Urinary Flashcards
(112 cards)
1
Q
What is the position in the body of the Kidneys?
A
They are Retroperitoneal organs. Left Kidney runs from T11-L2, Right Kidney runs from T12-L3. Lower due to the presence of the Liver on the right side of the body.
2
Q
What are the 4 layers of External protection the kidney has?
A
- Pararenal Fat (Posterior Kidney)
- Renal Fascia (Encloses Kidney + Adrenal Glands)
- Perirenal Fat
- Renal Capsule (Tough Fibrous layer)
3
Q
Describe the Drainage of the kidney
A
Drains through the pyramids into the Calyx, a few of these merge to form Major Calyx, a few Major Calyx form the Renal Pelvis. It then drains to the bladder via the ureters through the renal hilum
4
Q
Describe the Arterial Supply of the Kidneys
A
Renal arteries enter through the renal Hilum, divides into segmental arteries which divide further to interlobar which run along either side of each of the pyramids. Theses divide further into the Arcuate artery which divide further to form interlobular arteries. These divide finally to form Afferent arterioles
5
Q
Whats the difference in the path of the Ureters in Males + Females?
A
- In females they pass under the uterine arteries
- In men they pass under the Vas Deferens
6
Q
At what point are you most likely to get stones lodges in the Ureters?
A
In the Uteropelvic junction, Pelvic brim where it enters the pelvis, Entrance to the bladder
7
Q
What is the blood supply of the Ureters?
A
Branches of common + internal iliac arteries and uterine arteries
8
Q
What are the main structures of the Bladder?
A
- Apex - Located superiorly pointing towards the pubic symphysis, anchored by the median umbilical ligament
- Body - The main part of the bladder located between the apex + Fundus
- Fundus/Trigone - triangular shape between two ureters + Urethra
9
Q
What is the main muscle of the Bladder?
A
Detrusor muscle
10
Q
Whats the difference between Urinary Sphincters in males + females?
A
Both sexes have an External Urethral Sphincter under voluntary control. Males have an Internal Urethral Sphincter under autonomic control to prevent seminal regurgitation
11
Q
Describe the male Urethra + the 4 parts its divided up into
A
Approximately 15-20cm long
- Pre-Prostatic - Begins at the internal urethral orifice at neck of the bladder + ends at the Prostate
- Prostatic - Passes through the Prostate gland, the ejaculatory ducts and prostatic ducts drain here
- Membranous - Passes through the pelvic floor + deep perineal pouch, its surrounded by the external urethral sphincter.
- Spongy - Passes through the bulb + corpus spongiosum of the penis ending at the external urethral orifice
12
Q
What is the Cloaca?
A
The common cavity at the end of the digestive tract
13
Q
Describe the development of the kidney with the 3 kidney systems
A
- Pronephros - Never functional in humans, Pronephric duct extends from cervicle region to the Cloaca. It drives development of Mesonephros
- Mesonephros - The Mesonephric tubules + Mesonephric duct make up the embryonic kidney. Mesonephric duct sprouts the Ureteric bud which induces the development of the definitive kidney.
- Metanephros - Ureteric bud induces development of definitive kidney within intermediate mesoderm. Ureteric bud contacts mesanephric blastema + expands and branches producing the minor + major calyx’s
14
Q
Describe the ascent of the Kidney
A
It first appears in the pelvic region + undergoes a caudal to cranial shift crossing the arterial fork formed by vessels returning blood from the foetus to the placenta. As it ascends it creates new blood supplies + looses the lower ones, this is why you can have extra blood supplies to the kidney
15
Q
What can go wrong with the ascension of the Kidney?
A
- Renal Agenesis - Ureteric bud fails to interact with the mesoderm intermediate and kidney fails to form
- Splitting of Ureteric bud - This can produce extra lobes in the kidney or extra urethral openings, if these are bencher the external sphincter of bladder can cause incontinence
- Multi-cystic Kidney disease - Atresia (narrowing) of ureter prevents it from functioning correctly causing spontaneous abortion due to lack of amniotic fluid
- Horseshoe Kidney - This happens if two kidneys become to close together during the ascent, they become fused and get stuck under the Inferior Mesenteric Artery
16
Q
What are the two different types of Nephron and whats the difference between them?
A
- Cortical Nephrons - 90% of nephrons. Located in outer cortex with shorter Loop of Henle + small glomerulus
- Juxtamedullary Nephrons - Located on edge of cortex next to the Medulla. They have large Glomeruli + long Loop of Henle. Efferent arteriole leads to Vasa Recta which runs countercurrent along side of loop of Henle
17
Q
What 3 layers makes up the Filtration Barrier?
A
- Capillary Endothelium - Permeable to Water, Salts + Glucose
- Basement Membrane - Acellular gelatinous layer of collagen + glycoproteins. It is permeable to small proteins however the glycoproteins are negatively charged which glee’s to repel the movement of proteins
- Podocyte layer - Pseudopodia interdigitate to form Filtration Slits (Slit Diaphragms), this layer is Permselective which means it filters on size
18
Q
How does the body maintain a normal Glomerular filtration rate at different blood pressures?
A
Auto regulation using the contraction + relaxation of Afferent + Efferent arterioles
19
Q
What is Tubular Glomerular Feedback? What chemicals are released to induce vasoconstriction + vasodilation?
A
The distal tubule lies between the Afferent + Efferent Arterioles. An increase in arterial pressure results in an increased glomerular capillary pressure and an increased GFR. Increased GFR leads to increase in Na + Cl ions conc. in the DT. Macula Densa cells in the DT detect the rise in Cl via conc. dependant salt uptake through the NaK2Cl co-transporter. This then stimulates the Juxtaglomerular apparatus to release chemicals.
- Adenosine is released to promote Vasoconstriction
- Prostaglandins are released to promote Vasodilation
20
Q
What has been reabsorbed by the end of the Proximal Convoluted Tubule?
A
- 100% Filtered nutrients
- 67% Filtered Na+
- 65% Filtered Water, Cl, K
21
Q
Describe the Co-transport of Glucose into the Proximal Convoluted Tubule
A
Na-K ATPase on basolateral membrane pumps Na into interstitial space to create Na gradient. 2 Na ions + 1 Glucose molecule are transported into tubular cell against the Glucose concentration gradient by the Sodium Glucose Transporter SGLUT. Glucose leaves the tubular cell on the basolateral side by facilitated diffusion
22
Q
Describe the secretion of Organic Cations
A
Na/K ATPase pumps Na out of the basolateral membrane producing an electrochemical gradient which allows positive OC’s to diffuse in down their concentration gradient. Na/H anti porter on luminal membrane pumps H+ into the lumen driven by the low Na in the cell. OC’s are then secreted into the lumen by the H-OC exchanger.
23
Q
Give some examples of important Cations + Anions
A
- Cations (Ach, Dopamine, Adrenaline, Histamine, Morphine, Atropine, Sulphonamides)
- Anions (Urate, Bile salts, Penicillin, NSAIDs)
24
Q
What is Renal Clearance?
A
Renal clearance of a substance is the volume of plasma that is completely cleaned of a substance by the kidney per minute.
25
What sort of substance do you need to calculate GFR? What is the gold standard to measure GFR? What can be used as a replacement + why is it not as good?
- Freely filtered, Non Secreting, Non Reabsorbed
- Inulin is best to calculate accurately
- Creatinine can be used but is slightly secreted so produces an overestimate
26
What is Filtered Load? How is it calculated?
- Amount of a substance that is freely filtered that enters the renal tubule over a given amount of time
- Plasma concentration x GFR
27
What is Renal Threshold?
Plasma concentration where Transport maximum is reached and substance begins to spill into the urine
28
What 4 main things control medium + long term BP?
1. Renin Angiotensin Aldosterone System - Renin is released from Granular cells of the Juxtaglomerular apparatus, the release is stimulated by; Reduced NaCl delivery to the DT, Reduced perfusion detected by baroreceptors in the afferent arteriole, Sympathetic stimulation to the juxtaglomerular apparatus.
2. Sympathetic Nervous System - High levels of Sympathetic Innervation causes constriction of the arterioles reducing GFR. Activates Na/H exchanger on apical membrane of the PCT + increases activity of Na/K ATPase increasing Na reabsorption. Stimulates the release of Renin from Juxtaglomerular apparatus.
3. Antidiuretic Hormone (ADH) - Increases presence of Aquaporin channels in the collecting duct to increase water absorption. Stimulates Na reabsorption by stimulating Na/K/Cl co-transporter. The release of ADH is stimulated by an increase in plasma osmolarity or in cases of severe Hypovolaemia.
4. Atrial Natriuretic Peptides - Cause vasodilation of Afferent arteriole which increases GFR, also inhibits the reabsorption of Na along the nephron. They are synthesised + stored in atrial myocytes + released in response to stretch. Low pressure sensors means that with less stretch you have less released.
29
Describe the Activation of Angiotensinogen
Angiotensinogen --(Renin)--> Angiotensin I --(Angiotensin Converting Enzyme)--> Angiotensin II
30
What are the affects of Angiotensin II?
- Vasoconstriction of arterioles
- Stimulates Na reabsorption in the kidney (Stimulates Na/H exchanger in the apical membrane of PCT)
- Increased release of NA in the sympathetic nervous system
- Stimulates the release of Aldosterone
- Increases thirst sensation
31
What affect does Aldosterone have on the Kidney?
Acts on principal cells of the collecting duct. Activates Epithelial Na channels (ENaC), apical K+ channels + increases the basolateral Na extrusion via Na/K ATPase. This increases the reabsorption of Na + water
32
Other than the conversion of Angiotensin I to Angiotensin II how does ACE help to increase BP?
Breaks down Bradykinin which is a vasodilator so reduction of the presence of Bradykinin causes an increase in the Vasoconstriction effect
33
Why are Prostaglandins important in the kidney?
Act as vasodilators, important as they act as a buffer to excessive vasoconstriction caused by the sympathetic nervous system + RAAS. They enhance GFR and reduce reabsorption of Na
34
How can NSAID's be dangerous to the Kidney?
Inhibit the production of prostaglandins. Administration of these drugs when renal perfusion is compromised can further reduce GFR which can lead to Acute Renal Failure
35
What is the difference between Primary + Secondary Hypertension?
- Primary is when there is no definable source of hypertension. This accounts for 95% of primary hypertension
- Secondary is when there is a clear cause for the hypertension that can be treated
36
Give 3 main causes of Secondary Hypertension
1. Reno-vascular Disease - Occlusion of the renal artery causes a fall in renal perfusion. This leads to increased Renin production and activation of RAAS to increase Na retention
2. Renal Parenchymal Disease - Damage to the parenchymal cells, at early stages of hypertension may be due to a loss of the vasodilator substances Dopamine + Prostaglandins. Later due to reduced GFR
3. Adrenal causes
- Conn's Syndrome (Aldosterone secreting Adenoma - causes hypertension + Hypokalaemia)
- Cushing's Syndrome (Excess secretion of Glucocorticoid Cortisol acts on aldosterone receptors)
- Phaeochromocytoma (Tumour of adrenal medulla causing secretion of catecholamines Adrenalin + NA)
37
What are the 4 main pharmacological treatments for Hypertension?
1. Targeting RAAS - ACE Inhibitors prevent production of Angiotensin II, Angiotensin II receptor antagonists
2. Diuretics
3. Vasodilators - L-type Ca Channel blockers - Reduce Ca entry to vascular smooth muscle cells causing relaxation, α1 receptor blockers - reduce sympathetic tone causing relaxation
4. β Blockers - Blocking β1 receptors reduces effects of sympathetic output of the heart reducing HR + contractility
38
How is salt intake described?
Hedonistic Appetite (Regulatory appetite), a deficiency drives a need for it
39
Describe the affect of ADH
Causes vasoconstriction of arterioles. Increases Na, K + Cl absorption in the thick ascending limb, this produces a hypo-osmotic solution at the top of the ascending limb which increases absorption in the collecting tubule. In cortical collecting duct water reabsorption is increased as is K+ secreting. In medullary CD water + urea reabsorption increases
40
Describe how changes in blood pressure + volume effect how the body deals with changes in Osmolarity. Why is this?
- Reduced extra cellular volume - Set point for osmolarity is set to be lower, so even if you have a low osmolarity the body will continue to absorb H2O to prevent circulatory collapse.
- High BP - Set point is shifted to a higher osmolarity so less ADH is secreted even at high osmolarity.
The shifts in set point are because the blood volume is more important than osmolarity
41
What problems can there be with ADH secretion?
