1
Q
What are the 2 types of hypertension?
A
- Essential hypertension
- Secondary hypertension
2
Q
What are the causes of secondary hypertension?
A
- Primary hyperaldosteronism (primary cause)
- Primary chronic kidney disease
- Renal artery stenosis: ACEi/ARB can precipitate renal failure by causing a stenosis of renal artery because constriction of afferent and dilation of efferent
- Thyroid disease (hyperthyroidism causes cardiac hyperactivity and hypothyroidism increases peripheral resistance)
- Sleep apnoea
- Medication (oral contraceptives, NSAID, glucocorticoids, alcohol, cocaine)
- Pheochomocytoma (catecholamine secretion)
- Coarctation of aorta
- Cushing syndrome.
3
Q
When should we screen a patient to find out the cause of his hypertension?
A
We don’t screen everybody with hypertension, we screen:
- extremes of age
- sudden onset of HTN
- resistant HTN
- difficult to control HTN
- family history of secondary HTN and
- suggestive features on history, physical and investigations
4
Q
According to Canadian Guidelines, when do we initiate therapy for HTN?
A
- ≥140/90 mmHg for most patients
- ≥130/80 mmHg for diabetics
- ≥130 mmHg for certain high risk patients
- ≥160/100 mmHg for patients in low risk patients
5
Q
What are the treatments for hypertension?
A
- Pharmacological: diuretis, ACEi, ARB, CCB, B-blocker or combined pill, monotherapy is often not enough
- Non-pharmacological: diet (salt++), weigh, physical activity, alcohol and smocking cessation
6
Q
How do we diagnose HTN for a pregnate woman?
A
- Before 20 weeks of gestation: high BP is considered chronic HTN
- After 20 weeks of gestation
- Preeclampsia
Risk factors include primigravidy, extreme maternal age (<18 or >35), chronic HTN, gestational diabetes, obesity
- Gestational hypertension (transient but precursor to preeclampsia)
7
Q
When are how do we treat a pregnate women with HTN?
A
- Treat when BP >140/90 mmHg
- Aim for diastolic BP <85 mmHg
- Treatment is delivery of the baby, IV magnesium sulphate to prevent seizure, antihypertensive medications (NOT ACEi and ARBs) and supportive management
8
Q
What are some major challenges in regards to HTN?
A
- Making the diagnosis
- Measuring the BP correctly
- Instituting lifestyle changes
- Treating to target with medications
- Addressing other risk factors
- Ensuring adherance to treatment plan
- Identifying secondary HTN
- Pregnancy
9
Q
Players of continence?
A
- bladder (low pressure, compliant, sympathetic system promotes storage)
- sphincter
- peripheral nervous system
- central nervous system
10
Q
Lower urinary tract symptoms (LUTS)?
A
- Irritative: dysuria, frequency, incontinence, hematuria, urgency, nocturia
- Obstructive: frequency, retention, hesitancy, straining, intermittency, incomplete emptying, weakness of stream, terminal dribbling
11
Q
Causes of LUTS?
A
- Overactive bladder (when it fails to act as a low-pressure storage)
- Frequency, urgency ± incontinence
- Etiologies: neurogenic or myopathic
- Management: anticholinergic, catheterization, cystostomy, surgical bladder augmentation
- Obstruction (BPH)
- Retention
- Bladder problem: failure to empty
Neurogenic, pharmacologic or myopathic
- Outlet problem
Prostate obstruction, urethral stricture or bladder neck contracture orfailure of the sphincter to relax during voiding
- Incontinence
- Bladder problem
Neurogenic, myopathic, retention with overflow incontinence
- Outlet problem
Sphincter incompetence or stress incompetence
12
Q
What zone of the prostate comonly causes BPH?
A
Transitional zone
13
Q
What zone of the prostate commonly causes cancer?
A
Peripheral zone
14
Q
How do we diagnose BPH?
A
- A good history and a thorough physical examination are the keys to diagnosis
Must do both DRE and PSA to achieve a higher sensitivity of prostate cancer diagnosis
- AUA Symptom Score
- Another important tool is a self-reported voiding diary
- Record the volume of intake, urine flow, time and volume of urination over a period of 1 or few days
- Lab evaluations to confirm or rule out various diagnoses
- PSA helps detect prostate cancer, but is not cancer specific
15
Q
Treatment options for BPH?
A
- Non pharmacological: watchful waiting
- Pharmacological: 5-a-reductase inhibitors, a1-blockers
- Surgical: Transurethral Resection of Prostate, Transurethral Incision of Prostate, Laser or Open prostatectomy when prostate is very large
16
Q
What are the 2 screening urine tests ?
A
- Urinalysis
Dipstick, assess: pH, glucosuria, ketones, nitrites (infection), WBC, albumin, hemoglobin
- Urine microscopy (automated or manual)
17
Q
What are the Biopsy indication?
A
- Proteinuria is >1g/day
- Proteinuria is associated with hematuria or casts
- Renal disease in setting of systemic disease
- Unexplained AKI or CKD (normal renal imaging)
18
Q
What are the types of proteinuria?
A
- Functional
Fever, exercise, CHF, orthostatic
TRANSIENT AND NORMAL
- Overproduction
Protein produced in another part of the body are filtered and excreted by the kidney
- Tubular protein loss
Impaired reabsorption along the renal tubules (FANCONI’S SYNDROME)
- Glomerular protein loss
Loss of negative charges on the GBM, pore size- e.g. minimal change, focal glomerulosclerosis, membranous, diabetic renal disease
19
Q
Hematuria management?
A
20
Q
How are defined AKI?
A
- Increase in SCr by ≥ 26.5 µmol/l within 48 hours
- Increase in SCr to ≥ 1.5 times baseline, which is known or presumed to have occurred within the prior 7 days
- Urine volume, 0.5 ml/kg/h x 6 hours (<30 cc/h)
Further be classified as oliguric/non-oliguric:
- Urine output drop = oligura <30 cc/hour (Anuria is <50 cc/24 hours)
- <200 cc/8h shift
21
Q
What are the 3 most common problems in hospital?
A
- Acute tubular necrosis — 45 %
Muddy brown dead cell casts under microscopy
FENa > 2%
- Pre renal — 21 %
Urine Na is low <20
FENa <1 % suggests prerenal disease
- Acute on chronic renal failure — 13 %
22
Q
Examples of AKI?
A
- Multiple myeloma (plasma cell clone)
Test: Serum free light chains λ or κ
- Rhabodmyolysis
Skeletal muscle breakdown
Labs: Myoglobin very high, cola-colored urine, high creatinine kinase
3. TTP Thrombotic Thrombocytopenic Purpura– thrombi in the vessels
Fever, neurologi symptoms, renal failure
4. HUS- hemolytic uremic syndrome
Most common cause of acute kidney injury in children < 5 years, E.Coli causes microangiopathic
haemolytic anemia, thrombocytopenia and renal insufficiency
5. Acute Interstitial Nephritis
Allergic reaction to a drug in the kidney, inflammation, we give steroids
6. Aminoglycoside toxicity
Not an allergy, just toxicity
7. Contrast Nephropathy
Dye causes intrarenal vasoconstriction, prevention: IV hydration, hold ACEI/ARB and NSAID
8. RPGN Rapidly Progressive GN
Crescents
23
Q
When do we hemodialyse a patient with AKI?
A
- Hyperkalemia
- Fluid overload
- Uremic syndrome- pericarditis, CNS symptoms
24
Q
What are the 3 main causes of CKD?
A
- Hypertensive nephrosclerosis
- Diabetic nephropathy
- Glomerulonephritis
25
How do we differentiate the types of CKD?
