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Block 34 Metabolic Flashcards > Renal > Flashcards

Renal Flashcards

1
Q

What are the main causes of CKD

A

Diabetes
Hypertension
Glomerular disease (including glomeruloneprhitis)
Polycystic disease
Recurrent UTIs

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2
Q

How would CKD present or end stage renal failure

A
  • hypertension ( kidneys filtering ability decreases which means more fluid is retained leading to hypertension and oedema)
  • breathlessness due to anaemia

-palpitations and muscle cramps from hyper kalemia

  • fatigue and dizziness from less EPO
  • bone pain from decreased vitamin D
  • pruritus (from increases in urea)
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3
Q

The release of renin is controlled by what things

A
  • changes in pressure at afferent arteriole
  • sympathetic tone
  • changes in chloride and osmotic concentration detected by the macula densa
  • local prostaglandin release
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4
Q

What are the actions of angiotensin II

A
  • systemic vasoconstriction to increase blood pressure (specifically the efferent arteriole
  • increasing sodium and water retention
  • also increases aldosterone secretion by the adrenal cortex
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5
Q

What is the effect of endothelin on kidneys

A

Inhibits sodium and water absorption
Antagonises the action of ADH and aldosterone

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6
Q

What is the effect of prostaglandins on the kidney

A
  • causes vasodilation of the afferent arteriole increasing blood flow and GFR. Promotes diuresis

Nitric oxide works in a similar fashion to endothelis

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7
Q

How many stages are used to categorise CKD

A

5 stages
Stage 1 less than 90mL/min
Stage 3 split into 3a and 3b
Stage 5 less than 15mL/min

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8
Q

What is Fanconi syndrome

A

Disease affecting the PCT in which amino acids, bicarbonate, glucose, phosphate, proteins, and uric acid are not re absorbed leading to symptoms.

Can be inherited (mostly presents in children) or acquired later on in life in adults.

Acquired maybe due to drugs such as anti-virals, cisplatin or azathioprine

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9
Q

Red cell casts almost always diseased relating to which part of the nephron

A

Glomerulus

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10
Q

Features of nephrotic syndrome

A

Heavy proteinuria greater than 3.5g per day
Hypoalbuminaemia - leads to fluid overload and oedema
Hyperlipidaemia (increase in LDL +VLDL to compensate for lack of albumin as they are lipoproteins)

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11
Q

What things are included in the management of nephrotic syndrome

A
  • fluid restriction and low salt (to reduce oedema)
  • replacing lost albumin
  • diuretic like furosemide to get rid of excess fluid

Consider:

  • increase risked of thromboembolism as loss of anti thrombin in urine
  • increased risk of sepsis as loss of immunoglobins - decreased immunity
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12
Q

Most common of nephrotic syndrome in children

A

Minimal change disease

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13
Q

What is the most common cause of AKI

A
  • acute tubular necrosis
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14
Q

What are the 2 main causes of acute tubular necrosis

A
  • ischaemia caused by sepsis or shock
  • nephrotoxic substances such as aminoglycosides, myoglobin, radiocontrast agents and lead
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15
Q

What electrolytes changes are seen in ATN

A

Rise in urea, creatinine and potassium

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16
Q

What are the features of ADPKD

A
  • hypertension
  • recurrent uTIS
  • flank pain
  • haematuria
  • Palpable kidneys
  • Renal stones

Causes cysts in other organs such as the liver, spleen, pancreas.
May also cause berry aneurysms leading to subarachnoid haemorrhage

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17
Q

What is Alport’s syndrome

A

X linked genetic condition which leads to faulty formation of collagen in the glomerular basement membrane therefore leading to
microscopic haematuria
Progressive renal failure

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18
Q

What are the causes of AKI (pre-renal)

A
  • hypovolemia secondary to diarrhoea or vomiting
  • RA stenosis
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19
Q

Examples of renal causes of AKI

A
  • glomeruloneprhtis
  • ATN
  • AIN
  • rhabdomylosis
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20
Q

What are the post renal causes of AKI

A
  • kidney stone
  • BPH
  • external compression of the ureter
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21
Q

Who is at increased risk of AKI

A

-previous AKI
- other failures (heart, diabetes)
- recent use of nephrotoxic drugs
- CKD
-use of iodine contrast agents

