells. These provide help to self reactive B cells

212
Q

give some examples of autoimmune conditions and the infections that can cause them

A
213
Q

which 3 conditions are treated with removal of the antibody by plasmapheresis or IgG therapy

A
  • Guilian-Barre
  • Myasthenia gravis
  • Thrombotic thrombocytopenia purpura
214
Q

what autoimmune conditon is treated with anti-inflammatory drugs and NSAIDs, steroids and/or biologics

A

RA

215
Q

which 3 conditions have treatment to restore/reverse specific damge

A

Type 1 diabetes - insulin
Graves disease - carbimazole
hashimotos - thyroxine

216
Q

What antibiotic would you prescribe for an uncomplicated lower UTI for a patient taking methotrexate

A

Nitrofurantoin
dose 50mg QDS PO for 3 days (7 if pregnant or male)
OR
100mg modified release BD PO 3/7 days

217
Q

wahat antibiotic would you prescribe for a patient with a Lower UTI - no other notable issues

A

Trimethoprim (AKA Septrin
*200mg BD PO for 3/7 days) – 7/7 if complicated (male)

218
Q

what is co-amixicalv

A

amoxicillin and clavulanic acid

219
Q

how do you differentiate between lower and upper UTI

A

presenting symptoms:
U UTI - Rigors, vomiting, flank pain, high grade 38

220
Q

what antibiotic can you not use in Upper UTI

A

Nitrofuratoin - it cant act on kidneys

221
Q

what is 3rd line treatment for UTI

A

cephalexin

222
Q

what is the main complication of ciprofloxacin

A

achilis tendonitis

223
Q

what is a kidney stone usualy made of

A

calcium oxulate

224
Q

what 3 areas usually block with a kidney stone

A

Uretoesical junction UVJ, ureter and renal pelvis

225
Q

how do you image for kidney stones in females and males

A
  • Female – ultrasound plus x ray (don’t get high dose radiation of ovaries)
  • Male – CT KUB (kidneys, ureter and bladder)
226
Q

4 year old boy presents with generalised swelling
Urine dipstick testing shows 4+ protein
Blood tests: albumin 23, creatinine 40
What is the name of the syndrome?

A

Nephrotic syndrome
Proteinuria (>3.5g/24hrs)
Oedema Hypoalbuminaemia

227
Q

what is the most likely diagnosis?

A

Minimal change disease is commonest childhood cause (>75%)

228
Q

What is the management of minimal change disease

A

Empirical steroid therapy usually given to children; if no response consider further investigation for alternative cause
- Prednisolone 1-2mg/Kg

229
Q

what is the prognosis of Minimal change disease

A

Remission with treatment is usually the norm in minimal change disease; may relapse, but should not affect renal function

230
Q

65 year old woman presents with generalised swelling Urine dipstick testing shows 4+ protein Serum albumin 23
What is the differntial diagnosis

A

Membranous nephropathy
Minimal change disease
Focal segmental glomerulosclerosis (FSGS)
Amyloid
Diabetes
Mesangiocapillary glomerulonephritis (MCGN)

231
Q

To determine the diagnosis what further information and examination would be necessary

A
  • Drugs
  • Infection
  • Malignancy
  • Other systemic disorders

MBBS - Year 3 (13 decks)

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