Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MBBS - Year 3 > The Renal & Urological System - Abnormal Urine > Flashcards

The Renal & Urological System - Abnormal Urine Flashcards

1
Q

What features of blood are regulated by the kidneys

A

pH
Volume
Pressure
Osmolality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where are the kidneys located

A

Between T12 and L3 (retroperitoneal)
R sits slightly lower than L due to liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does the renal hilum act as entry and exit for

A

Ureter
Renal arteries
Renal veins
Lymphatics
Nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Layers of kidney

A

Renal facsia
Adipose capsule
Renal capsule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What % of cardiac output is received by kidneys and why

A

25% as kidneys filters ~150L of blood/ day
Flows into R and L renla arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are nephrons divided into

A

Renal corpuscles and renal tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Whats found in the renal corpuscle

A

Glomerulus and bowman’s capsule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Once fluid is passed through the renal corpuscle, what is it referred to

A

Filtrate (urine precursor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What do filtration slits allow the passage of

A

Water
Glucose
Ionic salts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the renal tubule surrounded with

A

Peritubular capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does the renal tubule consists of

A

Proximal convoluted tubule
DCT
Collection duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the role of the juxtaglomerular complex

A

Help regulate BP and GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Where is the juxtaglomerular complex found

A

Between afferent arteriole and DCT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the juxtaglomerular complex composed of

A

Macula dense cells - sense low [Na] & [Cl]
Juxtaglomerular cells - helps w/ signalling
Extraglomerular mesangial cells - senses low bP –> secretes renin –> increased Na absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Metabolic function of kidney

A

Gluconeogeneisis, esp in conditions of prolonged fasting
Vit D activation - controls Ca and phosphorus metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Main function of renal tubules

A

Recovering solutes filtered at glomerulus - occurs mainly in PCT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Main function of Loop of Henle

A

Forming concentrate or dilute urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Role of distal tubule and collecting duct system

A

Fine control of slat and water excretion
(Most hormones exert their main effects on electrolyte and water secretion here e.gh. aldosterone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What do the sympathetic fibres to the kidney regulate

A

Blood flow
Glomerular filtration
Tubule reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is renal blood flow proportional to

A

Pressure gradient
(Pressure in renal artery - pressure in renal vein)/ reisstance in renla arterioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How does increased renal blood flow, affect GFR

A

increases it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Which hormones affect renal arteriole reistsnace

A

Adrenaline and AngII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How does adrenaline affect arteriole resistance

A

Released when SNS is activated
Binds to alpha-1 adrenergic receptors on aff and eff arterioles –> constriction
Increased resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

When is angiotensin released and how

A

In response to low BP
Renin released for JG cells –> cleaves angiotensinogen to AngI (works on endothelial cells in blood vessels) –> ACE made in lungs, converts AngI to AngII
AngII binds to receptors on aff and eff arterioels –> constriction
Increased resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How is GFR maintained, in terms of hormones affecting arteriole resistance

A

Eff arterioles more receptive to AngII, when low levels only eff contracts –> less blood leaving glomerulus, preserving GFR
High levels cause both to constrict

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Role of ANP and BNP in regulating renal blood flow

A

Both release when there’s increased cardiac workload
Binds to receptors on smooth muscle and causes DILTATION of aff & CONSTRICTION of eff arterioles –> increasing renal blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Role of PGI2 and PGE2 in regulating renal blood flow

A

Produced during SNS stimulation
Dilates both arterioles to ensure renal blood flow isn’t too low during SNS response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Role of dopamine in regulating renal blood flow

A

Dilates small vessels around heart and kidneys (but constricts in skin and muscle)
Even low levels increases renal blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Autoregulation of kidneys

A

Mechanism within kidney to keep renal blood flow & GFR constant, despite systemic BP
Kidney adjusts own arteriole resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Two mechanisms involved in kidney autoregulation

A

Myogenic mechanism
Tubuloglomerular mechanism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Myogenic mechanism - autoregulation

A

Reflex of smooth muscle cells to contract when stretched (high BP, more contraction)
Leads to vasoconstriction of aff and eff arterioles
Increased resistance to decrease GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Tubuloglomerular mechanism - autoregulation