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22
Q

What meds should be stopped in AKI

A
  • NSAIDS. - (decrease renal perfusion)
  • aminoglycosides (
  • ACEi and ARBS -decrease renal perfusion
  • diuretics (decrease perfusion as lower blood pressure and volume)
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23
Q

What may have to stopped in AKI as there is risk of toxicity if it builds up

A

Metformin
Digoxin
Lithium

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24
Q

Hyperkalemia occurs in AKI. What is used to protect the myocardium

A
  • calcium gluconate
  • insulin and dextrose used to shift extraceullalr to inside.
  • calcium resonium used to remove potassium from the body
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25
Q

What are the features of Good pastures syndrome

A
  • causes pulmonary haemorrhage and rapidly progressive glomerulonephritis (blood and protein loss)
  • more common in men
  • associated with HLA DR2
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26
Q

What does renal biopsy show in GP syndrome

A
  • linear IgG deposits along the basement membrane
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27
Q

What is focal segmental glomerulosclerosis

A

Presents as haematuria (microscopic), proteinuria, hypertension, xanthelasma. This progresses to nephrotic syndrome with significant loss of albumin and then ESRD

Investigated by light microscopy which demonstrates regions of scarring within the renal tissue. The deep corticomedullary glomeruli are affected first

Causes can be primary which is genetic or secondary due to pre-existing renal disease, SCD,HIV and lupus and use of heroin

On renal biopsy glomeruli may appear glassy

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28
Q

What diseases cause nephrotic syndrome:

A

Primary
- minimal change disease
- focal segmental glomerulosclerosis
- membranous glomerulonephritis
- membranoproliferative glomerulonephritis

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29
Q

What are the secondary causes of nephrotic syndrome

A
  • diabetic nephropathy
  • lupus nephritis
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30
Q

What are the complications of nephrotic syndrome

A
  • thromboembolism - getting rid of anti-thrombin proteins
  • microcytic hypochromic anaemia
  • infections
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31
Q

What is the pathophysiology of diabetic nephropathy

A
  • excess glucose in the blood causes glycation of the proteins which causes the basement membrane to thicken. (Hyaline arteriosclerosis)
    This causes arteriole dilation to increase pressure and blood flow into the glomerulus) —> causes damage over time causing filtration slits to widen leading to loss of protein
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32
Q

What is the pathophysiology of FGS

A
  • cause is unknown but it causes focal sclerosis of the glomerulus.
  • foot processes of the podocytes become damaged.
  • proteins, lipids trapped within the glomeruli - hyalinosis occurs

Secondary causes include SCD, HIV, renal hyerfiltration (only having 1 kidney)

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33
Q

What are the risk factors for FGS

A

Black african descent

Morbid obesity

CKD

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34
Q

What is the pathophysiology of membranous glomerulonephritis

A

Primary - idiopathic

Secondary: infections, neoplasms , drugs, hearty metal poisonings and autoimmune diseases (SLE, RA and Sjögren’s syndrome)

-leads to deposition of complexes at basement membrane (spike and dome pattern) triggers immune response which releases cytokines and inflammatory cells causing damage — leads to protein loss

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35
Q

What are the main risk factors for MCD

A

Hodgkins lymphoma

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36
Q

What are the functions of the kidneys

A

Elimination of metabolic waste
Water homeostasis
Electrolyte homeostasis
Acid base homeostasis
Blood pressure control

Vitamin D
Erythropoiesis
Renin

Excretion of drugs and metabolites

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37
Q

What parameters are used to measure renal function in AKI

A

1) serum creatinine. (Can be influenced by gender, ethnicity, age, body mass, diet and exercise)

2) urine output

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38
Q

EGFR is used in CKD. What is it based on

A
  • creatinine, age, gender and ethnicity
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39
Q

Diagnostic criteria for CKD

A

EGFR of less than 60mL/min

Or

Kidney damage indicated by abnormal bloods, urine or imaging

Present for more than 3 months and tends to be irreversible

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40
Q

How many stages of CKD is there

A

5

Stage 5 (worst) = less than 15mL/min

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41
Q

CKD stages 3-5 increase with what

A

Age

Worse CKD staging also associated with lower SES

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42
Q

What are the risk factors for developing CKD

A

Increased age
Hypertension
Diabetes
Smoking
Poor education
Recurrent UTIs
Long term use of nephrotoxic meds