- Diabetes Insipidus - Where the pituitary gland doesn't produce enough ADH or there is an acquired insensitivity of the kidney to ADH. Due to the low amount of ADH water isn't adequately reabsorbed so large amounts of ruin is produced
- Syndrome of Inappropriate ADH Secretion (SIADH) - This is characterised by excessive release of ADH from the posterior pituitary gland or another source. This causes Hyponatremia (Low Na) due to increased secretion (ADH works on DCT + CD to retain water but not solute) + increase in total bodily fluid due to low secretion of water
42
What is an effective osmole?
Molecule that doesn't diffuse across the membrane easily _ doesn't have any transporters that easily transport it from one side of the membrane to the other
43
How is the Counter Current Gradient produced? How is it maintained? Describe the involvement of the Vasa Recta
- Ascending Limb is impermeable to water but permeable to NaCl + Urea. As urea is high conc. in interstitium it means Na + Cl can leave into medulla as urea enters (Urea then reabsorbed from the medullary collecting duct) Na is being pumped out of the ascending limb which raises the oncotic pressure outside + lowers it inside.
- Water flows out of the descending limb down the osmotic gradient raising oncotic pressure inside the tubule.
- Fresh fluid enters glomerulus pushing conc. fluid round into ascending limb where Na is pumped out into interstitium again.
- By the 3rd round the interstitial conc. is 700mOsm/L
- Its produced by the Loop of Henle but is maintained by the Vasa Recta which acts as a counter current multiplier.
- Descending limb of Vasa Recta - Blood is initially isosmotic. It runs past the Ascending limb where the interstitial conc. of Na, Cl + Urea is V. high. These diffuse into the Vasa Recta increasing the osmolarity.
- Ascending limb of Vasa Recta - Initially has a V. high osmolarity due to the high conc. of Na, Cl + urea. Due to the high osmolarity water flows in from the descending limb of the Loop of Henle.
44
Where is Calcium reabsorbed in the Kidney?
98% is reabsorbed
- 65% in proximal tubule coupled with Na + water
- 20% in ascending loop of Henle
- 15% in DCT
45
How is Vitamin D used in the body? How does Parathyroid Hormone affect calcium levels?
- It has a short half life so is converted to Calciferol in the liver to extend it. PTH (Parathyroid Hormone) regulates the conversion to its active form Calcitriol. Calcitriol works by binding Calcium in the gut to increase its absorption.
- PTH can increase release of Calcium from bone + increase its absorption in the PCT of the kidney. It also decreases the reabsorption of phosphate + bicarbonate as if they are in the blood Calcium stones will form
46
How does Calcitonin work?
Rises in plasma Ca2+ promotes secretion of Calcitonin. Causes a rapid fall in Calcium levels by preventing the resorption of bone + inhibiting renal reabsorption of Calcium allowing it to be secreted in urine
47
What can cause Hypercalcaemia? What are the Symptoms? How is it Managed?
- Hypercalcaemia of Malignancy - This comes from the production of Parathyroid hormone-related peptide. Due to having a similar structure it works as PTH and increases plasma conc. of Ca2+
- Primary Hyperparathyroidism (Usually caused by a tumour in the parathyroid gland)
- Haematological + Non-Haematological malignancies
Symptoms
- GI (Anorexia, Nausea/Vomiting, Constipation, Acute Pancreatitis), CVS (Shortened QT segment, Enhanced sensitivity to Digoxin [used to slow HR]), Renal (Polyuria, Polydipsia, Nephrocalcinosis), CNS (Cognitive difficulties, Depression, Drowsiness, Coma)
Management
- General Measures - Hydration, Loop Diuretics. Both of these increase secretion.
- Specific Measures - Bisphosphonates (Prevents breakdown of bone), Calcitonin (Opposes the action of PTH)
48
What is Alkalemia (Alkalosis)? What can it cause + how?
Alkalemia is when the pH of the blood rises above a pH of 7.45. As less H+ ions bind to albumin there is increased room for binding of Ca2+ so there is less free Calcium. This increases neuronal excitability, if pH>7.45 it can lead to paraesthesia + tetany. If pH rises to 7.55 there is a 45% mortality rate, 80% mortality rate at a pH of 7.65
49
What is Acidemia (Acidosis)? What can it cause + how?