A

Macula densa cells can sense when GFR increases due to [Na] and [Cl]
Increased BP —> increased renal blood flow –> more filtrate produced , w/ more Na and Cl –> MD cells release adenosine, diffuses to afferent arteriole (constriction) –> increases arteriole resistance –> decreased GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Layers of glomerular filtration barrier

A

Endothelium - fenestration allow solutes and proteins
Basement membrane - pores percent plasma proteins (-ve charge) entering filtrate
Epithelium - filtration slits of podocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Where does glomerular filtration membrane sit

A

Between blood and Bowman’s capsule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What does GFR represents

A

Total amount of filtrate produced bu all glomeruli in BOTH kidneys/ minute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How does oncotic pressure change in both arterioles

A

Low in aff and increase through glomerulus
Maximum at eff

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the. et filtration pressure at eff arteriole

A

0
Has reached filtration equilibrium, so blood is no longer filtered

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How does capillary hydrostatic pressure affect GFR

A

As it increases, as does GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How does capillary oncotic pressure affect GFR

A

As it increases, GFR decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

How does hydrostatic pressure in Bowman’s space affect GFR

A

As it increases, GFR decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What may cause increased hydrostatic pressure in Bowman’s space

A

Stone in ureter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Physiological buffers

A

Bicarb
Phosphate
Plasma proteins
Hb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Equation of bicarb buffer system

A

CO2 + H2O <—> H2CO3 <—-> H+ + HCO3-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Lines of defence against pH reduction

A

Lungs can blow off excess CO2
Kidneys reabsorb excess bicarb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What kind of acidosis is caused by disturbances of CO2

A

Primarily resp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What kind of acidosis is caused by disturbances of HCO3

A

Primarily metabolic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What must be equal to maintain pH and acid-base balance

A

Net endogenous acid production (NEAP) and renal net acid excretion (RNAE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Acidaemia

A

Arterial pH below normal range (<7.35)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Alkalaemia

A

Arterial pH above normal range (>7.45)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Acidosis

A

Process that tends to lower extracellular fluid pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Alkalosis

A

Process that tends to raise extracellular fluid pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

How do we produce H+

A

Tissue metabolism
Diet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Reclamation

A

Reabsoprtion of filtered bicarb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is required to neutralise NEAP

A

Reclamation and generation of new bicarb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Where does majority of bicarb occur in nephron

A

PCT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Bicarb reabsorption in PCT

A

Na-K ATPase creates Na gradient
Na/H transporter protein brings Na into tubular cell and H+ secreted out
H+ + HCO3- –> H2CO3 (in urinary space)
Carbonic anhydrase causes dissociation into H2O and CO2, these move into tubular cells
H2CO3 reforms in tubular cells before dissociating into H+ and HCO3-
Na+/HCO3- con transporter brings both into peritubular capillary
HCO3-/Cl- exchanger brings Cl- from peritubualr capillary into tubular cells and HCO3- into capillary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Bicarb reabsorption in DCT and CD

A

Same process as PCT but ATP pump in alpha0-intercalated cells pushes H+ into urinary space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Generation of new bicarb - urinary buffers

A

Urinary phosphate buffers –> acidosis stimulates excretion of urinary Pi buffers as acid
Synthesis of NH4+ from NH3 –> acidosis stimulates renal ammoniagenesis from glutamine
These allow H+ excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Urinary buffers - ammoniageneisis

A

Most important buffer mechanisms
PCT cells brake down amino acids into ammonia
NH3 diffuses into tubule and combines w/ H+ –> NH4+
NH4+ combines w/ Cl- in urine to create a weak acid - maintaining pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Urinary buffers - Pi

A

Phosphate ions enter tubules from plasma
Phophate ions poorly reabsorbed so builds up
Pi combines w/ H+ and lost through urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Why do we need urinary buffers

A

pH of urine cannot be reduced below 4.5
H+ builds up in urinary space so needs to be excreted as to not lower pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What would happen to urinary HCO3- excretion if a drug inhibiting carbonic anhydrase is administered

A

Metabolic acidosis
Lack of lumen reaction - increases H+ conc in tubular lumen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Calculating urine anion gap