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43
Q

What systemic diseases cause CKD

A

Diabetes
Hypertension

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44
Q

What immune mediated diseases cause CKD

A

Membranous nephropathy
IgA nephropathy
SLE

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45
Q

Which infections can cause CKD

A

HIV
HBV
HCV
Tb

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46
Q

What genetic diseases can cause CKD

A

Polycystic kidneys
Cystinosis

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47
Q

Complications CKD

A

Cardiovascular disease (inappropriate elevation of blood pressure puts strain on the heart. Also unable to get rid of water - fluid overload increases blood Pressure,
more prone to atherosclerosis as dyslipidameia occurs)
Metabolic acidosis ( can’t excrete H+ and reasborb bicarbonate )
Uraemia (failure to excrete urea)

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48
Q

What diagnostic measures confirm AKI

A

Stage 1 — creatinine 50-100% increase from baseline and less than 0.5ml/kg/hr for 6 hours urine output

Stage 2 — creatinine 100-200% increase from baseline and less than 0.5ml/kg/hr for 12 hours

Stage 3 — >200% increase. <0.3ml/kg/hr for 24 hours

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49
Q

What meds increase risk of AKI

A

Diuretics
Acei arbs
NSAID
Gentamicin
Vancomycin
Chemo

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50
Q

Diagnostic criteria for nephrotic syndrome

A

Proteinuria - more than 3g

Peripheral oedema

Hyperlipidaemia

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51
Q

What are the primary diseases causing nephrotic syndrome

A

FSGS
Minimal change disease
Membranous nephropathy

Damage to filtration barrier occurs leading to protein leak

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52
Q

What are the secondary causes of nephrotic syndrome

A

DM
Cancers
Drugs
Infections
SLE
Amyloidosis

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53
Q

What are the complications of nephrotic syndrome

A

Thromboembolism
DVT and PE
Infection
Hyperlipidaemia
AKI
CKD

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54
Q

Treatment of nephrotic syndrome

A
  • diuretics
  • salt restriction
  • reduce proteinuria by acei and arb
  • thromboprolylaxis
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55
Q

Diagnostic criteria for nephritic syndrome

A

Proteinuria less than 3g
Haematuria
Hypertension
Oedema
AKI/ckd

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56
Q

What are the causes of nephritic syndrome

A

Usually inflammatory or immune mediated

  • autoimmune
    SLE
    ANCA vasculitis
    Anti-glomerular basement membrane antibody disease

Infection related:
Post infectious glomerulonephritis
Bacterial endocarditis
HCV

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57
Q

What is the surgical triad which causes most AKIs in hospital

A

Post operative volume depletion

Infection

Nephrotoxic drugs

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58
Q

What % of akis are caused by parenchyma damage

A

Less than 5%

Post renal 10%

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59
Q

Which groups are at risk for AKIs

A

Elderly
Diabetics
Vasculopaths
Chronic renal impairment
Chronic liver disease
Cardiac dysfunction

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60
Q

What kind of drugs can impact the function of the kidneys

A

ACEI + ARBS

NSAIDS

PPIs cause interstitial nephritis

Aminoglycosides

Contrast medium

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61
Q

Remember a normal serum creatinine is not synonymous with a normal GFR

A
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62
Q

What are the life threatening complications of AKI

A

Hyperkalemia

Pulmonary oedema

Uraemic encephalopathy

Pericardial fluid

63
Q

Who is involved in MDT of renal patients

A

Nephrologist
Dietician
Transplant nurse
Dialysis technician
Clinical pharmacist
Community peritoneal dialysis staff
Haemodialysis staff
Surgeon

64
Q

Where does urea come from

A

Proteins are broken down into amino acids which are converted to ammonia which is very toxic so it is converted to urea. Conversion occurs in the liver but urea is excreted via the kidneys

