Kidney + Urinary Tract Flashcards

1
Q

Kidney Functions

A
  1. Elimination
    - Metabolic waste
    - Drugs & toxins
  2. Homeostasis
    - Electrolytes, water, pH, blood pressure (renin)
    - Bone metabolism
    — Vit. D activation
    — Ca+2 and PO4
    - Bone marrow RBC production (erythropoietin)
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2
Q

Kidney Gross Anatomy

A

The two kidneys are located in the posterior wall of the abdomen at the level of the 11th and 12th ribs and are wrapped by a protective layer of fat.

The kidney can be divided into the renal cortex (outer region, where most of filtration is) and the medulla (inner region).

The renal columns are connective tissue extensions that radiate downward from the cortex through the medulla to separate the most characteristic features of the medulla: the renal pyramids and renal papillae.

The papillae are bundles of collecting ducts that transport urine made by nephrons to the calyces of the kidney for excretion. The pyramids and renal columns taken together constitute the kidney lobes.

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3
Q

Glomeruli

A

Nephrons are the “functional units” of the kidney; they cleanse the blood and balance the constituents of the circulation.

The afferent arterioles form high-pressure capillaries called the glomeruli.

The rest of the nephron consists of a tubule whose proximal end surrounds the glomerulus—this is Bowman’s capsule.

The glomerulus and Bowman’s capsule together form the renal corpuscle.
- These glomerular capillaries filter the blood based on particle size.

After passing through the renal corpuscle, the capillaries form a second arteriole, the efferent arteriole.

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4
Q

Filteration of the Bowmans Capsule

A

One layer of the Bowman’s capsule is composed of uniquely shaped cells (podocytes) with extending finger-like arms to cover the glomerular capillaries. These projections interdigitate to form filtration slits, leaving small gaps between the digits to form a sieve. As blood passes through the glomerulus the plasma filters between these sieve-like fingers to be captured by Bowman’s capsule.

Overall, filtration is regulated by fenestrations in capillary endothelial cells, podocytes with filtration slits, and the basement membrane between capillary cells.

Filtration has:
- endothelial lining with fenestrations
- then, a protein meshwork called glomerular basement membrane. The fluid needs to get through this. It acts as a filter, and has a negative charge. So it is a physical and charge barrier
- then, there are epithelial podocytes with filtration slits

there is protein meshwork between the podocytes too

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5
Q

Structure of the Nephron

A

After leaving the renal corpuscle, the filtrate passes through the renal tubule in the following order: proximal convoluted tubule (found in the renal cortex), loop of Henle (mostly in the medulla), distal convoluted tubule (found in the renal cortex), collecting tubule (in the medulla), collecting duct (in the medulla).

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6
Q

Function of renal corpuscle

A

Production of filtrate

Squamous cells

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7
Q

Function of proximal convoluted tubule

A

Reabsorption of water, ions, and all organic nutrients

Cuboidal cells with abundant microvilli

And mitochondria

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8
Q

Function of distal convoluted tubule

A

Secretion of ions, acids, drugs, toxins

Variable reabsorption of water, sodium ions, and calcium ions (under hormonal control)

cuboidal cells with few microvilli

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9
Q

Function of nephron loop

A

Descending thin limb
- further reabsorption of water
- squamous cells

Thick ascending limb
- reabsorption of sodium and chloride ions
- low cuboidal cells

Ascending thin limb
- squamous cells

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10
Q

Function of collecting duct

A

Variable reabsorption of water and reabsorption or secretion of sodium, potassium, hydrogen, and bicarbonate ions

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11
Q

Function of papillary duct

A

Delivery of urine to minor calyx

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12
Q

Acute Kidney Injury

A
  1. Pre-Renal
    - decrease blood flow quickly before the blood goes to kidney
    - Shock, dehydration, hemorrhage, trauma, etc.
    - often related to the heart and the low cardiac output.
  2. Renal
    - directly damages kidney
    - Inflammation, infection, ischemia
    - Drugs and toxins
  3. Post-Renal
    - Acute urinary tract obstruction
    - impacts the collecting system
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13
Q

Chronic Kidney Injury

A
  1. Pre-Renal
    - Hypertension, diabetes
  2. Renal
    - Primary glomerulopathies
    - Chronic tubulointerstitial diseases
  3. Post-Renal
    - Chronic urinary tract obstruction
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14
Q

Acute vs chronic kidney injury

A

Acute kidney injury
*Acute onset of symptoms
*Potentially reversible
*if treated early enough the damage is not permanent

Chronic kidney injury
*Often asymptomatic at first
*Slowly progressive and irreversible damage
*Loss of glomeruli, chronic inflammation, scarring