A

[Urine sodium + urine potassium] - urine chloride

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What does a negative UAG indicate

A

Another cation (as opposed to Na+ and K+) is being excited e.g. ammonium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is the correct renal response to metabolic acidosis

A

Increased ammonium exertion
Implies tubular function is intact and cause of metabolic acidosis is extra-renal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Focal in terms of GN

A

Only affecting some glomeruli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Diffuse in terms of GN

A

Affecting all glomeruli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Segmental in terms of GN

A

Affecting only part of glomerulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Global in terms of GN

A

Affecting whole glomerulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Proliferation vs expansion in GN

A

Proliferation is increase in no. cells but expansion is increase in intercellular matrix

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Types of mechanisms underlying glomerulonephritides

A

Immune
Vascular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Indications for renal bx

A

Nephrotic syndrome (adults)
Renal dysfunction of unknown cause (esp a/c)
Dysfunction of transplant kidney
Guide treatment or assess prognosis where dx known
Haematuria/ proteinuria?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Complications of renal bc

A

Pain
Bleeding - macroscopic haematuria +/- clot retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Contraindications for renal bx

A

Abnormal clotting/ thrombocytopenia
Uncontrolled HTN
Single kidney - relative
Hydronephrosis
UTI (pyelonephritis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Hydronephrosis

A

Kidneys swell as a result of obstruction to urine output

76
Q

Interpretation of renal bx

A

Light microscopy
Immunostaining
Electron microscopy

77
Q

How may renal disease px

A

Haematuria
Proteinuria
Nephrotic syndrome
Nephritic syndrome
A/c renal
C/c renal failure

78
Q

What sx are involved in nephrotic syndrome

A

Proteinuria
Hypoalbuminamia
Oedema
Hypercholesterolaemia

79
Q

What sx are involved in nephritic syndrome

A

Haematuria
HTN
Renal impairment e.g. reduced urine output

80
Q

Commonest cause of nephrotic syn in children

A

Minimal change disease

81
Q

Bx findings for minimal change disease

A

Normal light microscopy
Fusion of podocytes on electron microscopy

82
Q

Causes of minimal change disease

A

Usually idiopathic
May be caused by NSAIDs or lymphoma
Associated w/ URTI

83
Q

Mx of minimal change

A

Usually steroid responsive
May relapse, requiring heavy immunosuppression
1% go on to end stage renal failure

84
Q

Px of focal segmental glomerulosclerosis

A

Nephrotic syn +/- renal impairment

85
Q

Associations w/ FSGS

A

Berger’s disease, sickle cell, HIV
More common in afro-caribbean population

86
Q

Bx findings for FSGS

A

Focal scarring
Segmental sclerotic lesion
C3 and IgM deposition

87
Q

Mx for FSGS

A

Steroids or cyclophosphamide/ ciclosporin
40% progress to end-stage renal dialler, may recur following transplant

88
Q

Types of FSGS

A

Primary or secondary - obesity, IVDU, HIV, pamidronate

89
Q

Commonest cause of nephrotic syn in Aleuts

A

Membranous nephropathy

90
Q

Associations seen in membranous nephropathy

A

Malignancy - lung, colon, breast
Infections - Hep B, malaria
AI teases - SLE, thyroid issue
Drugs - pencillamine, gold, captopril

91
Q

Bx for membranous nephropathy

A

Spikes on basement membrane - IgG deposition
Subepithelial immune complex deposits

92
Q

Rule of 1/3rd in membranous neohropathy

A

1/3 gets better speonatnouesy
1/3 stays the same
1/3 gets worse

93
Q

Px of mesnagiocapillaru (membranoprolofertaive glomerulonephritis )

A

Nephritic or nephrotic syn

94
Q

Bx findings for mesangiocapillary GN

A

Thckened capillary walls
‘Double contouring’ of basement membrane
+ve immunoflurosece (C3)

Serum complement levels may be low

95
Q

Associations w/ mesnagiocapillary GN

A

Infection - hep B/C, endocarditis, malaria
Cryoglobulinaemia
Malignancy

96
Q

Clinical features of diabetic nephropathy

A

Low level proteinuria - earliest sign
Pts usually have other micro vascular complications (retinopathy, peopgeral neuropathy, diabetic neohropathy)

97
Q

Histology for diabetic nephropathy

A

Kimmelsteil-Wilson lesions

98
Q

How may amyloidosis present

A

Heavy proteinuria +/- nephrotic syndrome & renal failure

99
Q

What does amyloidosis stain with

A

Congo red
Apple green birefrigence under polarised light

100
Q

Commonest form of glomerulonephritis WW

A

IgA nephropathy (Berger’s disease)

101
Q

Px of IgA nephropathy

A

Ranges drom microscopic haematuria to paroxysmal macroscopic haematuria (e.g. exercise, resp tract infection) and progressive c/c renal failure

102
Q

Bx findings for IgA nephropathy

A

IgA deposition in mesangial area

103
Q

Associations w/ IgA nephropathy

A

C/c li9ver disease
Henoch Schonlein Purpura

104
Q

When does post-stop GN px

A

2/3 weeks after Gp A strep infection (throat. skin)
Usually px as neohritic illness

105
Q

Investigative findings for post-stop GN

A

Low C3
Normal C4
+ve ASO titre (anti-streptolysin O)

106
Q

IgA nephropathy vs post-strep GN

A

IgA occurs 3-4 days after and post-strep is 2/3 weeks

107
Q

Mx for post-strep GN

A

Supportive

108
Q

How does renal involvement of systemic vascilutis (GPA and MPA) px

A

Nephritic illness

109
Q

Goodpasture’s disease pathophys

A

AKA anti-glomerular basement disease
Antibodies to tupe IV collagen (found in glomerular and alveolar basement membrane)

110
Q

Px of Goodpasture’s disease

A

A/c renal failure (often absolute anuria) and/ or pulm haemorrhage (in smokers)

111
Q

Rapidly progressive GN

A

Clinical syn of nephritis w/ rapid decline in renal function
Often associated w/ presents on bx - cellular proliferation in Bowman’s space

112
Q

Causes of rapidly progressive GN

A

Can be due to many causes incl systemic vasculitis and Goodpasture’s

113
Q

Ix for pts w/ glomerular disease - urine

A

Dipstick
Microscopy and culture
Electrophoresis (light chains - Bence Jones proteins)
Protein quantification

114
Q

Ix for pts w/ glomerular disease - bloods

A

Haem - FBC, ESR, coagulation, blood film
Biochem - U&Es, LFTs, Ca, PO4-, CRP
Immunology
Microbio - blood cultures, serology (Hep B/C, HIV, ASO titre)

115
Q

Imaging for pts w/ glomerular disease

A

CXR
Renal ultrasound
Other (CT, MRI, angiography)

116
Q

Normal urine protein

A

<150mg/ day (usually 40-80mg/day)

117
Q

Urine proteins

A

Albumin - highest %
Low molecular weight proteins - beta2 microglobulins, polypeptides
Secreted proteins e.g. immunomodulatory

118
Q

Calculating excretion in neohron

A

Filtration - rebaosrption + secretion

119
Q

How does proteinuria present

A

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

120
Q

Advantages of urine dipstick

A

Simple bedside tetst
Rapid dx
Inexpensive

121
Q

Disadvantages of urine dipstick

A

Operator dependent
Semi-quantitive
Insensitive to low level proteinuria
Doesn’t detect non-albumin proteinuria

122
Q

Ways of detecting proteinuria

A

Urine protein: creatinine ratio and albumin: creatine ratio - spot urine sample
24hr urine protein collection

123
Q

Which types of dysfunction mechanisms cause proteinuria

A

Glomerular
Tubular
Overflow
Post-renal

124
Q

Glomerular mechanism for proteinuria

A

Disruption in glomerular filtration barrier (loss of structural/ functional integrity)

125
Q

Tubular mechanism for proteinuria

A

Defects in reabsorption and secretion (infl condns can cause this)

126
Q

Overflow mechanism for proteinuria

A

Production of excess amounts of protein - overwhelms filtration and tubular reabsorption (associated w/ myeloma and massive hameolysis)