65
Q

What test is used to measure urea levels

A

BUN blood urea nitrogen

66
Q

What is oliguria

A

Volume of urine below which body cannot excrete products of metabolism

67
Q

Why might acutely sick patient in AKI become acidotic

A

Failure to remove acid from the body via H+ excretion

Production of other acids such as lactic acid from tissue hypoxia

68
Q

What ECG changes occur in Hyperkalemia

A

Tall tented T waves

Wide WRS and disappearance of P wave

Sine waves

69
Q

What methods are used to assess intravasular volume

A

Body weight
Skin turgor
Postural blood pressure
Mucous membranes
JVP
Lung bases

70
Q

What complications occur in CKD

A

Anaemia
Renal bone disease (Vit D)
Acidosis
Hypertension (fluid overload
Malnutrition
Uraemia

71
Q

What can cause haematuria

A

Infections - carry out urine microscopy and culture

Renal stones:

Urothelial malignancies

BPH or strictures

72
Q

What does absolute anuria mean

A

Urinary tract obstruction

73
Q

What happens in Fanconi’s anaemia in relation to the bone marrow vs Fanconi syndrome

A

Anaemia - Type of bone marrow failure in which DNA repair machinery is faulty leading to pancytopenia.

Syndrome : Significant renal involvement occurs in which the PCT is not able to re absorb required electrolytes and substances

74
Q

What classification is used to assess the severity of AKI

A

RIFLE
Risk
Injury
Failure
Sustained loss
End stage renal disease

75
Q

What are examples of true and relative hypovolemia

A

True -
GI (diarrhoea and vomiting)
Burns
Haemorrhage

Relative
Heart failure
Septic shock
Hepatorenal failure

76
Q

What are the clues to renovascular disease

A

Atherosclerotic disease elsewhere
Hypertension
Vascular bruits on examination abdominal

77
Q

What parts of the nephron may be affected in renal disease

A

Glomeruli
Tubules
Intersitium
Blood vessels

78
Q

What diseases can impact tubular function

A

Ischaemic ATN

Nephrotoxic ATN

Intratubular obstruction like crystals, myoglobin and myeloma

79
Q

What can impact the interstitum in terms of renal causes of AKI

A

Acute pyelonephritis

Acute interstitial nephritis (infection or drugs)

80
Q

What can impact the vascular compartment in terms of renal causes of AKI

A

Vasomotor drugs that reduce perfusion to the kidneys

Malignant hypertension

Vasculitis

Micro vascular obstruction like an emboli

81
Q

Microalbuminuria is associated with what conditio

A

Early diabetic nephropathy

  • can be measured via albumin: creatinine ratio

Urine dipstick will be negative

82
Q

Visible haematuria indicates bleeding within the urinary tract whilst microscopic haematuria indicates..

A

Glomerular haematuria

83
Q

What kind of things can cause obstruction

A

Tumours
Stones
Prostatic hypertrophy

In urethra tumours, valves (in young boys congenital condition), strictures and foreign bodies

84
Q

What are the signs and symptoms of uraemia

A

Anorexia
N+V
Pruritus
Neuropathy
Pericarditis
Confusion
Encephalopathy
Coma

85
Q

Impact of kidney failure on other body systems

A

Causes hypertension and left ventricular hypertrophy
Peripheral oedema
Pulmonary oedema

86
Q

How does renal failure cause bone disease

A

Decreased D3 means that less calcium is absorbed. This triggers PTH which causes resorption of bone to release calcium into the blood — this may lead to vascular calcification

Increased. Phosphate triggers PTH release. — renal osteodystrophy

87
Q

What is renal osteodystrophy

A

Due to low levels of calcium and vitamin d and other altered electrolytes there is changes to bone mineralisation leading to bone pain and pathological fractures

Signs of low calcium also occur (abdominal pain, cramp, seizures)
Chovsteks sign
Trousseaus

88
Q

What is the treatment of chronic Hyperkalemia

A

Loop diuretics flush out potassium

Consider dietary potassium restriction

89
Q

How is acidosis treated in ckd

A

Sodium bicarbonate

90
Q

What ECG changes are seen in Hyperkalemia

A

Tall tented T waves

Wide QRS

Absent p waves

Sine waves

91
Q

What are the advantages of renal transplant

A
  • don’t need dialysis lifelong
  • improves renal clearance
  • restores endocrine functions of the kidney
  • improves LE
92
Q

