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MD2 > Renal > Flashcards

Renal Flashcards

1
Q

Pre-renal causes of renal disease

A

Decr blood flow to kidneys:

  • Shock
  • Heart Failure
  • Hypotension
  • Renal artery stenosis
  • Dehydration
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2
Q

Renal Causes of Renal Disease

A

GN (nephritic/nephrotic)

ATN

Interstitial disease

  • Vascular (vasculitis, thrombus/dissection)
  • Infiltration (sarcoid, Tb)
  • Systemic (SLE, DM)
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3
Q

Post-renal causes of renal disease

A

Urinary tract obstruction:

  • prostate obstruction
  • strictures
  • stones
  • clots
  • malignancy
  • sloughed papillae occluding lumen (DM)
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4
Q

Causes of glomerular nephritis

A 
Autoimmune (SLE, HSP)
Drugs
Infection
Malignancy
Primary GN
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5
Q

Causes of ATN

A

Pre-renal damage

Nephrotoxins (aminoglycosides)
Contrast medium
Rhabdomyolysis (muscle breakdown) !!

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6
Q

Interstitial disease causes

A

Drugs (penicillin allergy)

Infiltration (lymphoma, infection-Tb, post-chemo, Sarcoid)

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7
Q

Causes of renal vascular damage to kidneys

A

Vasculitis
Malignant HTN
Large vessel occlusion (thrombus, dissection)

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8
Q

What does a urine dipstick detect?

A

Leucocytes
Nitrates
Blood
Protein

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9
Q

RAAS

A

JGA detects decr in renal perfusion -> activates RAAS:
Renin secreted from kidneys -> converts angiotensinogen to angiotensin 1 -> ACE converts angiotensin 1 to angiotensin 2 -> Ang II does the following to incr BP:

  1. incr symp activity
  2. Incr Na/H20 reabsorption; incr K excretion
  3. Aldosterone secretion from adrenals
  4. Vasoconstriction to increase BP
  5. ADH/vasopression secretion from posterior pituitary -> aquaporins inserted into collecting duct increases Na reabsorption

1-5 increase circulating volume and BP leading to reperfusion of JGA

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10
Q

What is the commonest renal cause of kidney disease?

A

ATN

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11
Q

Nephrotic Syndromes

A
  1. Membranous nephropathy most common cause for adults
  2. Minimal change disease most common cause for kids
  3. FSGS
  4. Membranoproliferative GN
  5. Secondary causes due to hepB/C, SLE, NSAIDs, neoplastic syndrome, diabetic nephropathy, amyloidosis
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12
Q

Nephritic Syndromes

A
  1. IgA nephropathy most common cause for adults
  2. Post-infectious (strep) GN
  3. Rapidly progressive GN (IgA, vasculitis, anti-GBM/Goodpastures GN)
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13
Q

Ways to evaluate volume status

A

Capillary refill, Mucus membranes and skin turgur, urine output

Peripheral oedema, JVP

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14
Q

What is the protein deposited in the kidneys in Multiple Myeloma called?

A

Bence Jones Protein or M protein (light chains) or paraprotein

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15
Q

Blood tests in kidney disease

A 
UE
FBC
LFT
Clotting
CRP
ABG 
If systemic cause suspected: Ig and paraprotein electrophoresis, C3/C4, autoantibodies (ANCA, ANA, Anti-GBM), blood culture
- low C3 indicates immunological cause
- low C4 indicates SLE
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16
Q

Investigations for kidney malfunction

A

Renal USS shows cysts/small kidneys/masses
CTKUB: obstruction (non-contrast) or IVU (contrast for strictures)
XRKUB: stones

Urine dipstick (proteinuria, haematuria)

Urine spot test (microalbuminuria)

Urine MCS (glomerular in origin, infection?)