127
Q

Post-renal mechanism for proteinuria

A

Characterised by infl in urinary tract AFTER level of nephron

128
Q

Types of benign proteinuria

A

Orthostatic proteinuria
Transient proetinuria

129
Q

Orthostatic proteinuria

A

Children and adolescent
Usually <3.5g/day erect but not supine

130
Q

What may transient proteinuria be due to

A

Fever
Heavy exercise
Vasopressor
IV albumin

131
Q

Primary glomerulonephritides

A

Minimal change disease
1’ FSGS
Idiopathic membranous nephropathy
IgA nephropathy
Idiopathic mesangiocapillary GN

132
Q

Secondary glomerulonephritiides

A

DM
Systemic amyloidosis
2’ FSGS e..g obesity, HTN, HIV infection
AI disease e.g. SLE
2’ membranous nephropathy e.g. cancer, drugs
Mesangiocapillary GN - Hep B/C

133
Q

Tubular proteinuria

A

Usually 1-2 g/ day
Low molecular weight proteins are filtered at glomerulus an reabsorbed by proximal tubules so proximal tubular function can be tested by looking ta levels of LMWP

134
Q

Causes of tubular proteinuria

A

Tubulo-intertstitial nephritis caused by infl reaction

135
Q

Causes of tubulo-interstitial nephritis

A

Drugs - e.g. abx, NSAIDs, PPis
AI disease - Crohn’s, sarcoidosis, Sjorgen’s disease
Infections - TB, CMV infection, Leptospirosis

136
Q

Overflow proteinuria

A

Excess production of LMWP exceeds reabsorptive capacity of tubules

137
Q

Condns causing overflow proteinuria

A

MM (free light chains)
Rhabdo (myyoglobin)
Haemolysis (Hb)

138
Q

What may post-renal proteinuria be caused by

A

Infl of lower urinary tract - infection, stones

139
Q

Clinical significance of proteinuria

A

Proteinuria is a risk factor for CDV disease and progressive CKD

140
Q

Assessment of a pt w/ proteinuria

A

Hx
Physical exam
Urine dipstick and quantification
Assessment of renal function - creatinine and GFR
Renal imaging - USS
Relevant bloods
Renbal bx - definitieve test

141
Q

Reevant bloods for proteinuria

A

ANA
ANCA
Anti GBM
Serum protein electrophoresis and free light chain ratio
Hep B/C serology
Complement
Anti-PLA2 (membranous nephropathy)

142
Q

Complication of nephrotic syn

A

Infection
Thrombosis
Renal failure

143
Q

Infection as a complication of nephrotic syn

A

Loss of albumin accompanied w/ loss of immunomodulatory proteins (Ig)

144
Q

Thrombosis as a complication of nephrotic syn

A

Loss of anticoagulant proteins (protein C, protein S, antithrombin III) creates pro-thrombotic state

145
Q

Renal failure as a complication of nephrotic syn

A

Proteinuria causes reduction in GFR –> CKD

146
Q

Renal pathophys of nephrotic syn

A

Disruption of glomerular filtration barrier w/ podocyte effacement

147
Q

Rarer clinical features of nephrotic syn

A

Pulm oedema and pleural effusion
Hyperlipidaemia
Thromboses

148
Q

Why is hyperlipidaemia seen in nephrotic syn

A

Possible 2’ to increased hepatic lipoprotein synthesis - up-regulation of synthetic function of liver (goal is increased albumin)

149
Q

Causes of nephritic syn

A

SLE
Henoch-Schonlein Purpura
Anti GBM
Rapidly progressive GN
Post-strep GN
Alport syn
IgA nephropathy
Membranoproliferative GN

150
Q

Alport syndrome

A

Genetic disease that affects renal blood vessels leading to GN and defness
May also cause catracts and bulging of the lens

151
Q

Pathophys of Alport syn

A

X-inked disease causing mutation of type 4 collagen
Abnormal collagen of basement membrane of kidneys, ears and eyes

152
Q

Management of nephrotic syndrome

A

Low Na diet and fluid restriction due to 2’ hyperaldosteronism
Diuretics
BP control
Statin
Anticoagulant