Disadvantages of renal transplants

A

Perioperative mortality risk (CV mortality)

Lifelong immunosuppression

Cancer risk for lymphoma

New onset post transplant diabetes

93
Q

What are the contraindications for renal transplant

A

Active infections
Active cancer
Active drug misuse
Uncontrolled major psychiatric disease
Non concordance with treatment
Short LE <5yr

94
Q

What is tissue typing (HLA compatibility)

A

All cells in the body have antigens that allows the body’s immune system to differentiate its own cells from non self or foreign. If a tissue is introduced that will trigger an antibody response. Antigen is presented to T cell by antigen presenting cells ( class II MHC molecules and co-stimulatory molecules). This T cell will then undergo IL-2 mediated clonal expansion and recruit other immunoreactive cells

In this test the recipient is tested to see whether they have antibodies against the antigens on the donors tissue/organ

For renal transplant ABO blood group must match as well

95
Q

What kind of drugs are used to prevent rejection following transplant

A

Calcineurin inhibitors

MTOR inhibitors

Anti-metabolites

Monoclonal antibodies

Steroids

96
Q

Mechanism of hyper acute rejection

A

When recipeient has pre-formed antibodies to donor kidney
Complement activation and infmamotyr cell infiltration results in endothelial damage

97
Q

What occurs in acute rejection

A

Antigen is presented to T cell — clonal proliferation

T helper recruit cytotoxic T cells — cellular toxicity

B cells produce donor specific antibodies

98
Q

Examples of calcineurin inhibitors and how they work to prevent organ rejection

A

Cyclosporine
Tacrolimus

Inhibit calcineurin which is an enzyme required for the activation of T cells .
Inhibiting calcineurin leads to decreased production for IL-2 which is required for clonal expansion of T cells

99
Q

How does sirolimus work

A

Inhibits MTOR pathway which is needed for cell cycle in T cells
Also affects B cells
Blocks response of T cells to IL-2

100
Q

How does azathioprine work

A

Is a pro drug which must be activated into 6 mercaptopurine

Inhibits the synthesis of purines A+G which are needed for DNA synthesis. This prevents the cells from dividing and prevents T and B cell proliferation

101
Q

How does mycophenolic acid work

A

Blocks IMPDH enzyme responsible for purine synthesis. Cell cannot divide with DNA replication and synthesis.

B and T cells cannot proliferate

102
Q

How does leflunomide work

A

Inhibits DHODH enzyme which is responsible for synthesis of pyrimdines. Cell cycle cannot progress

b and T cells can’t proliferate

103
Q

Mechanism of action of alemtuzunab

A

Monoclonal antibody binds to glycoprotein CD52 on surface of immune cells triggering self destruction of these cells

104
Q

Mechanism of action of basiliximab

A

Monoclonal antibody which binds to CD25 part of IL-2 receptor thus preventing IL-2 from binding.

IL-2 is required for clonal expansion of T cells

105
Q

What is the treatment of FSGS

A
  • immunosuppressants - pred
  • dietary restriction of salt.
106
Q

Post strep glomerulonephritis presentations and diagnostic test

A
  • headache
  • sore throat
  • non-specific joint pain
  • hypertension
  • haematuria
  • renal biopsy is the diagnostic test
107
Q

Fever can cause hypotension

A
  • causes vasodilation which reduces blood pressure
  • also through sweating which causes fluid loss — lower BP
108
Q

Losses:

A

Sensible: loss of fluid from tubes within the body (can be measured)
( vomiting, urine output, diarrhoea + blood)

Insensible ( sweating and breathing (mouth - lose water)

109
Q

Sepsis can cause intrinsic renal failure: T or F

A

True

110
Q

Specific gravity will be raised in pre - renal failure T or F

A

T

As the urine is more concentrated (more solutes)

111
Q

Causes of anaemia 3 Hs

A

H - haematopeeitic - can’t make red cells ( deficiencies, CKD, malabsorption, BM failures)

H - haemolytic - breaking down of the red cell

H aemorrhagic - loss of blood cell

112
Q

ACEi in acute vs chronic renal failure

A

Nephrotoxic in acute

Protective in chronic renal failure

113
Q

Management of Hyperkalemia FAR

A

F - force potassium into cells (takes seconds to minutes)
( glucose with insulin) 10ml of 10% of glucose with 10 units of insulin
(Sodium bicarbonate )
B2 agonist - salbutamol (IV or nebs)

Antagonise potassium on cells: hours
- calcium gluconate IV

Remove K from blood:
- dialysis
- Na/ Ca resonium suppository

114
Q

What are the 4 acute life threatening complications of CKD

A

1) Hyperkalemia

2) hyperphosphatemia

3) fluid overload

4) uraemic encephalopathy

115
Q

Management of hyper phosphate

A

Phosphate binders ( calcium acetate)

116
Q

Treatment of fluid overload

A
  • consider ventilation
  • consider therapy for hypertension
    Renal dialysis
117
Q

Treatment for uraemic encephalopathy

A
  • dialysis
118
Q

What form of heart failure do patients with chronic renal failure develop

A

Concentric left ventricular hypertrophy

Sub endocardial region is not well perfused due to thickened ventricular wall. So more susceptible to MI in this region - non ST elevation presentation

Muscle is not relaxing very well during diastole leading to hypo-perfusion

119
Q

Radio-femoral delay is indicative of what disease

A

Coarctation of the aorta:
Tear in the intima of the aorta - blood separates into two - radial artery gets blood earlier

120
Q

ACEi and ARBS are absolutely contraindicated in what condition

A

Renal artery stenosis

121
Q

What are the contraindications for dialysis

A

No absolute

Do consider age, cause of ESRD, prognosis….

122
Q

Indications for urgent dialysis

A

Pericarditis

Uraemic encelopathy

Fluid overload unresponsive to diuretics

Poorly controlled hypertension despite treatment

Persistent metabolic disturbances despite treatment

123
Q

What is the difference between haemodialysis and haemofiltration

A
  • haemofiltration occurs in patients who are not cardiovascularlly stable
  • haemodialysis - diffusion - better at acid base issues
  • haemofiltration - convection - better at water + solute issues
124
Q

Contraindications to renal transplant:

A

Contraindications to surgery —- CVD, morbid obesity, hepatic disease, CJD

To immunosuppression: aucte infection, malignancy, HIV

Recurrent renal disease:
- IgA nephropathy
- diabetic nephropathy
- hereditary oxalosis

  • substance abuse
125
Q

What is the effect of PPIs on the kidneys

A

Can cause acute interstitial nephritis

126
Q

What is normal GFR

A

120ml/min

127
Q

Diabetic nephropathy pathology

A

Increased blood sugars increases tonicity of the fluid which results in greater flow through the glomerulus — increased pressure and constant stretching of the glomerulus causes slits in membrane to become wider — proteinuria

128
Q

PCR & ACR

A
  • acr better measure in diabetes as albumin is more affected
129
Q

What are the issues with SGLT-2 inhibitors

A

Glycosuria increases risk of infections

Normoglycaemic ketosis

130
Q

How do GLP1 agonists work

A

Incretin hormones like GLP-1 and GIP stimulate the release of insulin after glucose intake.
Inhibit release of glucagon
Delay gastric emptying and
Increase glucose uptake from muscles
Decrease glucose production in the liver

131
Q

Hypertensive renal disease

A

Intimal thickening of small vessels

Onion skin large vessels

Kidneys become smaller

Glomerulosclerosis

Fibrinoid necrosis

132
Q

Side effects of ACEi

A

Hyperkalemia
Dry cough

133
Q

Manifestations of nephritic syndrome

A

Haematuria
Uraemia
Hypertension
Hyperlipidaemia

134
Q

Types of vasculitis

A

*** add notes

135
Q

Types of vasculitis

A

*** add notes

136
Q

P - ANCA test for..

A

Small vessel vasculitis

137
Q

C -ANCA

A

Large vessel vasculitis

138
Q

HUS

A

Occurs in children under 10 mostly after shiga toxin producing E.coli infection
Shiga toxin - release of inflammatory cytokines which causes vascular injury leading to formation of microthrombi
Enters cell and binds to ribosome causing destruction of the cell.