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15
Q

Consequences of Kidney Injury

A
  1. Loss of water regulation - Edema, often exacerbated by protein loss in the urine.
  2. Electrolyte disturbances - minerals lost Na+, K+ , Ca2+, PO4
  3. Lower Blood pH - Acidosis
  4. Increased Waste products
  5. Anemia - due to loss of vitamin D.
  6. Lower bone density- due to loss of vitamin D.
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16
Q

Management of Chronic Renal Failure

A
  1. Medication
  2. Dialysis
  3. Transplant
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17
Q

Glomerular Diseases

A
  1. Primary glomerulopathy:
    - Affect kidney primarily or exclusively
  2. Secondary glomerulopathy:
    - Systemic diseases that affect multiple organs
    - E.g. diabetes, systemic lupus, vasculitis
18
Q

Glomeruli diseases are associated with several complications

A

Majority are immune mediated
- Immune Mechanisms underlie Most types of primary glomerular diseases and many of the secondary glomerular diseases. (ex. Poststreptococcal glomerulopathy)

Most damage the glomerular filter in some way
- The deposition of circulating immune complexes in the glomerulus initiates complement and/or Fc receptor-mediated leukocyte activation resulting in glomerular injury.

19
Q

Investigations for renal disease

A

Urinalysis:
- Hematuria (blood in urine)
- Proteinuria (protein in urine)

Blood:
- Increased Creatinine and urea (impaired waste elimination)

Kidney biopsy:
- Needed for definitive diagnosis
- Use light microscopy, immunofluorescence and electron microscopy

20
Q

Kidney biopsy results

A

Light Microscopy:
* Inflamed, causes more cells than usual
*Thickened matrix, obscured capillaries
* more pink

Immunofluorescence
*Immune complex deposition (IgA)
* can check for diff immune complexes

Electron Microscopy
*Abnormal proteinaceous deposits in the glomerulus

21
Q

Tubular Diseases

A

The proximal tubular epithelium is quite sensitive
- it works hard to resorb certain substances and get rid of some substances
- it is sensitive to ischemic insult and toxic insult. you may get death of the tubular epithelium or it may get patchy and parts of it becomes lost

Acute Tubular Necrosis (ATN): Acute tubular injury (ATI/ATN) is a clinicopathologic entity characterized by damage to tubular epithelial cells and an acute decline in renal function.
- ATN is potentially reversible

  1. Ischemic injury (decreased blood flow to kidney)
    Caused by:
    - Low cardiac output (heart failure)
    - Low blood volume (hemorrhage)
    - Vasodilation (sepsis, anaphylaxis)
  2. Nephrotoxic injury
    - Exogenous (drugs, toxins)
    - Endogenous (muscle injury, transfusion reaction)

Consequences of acute kidney injury, specifically acute tubular necrosis:
- things get clogged up, there is sloughing of dead ep cells
- that causes low urine output (called oliguria)
- thus, there is buildup of back pressure because you are not filtering nor excreting your waste products; this causes high pressure
- there is also decreased blood pH (called metabolic acidosis)
- messing up electrolyte balance (hyperkalemia - increased potassium)
- azotemia is nitrogen containing blood

22
Q

Kidney Cyst

A

Cystic diseases of the kidney are a heterogeneous group comprising hereditary, developmental, and acquired disorders.

Acquired
- Simple
- End-stage failure

Genetic
- Polycystic kidney diseases

Neoplastic
- Renal carcinoma variant

Developmental
- Congenital syndromes

23
Q

Pathogenesis of Kidney Cysts

A

Altered growth and differentiation of tubular epithelium.

Then there is fluid secretion

And the fluid builds up in the cyst

24
Q

Acquired Simple Cyst

A

Simple cysts are generally innocuous lesions that occur as multiple or single cystic spaces of variable size.

Simple cysts are a common postmortem finding that has no clinical significance.

25
Q

Adult Polycystic Kidney Disease

A

Acquired cystic kidney disease: occurs in patients with end-stage renal disease who have undergone dialysis for many years. Multiple cysts may be present in both the cortex and the medulla and may bleed, causing hematuria.

Too many cysts will replace the functional kidney tissue and impair function

26
Q

Vascular Diseases of the Kidney

A

Atherosclerosis
- Embolic infarcts
- Artery narrowing (low perfusion, atrophy)

Hypertension
- Thickening of small vessel walls

27
Q

Aortic Atherosclerosis

A

Plaques on the lining of the renal artery result in its narrow and lower perfusion of the kidney. Grossly the kidney’s topography will no longer be smooth.

This can also lead to renal atrophy due to chronic hypoxia, where one kidney will appear to be smaller in size. (Atherosclerosis Related Kidney Atrophy)
- renal artery stenosis on one side but not the other side can cause the side with the stenosis to have smaller kidney but other side stays normal

Embolic infarct
- atherosclerotic plaque is broken off and dislodges
- then it causes an area of infarction that is white colored and causes white scar in the subsequent blood vessels that have no blood anymore

28
Q

Hypertensive Kidney Disease

A

Thickening of the vessel walls can result in increased pressure.