Renal biopsy -> immunohistochemistry

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17
Q

Signs of chronic kidney disease

A 
Small kidneys on USS
Anaemia
Low Ca, high PTH
High phosphate 
High creatinine/low GFR
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18
Q

Complications of AKI

A
  1. Electrolyte imbalance: Hyperkalaemia, hypnatraemia
  2. Acid base: metabolic Academia
  3. Fluid balance: Pulmonary Oedema from fluid overload (need diuretics or dialysis)
  4. Uraemia (need dialysis at this stage)
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19
Q

Nephritic syndrome criteria

A 
Haematuria mostly
Oedema
HTN
Mod-severe decr GFR
Non-nephrotic range proteinuria
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20
Q

Nephrotic syndrome criteria

A

Proteinuria mostly
Hypoalbuminaemia -> pitting oedema
Hypercholesterolaemia
Normal-mild decr GFR

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21
Q

Most common cause of childhood nephrotic syndrome and prognosis/treatment

A

Minimal change disease

- Good prognosis with steroids

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22
Q

Most common cause of adult nephrotic syndrome and prognosis/treatment

A

Membranous nephropathy (primary/secondary causes)

Prognosis: 1/3 get better on own w supportive care; 1/3 relapse/remit; 1/3 progressive renal failure

Treatment: BP control, supportive measures only

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23
Q

Complications of CKD

A

CV disease leading cause of death due to poorer prognosis after AMI

Dyslipidaemia

Oedema

Metabolic Acidosis due to increased H retention

Anaemia due to Epo deficiency and decreased RBC survival time

Hyperkalaemia due to reduced K excretion

CKD mineral and bone disorder due to incr PO4 which suppresses Ca which stimulates rise in PTH to stimulate Ca resorption from bone -> SECONDARY HYPERPARATHYROIDISM and calcification of soft tissues and vasculature

Vitamin D deficiency due to inability to add the second OH onto 25 hydroxyvitamin D -> OSTEOMALACIA

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24
Q

What are medications that impair K excretion?

A

K sparing diuretics
ACE inhibitors
NSAIDs

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25
Q

Treatment of CKD mineral and bone disorder

A

Phosphate binders (prevent dietary absorption of PO4) + Restrict dietary PO4 (milk, cheese, eggs)

1,25 OH Vit D analogues
Cinacalcet (allosteric activator of Ca-sensing R on body tissues)

+/- subtotal parathyroidectomy

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26
Q

Hyperkalaemic ECG changes

A

Widened QRS
Tall peaked T waves
Depressed ST segment

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27
Q

Treatment of CKD metabolic acidosis

A

Sodium bicarbonate

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28
Q

Lifestyle factors to adjust in CKD

A

SNAP: smoking, nutrition, alcohol, physical activity

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29
Q

Nephrotoxic drugs

A 
ACE inhibitors
NSAIDs
Amino glycosides (gentamycin)
Amphotericin (anti-fungal)
Lithium
IFNalpha

+ penicillin (allergic interstitial nephritis), flucloxacilin (in pre-existing RF), BActrim

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30
Q

Role of PTH including the organ that produces it

A

Parathyroid gland produces PTH when serum Ca low -> leads to bone resorption of Ca to incr serum Ca -> inhibits PTH production

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31
Q

What is the active form of vitamin D called?

A

1,25 hydroxyvitamin D3

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32
Q

How is the active form of vitamin D produced?

A

Vitamin D is made in the skin as calcitriol and converted to cholecalciferol or vitamin D3 via sunlight -> liver hydroxylates this to 25-hydroxyvitaminD3 and then kidney adds a second OH to form 1,25 hydroxyvitaminD3

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33
Q

Actions of 1,25 hydroxyvitamin D3

A

Increased intestinal absorption of Ca and Phosphate

Incr Bone mineralisation

Incr bone resorption (remodelling)

Immunity

Muscle and bone health/strength

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34
Q

What happens if you are deficient in vitamin D?

A

Can result from lack of sunlight exposure.

Leads to bone softening diseases such as
Osteomalacia (Adults)
Ricketts (kids)

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35
Q

Pathology seen in glomerulonephritis

A

Acute:

  • proliferation of mesangial or endothelial cells
  • WBC infiltration
  • Crescent formation
  • Ab deposition, immune complex formation, C’ activation

Chronic:

  • Hyalinosis
  • Sclerosis
  • BM thickening
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36
Q

What is the definition of rapidly progressive GN?

A

ARF + blood and protein in urine (nephritic)

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37
Q

What is the definition of chronic glomerulonephritis

A

CRF caused by glomerulonephritis + HTN + proteinuria + SMALL AND SHRUNKEN KIDNEYS

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38
Q

What is the most common cause of macroscopic haematuria?

A

UTI

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39
Q

What is the most common adult glomerulonephritis? and common symptoms of this

A

IgA nephropathy (may be asymptomatic/have macroscopic haematuria or nephritic syndrome)

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40
Q

What is the pathophys of IgA nephropathy?

A

IgA + C3 forms immune complexes and deposits in mesangial cells
Mesangial proliferation

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41
Q

What is the treatment for IgA nephropathy?

A

Ace inhibitors or ARBs to lower bP and thus amt of protein in urine

Fish oils

Corticosteroids with rapidy progressive RF

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42
Q

What electrolytes are commonly deranged in kidney disease?

A

Na, K, Ca

Phosphate and Mg

43
Q

What hormones control sodium?

A

Aldosterone - Na/K exchange in DCT
Angiotensin
Renin

44
Q

What hormone controls water content and how?

A

Vasopressin/ADH

Inserts aquaporins in collecting duct.

45
Q

Where is ADH made and secreted from?

A

Made in hypothalamus, stored and secreted in posterior pituitary

46
Q

Where is aldosterone secreted from?

A

Adrenal cortex

47
Q

What determines serum osmolarity?

A

Na
K
Glucose
Urea

48
Q

Difference btw AKI and CKD in terms of

  • definition
  • urine output
  • SX
A

AKI: low urine output with general SX of malaise (nausea, vomiting etc)
- rapid reduction in kidney function over hours to days as measured by increase in serum urea and creatinine (>x1.5 baseline)

CKD: normal to high urine output with NO SX due to adaptation
- Impaired renal function (evidence of renal damage) >3mo
○ Microalbuminuria
○ Proteinuria
○ Glomerular haematuria
○ Pathological abnormalities on renal biopsy
○ Anatomical abnormalities (cysts on ultrasound etc)
- OR GFR <60ml/min/1.73m^2 for >3 mo with or without evidence of kidney damage

49
Q

Complications of nephrotic syndrome

A
  • susceptible to infection (loss of Ig in urine, and steroid use)
  • hyperlipidaemia
  • hyper coagulable state -> incr risk of VTE
50
Q

What do you think of if a patient presents with haematuria a few weeks after infection?

A

post-strep glomerulonephritis

51
Q

What do you think of when a patient presents with a purpuric rash and macroscopic haematuria?

A

Hence Schonlein -> IgA nephropathy

52
Q

What do you think of when a patient presents with a purpuric rash and macroscopic haematuria?

A

Henoch Schonlein -> IgA nephropathy

53
Q

At what stage do patients need dialysis or renal transplant?

A

Stage 5 CKD (when eGFR<15ml/min) = ESRF

54
Q

What are the various stages of CKD

at what stage do sx/signs become evident?

A

1-2: GFR is >60 with evidence of renal damage (proteinuria, haematuria or abnormal anatomy or systemic disease)

3: GFR 30-60 with/without evidence renal damage
4: GFR 15-30 Sx/signs
5: ESRF (GFR<15) sx/signs

55
Q

SYMPTOMS of CRF

A

Polyuria, nocturia

+/- Macroscopic haematuria

Uraemia symtoms

  • lethargy, malaise
  • fluid overload
  • pruritus
  • seizures and restless legs + peripheral neuropathy
  • anorexia, N&V
56
Q

Broad classes of causes of CRF

A
  1. Diabetic nephropathy (2>1)
  2. Glomerulonephritis
    - IgA nephropathy, membranous nephropathy, FSGS
  3. Hereditary disorders (PCOS, familial nephritis, reflux nephropathy)
  4. Analgesic (drugs) -> interstitial nephritis
    - most commonly chronic NSAID overuse (women in 50s and 70s)
  5. Hypertensive nephrosclerosis
57
Q

What are the histopathological features of diabetic nephropathy

A
  • Arterial hyalinisation
  • Thickening of GBM and mesangial matrix
  • Nodular Kimmelstiel-Wilson glomerulosclerosis OR diffuse glomerulosclerosis
  • Papillary necrosis
58
Q

Progression of Diabetic nephropathy (4 stages)

A
  1. Elevated GFR (transient, early on)
  2. Glomerular hyperfiltration due to increased mesangial matrix
  3. Microalbuminuria (GFR normal)
  4. Macroalbuminuria = overt nephropathy (GFR decr, proteinuria incr)
59
Q

Pathophysiology of membranous nephropathy

A

Diffusely thickened GBM

Sub epithelial IgG+C3 deposits

60
Q

Hereditary disorders of CRD

A

Adult polycystic kidney disease

Familial nephritis

Reflux nephropathy with vesicoureteric reflux

61
Q

How does PKD present ?

What does renal US show?

A

Autosomal dominant:
- abdo pain +/- haematuria (bleeds into cyst), cyst infection, renal calculi, HTN, progressive renal failure

Recessive often presents in infancy with multiple renal cysts and congenital hepatic fibrosis

Renal U/S: kidneys enlarged and full of cysts

62
Q

What other medical conditions are associated with PKD?

A

Liver cysts
Diverticular disease
Ovarian cysts
Intracranial aneurysm -> SAH

63
Q

At what age do people with PKD typically reach ESRF?

A

mutation in:

  • PKD1 (85%): by 50s
  • PKD2 (15%): by 70s
64
Q

Management of CRF

A

Identify and treat cause!

Control HTN (SBP<130)
- ACEi or ARB (second line is CCB)
BSL control

Fluid balance

  • loop diuretics
  • salt and fluid restriction

Diet

  • low protein diet to reduce nitrogenous wastes (urea, uric acid)
  • restrict K and PO4

Adjust meds (avoid nephrotoxic and renally excreted meds)

Manage complications

  • Vit D and Ca supplements
  • phosphate binders
  • Epo +/- Iron
  • sodium bicarbonate
  • statin

Dialysis when GFR <15ml/min or uraemic SX onset

65
Q

What are the different types of dialysis and what are the main concepts of each?

A

Haemodialysis:

  • blood circulates at high volume through a dialysed composed of many tubes of semi-permeable membranes
  • solutes move by osmosis
  • fluid moves by ultrafiltration

Peritoneal dialysis

  • dialysis solution infused into peritoneal cavity, left to dwell for equibrilation of solutes and fluids, then the used dialysate is discarded
  • semi permeable membrane is the visceral capillary wall lining the peritoneal cavity
  • solutes leave blood via diffusion
  • fluids leave blood by mix of osmotic and hydrostatic pressure
66
Q

Complications of renal transplant

A
  • Graft rejection
  • surgical complications
  • drug toxicity
  • infection (opportunistic due to long-term immunosuppression)
  • malignancy 5x increased risk
  • CV disease
67
Q

Absolute CI to renal transplant surgery

A

Cancer
Active infection
Severe comorbidity

68
Q

What is the leading cause od death amongst CKD patients?

A

CVD

69
Q

What is hypertensive nephrosclerosis?

What does it feature?

How can it present?

A

Damage to kidney resulting from chronic high BP

Features renal hyaline arteriolosclerosis -> narrows arteriole lumina -> ischaemia -> tubular atrophy, interstitial fibrosis and glomerulosclerosis

Presents in hypertensive patient as mild proteinuria OR haematuria and proteinuria

70
Q

Risk factors for renal stones

A 
White male
High protein, salt, Ca intake
dehydration
Metabolic abnormalities (can be hereditary)
Urinary tract abnormalities
Medication (loop diuretics)
71
Q

Clinical presentation of renal stones

A

Asymptomatic

Acute severe flank pain or waxing and waning severe loin to groin pain
Haematuria (90% microscopic)
Nausea, vomiting
+/- Frequency, urgency (LUTS from bladder stones)
Fever, hypotension, tachycardia and tachypnoea

72
Q

Types of bladder stones and their treatment.

radio-opaque or lucent on KUB?

A

Analgesia and fluids for all +/- antiemetics

Calcium (75%) - incr fluid +/- thiazides, Ca channel blockers or alpha blockers to promote stone passage
- radiopaque on KUB

Uric acid (5-10%) - incr fluid intake and alkalinise urine +/- allopurinol 
- radiolucent on KUB

Struvite (5-10%) - often harbour bacteria, needs removal and ABx

Cysteine (1%) - incr fluid intake and alkalinise urine

73
Q

What is the order of investigations for suspected renal stones?

A
  1. Non-contrast helical CT of abdo/pelvis is first line!

If CT shows stone:

  1. KUB X-ray (for follow up)
    - intervention required if solitary kidney/bilateral stones/ARF/intractible pain OR low likelihood of stone passage.

If recurrent Ca stone formation, investigate for metabolic causes

  • 2x 24 hour urine
  • PTH
  • Cr
  • Ca, Na, Ph, Mg
  • Oxalate, citrate, cysteine
74
Q

Risk factors for RCC

A

Smoking, HTN, obesity
Male and >50
Haemodialysis (15%)

75
Q

Where does RCC metastasise to?

A

Lungs first -> cough -> CXR -> cannon ball mets
Bone -> bony pain
Liver

25% at presentation have metastatic disease

76
Q

Paraneoplastic syndromes (SX of cancer not explained by its anatomical position)

A

PUO/flu-like illness

Hematopoietic:

  • anaemia
  • polycythemia
  • raised ESR

Endocrinopathies

  • hypercalcaemia
  • incr epo
  • incr renin -> HTN
  • incr prolactin, gonadotropins, TSH, insulin, cortisol

Hepatic cell dysfunction w abdominal LFTs and reversible areas of hepatic necrosis

77
Q

How does RCC present?

A
  1. Commonly asymptomatic - detected incidentally by U/S or CT
  2. Loin pain/ flank pain
    gross haematuria
    palpable mass
  3. Weight loss, weakness, bone pain, anaemia
78
Q

Treatment for RCC

A

Systemic therapy (immunotherapies and chemo) doesn’t work!

Surgery the only curative treatment
-> remove the kidney (or partial nephrectomy if bilateral tumour or only one remaining kidney) and solitary mets

+ targeted therapies (T kinase, MTOR, anti-VEGF inhibitors) for advanced stage disease
+ pal care

79
Q

Differentials for haematuria

A

Urothelial malignancy

  • TCC (bladder)
  • RCC (kidney)
  • Prostate
UTI, cystitis, pyelonephritis
BPH
Stones
Trauma (surgery or blunt trauma)
PCKD/simple renal cyst 
GN or IN 
Systemic disease 
- SLE, autoimmune
80
Q

Investigations for haematuria

A

Dipstick - nitrates, WCC, protein, microscopic haematuria (nephrological)

Urine MCS (cytology for cancer cells)

FBE - anaemia, WCC
UEC

Imaging: U/S first line +/- IVU (CT + contrast)
+ CYTOSCOPY (unless <40)

81
Q

What is the most common form of carcinoma of the renal pelvis and ureter?

What are clinical features?

A

Papillary urothelial carcinoma

Gross/microscopic hematuria
Flank pain
LUTS
Flank mass +/- hydronephrosis

Investigate w IVU + cystoscopy and retrograde pyelogram

82
Q

Risk factors for bladder common

A 
Smoking
Aromatic amines 
Cyclophosphamide
Pelvic Radiation 
Chronic irritation: cystitis, chronic catheterisation, bladder stones
83
Q

What are the 2 most common forms of bladder cancer?

A

TCC >90%

SCC 5-7%

84
Q

Clinical features of bladder cancer

A

HAEMATURIA!! Painless (50%) or painful (50%)

Cystitis like symptoms with no infection on urine test (storage LUTS)

Advanced disease: bony pain, ureteric obstruction

85
Q

Treatment for bladder cancer

A

Depends on stage

Superficial (non-muscle invasive):

  • TURBT + adjuvant intravesical therapy (6 week course of BCG or mitomycin C to decrease recurrence)
  • cystectomy with high grade disease or non-responders

Invasive disease
- radical cystoprostatectomy + neoadjuvant chemo-radiotherapy

86
Q

Investigations for RCC

A

U/A, Urine MCS and urine cytology

U/S bladder
IVP (filling defect)
Cystoscopy with bladder washings GOLD STANDARD
Biopsy - establish diagnosis and determine staging
Bladder tumour markers

CT/MRI, CXR, LFTs etc for invasive disease

87
Q

Investigations for prostate cancer

A

DRE and PSA
TRUS-guided needle biopsy
Bone scan if PSA >10
CT scan (mets?)

88
Q

What scoring system is used to assess mortality risk of prostate cancer?

A 
Gleason score!
Scale of 10 - GRADE the 2 most common histological patterns on a scale 1-5 on biopsy and add the scores to get the gleason score
<7 low risk
7 moderate risk
8-9: high risk
89
Q

Treatment options for prostate cancer

A 
Prostatectomy
Hormone therapy (androgen deprivation therapy)
90
Q

Side effects of androgen deprivation thearpy

A

Hot flushes
loss of libido, impotence
tiredness, loss of muscle, osteoporosis
cognitive dysfunction

91
Q

Why is prostate cancer screening poor?

A

We are over diagnosing low grade and under diagnosing aggressive high grade cancers.