Microthrombi and damaged Rbc become stuck in glomerulus — complement activated — renal damage and necrosis
Presents as bloody diarrhoea, abdominal pain and vomiting and fever. + oliguria and oedema + bruising

139
Q

TTP thrombotic thrombocytopenic purpura

A

Blood clots form in small vessels which might block blood flow to major organs.

This is caused by deficiecies or changes to an enzyme which controls the blot clotting process

Genetic
Acquired: can be caused by drugs like chemo. Cancer, HIV, lupus may trigger this

More common in women

140
Q

Antibodies in SLE

A

ANA - general

Anti double stranded DNA - more specific

141
Q

What is plasmapheresis

A
142
Q

What is the presentation of IgA nephropathy: Berger’s disease

A

Caused by abnormal activation of the immune system which results in deposition of igA complexes in the kidneys.

This then triggers complement cascade C3 or C4 which causes damage leading to haematuria, hypertension and proteinuria

Usually after an infection like URTI, or gastroenteritis

Is the most common cause of glomerulonephritis in adults

143
Q

Characteristics of post infection glomerulonephritis

A

Haematuria
Ödema
Hypertension
Proteinuria
Occurs mostly in children 1-2 weeks after strep throat

Presence of immune complexes causes complement activation which causes damage to the glomerulus leading to symptoms of nephritic syndrome

On microsocopy there is subepithelial humps which are electron dense deposits near the BM.
IgG and C3 deposits are found on microscopy

144
Q

what are the characteristics of membranoproliferative glomerulonephritis

A

Has features of both nephritic and nephrotic syndrome
mesangial cells proliferate + immune deposition in the sub-endothelial space

145
Q

What is the presentation and pathology of ANCA gomerlonephritis

A

Haematuria,
Proteinuria
Hypertension
Oedema

Autoimmune condition in which antibodies released by plasma cells activate neutrophils to release granules wich cause damage to the glomerulus — inflammation, fibrosis and scarring occurs leading to renal impairment

146
Q

Examples of large vessel vasculitis

A

1) giant cell arteritis

Affects large arteries specifically temporal artery
Causes headaches, jaw pain, vision probs, fatigue

147
Q

Examples of medium vessel vasculitis

A

1) polyarteritis nodosa

Mostly affects skin, kidneys, nerves and GI system. Causing muscle pain, fatigue, weight loss, nerve damage leading loss of sensation and abdominal pain
Associated with Hep B + C

2) kawasakis disease - children

Especially affects coronary arteries (complications is CA aneurysm if untreated)
High fever, strawberry tongue, swollen hands,feet and lymph nodes

148
Q

Examples of small vessel vasculitis

A

1) granulomatosis with polyangitis (wegeners)

Affects. Arterioles, venules and capillaries in which grnaulomas form.

Typically affects resp tract: chronic sinusitis, nosebleeds, cough, haematuria, SOB
Affects bilaterally represented organs

Associated with C-ANCA

2) microscopic polyangitis
Kidneys and lungs affected. Haemoptysis + haematuria, proteinuria, fever + weight loss

Associated with P-ANCA

3) churg-Strauss syndrome (eosinophilic granulomatosis with polyangitis)

Only affects individual with asthma or allergic rhinitis

Associated with p-ANCA

4) henoch schonlein Purpura / IgA vasculitis
Deposition of igA

149
Q

What causes variable vessel vasculitis

A

BEHCETS disease

Painful oral and genital ulcers, uveitis, skin lesions etc

150
Q

What is MPGN type I

A

Damage occurs as immune complexes and C3 proteins are deposited in subendothelial space

Associated with chronic infections, SLE and multiple myeloma

151
Q

What is MPGN type II

A

No immune complexes deposition occurs. Abnormal activation of complement causes glomerular damage causing both nephritic and nephrotic syndrome symptoms

152
Q

what causes the production of struvite stones

A

caused by GR-ve urease producing bacteria that convert urea to ammonia.

pseudomonas
proteus
klebsiella

153
Q

what are the risk factors for urolithiasis

A

= anatomical variations that lead to stasis

= low urine volume

= recurrent UTIs

= meds - anti virals

= hyperparathyroid, metabolic syndrome, gout,

= acidic urine (increased protein intake)

= genetic disorders affecting cysteine metabolism

154
Q
A

Block 34 Metabolic Flashcards (5 decks)

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