Acidosis is when the pH of the blood falls below 7.35. The excess H+ ions are buffered inside cells by the exchange of K+ ions into the extracellular fluid. The high K+ effects excitability especially in the cardiac muscle causing arrhythmias. Increasing H+ denatures proteins which disturbs enzymes, affects contractility of muscles. Effects are severe below pH 7.1 + life threatening below a pH of 7.0
50
What is Metabolic Acidosis?
Metabolic acidosis is a fall in pH due to a fall in [HCO3-]. Acid produced in tissues reacts with HCO3 to produce H2) and CO2 which can be blown off at the lungs. Metabolic acidosis can be compensated for by increasing the respiratory rate. Peripheral chemoreceptors detect the changes in plasma pH and Respiratory neurones in the medulla are stimulated causing an increase in ventilation
51
What is Metabolic Alkalosis? How can it be caused?
Rise in [HCO3-] causes a rise in plasma pH.
| Can be caused by repeated vomiting.
52
How is HCO3 made in the Kidney?
Kidneys have a high metabolic rate so produce lots of CO2, this is reacted with water to produce HCO3- and H+. H+ is pumped into the urine and HCO3- enters the blood. It can also produce it from amino acids which produces NH4+ which enters the urine
53
How is HCO3- recovered from the Kidney?
- Na moves into the cell from the lumen down the concentration gradient created by the Na/K ATPase through the Na/H exchanger pumping H+ into the lumen.
- H+ in the lumen reacts with HCO3- to produce CO2
- CO2 moves freely into the cell + reacts with water to become HCO3- again
- HCO3 moves across the basolateral membrane through the Na/HCO3 co-transporter
54
How can HCO3 be produced in the Proximal Convoluted Tubule?
Glutamine is metabolised to α-ketogluterate to produce HCO3 + NH4+
55
What happens to the Na gradient in the Distal Tubule? How can the urine be buffered if the pH is too low?
Na gradient is no longer strong enough to drive the secretion of H+ so it is actively secreted through H+ ATPase. If the pH of the urine is to low it can cause damage to the cells. It combines with NH3 to form NH4+, as its now charged it can't diffuse back out of the lumen. It can also be combined with HPO4(2-) to form H2PO4-.
56
Whats the Intracellular + Extracellular concentration of K+?
```
Intracellular = 120-150mmol
Extracellular = 3.5-5mmol
```
57
How does K+ get in and out of cells? What factors can increase the uptake into cells?
- Movement into the cell is mediated by Na/K ATPase
- Movement out of the cell is mediated by K+ channels (ROMK)
- Factors that increase the uptake of K+; Hormones act on Na/K ATPase (Insulin, Aldosterone, Catecholamines), Increased K+ conc. in ECF, Alkalosis (Low conc. of H+ in ECF, H+ moves out of cell and K+ moves in)
58
What factors promote the movement of K+ out of the cell?
- Exercise - Skeletal muscle contraction causes the net movement of K+ out of the cell during recovery phase of the action potential. Uptake of K+ from non contracting cells helps to offset the increase. Exercise + trauma also cause the release of Catecholamines which cause increase in Na/K ATPase
- Cell Lysis - Trauma to skeletal muscle causing cell necrosis (Rhabdomyolysis). Cancer chemo causing tumour cell lysis. The break down of cells causes release of K+ into ECF
- Increased Tonicity - Increase in plasma + ECF tonicity causes water to leave cell into ECF which increases [K+] so it leaves cell down its concentration gradient. This is relevant in Diabetic Ketoacidosis as the high level of glucose increases tonicity.
59
How is Potassium handled by the Kidney?
K+ is freely filtered at the Glomerulus. K+ is then reabsorbed in the PCT + Loop of Henle.
Its secreted from the Distal Tubule + Cortical Collecting Duct.
60
How do Principal cells of the Collecting duct effect K+?
They secrete K+.
- Increased ECF [K+] directly stimulates Na/K ATPase + increases permeability of apical membrane to K+. Also causes secretion of Aldosterone (Increases transcription of ENaC, K+ Channels + Na/K ATPase)
- Na/K ATPase increases the intracellular [K+] and decreases [Na+]
- Na diffuses down conc. gradient into cell producing electrical gradient
- K+ then moves down the electrical + chemical gradient into the lumen
61
What can cause Hyperkalaemia?