Due to lead time and lag time bias.
□ Likelihood of getting aggressive fast growing cacner whilst it is curable and screenable is very low. These men are missed with screening, and these are the people that need treatment most.
Vs much higher likelihood with slow growing cancers because the window of time that it is curable and screenable is much longer. But these are the men that would do well anyway.

92
Q

Treatment of Prostate cancer

A

○ Watchful waiting - no treatment or monitoring
§ Wait for symptomatic disease and then paliate

○ Active surveillance - monitor tumour for signs of growth or symptoms to appear
§ Serial PSA, DRE, repeat biopsies
§ Goal is to avoid overtreatment and side-effects

§ Radical prostatectomy (high-risk disease or young patients)

§ Radiation therapy (brachytherapy etc) - for low volume, low grade cancer

§ Chemotherapy

§ Hormonal therapy (anti androgens, GnRH agonists, oestrogens, bilateral orchidectomy removes 90% of testosterone )

93
Q

When to start screening for prostate cancer?

A

All men at age 50 + if >10 year life expectancy.
Initial screening involves serum PSA and DRE

High risk individuals at age 40

94
Q

Clinical presentation of urinary retention

What presentation is a medical emergency?

A 
Poor urinary stream w intermittent flow
Strain
Sense of incomplete voiding
Hesitancy
Incontinence, nocturia, frequency

ANURIA and suprapubic, dull constant pain is a medical emergency!

95
Q

Investigations for suspected urinary retention

A

U/S bladder
PSA (raised in prostate cancer, BPH and prostatitis)
CT
MRI if cauda equine syndrome suspected

96
Q

Causes of urinary retention

A

Bladder

  • trauma
  • scarring of bladder neck (iatrogenic causes)
  • neurogenic bladde (splanchnic nerve damage or cauda equina syndrome)
  • detrusor sphincter dyssynergia

Prostate

  • BPH
  • Prostate cancer
  • Prostatitis

Penile urethra

  • congenital
  • phimosis or pinhole meatus
  • circumcision
  • obstruction
  • Gonorrhoea, chlaymadia

Other

  • drugs
  • psychogenic
97
Q

Treatment of urinary retention

A

URinary catheter to empty bladder OR suprapubic puncture if can’t catheterise

+ Alpha blockers and TOV

Acute surgery - Prostatic stent, TURP, laser, open prostatectomy etc
Treat the underlying cause (BPH etc)

bladder outlet surgery

98
Q

Complications of urinary retention

A

Acute

  • bladder rupture
  • hydronephrosis and pyonephorisis leading to ARF
  • Sepsis

Chronic

  • bladder damage
  • CKF
  • bladder stones
  • hydronephrosis
  • diverticula in bladder wall -> stones, infection
99
Q

LUTS

A

Voiding SX

  • hesitancy
  • slow or intermittent stream
  • incomplete emptying
  • terminal dribbling

Storage SX

  • frequency
  • urgency
  • nocturia
  • incontinence
100
Q

Aetiology of problems with ‘waterworks’ in males

A

Obstructive

  • BPH or prostate cancer
  • stricture

Irritative

  • secondary to obstruction
  • UTI
  • Bladder cancer
  • stone
  • diabetes
  • TB
  • medical causes (diuretics, anticholinergics); caffeine and alcohol etc
101
Q

Treatment of BPH

A

Alpha blockers (relaxes smooth muscle of urethra)
+/-
5 alpha reductase inhibitors (blocks conversion of testosterone to DHT) reduces prostate volume.

Surgical

  • TURP
  • open prostatectomy
102
Q

What type of bladder retention is painful and which is more dangerous?

Which is associated with bed wetting?

A

Acute retention for both pain and dangerousness.

Chronic assoc w bed wetting due to overflow. Not painful.

103
Q

Causes of acute bladder retention

A

BPH, prostate cancer, stricture
Weak detrusor muscle due to old age

Acute precipitants:
- UTI (urethritis)
- diuresis (alcohol)
- drugs (anticholinergic)
- post-op
- prolapse in women
Neurological
- DM
- Stroke
- PD
- spinal cord compression
104
Q

How is obstructive nephropathy defined?

A

Elevated Creatinine
Bilateral hydronephrosis

Due to significant back pressure from bladder (AUR) causing renal dysfunction

MX: admit, monitor urine output and U&Es regularly and replace urine output with normal saline + electrolytes as needed.

MD2 (16 decks)

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