Brainscape's Knowledge GenomeTM

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


See full index

RACP > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Gaddolinium contrast load in CKD

A

Causes Nephrogenic Systemic Fibrosis

Symmetrical skin involvement with waxy, thickened and hardening of extremities and torso

Can have fibrosis of deeper structures such as lung, heart, fascia, muscles

CD34 + fibrocytes

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

HLA sub-typing and risk of rejection

A

Complement Dependent Cytotoxicity (CDC) - Highest risk if Positive (holds most weight on decision!)

Flow

Virtual - Lowest risk if positive

Most important HLA group is HLA DQ

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

Induction therapies in Renal transplant

A

Basilixumab - Bind IL2 recetor to inhibit CD25 on T cells

Anti-Thymboglobulin (ATG) - Rabbit Thymoglobulin Ab - Mechanisms; Antibody dependent cell mediated cytotoxicity & complement dependent cytotoxicity

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

Most common treatment regime in renal transplant

A
  • Basilixumab
  • Prednisolone
  • Tacrolimus
  • Mycophenolate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

MOA Tacrolimus

A

Calcineurin inhibitor; inhibit activation of NFAT (Nuclear Factor activated T cells) and reduce trascription of cytokines including IL2

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

MOA mTORi

A

i.e. Everolimus, Sirolimus

Binds FK receptor to inhibit mTOR (mammalian target of rapamycin) and arrest the T cell cycle to prevent proliferation (arrest of cell cycle at G1) -> which would normally be stimulated by IL2

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

Tacrolimus side effects

A

ā€œTACROLIMUSā€

Tremor
Alopecia
Cardiovascular - HTN
Renal insufficiency
Oncological risk - skin cancers
Lipid elevation
Insulin dependent diabetes (depletion not resistance)
Magnesium wasting
Uric acid elevation
Seizures

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

Cyclosporin Side effects

A

Gum Hypertrophy
Hirsutism

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

Mycophenolate MOA

A

Pro-drug of Mycophenolic Acid. Inhibits Inosine-5- Monophosphate dehydrogenase (IMPDH) to reduce purine synthesis (Guanine) and cell replication of T and B cells

Side effects are diarrhoea and BM suppression (within 6 months)

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

Types of renal transplant rejection

A

T- Cell (Donar APC: Host T cell)-> treat with pulse methyl pred +/- thymoglobulin and increase maintenance therapy.

Antibody mediated (Host APC: Host T cell) -> requires IVIG or PLEX +/- Rituximab. C4D+

Mixed

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

CMV prophylaxis indications

A

D + / R - = 6 months
D - / R + = 3 months
D - / R - = no prophylaxis unless

Oral Valganciclovir

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

CMV treatment

A

Double dose of prophylaxis with PO Valganciclovir or IV Ganciclovir, cautiously reduce immunosuppression, switch to mTORi, if resistance - Foscarnet or Cidofivor (but nephrotoxic!)

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

CMV treatment

A

Double dose of prophylaxis with PO Valganciclovir or IV Ganciclovir, cautiously reduce immunosuppression, switch to mTORi, if resistance - Foscarnet or Cidofivor (but nephrotoxic!)

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

Immunosuppressant with low risk skin cancer

A

mTORi (Everolimus, Sirolimus) - if skin cancer -> change AZA to mTORi

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

BK Virus

A

Polyoma virus
Post transplant nephropathy

Risk factors; female, HLA mismatch, Older age, immunosuppression

Ix;
- SV 40 stain shows intracellular inclusions on biopsy
- BK Virus PCR (100% of patients!), should be screened at 12 months
- Viral load

Rx with reduction in immunosuppression, Cidofovir, Ciprofloxacin

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

RIFLE Criteria

A

for AKI (injury within 7 days);
Risk - 1.5 x Cr, UO < 0.5ml/hr/kg for 6 hours
Injury - 2 x Cr, UO < 0.5ml/kg/hr for 12 hours
Failure - 3 x Cr, UO < 0.3ml/kg/hr for 24 hours, anuria for 12 hours
Loss - Persistent renal failure for 4 weeks
ESRD

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

Management AKI; Type fluid, BP target, Dialysis commencement time

A
  • Resuscitation with N.Saline - Albumin had increased mortality
  • Aim MAP 65mmHg
  • Dialysis - NO benefit with early dialysis < 48 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Rx contrast induced nephropathy

A

IVH, no benefit from other therapies

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

Rhabdomyolysis in AKI

A
  • Dehydration with renal hypoperfusion
  • Increased water resorption with precipitation of tubular casts
  • Cast nephropathy

= Tubular ischaemia due to casts and hypoperfusion

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

Secondary causes of minimal change disease

A

Presents as acute onset Nephrotic Syndrome, with effacement of foot podocytes on light microscopy

  • NSAIDs
  • Lithium
  • Lymphoma
  • Thymoma
  • Infection
  • Atopy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Membranous Nephropathy

A

Nephrotic syndrome

ā€œSā€
Staining PLA2R
Subepithelial immune deposition
SLE
Screen for malignancy

Rx with observation +/- ACE or ARB for proteinuria. Immunosuppression if not resolved > 12 months

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

Secondary causes Membranous Nephropathy

A

Malignancy
SLE

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

Causes of FSGN

A
  • Genetic predisposition - APOL1 gene in young Africans
  • SuPAR (soluble urokinase-dupe plasminogen activator)
  • Shear stress - HTN, prematurity, Obesity, single kidney
  • Drugs - Lithium, Pomidronate, IFN, heroin
  • HIV
23
Q

Biopsy findings FSGN

A

Focal segmental sclerosis in < 50% glomerulus

24
IgA GN pathophysiology
Nephritic disease Defect in IgA1-secreting cells forming an IgA that creates immune complexes with mesengial cells Post-infectious Worse prognosis if > 1g protein/day
25
Types of Lupus Nephritis
"No Man Faces Diffuse Menstrual Situations" 1. Normal - conservative Mngmt + ACE/ARB 2. Mesingial - conservative Mngmt + ACE/ARB 3. Focal Proliferative - Medical Mngmt 4. Diffuse - Medical Mngmt 5. membranous - Medical Mngmt 6. Sclerosing - requires preparation for dialysis
26
Indications for renal biopsy in SLE
If proteinuria > 0.5g/day
27
Management Lupus nephritis
For Class 3-5 Induction - Steroids (Methyl pred or pred) + Mycophenolate or cyclophosphamide Maintenance - Mycophenolate or Azathioprine Resistant - consider Rituximab
28
Pathognomonic features: Minimal Change Disease
- Nephrotic syndrome - Young - Podocyte effacement on light microscopy - Due to; Thymoma, Lymphoma, Atopy, NSAIDs, Lithium
29
Pathognomonic features: Membranous
Nephrotic syndrome Old -> middle age PLA2R serology & staining at subepithelium Causes: Malignancy & SLE
30
Pathognomonic features: Focal Segmental GN
Nephrotic syndrome < 50% sclerosis on biopsy Associated with APOL1 gene commonly in Africans Due to: - Shear stress; Obesity, HTN, Solo Kidney - SuPAR - Lithium, HIV, Pamidronate, IFN Heroin
31
Pathognomonic features: IgA nephropathy
Nephritic Syndrome 2-4 weeks post-URTI IgA-1 and complement deposits in mesengium
32
Pathognomonic features: MPGN
Rapid Nephritic/nephrotic syndrome Associated with Hep C, Chronic infection and Cryoglobulins Type 1 - Immune complex deposits (IgG and C3) Type 2 - Complement deposits (C3 only - dense deposit disease) Tram Tracking with immune deposition on Biopsy
33
Anti-GBM target
Alpha 3 chain of type 4 collagen
34
Risk factors Anti-GBM
- Male - HLADR2 - Alemtuzumab use - Hydrocarbons - Influenzae A - Smoking
35
Lipid changes with Nephrotic syndrome
- Unchanged HDL - Increased LDL - Increased TAGs - Increased Lipprotein A
36
Common associations hypercoaguable state of nephrotic syndrome
- Most commonly due to membranous nephropathy - Renal Vein thrombosis most common site - Proportional to hypoalbuminaemia
37
Management of Membranous Nephropathy
DO NOT USE STEROIDS ALONE - no evidence - Observe for 6 - 12 months - Immunosuppression w calceinerin inhibitors in combination with prednisolone - Anticoagulation (given highest risk prothrombotic state with renal vein thrombosis)
38
Pathognomonic features: Anti- GBM GN
- Anti- GBM + - Linear IgG staining - HLA DR2 - Use Alemtuzumab - Hydrocarbon exposure - Pulmonary-renal syndrome
39
Diagnosis Polycystic Kidney Disease
Positive FHx; On USS - > 3 cysts/total < 40 years age - > 2 cysts/kidney 40-60 years - > 4 cysts/kidney > 60 years On MRI > 10 cysts by age 40 If no cysts by 18 years of age, diagnosis unlikely Negative FHx; On USS Enlarged kidneys, with > 10 cysts/kidney
40
PCKD inheritance
Autosomal Dominant, point mutations, with complete penetrance; - PKCD type 1 - Polycystin -1 on Chromosome 16 (severe), ESKD by 50's - PKCD type 2 - Polycystin-2 on chromosome 4 (less severe), milder - ESKD by 70's *Non-truncated genes have milder phenotype (40%) *Variant of autosomal recessive but often causes fetal death
41
Worse prognosis in PCKD
- Truncated, PKD1 mutation - Male (but polycystic liver disease more common in women) - Obesity - HTN - Degree Proteinuria - Larger kidney size - FHx ESRD < 55 - Earlier onset symptoms
42
Extra-renal manifestations of PCKD
- Liver cysts - most severe in women due to oestrogen - Pancreatic cysts - Brain Aneurysms - Aortic Aneurysm - Valvular pathologies - most often mitral valve prolapse and AR - Seminal Vesicle cysts - Diverticular disease - Hernias
43
Tolvapton
Vasopressin 2 receptor antagonist Used in PCKD to reduce cyst size causes hypotonic urine Aim Urine Osmo < 280
44
Dialysis Disequilibrium Syndrome
Aggressive dialysis causing cerebral oedema. Decrease in Urea in blood post-dialysis but persistent Urea in brain therefore osmotic shift of fluid across BBB
45
Kt/V
Clearance of Urea in the context of time on Dialysis
46
ANP
Released from atria with stretch Atrial Natriuretic peptide - decreases extracellular fluid volume by increasing GFR through dilation afferent arteriole and inhibition of Na resorption at ENAC and Na/K+ channels. inhibits Renin.
47
Types of Vasopressin receptors
V1 - smooth and cardiac muscle V2 - thick ascending LOH, DCT, medullary & cortical collecting duct (target for Talvaptan) V3 - anterior pituitary - releases ACTH, prolactin
48
Carbonic Anhydrase inhibitors
Act at proximal convoluted tubule - Inhibit HCO3- resorption, leading to decreased activity of Na/H+ exchange and more to more urinary Na having a weak diuretic effect I.e. Acetazolamide and Topiramate Will cause a metabolic acidosis (Type 2 renal tubular acidosis)
49
Sites of Na resorption Kidney
65% PCT 25% Thick ascending LOH 5% DCT 3% Cortical collecting duct 1% Medullary collecting duct
50
Bartter Syndrome
Autosomal recessive Ineffective Na/K/Cl transporter at LOH - mimicking loop diuretics - Young children with growth and mental delays - Interrupts gradient for Mg, Ca - Low volume leads to hyperaldosteronism & increased Na uptake with H+ secretion. - Increased renin with high prostaglandins Leads to - Low K - Low H+ with metabolic alkalosis - Low Mg - Low Ca Treat with NSAIDs to block prostaglandin production. Replace electrolytes
51
Gitelman Syndrome
Autosomal recessive Interrupts Na/Cl- transporter at DCT to mimic thiazide diuretics Presents in adulthood with polyuria and craps Interrupts the electrochemical gradient of Mg resorption causing hypomagnesium
52
Type 1 RTA
- Loss of H+ ATPase at collecting duct - Increased retention H+ with metabolic acidosis - Decreased Na+/H+ exchange, leading to overactivity of Na+/K+ exchange and hypoklaemia - Hypercalcaemia as Ca drawn from bones to buffer H+, but consequence of reduced renal reabsorption calcium leading to Nephrocalcinosis Electrolyte disturbances - NAGMA - Hypokalemia, urine pH > 5.5 - Hypercalcaemia Rx with HCO3- which will increase urine pH and drive H+ excretion, reduces need for Na+/K+ exchange and decreasing hypokalaemia Causes - Autoimmune conditions - Sjogrens, RA
53
Type 2 RTA
Decreased capacity to resorb HCO3- at proximal tubule resulting in increased K+ secretion at DCT as compensatory mechanism Electrolyte disturbance - Hypokalaemia - made worse with BiCarb Rx given ++ renal wasting - Serum bicarb 12-20 - Lower urine pH - Can occur with other defects including impaired resorption of phosphate, glucose, uric acid and amnio acids Due to Fanconi's syndrome, monoclonal gammopathies, Tenofovir
54
Type 3 RTA
Combination of Type 1 and 2
55
Type 4 RTA
Hyperkalemia NOT hypokalaemia as with other RTA. Can be secondary to Heparin Due to hypoaldosteronism Rx Fludrocortisone (has mineralocorticoid activity)
56
Causes of Type 4 RTA
NSAIDs Calcineurin inhibitors - i.e Tacrolimus Chronic interstitial nephritis DM nephropathy Acute GN Heparin -> which has a toxic effect on adrenal glomerulosa cells Primary adrenal insufficiency/Addisons disease Ang2 inhibitors Potassium sparing diuretics

RACP (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions