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PCL 412 > Renal System Disorders > Flashcards

Renal System Disorders Flashcards

The kidney and kidney diseases.

1
Q

The kidneys are paired organs located where?

A

Retroperitoneally on either side of the vertebral column.

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2
Q

The renal parenchyma consists of an outer ______ and an inner ______.

A

Outer cortex
Inner medulla

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3
Q

The functional unit of the kidney is the nephron. Each kidney contains approximately how many nephrons?

A

Approximately 1 million.

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4
Q

_________ supply blood to the the kidneys.

A

Renal arteries.

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5
Q

What is the sequence of flow of blood through the kidney?

A

Renal artery > afferent arterioles > glomerulus > efferent arterioles.

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6
Q

Each nephron has:

A
  1. The glomerulus lying within the Bowman’s capsule
  2. Proximal convoluted tubule
  3. Loop of Henle
  4. Distal convoluted tubule
  5. Macula densa in the juxtaglomerular apparatus, situated on the afferent arteriole.
  6. Collecting duct
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7
Q

Each nephron is surrounded by a network of blood vessels called the _______.
What do they do?

A

Vasa recta
They supply a large volume of blood. (25% of Cardiac output ~1300ml/min)

A complex exchange of ions, molecules and waste products exits between the loop of Henle, vasa recta and collecting duct.

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8
Q

The functions of the kidney are classified into 3 main categories, which are:

A
  1. Excretory functions: the kidneys form and concentrate urine for the excretion of waste products such as water, urea, ammonia, uric acid and creatinine.
  2. Endocrine functions
  3. Maintaining homeostasis
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9
Q

The kidneys’ excretory ability is measured by glomerular filtration rate. What are the methods of measuring GFR?

A
  1. Creatinine clearance (Cockroft-Gault equation)
  2. Modification of diet in renal disease (MDRD) equation
  3. CKD epidemiology (CKD-EPI) collaboration equation
    *The above 3 are eGFR methods used in individuals 18 and above.
    *MDRD and CKD-EPI account for age, sex and race.
  4. Bedside Schwartz equation
    *This is used in children.
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10
Q

What are the endocrine functions of the kidney?

A
  1. Renin Angiotensin Aldosterone System (RAAS)
  2. Erythropoietin production
  3. Vitamin D metabolism
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11
Q

Describe the RAAS.

A
  • When the macula densa detects hypotension, hypovolemia, or hyponatremia, it signals the conversion of prorenin into renin by the juxtaglomerular apparatus (Prorenin is cleaved into active renin which is stored as granules in juxtaglomerular cells)
  • Renin release is influenced by sympathetic tone, local prostaglandins and nitric oxide release; these all affect blood pressure.
  • Renin then converts Angiotensinogen, which is of hepatic origin, to Angiotensin I (AT I), which is further converted to Angiotensin II (AT II) by Angiotensin-converting enzyme (ACE- present in lungs and vascular epithelium)
  • AT II binds to Angiotensin receptors located in the heart, lungs, blood vessels, brain, kidney, resulting in rapid powerful vasoconstriction.
    AT II also stimulates the Adrenal Zonal Glomerulosa in the Adrenal cortex to increase aldosterone production leading to Na+ and water retention.
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12
Q

What are the pharmacological agents that block certain points in the RAAS?

A
  1. Renin inhibitors e.g. Aliskiren
  2. ACE inhibitors e.g. Lisinopril, ramipril, perindopril
  3. Angiotensin II receptor blockers (ARBs) e.g. Valsartan, Losartan, Telmisartan, Candesartan
  4. Aldosterone antagonists e.g. Spironolactone
    Eplerenone: they competitively bind to aldosterone receptors in the DCT, preventing reabsorption of Na+Cl- and H20.
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13
Q

What is the function of Erythropoietin?

A

It is responsible for erythropoiesis – RBC production.

It is a glycoprotein produced primarily by fibroblast-like cells in renal interstitium that promotes the formation of RBCs by the bone marrow.

Under hypoxic conditions, EP is produced and binds to erythroid precursor cells (immature cells that give rise to erythrocytes)

Loss of renal function my impact erythropoietin, leading to normocytic, normochromic anemia.

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14
Q

Describe the function of the kidney in vitamin D metabolism, regulation of calcium metabolism and bone mineralisation.

A

The kidneys produce Vitamin D3 1α-hydroxylase, mainly in the DCT and Collecting ducts.
This enzyme activates Vitamin D3 (Cholecalciferol) in the liver to 1,25-dihydrocholecalciferol (1,25-(OH2 D3), which promotes the absorption of calcium and phosphate in the GIT, enhancing bone mineralisation.