Grossly the cortex of the kidney appears to be scarred and granular.

Microscopically the glomeruli show scarring and we can see fibrosis of the interstitium.

29
Q

Bladder Gross Anatomy

A

The urinary bladder collects urine from both ureters.

In males, the anatomy is similar, and with the addition of the prostate inferior to the bladder.

The bladder is partially retroperitoneal (outside the peritoneal cavity) with its peritoneal-covered “dome” projecting into the abdomen when the bladder is distended with urine.
- The inner lining of the bladder is a layer of epithelial cells making the urothelial layer

30
Q

Vesicoureteral Reflux

A

Ureter orfices are usually a one-way valve
- urine goes down through the valve
- urine flowing backwards is retrograde flow (not normal) and this is prevented with a valve

In some people, the valve does not work well, resulting in Vesicoureteral Reflux (urine goes back up)
- pressure in outflow increases
- leads to infection
- leads to renal inflammation and scarring

There are diff grades of severity of Vesicoureteral Reflux
- depends on how far urine backs up

31
Q

Kidney Stones

A

Urolithiasis is calculus formation at any level in the urinary collecting system, but most often calculi arise in the kidney.

Pathophysiology
- increased Stone-forming substances
- decreased Precipitate inhibiting buffer agents

Risk Factors
- Hereditary
- Underlying condition (hypercalciuria, gout etc.)
- Low fluid intake
- Infection (urea splitting bacteria)
- Urinary flow abnormality
- Diet in ‘at risk’ population (Ca+2, oxalate, protein, citrate)

Treatment:
- drink water if small
- blast them with shock waves if big
- surgical removal

32
Q

There are three major types of renal stones

A

About 75% are composed of either calcium oxalate or calcium oxalate mixed with calcium phosphate.

About 15% are composed of magnesium ammonium phosphate (Struvite).
- struvite is a substance that you get when you have repeated infections of bacteria infecting the urine
- the bacteria can split urea, and the byproduct is struvite

Approximately 6 to 8% are either uric acid or cystine stones.

33
Q

Bladder Cancer

A

Also known as: Urothelial Carcinoma

Effects Bladder and urinary tract

Elderly, Caucasian, male

Risk factors:
- Smoking (strongly linked)
- Industrial chemicals

Presentation:
- Blood in urine
- Urinary irritation symptoms

34
Q

Grading of Urothelial Carcinoma

A

Low grade:

  • Papillary
  • Superficial
  • Multifocal
  • Slow growing

High grade:

  • More invasive
  • Aggressive
35
Q

Treatments of Urothelial Carcinoma

A

Local disease:
* Conservative (excise, cauterize etc.)

Advanced disease:
* Removal of bladder and nodes
* Chemotherapy or radiation

36
Q

Urinary Tract Obstruction - Intrinsic and extrinsic causes

A

Strictures and scarring

Stones (Intrinsic)

Tumors

Prostate enlargement

Structural anomalies

37
Q

Urinary Tract Obstruction - symptoms

A

Depends on:

  • Acute vs. chronic
  • Partial vs. complete
  • Unilateral vs. bilateral

Can include

  • Nausea & vomiting
  • Hematuria
  • Pain radiating in the flank area
  • Sharp Sudden and radiating pain.
38
Q

Urinary Tract Obstruction - Complications

A

Proximal dilatation (Hydronephrosis)

Stones

Infection

Inflammation

Scarring & atrophy

39
Q

IgA Nephropathy

A

One of the most common of the primary glomerulopathy

Presents in childhood
- microscopic OR gross hematuria (gross = naked eye)

Develops during infection of mucosal lining

  1. Infection of GI tract or respiratory tract
  2. IgA1 production that is abnormal IgA
  3. Immune complex deposits in Glomerular Mesangium
  4. Inflammation
40
Q

Patients with glomerulopathy can present one of 2 ways

A
  1. Nephritic syndrome
    - inflammation of glomeruli
    - hypertension (high blood pressure)
    - cola-coloured pee (dark pee color aka hematuria)
    - oliguria (decreased urine output)
    - Berger’s disease (IgA nephropathy) is the most common cause of primary glomerulonephritis
  2. Nephrotic syndrome
    - hypoalbuminemia (decreased blood protein)
    - hyperlipidemia (increased lipid production)
    - peripheral edema
    - massive proteinuria (lots of protein in urine, so lose lots of protein)
41
Q

Kidney disease progression in ADPKD

A

Over time, cysts become more numerous and get even bigger
- eventually, there is kidney impairment, then kidney failure

Patients may have pain, hematuria, urinary tract infection, cyst infection, kidney stones

Eventually, dialysis is required

It is autosomal dominant form of inheritance
- so families need to be screened