WEEK 3 Flashcards

(64 cards)

1
Q

KIDNEY BACKGROUND

A
  • Maintain stable internal environment for cell/ tissue metabolism→ filter blood and eliminate waste
  • Produce urine; contributes to homeostasis of blood volume
  • Waste products→ metabolites formed during chemical reactions, toxins, excess electrolytes
  • Endocrine function→ secrete hormones→
    Renin (blood pressure)
  • Erythropoietin (erythrocyte production)
    1.25-dihydroxyvitamin D3 (calcium metabolism)
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2
Q

KIDNEY ANATOMY

A
  • 3 distinct sections→ cortex, medulla and pelvis
  • Outer layer of kidney→ cortex
  • Medulla→ inner part of kidney and consists of regions called pyramids (cone shaped structures)
  • Minor and major calyces are chambers that receive urine and form the entry into the renal pelvis
  • The pelvis connects to the ureters for urine to flow into the bladder for storage
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3
Q

NEPHRON

A
  • Functional unit of the kidney (Each kidney has over 1 million nephrons)
  • Units are responsible for producing urine → glomerular filtration and tubular reabsorption and secretion
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4
Q

3 PROCESSES IN THE FORMATION OF URINE

A
  • Glomerular filtration: Filtration of plasma at the glomerulus
  • Tubular reabsorption: Reabsorption of various substances along tubular structures
  • Tubular secretion: Secretion of solutes into the tubules
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5
Q

3 PROCESSES IN THE FORMATION OF URINE: Glomerular filtration: Filtration of plasma at the glomerulus

A
  • Passive process; fluid and solutes (filtrate) move across membrane by hydrostatic pressure
  • Filtrate contains electrolytes (sodium, chloride, potassium) and organic molecules (creatinine, urea, glucose)
  • 2 forces oppose filtration effects of glomerular capillary hydrostatic pressure
    Hydrostatic pressure in the glomerular space
  • Osmotic pressure of the glomerular capillary blood
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6
Q

3 PROCESSES IN THE FORMATION OF URINE: Tubular reabsorption: Reabsorption of various substances along tubular structures

A
  • Filtrate flows into proximal convoluted tubule ready for reabsorption
  • Due to processes such as simple diffusion, facilitated diffusion, active transport, co-transport and osmosis
  • A large amount is reabsorbed back into the blood
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7
Q

3 PROCESSES IN THE FORMATION OF URINE: Tubular secretion: Secretion of solutes into the tubules

A
  • Molecules move into the tubules FROM the peritubular capillaries
  • These are usually metabolism by-products that the body needs to remove
  • Allows for other substances to be secreted AFTER glomerular filtration occurs
  • Unlike glomerular filtration, this secretion process is selective
  • Kidneys are an important organ in eliminating drugs from the body; these drugs are secreted in the tubules to be added to the urinary filtrate
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8
Q

TYPES OF CAUSES OF ACUTE RENAL FAILURE (3)

A
  • Prerenal
  • Intrarenal
  • Postrenal
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9
Q

TYPES OF CAUSES OF ACUTE RENAL FAILURE: Prerenal description

A
  • Problems upstream of kidneys→ alterations in renal blood flow
  • Decreased blood flow to kidneys from
    Trauma/ Major surgery
  • Water loss from blood; dehydration or burns
  • Heart Disease/ Decreased cardiac output
  • Occlusion of small blood vessels in kidney
  • Tubular necrosis can occur→ tubule cells sensitive to hypoxia
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10
Q

TYPES OF CAUSES OF ACUTE RENAL FAILURE: Prerenal clinical manifestations

A
  • Hypotension→ increase blood loss post surgery, severe burns or infection (sepsis) causing vasodilation
  • Tachycardia
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11
Q

TYPES OF CAUSES OF ACUTE RENAL FAILURE: Prerenal management

A
  • Correction of fluid volume deficit
  • Improvement of pump failure using inotropic agents
  • If ischemia is fixed, patient supported on dialysis→ kidney function returns over next weeks
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12
Q

TYPES OF CAUSES OF ACUTE RENAL FAILURE: Intrarenal description

A
  • Associated with damage to kidney tissues
    May occur as result of diseases affecting nephrons
  • Glomerular disease, Medullary disease or Immune hypersensitivity disorders
  • Toxic chemicals
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13
Q