In kidney disease, this process becomes impaired, leading to:
- hypocalcemia
- hypophosphatemia
- bone dimineralisation
- increased risk of fracture

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15
Q

Mention 4 homeostatic functions of the kidney.

A
  1. Regulation of electrolytes
  2. pH regulation
  3. Blood pressure regulation
  4. extracellular fluid regulation
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16
Q

What are the investigations of kidney disease?

A

-Examination of the urine
1. Apperance: overt bloody urine in haematuria
2 Volume: In diseases such as CKD and diabetes insipidus, the concentrating ability of the kidney is impaired, leads to passage of increased volumes of urine.
Normal range in temperate regions is 800-2500ml
3. urine pH
4.Gluocosuria
5. Bacteriuria
6. Proteinuria: using Stix testing
7. Microalbuminuria: albumin > 20mcg per minute is an early indicator of diabetic glomerular disease.
8 Specific gravity and osmolality
9. Microscopy

-Examination of blood
1 BUN: increased BUN. Normal range is 20-40mg/dL

  1. Creatinine: increased creatinine levels. Normal range is 1.0-1.2mg/dL
17
Q

Define Acute Kidney Injury (AKI).

A

Acute Kidney Injury is defined as an abrupt (within 48 hours) reduction in kidney function based on an elevation of serum creatinine level with or without a decrease in in urine output, the need for dialysis, or a combination of these factors.

18
Q

What are the manifestations of AKI?

A

The condition is marked by
- increased serum creatinine
- increased BUN
- decreased urine output

However, immediately after AKI, serum creatinine and BUN levels may be normal, and the only sign of AKI may be decreased urine production.

19
Q

Define oliguria and anuria.

A

Oliguria: urine volume of <400mL/day.

Anuria: urine volume of <100mL/day.

20
Q

Name the 2 classification systems for AKI.

A
  1. Acute Kidney Injury Network (AKIN) Classification/Staging System
  2. RIFLE Classification System
21
Q

AKI can be caused by:

A
  • Drugs
  • Diseases
  • Infections e.g. malaria, syphilis, UTIs
  • Obstruction e.g. kidney stones, fibrosis, tumor, bladder neck obstruction.
22
Q

Mention 5 drugs that may cause AKI.

A
  1. NSAIDs e.g. piroxicam, naproxen
  2. Amphotericin B
  3. Calcineurin inhibitors e.g. cyclosporine
  4. Radiocontrast agents
  5. Aminoglycosides e.g. streptomycin, neomycin
23
Q

Mention 4 diseases that can lead to AKI.

A
  1. Malignant hypertension.
  2. Preeclampsia
  3. Liver failure
  4. Renal artery obstruction
24
Q

What are the 2 primary goals of treatment of AKI?

A
  1. To maintain volume homeostasis
  2. To correct biochemical abnormalities.
25
Q

What the measures taken in achieving the primary goals of AKI treatment?

A
  1. Correction of fluid overload - diuretics
  2. Correction of severe acidosis with bicarbonate administration - this can be important as a bridge to dialysis
  3. correction of hyperkalemia:- 5-10 IU of regular insulin and 50% dextrose intravenously can shift K+ out of circulation, into cells
  4. Correction of hematological abnormalities e.g. anemia, uremic platelet dysfunction with measures such as transfusion.
26
Q

What are the therapies used in AKI treatment?

A
  1. Diuretics e.g. Furosemide (Lasix®):- Aid fluid homeostasis and reduce the need for dialysis.
  2. Inotropic agents e.g. Dopamine (Intropin®):- Dopamine in small doses causes selective dilation of renal vasculature, enhancing renal perfusion. It also reduces Na+ absorption, reducing the burden on the damaged tubules
  3. Vasodilators e.g Fenoldopam (Corlopam®):- Decreases systemic vascular resistance and increases renal blood flow to the cortex and medulla. It is 6-times more potent than dopamine in causing vasodilation with minimal adrenergic effects. It is indicated for treatment of severe hypertension in patients with renal compromise.
  4. Calcium Channel Blockers e.g. Nifedipine (Adalat®):- They relax smooth muscles and produce vasodilation, which improves perfusion
  5. Dietary Modifications:- Restriction of salt and fluid is critical in oliguric renal failure.
    Restriction of potassium and phosphorus too may be necessary, as excretion of these electrolytes is not optimal in AKI.
  6. Dialysis.
26
Q

What are the indications for Renal replacement therapy (dialysis) in patients with AKI?

A

i. Volume expansion that cannot be managed with diuretics
ii. Hyperkalemia unresponsive to medical therapy
iii. Sever pH imbalance unresponsive to medical therapy
iv. Severe azotemia
v Uremia

PCL 412 (6 decks)

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