Kidney Flashcards

1
Q

Name the retro-peritoneal adominal viscera

A
SAD PUCKER
S=suprarenal (adrenal) glands
A=Aorta/IV
D=duodenum (except duodenal cap- first 2cm)
P=Pancreas (except tail)
U= Ureters
C= colon (ascending and descending)
K=Kidneys
E=(O)esophagus
R=Rectum 

The rest are intra-peritoneal

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

At what spinal levels do the kidneys usually lie within

A

T12 to L3. Right kidney usually lower due to liver. Usually 3 vertebrae in length

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

Layers of fascia and fat around kidneys (deep to superficial)

A

Renal capsule – Tough fibrous capsule.
Perirenal fat – Collection of extra-peritoneal fat.
Renal fascia – Encloses the kidneys and the suprarenal glands.
Para-renal fat – Mainly located on the posterolateral aspect of the kidney.

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

Arterial supply and venous drainage of the kidneys

A

Arterial supply:
Renal arteries from abdominal aorta
Splits into: segmental -> interlobar -> arcuate -> 90 degrees interlobular arises -> afferent arterioles

Venous drainage:
Left and right renal veins

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

Define nephrotic syndrome

A
  1. presence of proteinuria (>3.5 g/24 hours)
  2. hypoalbuminaemia (<30 g/L),
  3. peripheral oedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Nephrotic syndrome-associated diseases

A

Primary
Minimal change disease
Focal segmental glomerulosclerosis
Membranous nephropathy

Secondary
Amyloidosis
SLE
Hep B and C (rare)
Diabetic nephropathy
Malignancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Reason for proteinuria, hypoalbuminaemia and oedema

A

proteinuria is a result of damage to the glomerular resulting in ability for protein to squeeze into nephron. The worse the protein loss the more likely nephrotic syndrome

Hypoalbuminaemia due to urinary loss of albumin. Liver compensates by synthesis of more albumin and other proteins in particular lipoproteins hence lipid abnormalities (hypercholesterolaemia)

oedema is due to a combination of a decrease in oncotic pressure from the hypoalbuminaemia, as well as a primary renal sodium retention in the collecting tubules

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

Drugs associated with nephrotic syndrome

A
Pamidronate
Lithium 
Gold
Penicillamine
NSAIDS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Causes of glomerulonephritis

A

Systemic lupus erythematosus
Rheumatoid arthritis
Infections
Drugs (Penicillamine, gold, heroin, NSAIDs, Cyclosporin)
Metabolic disorders (Diabetes, HTN, thyroiditis)
Malignancy (lung and colorectal cancer, melanoma, and Hodgkin’s lymphoma)

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

Pathophysiology of glomerulonephritis

A

cellular immune response results in infiltration of mononuclear inflammatory cells (lymphocytes and macrophages)

humoral immune response leads to immune deposit formation and complement activation in glomeruli.
Injury usually occurs as a consequence of the activation and release of a variety of inflammatory mediators

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

Common signs and symptoms of glomerulonephritis

A
Haematuria
Oedema 
HTN
Oliguria
Anorexia
Nausea
Malaise
Weight loss
Fever
Skin rash
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Risk factors of glomerulonephritis

A
  1. Group A beta-haemolytic Streptococcus
  2. Respiratory infections
  3. GI infections
  4. Hep B, C
  5. HIV
  6. SLE
  7. Infective endocarditis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is minimal change disease?

A

Most common form of nephrotic syndrome in children.

Characteristics only seen under an electron microscope (can see foot process effacement/thinning)

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

Cause of minimal change disease

A
Idiopathic (primary)
Secondary:
Drugs (NSAIDs, lithium, bisphosphonates)
Malignancy (Leukemia, Lymphoma)
Infection (Syphillis, HIV, Hepatitis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Treatment of minimal change disease

A
Prednisolone 
Fluid restriction
Low salt diet
Albumin and Furosemide
Corticosteroid sparing therapy (Ciclosporin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Amyloidosis

A

Group of rare yet serious disease characterised by deposits of amyloid protein.

Amyloid is a description of proteins which have folded abnormally and then collected together.

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

Classifications of amyloidosis

A

Primary amyloidosis (AL): Aetiology unknown

Secondary amyloidosis (AA): 2 to RA, PA, ankolysing spondylitis, chronic infections, IBD
Familial Mediterranean fever
Tumour necrosis factor receptor-associated periodic fever syndromes
Muckle-Wells syndrome
Hyper-IgD syndrome

Inherited amyloidosis (AF):
Mutations of transthyretin leading to progressive cardiomyopathy or progressive neuropathy or both
Mutation of fibrinogen A alpha-chain leading to renal involvement
Mutation of apolipoprotein A
Mutation of lysozyme

Senile amyloidosis (SSA)

18
Q

Signs and symptoms of amyloidosis

A
Lower extremities oedema
Periorbital purpura
Raised JVP
Macroglossia (enlarged tongue in primary)
Fatigue
Weight Loss
SOBOE
19
Q

Investigations for amyloidosis

A

Urine fixation: light chain protein in the urine is suggestive of multiple myeloma and amyloidosis.

Serum fixation: Presence of monoclonal Ab

Immunoglobulin free light chain assay: abnormal lambda to kappa ratio

20
Q

Definition of diabetic kidney disease (DKD)

A

Macroalbuminuria (Alb:Creat ratio >34mg/mmol)

or

Microalbuminuria (3-34mg/mmol) + associated retinopathy or T1DM >10 years.

21
Q

DKD pathophysiology

A

Hyperglycaemia and HTN cause glomerular mesangium expansion via increase mesangial growth.