\> 3 g per day: Glomerulonephritis, need biopsy
1-2 g per day: Could be tubular or glomerular
\< 1g per day: No biopsy, hypertension
26
On what depends the prognosis of CKD?
1. Proteinuria
2. Lower GFR (patients with a GFR \< 30 ml/min have a high prevalence of cardiovascular mortality and hospitalized frequently)
3. Younger age
27
General management principles of CKD?
1. Blood pressure control – MOST IMPORTANT
140/90, but 130/80 with albuminuria
1. Blood sugar control
2. RASS inhibition (ACEi or ARBs is proteinuria, STOP IF EPISODE OF VOLUME DEPLETION)
3. Prevention of AKI – VERY IMPROTANT (avoid NSAIDs)
28
How do we manage stage 4 and 5 CKD?
1. Treatment of metabolic and volume complications (Na and fluid restriction)
2. Reduction of CV risk
3. Prevention of other complications (anemia, calcium, potassium, metabolic acidosis, medication review, vaccination)
4. Preparation for ESRD (\< 15 ml/min)
29
Common congenital renal anomaly that are likely to have a genetic etiology?
**Unilateral renal agenesis**
* Usually no symptoms
**Bilateral renal agenesis (Potter’s sequence)**
* Not compatible with extra uterine life
* Lung hypoplasia and severe oligohydrammnios
**Horseshoe kidney**
* Kidneys fuse
* Not always symptoms
**Turner syndrome**
* Dysmorphic and sexual features
* 40% have congenital abnormality of urinary system
30
Autosomal dominant polycystic kidney disease (ADPKD)?
* A systemic disease characterized by the progressive development of fluid filled cysts in the kidneys, cardiovascular disease and cyst formation in the liver and pancreas (polycystic and vascular complications).
* ADULT and fully penetrant by 30 years old, football kidney
* Two main genes: PKD1 & PKD2, encodes for polycystin
* As cysts accumulate fluid, they enlarge, compress the neighboring normal renal parenchyma, and progressively compromise renal function: glomerular filtration rate declines + inflammation and fibrosis + apoptosis of the tubular epithelial cells
* Genetic testing can be pertinent, but sensitivity is not 100% so can’t rule out
31
Autosomal recessive polycystic kidney disease (ARPKD)?
* More severe and rare
* Gene: PKHD1*,* encodes fibrosystin protein
32
Alport syndrome?
* Abnormal type IV collagen
* Renal failure, occular abnormality and sensorineural hearing loss
* Clinical presentation: microscopic hematuria, proteinuria, hypertension and renal insufficiency
* Several genes: COL4A3, COL4A4, COL4A5
* Typically X-linked
33
What is the approach when we suspect that a renal syndrome is genetic?
* Isolated or part of a syndrome?
* Is there a family history?
* Renal ultrasounds in both parents can help
* Karyotype or aCGH if suspect chromosome abnormality
* Targeted DNA testing if suspect specific genetic disorder
34
Causes of bladder dysfunction in children?
1. **Neurogenic causes**: congenital anomalies that affect spinal cord (spina bifida), trauma to Central Nervous System (CNS) or Peripheral Nervous System (PNS), tumors that affect CNS or PNS.
2. **Anatomic causes**: never acquire voluntary control of bladder function
- Anatomic defect bypasses the bladder outlet with ectopic ureter with insertion distal to the bladder neck;
- Obstruction to bladder outlet e.g. posterior urethral valves;
- Vesico-ureteric reflux;
- Polyuria from renal failure
3. **Functional causes**: MOST COMMON-no known anatomic or neurological cause
35
What is vesico-ureteric reflux (VUR)?
A congenital defect of the uretero-vesical junction (UVJ). Associated with bladder dysfunction, congenital renal malformations, recurrent urine infections, hypertension, reflux nephropathy, and end-stage renal disease. Treatment includes **antibiotic prophylaxis** (because it presents in UTI) and **surgical therapy** to correct the UVJ defect.