TYPES OF CAUSES OF ACUTE RENAL FAILURE: Intrarenal Clinical Manifestations

A

Hypertension

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14
Q

TYPES OF CAUSES OF ACUTE RENAL FAILURE: Intrarenal Management

A
  • Identification and removal of nephrotoxic agent

- Potentially dieuretics

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15
Q

TYPES OF CAUSES OF ACUTE RENAL FAILURE: Postrenal Description

A
  • Problems downstream of kidneys; obstructions to urine flow
  • Caused by urine flow obstruction from both kidneys, at level of ureters urinary bladder or urethra
    Hypertension (upstream)
  • Damages blood vessels
  • Causes decreased glomerular blood flow
  • Stimulates the secretion of renin
  • Causes further upstream effects → increased BP
  • Ischaemic damage occurs within the kidney
  • Kidney stones
  • Enlargement of the prostate gland impedes the flow of urine in the urethra (downstream)
  • Results in back pressure up the urinary tract
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16
Q

TYPES OF CAUSES OF ACUTE RENAL FAILURE: Postrenal Clinical manifestations

A
  • Hypertension by decreasing GFR
  • Hydronephrosis→ When a kidney swells due to urine failing to properly drain from the kidney to the bladder as a result of a blockage /obstruction in urinary tract
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17
Q

TYPES OF CAUSES OF ACUTE RENAL FAILURE: Postrenal Management

A

Identification and removal of cause of obstruction

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18
Q

TYPES OF CAUSES OF ACUTE RENAL FAILURE: IRRESPECTIVE OF THE CAUSE→ CLINICAL MANIFESTATIONS

A
  • Uraemia→ increased urea
  • Pruritus→ Itching due to waste build up
  • Oliguria or anuria→ little or no urine production
  • Azotaemia→ High levels of nitrogenous compounds (e.g. urea, creatinine)
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19
Q

CHRONIC RENAL FAILURE: DESCRIPTION

A
  • It is the long term progressive and permanent loss of nephrons evident at >80% lost
  • Nephron function is unrecoverable
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20
Q

CHRONIC RENAL FAILURE: CAUSES

A
  • Chronic glomerular disease
  • Chronic medullary disease
  • Diabetes mellitus
  • Chronic hypertension
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21
Q

CHRONIC RENAL FAILURE: MANAGEMENT

A

Management is dependent on reducing or stopping the disease progression

Cardiovascular issues

  • Antihypertensives
  • Erythropoietin injections

Electrolyte issues

  • Low potassium diet for management of hyperkalemia with
  • Phosphate binders for hypocalcemia and hyperphosphatemia

Renal issues
- A low protein diet for proteinuria

Metabolic Issues

  • Dialysis for uraemia and acidosis
  • Sodium bicarbonate for acidosis

Other Issues

  • EMLA cream and ultraviolet- B therapy for pruritus
  • Management of calcium and phosphate levels for restless legs
  • Dialysis→ haemodialysis and peritoneal dialysis
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22
Q

BACTERIAL UTIs: DESCRIPTION

A
  • Kidneys, ureters, bladder, urethra usually sterile→ maintained by frequent flushing action of urine
  • Some resident bacteria exist in the distal urethra (near opening)
  • UTI’s usually caused by bacteria and most arise from patients own bowel flora
  • Pathogenic microbe enters urinary tract→ damages urethra lining→ ascends tract→ enters urinary bladder→ damage to bladder lining→ inflammation (cystitis)
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23
Q

BACTERIAL UTIs: MECHANISMS OF SPREAD

A
  • Haematogenous→ less often, the pathogen may be carried by the bloodstream from a distant focus of infection to the kidney in the bloodstream
  • Ascending→ Most UTIs arise from patients own bowel flora. Bacteria from faeces can enter urinary tract at urethral opening, and ascend to bladder→ sometimes progresses higher up to kidneys
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24
Q