153
Q

How does angiotensin increase GFR

A

Constricting the eff arteriole increases pressure in glomerulus

154
Q

How does angiotensin decrease proteinuria

A

By dropping pressure in glomerular capillariess

155
Q

What antibody be tested for in primary membranous nephropathy

A

Anti-PLA2R

156
Q

How is diabetic nephropathy managed

A

Glycaemic control
BP control
RAAS inhibition

157
Q

AL amyloidosis

A

Raised by light chain deposition (closely related to MM)

158
Q

AA amyloidosis

A

2’ amyloidosis caused by protein serum amyloid A released in c/c infl (infection, CTD)

159
Q

Which cells release renin

A

Juxtaglomerular cells release renin (via exocytosis)

160
Q

How is pro-renin converted to renin

A

By proteolytic enzymes

161
Q

Factors that will increase renin release

A

Decrease in arterial BP
Decreased BP in glomerular vessels
Increased loss of Na and water
Increased sympathetic activity

162
Q

Factors that decrease renin release

A

Na and water retention
Increased BP
Activation of AngI receptors (short loop -ve feedback)

163
Q

Which pathways control renein secretion

A

Macula densa
Intrarenal barorecptor
Beta-receptor

164
Q

Macula densa pathway of renin release

A

Reabsorption of Na Cl occurs via MD cells
Changes in Na reabsorption modifies release by JG cells
Increase in NaCl reabsorption inhibits renin release and vice versa

165
Q

Which ion conc is mainly required for macula dense pathway of renin release

A

Cl- rather than Na
[CL-] required for saturation of symporter are high so changes in conc mainly effect MD mediated renin release
[Na+] in tubular lumen is higher than required for symporter

166
Q

What modulates the macula densa pathway for rent please

A

ATP
Adenosine
PGI2

167
Q

Intrarenal baroreceptor pathway for renin release

A

Increase in BP or renal perfusion pressure in preglomeruluar vessels inhibit renin release and vice versa

168
Q

What may modify the intrarenal baroreceptor pathway for renin release

A

Stretch receptors in arterial walls and.or by PG synthesis

169
Q

Beta receptor pathway for control of renin related

A

Via beta-1 receptors on JG cells

170
Q

-ve feedback for renin release

A

Increased renin secretion enhances formation of AngII which is responsible for short loop -ve feedback

171
Q

Other factors causing -ve feedback for renin release (NOT renin secretion)

A

Activating high pressure baroreceptors and thereby reducing renal sympathetic tone
Increasing pressure in pre-glomerular vessels
Reducing NaCl reabsorption from proximal tubule (pressure natriuresis) thereby reducing MD pathway

172
Q

Physiological factors affecting renin release

A

Systemic blood pressure
Dietary salt intake
Pharmacological agents

173
Q

Pharmacological agents modifying renin release

A

NSAIDS
Loop diuretics
ACEi, ARBs, renin inhibitors
Centrally acting sympatholytic agent and beta blockers

174
Q

How do NSAIDs affect renin release

A

NSAIDS inhibit PG synthesis –> decreased renin release

175
Q

How do loop diuretics affect renin release

A

Loop diuretics decreased BP and increase NaCl reabsorption
Causing increased renin release

176
Q

How doe centrally acting sympatholytic agents and BBs affect renin release

A

Decreased renin secretion by reducing beta-receptor activation

177
Q

Role of ACE

A

Convert AngI to AngII
Also inactivates vasodilators (identical to kinin 2)

178
Q

Where is angiotensinogen made

A

Liver

179
Q

Where is the major site of conversion of AngI to AngII

A

Lungs

180
Q

What is the local (tissue) renin-angiotensin system important for

A

Its role in hypertrophy, infl and remodelling and apoptosis

181
Q

Which tissue can local RAAS occur in

A

Brain
Pituitary blood vessels
Heart
kidney
Adrenal glands

182
Q

Extrinsic vs intrinsic local RAAS

A

Extrinsic - vascular endothelium of the tissues
Intrinsic - tissues having mRNA expression

183
Q

Local (tissue) RAAS

A

Binding of renin or pro-renin receptors located on cell surface

184
Q

Enzymes that act as alternative conversion of angiotensinogen to AngI or AngII

A

Cathepsin
Tonon
Cathepsin G
Heart chemise

185
Q

Angiotensin receptors

A

Most effects of AngII are mediated by AT1

MBBS - Year 3 (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions