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)
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
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
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
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
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
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
8
Q
TYPES OF CAUSES OF ACUTE RENAL FAILURE (3)
A
- Prerenal
- Intrarenal
- Postrenal
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
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
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
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
13
Q
TYPES OF CAUSES OF ACUTE RENAL FAILURE: Intrarenal Clinical Manifestations
A
Hypertension
14
Q
TYPES OF CAUSES OF ACUTE RENAL FAILURE: Intrarenal Management
A
- Identification and removal of nephrotoxic agent
- Potentially dieuretics
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
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
17
Q
TYPES OF CAUSES OF ACUTE RENAL FAILURE: Postrenal Management
A
Identification and removal of cause of obstruction
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)
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
20
Q
CHRONIC RENAL FAILURE: CAUSES
A
- Chronic glomerular disease
- Chronic medullary disease
- Diabetes mellitus
- Chronic hypertension
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
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)
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
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
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
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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
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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