Works by:

  1. PDGF and transforming growth factor (TGF-b) stimulate collagen and fibronectin synthesis and decreased matrix degradation.
  2. Glucose binds to proteins forming advanced glycation end products (AGEs)
  3. AGEs crosslink and activate downstream cytokines such as TGF-b.
  4. AGEs modify or impair the function of the proteins (such as laminin and type IV collagen).
  5. Results in increase in permeability of glomerular basement membrane.
22
Q

Signs and Symptoms of DKD

A
HTN
Oedema
Retinal findings: dot and blot haemorrhages, microaneurysms (background retinopathy), and/or neovascularisation (proliferative retinopathy).
Poor vision
Numbness or pain in lower extremeties
Foot ulcers, Charcot joints
23
Q

Investigations to order for DKD

A

Urinalysis (Proteinuria)

Urinary creatinine to albumin ratio: elevated

Serum Creatinine (GFR estimation): elevated. GFR raised in patients with CKD 1, normal in CKD 2, low in CKD 3-5

Kidney ultrasound:
normal-to-large kidneys with increased echogenicity; may show hydronephrosis if vesiculopathy and/or obstruction is superimposed

24
Q

Management of type 1 DKD, not on dialysis

A

Insulin lipro & Insulin glargine
ACEi, (add more anti hypertensives depending on BP)
Statin,
Nutrition (low protein, low salt and low unsaturated fats diet)
Smoking cessation

25
Q

Management of patient on dialysis

A

Insulin lipro and Insulin glargine
(Can add sitagliptin or glipizide for T2DM)
ACEi, (add more anti hypertensives depending on BP)
Statin,
Nutrition (low protein, low salt and low unsaturated fats diet)
Smoking cessation
If all else fails consider pancreas, kidney transplant.

26
Q

Management of type 2 DKD not on dialysis

A

Metformin or glipizide or sitagliptin or repaglinide
(Insulin lipro and insulin glargine can be added as well)
ACEi or ARB (add more anti hypertensives if needed)
Nutrition (low protein, low salt and low unsaturated fats diet)
Smoking cessation

27
Q

What is pyelonephritis?

A

Infection of the kidneys resulting in inflammation of the renal parenchyma, calices and pelvis.

28
Q

Major causative pathogens of pyelonephritis

A
Gram negative
E.coli (60-80% of uncomplicated)
Proteus Mirabilis (15%)
Klebsiella (20%)
Pseudonomas, Enterobacter species 
Gram positive (less common)
Enterococcus faecalis, Staphylococcus saprophyticus, and S aureus
29
Q

Signs and symptoms of pyelonephritis

A

Fever
Vomiting & Nausea
Flank pain costovertabral angle tenderness.
Dysuria, frequency or urgency.

30
Q

Risk factors for pyelonephritis

A
Frequent sexual intercourse
UTI
Diabetes
Catheter, Calculus (stone)
Immunosuppressive state 
Pregnancy
31
Q

Investigation to order for pyelonephritis

A
Urinalysis: WBC >10, RBC >5
Gram stain (Most common gram negative rods)
Urine culture >100,000 CFU/ml
FBC: Raised leukocytes
ESR, CRP elevated
32
Q

Management of pyelonephritis

A

On assumption: Empirical antibiotic

Once culture has been grown used sensitive antibiotics

33
Q

Nephrolithiasis (kidney stones)

A

Stones in the urinary system usually in response to elevated levels of urinary solutes such as calcium, uric acid, oxalate, and sodium, as well as decreased levels of stone inhibitors such as citrate and magnesium

34
Q

Risk factors for nephrolithiasis

A

High protein or salt intake
Male sex (ratio of 3:1 male to female)
Dehydration
Obesity

35
Q

Signs and symptoms

A
Acute severe flank pain. Radiates to ipsilateral groin
Nausea and Vomiting
Haematuria
Testicular pain
Urinary frequency/ urgency
36
Q

Management of nephrolithiasis

A
non pregnant, acute: 
Hydration, pain control , anti-emetic. Abx (Trimethoprim or Nitrofurantoin)
Surgical decompression
Alpha blocker: (Tamsulosin, Afluzosin)
Surgical removal

Non pregnant, ongoing,uric acid stone:
Alkalinisation (Potassium citrate, Sodium Bicarbonate) with or without allopurinol

Non pregnant, ongoing, hypercalcuria:
chlortalidone
hydrochlorothiazide
indapamide

For the rest see BMJ

37
Q

Cystitis

A

Infection of the bladder mainly affects young, sexually active women.

38
Q

Causative organism of cystitis

A

E.Coli (80%)
Staphylococcus saprophyticus, Klebsiella pneumoniae, Proteus mirabilis, Pseudomonas, Enterococcus, Enterobacter, and group B streptococci.

39
Q

Pathophysiology of cystitis

A

E coli or other bacteria that are normally found in the GI tract or vagina can be introduced into the urethra. This may happen during sexual intercourse, or through gradual colonisation of the adjacent tissues. Bacteria may also be introduced into the normally sterile urinary tract through instrumentation, as in cystoscopy or use of a urinary catheter

40
Q

Signs and symptoms of cystitis

A

Dysuria
Suprapubic pain
Urgency
Frequency

41
Q

Risk factors of cystitis

A
Frequent sexual intercourse
Hx of UTI
Congenital abnormalities
Urinary catheter
Diabetes
Age
Pregnancy
Spinal injury 
Immunodeficiency
Uncircumcised
42
Q

Investigations to order if suspecting cystitis

A

Pregnancy test
Urinalysis: Leukocyte esterase, nitrites, haemoglobin
Urine microscopy: RBCs, WBCs (>10), bacteria
Urine culture with sensitivity: 10^3 CFU/mL

Treatment similar to UTI treatment