36
Evaluation of bladder dysfunction in children?
* Growth? Height, weight, percentiles, neurological and physical, neurodevelopmental delay?
* Polydipsia (do they prefer to drink water? do they wake up to drink during the night), polyuria?
* Voiding schedule? (voiding diary)
* Blood pressure
* Symptoms of bladder dysfunction? Urinary tract infections? Vesico-ureteric reflux (VUR)?
* Bowel habits? (frequency, consistency, caliber and size), pain during defecation, fecal incontinence, soiling (Bristol stool chart)
* Perinatal and neonatal history? (birth insults?)
* Diet intake-amount of fluid, fiber in diet
* Medications?
* Toilet-training schedule?
* Family history?
* Physical exam: external genital lesions, bladder palpable
* Psychosocial
* Lab tests: urinalysis, urine culture, serum electrolytes, blood gas, creatinine, lumbosacral spine films, abdominal film, ultrasonography, voiding cystourethogram
37
What is the principles of dyalisis?
38
On what relies the choice of dialysis modality?
* Technical feasibility
* Degree of patient autonomy
* Personal preference
* Technique complications
39
What is an Arteriovenous fistula?
* A bypass between artery and vein to arteriolize the vein
* Surgically created
* Takes several weeks to months to mature
* Provides reliable long-term access for chronic hemodialysis
* Must be protected from compression to prevent thrombosis
40
How do molecules are dialized?
* Diffusion (gradient, molecular weight and membrane characteristics)
* Ultrafiltration (removes water)
* Convection (pressure that drives plasma trough the membrane)
41
What is the best option is ESRD?
Transplant with an alive donor
42
When do you consult urology for decompression?
* **Obstructing ureteral stone with infection (MOST IMPORTANT)**
* Impending renal deterioration/failure
* Pain refractory to analgesics
* Intractable nausea/vomiting
* Patient preference (multiple ED visits)
43
How do we prevent kidney stones?
1. Fluid intake
2. Reduce salt
3. Reduce animal protein
4. Citrate-rich fluids
5. Moderate consumption of high-oxalate content foods
6. Limit vitamin C intake to 1000 mg daily
7. Moderate calcium intake do NOT stop calcium supplement
8. Vitamin D
44
3 urological procedures used to treat stones?
1. Shock-Wave Lithotripsy (60-70% efficacy)
2. Ureteroscopy (90% efficacy for small stones but high risk of complications)
3. Percutaneous Nephrolithotomy (most invasive, 90% efficacy)
45
When do you consult nephrology for work-up?
* Recurrent, multiple or bilateral stones
* Stones in pregnancy
* Stones in children (\<18 years old)
* Non-calcium stones (e.g., cystine, uric acid)
* Strong family history (≥1 first-degree relative)
* Solitary kidney or anatomical abnormalities
* Renal insufficiency
* Systemic diseases (gout, IBD, RTA type I)
* Critical occupations (pilots, sailors, firemen)
46
What is the gold standard imaging study to dx kidney stones?
Low dose CT scan
47
Demographics of ESRD in Indigenous peoples?
* 3 times more likely to have ESRD
* Younger than non-Indigenous patients with ESRD
* More likely to have to travel further for care
* Less likely to receive a kidney transplant
* Lower survival rates in the period after starting dialysis
* Similar survival rates post-transplant
* More men than women
* Main factors and diabetes and obesity
* Main diagnosis for Indigenous children and youth with ESRD is glomerulonephritis
48
* Most Indigenous patients receive hemodialysis; less likely to receive peritoneal dialysis
* Indigenous ESRD patients are 50% less likely to receive kidney transplantation compared to non-Indigenous patients
WHY?
* Diabetes +++
* Language and cultural barriers
* Cultural differences on transplantation
* Distance (for children and nephrology consults)
Bloc D - Renal
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Decks in class (7)
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