BACTERIAL UTIs: DIAGNOSIS

A
  • Investigations of urine (colour, smell and transparency)
  • Test with a urinary dipstick to determine positive results for blood and nitrate (a characteristic product of bacterial metabolism)
  • A midstream urine (MSU) sample
  • A culture of the urine sample to identify the pathogen and determine its antibiotic sensitivity
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25
BACTERIAL UTIs: MANAGEMENT
- Removal or replacement of the catheter (often resolution of a UTI) - Initial antimicrobial therapy with a broad-spectrum agent - Encouraging fluid intake in order to help flush bacteria - Urinary alkalisers may assist in reducing dysuria - Cranberry as a supplement to reduce the adhesion of bacteria to the epithelial lining of the urinary tract
26
KIDNEY MEDULLARY DISORDER: PYELONEPHRITIS: DESCRIPTION
- An infection and inflammation of the kidney | - Progression to chronic renal failure is inevitable
27
KIDNEY MEDULLARY DISORDER: PYELONEPHRITIS: ACUTE
- An acute inflammation in the renal tubules and the interstitium due to a infectious cause - The infection settles in the renal parenchyma→ Acute inflammation with neutrophils & oedema in the interstitium - Phagocytes and inflammatory exudate move from the blood into the affected area, impeding tubule function. - The papillae of the medullary pyramids may become necrotic
28
KIDNEY MEDULLARY DISORDER: PYELONEPHRITIS: CHRONIC
Repeated infection causes gradual damage and loss of functional kidney tissue which is replaced by scar tissue
29
KIDNEY MEDULLARY DISORDER: PYELONEPHRITIS: CLINICAL MANIFESTATIONS
- Dysuria- painful to urinate, - Frequency and urgency of urination - Flank pain - High fever - Tachycardia
30
KIDNEY MEDULLARY DISORDER: PYELONEPHRITIS: MANAGEMENT
- Antibiotics, Analgesia, Increase their fluid intake (oral/IV) If septic: - Haemodynamic monitoring measure BP and blood flow - Inotropic/catecholamine support - Fluid support
31
KIDNEY MEDULLARY DISORDER: TUBULOINTERSTITIAL NEPHRITIS: DESCRIPTION
An infection and inflammation of the tubules and associated structures of the medulla
32
KIDNEY MEDULLARY DISORDER: TUBULOINTERSTITIAL NEPHRITIS: ACUTE
- A hypersensitivity reaction - Phagocytes and inflammatory exudate move from the blood into the affected area, impeding tubule function - Eosinophils (WBC) play a large role in these hypersensitivity reactions - Can result in acute renal failure
33
KIDNEY MEDULLARY DISORDER: TUBULOINTERSTITIAL NEPHRITIS: CHRONIC
Gradual replacement of functional structures with fibrous scar tissue following repeated episodes of acute inflammation
34
KIDNEY MEDULLARY DISORDER: TUBULOINTERSTITIAL NEPHRITIS: CLINICAL MANIFESTATIONS
- Proteinuria and haematuria - Oliguria - Anuria - Increased haemolysis - Fluid overload→ hypertension, pulmonary oedema - Uraemia (increased urea in blood) - Rash - Anemia→ increased haemolysis and RBC loss
35
KIDNEY MEDULLARY DISORDER: TUBULOINTERSTITIAL NEPHRITIS: MANAGEMENT
- Identify and remove causative substance - Support renal function: Dialysis - Red blood cell transfusion - Antihypertensives
36
DISORDERS AFFECTING THE GLOMERULUS: GLOMERULONEPHRITIS: DESCRIPTION
- Glomerulus becomes actively inflamed - May result from an immune process (Type III hypersensitivity reaction) - Immune complexes build up on basement membrane of blood vessels causing inflammation and damage to tissue Characterised by - Decreased glomerular filtration - Leaky filtration membrane allowing proteins and blood cells through
37
DISORDERS AFFECTING THE GLOMERULUS: GLOMERULONEPHRITIS: CLINICAL MANIFESTATION
- Hypertension (headache) - Oedema (peripheral or pulmonary oedema - Shortness of breath) - Anaemia due to fluid retention which leads to hemodilution - Nausea and vomiting - Anorexia - Oliguria (decreased urine production)
38
DISORDERS AFFECTING THE GLOMERULUS: GLOMERULONEPHRITIS: MANAGEMENT
- Antibiotics - Fluid restriction - Loop diuretics - Antihypertensives - Corticosteroids
39
ACUTE TUBULAR NECROSIS: DESCRIPTION
- Results from chemical damage, immune attack and renal ischaemia - Characterized by destruction of epithelial cells that make up tubule of nephron (very sensitive to hypoxia)
40
ACUTE TUBULAR NECROSIS: CLINICAL MANIFESTATIONS
- Oliguria - Ischaemia due to hypovolemic shock→ may also have hypotension and tachycardia - If ischaemia due to distributive shock→ may also have fever, rash - If disseminated intravascular coagulopathy, may also have→ petechiae, effects of increased blood clotting time and microthrombi
41
ACUTE TUBULAR NECROSIS: MANAGEMENT
- Support of blood volume and pressure - Identification and removal of toxic agent - Diuretics - Haemodialysis - Potassium binding resins - Insulin and glucose infusion - Cessation of further nephrotoxic drugs
42
POLYCYSTIC DISEASE: DESCRIPTION
- Hundreds of cysts develop from nephrons→ expand into tissue; surrounding cells are compressed and die - In time, kidneys may fail- transplant or lifelong dialysis required
43
POLYCYSTIC DISEASE: CLINICAL MANIFESTATIONS
- Hypertension - Enlarged painful abdomen - UTIs - Haematuria - Flank pain - Renal failure - Dry skin - Oedema - Uraemia (raised amount of urea in bloodstream)
44
POLYCYSTIC DISEASE: MANAGEMENT
- Annual renal function tests and ultrasound - Antihypertensive agents- hypertension exacerbates renal failure - Narcotic analgesics- pain relief (AVOID NSAIDS→ risk of nephrotoxicity) - Surgical intervention→ Nephrectomy - Transplant - Dialysis
45
RENAL CELL CARCINOMA
- Originates from epithelial cells of the tubule→ Relatively uncommon but it is an aggressive malignancy - Most common sites→ lymph nodes, bones, lungs - Twice as frequent in men than in women - Clinical manifestations include: haematuria, flank pain, hypertension, weight loss, fever - Management include→ surgery, chemotherapy, immunomodulators (chemical agents that modifies the immune response)
46
BLADDER CANCER
- Usually begins in epithelial lining- urothelium - Major factors→ cigarette smoking, exposure to certain industrial dyes, drugs for treatment of some cancers and autoimmune disorders - May arise as a consequence of chronic bladder inflammation by parasites→ rate of mitosis increases in surviving cells in an attempt to replace lost cells through infection and inflammation→ may lead to spontaneous mutations - Clinical manifestations→ haematuria, dysuria, increased frequency of urination - Diagnosis→ Urinalysis for UTI, X-ray (kidneys, ureters and bladder) Ultrasound - Management→ Surgery- resection of bladder tumour or cystectomy, chemotherapy, Immunomodulation with interferons
47
URINARY CALCULI
- Insoluble stones may form in urinary tract→ usually in renal pelvis, as ions precipitate from solution in urine - Major component of kidney stones is calcium→ Hypercalciuria increases risk - Small stones may be asymptomatic, larger stones→ cause urinary tract obstruction and damage - Causes intense pain that originates at the ureter and often radiates considerable distances - Clinical manifestations→ haematuria, fever, chills, bad smelling or cloudy urine, dysuria (burning feeling on urination)
48
TYPES OF STONES: Calcium stones
- Most common (70-80%) - Usually calcium oxalate or calcium phosphate - Increased calcium, bone disease, hyperparathyroidism
49
TYPES OF STONES: Magnesium ammonium phosphate stones (Struvite stones)
- Usually referred to as staghorn stones and associated with UTIs - Bacteria break urea into ammonia and carbon dioxide - Ammonia then takes up hydrogen ion increasing urine pH
50
TYPES OF STONES: Uric acid stones
- Small in structure - Develop in gout and form in urine with pH 5.1-5.9 - Thus can be treated by raising pH to 6 to 6.5 with potassium alkali salts
51
TYPES OF STONES: Cystine stones
- Cystinuria→ rare and result from genetic disease in renal transport of cystine - Autosomal recessive disease
52
MECHANISMS OF FORMATION: Saturation Theory
- Urine is supersaturated with stone components | - Greater the concentration of two ions; more likely for precipitation to occur (e.g. calcium or sodium oxalate)
53
MECHANISMS OF FORMATION: Matrix Theory
- Mucopolysaccharides derived from epithelial cells that line the tubules act as a nidus for stone formation - Unsure to whether material contributes to initiation of stone formation or is merely entrapped in stone
54
MECHANISMS OF FORMATION: Inhibitor Theory
- Persons have a deficiency of substances that inhibit stone formation - E.g. urinary citrate which stops calcium oxalate crystal forming
55
MECHANISMS OF FORMATION: Decrease levels of chelators (e.g. citrate)
- Form complexes with soluble ions and in so doing inhibi nuclei formation and thus renal calculi formation
