Urinary and Renal diseases Flashcards

1
Q

Renal blood Circulation

A

~ 20-25% Cardiac output
>90% to cortex (filtration takes place here)
Filters ~1200 mls/min

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2
Q

Renal Failure

A
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

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3
Q

How do the kidneys contribute to congestive heart failure?

A

Systemic hypertension —> left ventricular failure

By kidneys activating RAAS

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4
Q

Explain the impact that renal failure has on the rest of the body.

A

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

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5
Q

What are the main malignancies that affect the male & female urinary systems?

A

Transitional cell carcinoma - renal calyces, pelvis, ureter and baldder
Renal cell carcinoma : - Clear cell carcinoma
- Papillary renal cell
- Chromophobe renal
Prostate cancer (adenocarcinoma)
Nephroblastoma

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6
Q

What are common causes of glomerulonephritis & possible consequences?

A

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

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7
Q

Why is the renal papilla susceptible to toxic injury & ascending infections?

A

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
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8
Q

What are the possible consequences of urinary stones?

A

One stone predispose to more stones

Haematuria

Pain

Hydronephrosis

Cancer

Obstruction in kidney means more likely to get infections

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9
Q

Why are ascending infections more common in females than males?

A

Urethra much shorter in women. Women do not have prostate which helps counter microbials. Trauma during birthing and sexual intercourse. Proximity to anal canal

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10
Q

Descending infection

A

infection is travelling in blood. Renal failure.

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11
Q

Causes of Chronic Renal Failure

A
  • 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)

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12
Q

Common symptoms of chronic renal failure

A
Azotaemia/Uraemia: increased waste in blood 
Systemic Hypertension
Oedema
Acidosis
Hyperkalaemia (Potassium)
Muscle, Heart arrhythmias
Hyperphosphatemia
Muscle, nerves, bone 
Anaemia
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13
Q

Renal physiology

A

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

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14
Q

Ligand

A

hormone or growth factor interacting with receptors

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15
Q

Agonist

A

drug that binds to receptor and stimulates it

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16
Q

Antagonist

A

drug that binds to receptor and blocks it

17
Q

RAAS System

A

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

18
Q

Oedema relationship with renal failure

A
  • 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)
19
Q

Causes of Circulatory disease

A

Benign nephrosclerosis - Focal ischaemia & atrophy

Malignant- Damages renal arteries, arterioles & glomeruli
Rapid ↑ BP

Diabetes - atherosclerosis, systemic hypertension, lesions (aging) of kidneys

20
Q

Alterations in renal failure

A

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

21
Q

Endocrine problems caused by renal failure

A
Increased renin-angiostenin-aldosterone (systemic hypertension)
Decreased Erythropoietin (anaemia)
Decreased activation of vit D (renal osteodystrophy)
22
Q

Renal Pathology

A

Congenital and Cystic Diseases
Glomerular Diseases
- Immunologically mediated

Tubular and Interstitial Diseases
- Infection & toxins

Circulatory Disorders

Stones & Tumours
- Obstruction

23
Q

Developmental disorders

A

Renal agenesis - bilateral or unilateral
Horseshoe kidney
Polycystic kidney disease
Nephroblastoma

24
Q

Cystic Disease

A

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

25
Q

Tubular and interstitial disease

A
Does not cause renal failure 
Tubules  Interstitium
Inflammatory
- Tubulointerstitial Nephritis
- Pyelonephritis (ascending infection, coming from lower urinary tract)
26
Q

Pyelonephritis

A
Bacterial infection in the kidney
Effects pelvis tubules & interstitium
Acute : Bacterial infection
Chronic: Repeated infections
Obstruction
Symptom: fever
27
Q

Carcinoma of the prostate

A
Most common
Unknown cause and risk factors
Hormonal inluences
Racial differences
Genetics
Cancer as a chronic disease
28
Q

Calculi composition

A
  • Calcium oxalate and phosphate (70%)
  • Magnesium ammonium phosphate (15%)
    Uric acid (6%)
29
Q

Urinary tract obstruction and causes

A
  • 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
30
Q

Process of EPO

A

Hypoxia —> Kidney —> EPO —> Increased RBC production

Hypoxia —-> kidney —> no EPO —> Anaemia

31
Q

Process of Vitamin D increase in blood

A

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