Urinary and Renal diseases Flashcards
Renal blood Circulation
~ 20-25% Cardiac output
>90% to cortex (filtration takes place here)
Filters ~1200 mls/min
Renal Failure
Renal diseases very common
• Acute
Hours-days
Pre-renal
Renal
Postrenal
Predispose to chronic renal failure
• Chronic
Weeks, months, years
Acute —> Necrosis —> clogs up nephron—> decrease in filteration rate and urine formation
Injury —> RAAS activated —> systemic hypertension, reduced urine formation
How do the kidneys contribute to congestive heart failure?
Systemic hypertension —> left ventricular failure
By kidneys activating RAAS
Explain the impact that renal failure has on the rest of the body.
Overactivation of RAAS
When PTH hormone is released, kidneys activate more vitamin D, without it, calcium is not absorbed
passively, kidneys allow calcium to be lost in urine. Leads to soft tissue calcification and osteomalacia. Increase in phosphate
Lack of EPO —> Anaemia
Acidosis —> hyperkalaemia—> predispose to arrhythmia
Increase in built up waste in blood
What are the main malignancies that affect the male & female urinary systems?
Transitional cell carcinoma - renal calyces, pelvis, ureter and baldder
Renal cell carcinoma : - Clear cell carcinoma
- Papillary renal cell
- Chromophobe renal
Prostate cancer (adenocarcinoma)
Nephroblastoma
What are common causes of glomerulonephritis & possible consequences?
Blood borne. Chronic impacting functional units due to special cases (autoimmune disorders)
Caused by: swelling of endothelium, decreased blood flow, inflammation altering permeability, focal loss of epithelium and endothelium
Consequence: Renal Failure
Bilateral , decreased urinary output, proteinuria, haematuria, hypertension and headaches
Why is the renal papilla susceptible to toxic injury & ascending infections?
Renal pyramid protruding into waiting calyx
- First point of vulnerable tissue that ascending infections hit (from lower urinary tract)
- Urine is most concentrated
- Susceptible to injuries from drugs
What are the possible consequences of urinary stones?
One stone predispose to more stones
Haematuria
Pain
Hydronephrosis
Cancer
Obstruction in kidney means more likely to get infections
Why are ascending infections more common in females than males?
Urethra much shorter in women. Women do not have prostate which helps counter microbials. Trauma during birthing and sexual intercourse. Proximity to anal canal
Descending infection
infection is travelling in blood. Renal failure.
Causes of Chronic Renal Failure
- Hypertension
- Diabetes
- Obeseity
- Heart disease
- Smokers
- Over 60
- Aboriginals
- Family history of CKD
- Personal history of ARF
1 in 3 at risk (1.7mil australians)
Common symptoms of chronic renal failure
Azotaemia/Uraemia: increased waste in blood Systemic Hypertension Oedema Acidosis Hyperkalaemia (Potassium) Muscle, Heart arrhythmias Hyperphosphatemia Muscle, nerves, bone Anaemia
Renal physiology
Formation of urine – removal of wastes
Regulates plasma ions (Na+, Cl-, PO43-, K+, Ca2+)
Regulates pH (H+, HCO3-)
Endocrine Function (Vitamin D, RAAS, EPO)
Regulation of blood volume
Regulation of blood pressure
Metabolism – Deamination of αα, detoxification of drugs/toxins
Ligand
hormone or growth factor interacting with receptors
Agonist
drug that binds to receptor and stimulates it
Antagonist
drug that binds to receptor and blocks it
RAAS System
RAAS —> renin—> angiostenin ii —-> aldosterone —> increase water or sodium intake—> increase blood volume
RAAS —> renin—> angiostenin ii —-> vasoconstriction —> vas resistance
RAAS —> renin—> abgiostenin ii —-> SNS activated—-> increased sympathetic tone —> increased HR —-> increased vascular resistance
Oedema relationship with renal failure
- Due to increased HP
- Decrease in colloidal pressure
- Due to RAAS, increase in HP (constricted vessels and increased blood volume)
- Proteinuria Reduced colloidal Pressure
Renal failure —> systemic oedema happens through RAAS (retention of H20 and NA)
Causes of Circulatory disease
Benign nephrosclerosis - Focal ischaemia & atrophy
Malignant- Damages renal arteries, arterioles & glomeruli
Rapid ↑ BP
Diabetes - atherosclerosis, systemic hypertension, lesions (aging) of kidneys
Alterations in renal failure
Increased Na+ Increased H2O
Increased H+ Increased K+
Decreased Ca2+ Increased PO43-
Leading to acidosis
Increased hydrogen level can be replaced by potassium and leads to hyperkalaemia, predispose to cardiac arrhythmia
Endocrine problems caused by renal failure
Increased renin-angiostenin-aldosterone (systemic hypertension) Decreased Erythropoietin (anaemia) Decreased activation of vit D (renal osteodystrophy)
Renal Pathology
Congenital and Cystic Diseases
Glomerular Diseases
- Immunologically mediated
Tubular and Interstitial Diseases
- Infection & toxins
Circulatory Disorders
Stones & Tumours
- Obstruction
Developmental disorders
Renal agenesis - bilateral or unilateral
Horseshoe kidney
Polycystic kidney disease
Nephroblastoma
Cystic Disease
Cystic Renal Dysplasia
Autosomal Dominant (Adult) Polycystic Kidney Disease: born with normal kidneys, has genetic mutation. After birth, cysts forms. Loss of function. Significant level in Australia
Autosomal Recessive (Childhood) Polycystic Kidney Disease
Diseases of the Renal medulla
Tubular and interstitial disease
Does not cause renal failure Tubules Interstitium Inflammatory - Tubulointerstitial Nephritis - Pyelonephritis (ascending infection, coming from lower urinary tract)
Pyelonephritis
Bacterial infection in the kidney Effects pelvis tubules & interstitium Acute : Bacterial infection Chronic: Repeated infections Obstruction Symptom: fever
Carcinoma of the prostate
Most common Unknown cause and risk factors Hormonal inluences Racial differences Genetics Cancer as a chronic disease
Calculi composition
- Calcium oxalate and phosphate (70%)
- Magnesium ammonium phosphate (15%)
Uric acid (6%)
Urinary tract obstruction and causes
- Unilateral
- Urinary calculi/stones
- M>F & usually >30 years (male more likely)
- Any level (renal pelvis to bladder)
Predisposition • Stasis (obstruction) • Mucoproteins • pH • Infection • Dehydration • Calcium metabolism disorders • Metabolic pyrophosphates & citrates inhibit formation
Process of EPO
Hypoxia —> Kidney —> EPO —> Increased RBC production
Hypoxia —-> kidney —> no EPO —> Anaemia
Process of Vitamin D increase in blood
Kidney —> does not activate vitamin D —> Gut does not increase calcium intake
Increased phosphate, decreased calcium —>PTH stimulated —> Increase in calcium –>soft tissue calcification, osteomalacia