56
TREATMENT FOR RENAL CALCULI
- Prompt removal may be required→ Reasons include; - Taking too long for the calculus to redissolve/reduce in size; pain has become unmanageable - Calculus is judged to be too large to rely upon solubilisation for its removal - The calculus is lodged in a part of urinary system where it is recalcitrant to becoming dislodged - The person cannot urinate - A UTI develops - The calculus is lodged such that there is damage to the kidney and/or persistent blood loss - Over time, the calculus is increasing in size - Previously removal by open surgery with a four to six week recovery period→ nowadays less invasive and even non-invasive alternatives are available - Extracorporeal shock wave lithotripsy (ESWL) - Device delivering acoustic shock waves outside the body that can travel to site of the calculi and cause them to shatter - Sometimes the ureter will be stented to aid the fragments passing out the body - Percutaneous Nephrolithotomy→ Key hole surgery; incision in patients back, probe inserted to break up calculus into smaller fragments before removal - Ureteroscopic stone removal→ cystoscopy inserted into ureter to locate sone; cage like tool then traps stone and draws out calculus to shatter the stone
57
HYDRONEPHROSIS
- Swelling of the kidney from inability of urine to drain from the kidney into the bladder - Enlarged kidney; Ureter is obstructed and renal pelvis and calyx are distended
58
STAGHORN CALCULI
Calculi have grown and moulded into the renal pelvis and calyces to resemble the antlers of a stag
59
DIABETIC GLOMERULOSCLEROSIS
- Damages blood vessels, impedes glomerular filtration and causes ischaemic damage to medulla and cortex - Results in loss of protein (albumin) leading to hypoalbuminemia - Increased extracellular deposits inside the renal corpuscle, with decreased surface area available for filtration - Thickening of the glomerular capillary wall injured by diabetes
60
FILTRATION MEMBRANE: DESCRIPTION
- Endothelial cells→ stop all cells and platelets - Basement membrane→ stops large plasma proteins based on size (MW >69,000- collagen and lamina) Also contains heparin sulphate which excludes particles based on charge - Podocytes→ stop medium sized proteins, not small ones
61
FILTRATION MEMBRANE: DIAGNOSIS
- Full blood count and electrolyte levels - Renal function and liver function tests - Urinalysis- haematuria - WBVs - Poteinuria. Imaging studies→ Ultrasound, MRI
62
FILTRATION MEMBRANE: MANAGEMENT
- Aims to reduce progression of disease or stopping its progression if possible Systemic issues - Antihypertensive agents→ controls hypertension - Erythropoietin injections- management of anaemia Electrolyte issues - Low potassium diet→ for hyperkalemia - Control hypocalcemia and hyperphosphatemia with phosphate binders (e.g. aluminium hydroxide, magnesium hydroxide and simethicone) - Low protein diet to decrease proteinuria so as to decrease catabolism - Dialysis→ can manage the uraemia - Sodium bicarbonate will also also assist with the acidosis - Antiemetic agents to control nausea and vomiting
63
HYPOALBUMINEMIA (Albumin in blood is too low)
- Proteinuria contributes to nephron damage, hypoalbuminemia leading to oedema In glomerulosclerosis - Basement membrane of the glomerulus becomes thicker→ but→ - More permeable to proteins as it loses its negative change→ as a result→ - Large amounts of plasma protein are lost in the urine (proteinuria) → and→ - Protein level in the blood falls (hypoalbuminaemia) to a much greater extent than in glomerulonephritis In Nephrotic Syndrome - Increased susceptibility to infection→ As antibodies and complement proteins are lost in the urine - Hyperlipidaemia→ as the liver exports large amounts of lipoproteins to the blood in an attempt to compensate for lost plasma protein
64
HYPERTENSION AND THE NEPHRON
- Small blood vessels become damaged over time in hypertension - The consequence for the nephron is always: - Decreased blood flow through the glomerulus→ in the long term - Ischaemia will damage the nephron→ more immediately - When the juxtaglomerular apparatus senses the decrease in blood flow→ it will→ - Secrete renin, which will cause blood pressure to rise - A cycle of worsening hypertension and increased kidney damage will develop