- Increased intake - This can only cause Hyperkalaemia if there is renal dysfunction unless its given in to high concentration IV
- Decreased Renal Excretion - Acute/Chronic Kidney injury. Normal kidneys on drugs which block K+ secretion (ACE Inhibitors, K+ Sparing diuretics), Patients in a low aldosterone state.
- Diabetic Ketoacidosis (No insulin so reduced K+ Absorption + Increased glucose causes hyperosmolarity
- Cell Lysis
- Metabolic Acidosis
62
What can Hyperkalaemia cause?
- Depolarisation of cardiac tissue so more fast Na channels remain in active form so the heart is less excitable which produces heart block + arrhythmias
- Neuromuscular dysfunction can lead to paralytic Ileus (Intestinal Blockage)
- Acidosis
63
What changes would you see on the ECG of a patient at varying levels of K+?
- 4-5mEq/L (Normal)
- 7mEq/L (High T wave)
- 8mEq/L (Prolonged PR interval, Depressed AT segment, High T wave)
- 9mEq/L (Atrial Stand still, Intraventricular block)
- 10mEq/L (Ventricular Fibrillation)
64
What is the Emergency Treatment of Hyperkalaemia?
1. Reduce K+ effect on the heart with IV Calcium Gluconate
2. Shift K+ into cells with IV Insulin + Nebulised β-antagonists (Salbutamol)
3. Remove excess K+ (Dialysis)
65
What host factors contribute to UTI's?
- Shorter Urethra in females
- Obstruction (Enlarged Prostate, Pregnancy, Stones, Tumours) causes reduced clearance which increases infection rates
- Neurological - Incomplete emptying
- Uteric Reflux - Causes ascending infection from bladder (Pyelonephritis), especially in children
66
What bacterial factors contribute to UTI's?
- Faecal flora - colonise Periurethral area
- Adhesion - Fimbriae + adhesins allow attachment to urethral + bladder epithelium
- K Antigen - Allows some E. coli to resist host defences by producing a polysaccharide capsule
- Haemolysins - damage membranes + cause renal damage
- Urease - allows some bacteria to break down urea for energy
67
What different types of Lower UTI's are there? What are their symptoms?
- Bacterial cystitis (Polyuria, Dysuria, Pyuria, Haematuria)
- Abacterial cystitis (Same as above without Bacteriuria)
- Prostatitis - Inflammation of prostate gland (Polyuria, Fever, Dysuria, Perineal pain, Lower back pain)
68
What different types of Upper UTI's are there? What are their symptoms?
- Acute Pyelonephritis Bacterial invasion of the renal parenchyma, this is a life or organ threatening infection (Symptoms of cystitis with Fever + Loin to Groin pain)
- Chronic Interstitial Nephritis - Renal failure caused by inflammation of the interstitium of the kidney surrounding the tubules. Commonly caused by infection (Normally asymptomatic)
69
What is an Uncomplicated UTI and how would it be investigated? How is it treated?
- A UTI in a healthy woman
- No need to culture urine in uncomplicated UTI's, infection is indicated by Nitrite + Leucocyte Esterase dipstick testing. Nitrite indicates presence of of Nitrite reducing bacteria. Leukocyte Esterase shows presence of WBC's.
- Treated with 3 day course of antibiotics, 3 days to reduce selection pressure for antibiotic resistance
70
What is a Complicated UTI and how would it be investigated? How is it treated?
- A UTI in Pregnancy, Treatment failure, Suspected Pyelonephritis, Children or Men
- Mid stream urine sample collected, so you don't get normal flora. Adhesive bag can be used for children. Catheter samples can be taken by a needle up the catheter. Supra-pubic aspiration can be used to get a sample through the abdominal wall.
- Treated with 7 day course of antibiotics, Amoxicillin is not used as 50% of causes are resistant
71
How are Urine samples transported and why?
At 4 degrees with a little Boric acid in the collection tube to prevent bacterial division to keep a representative sample
72
When is Microscopy used to investigate UTI's?
- Kidney disease (Loin pain, Nephritis, Hypertension, Toxaemia, Renal Colic, Haematuria, Renal TB, Casts)
- Suspected Endocarditis
- Children under 6
- Schistosomiasis
73
What is Sterile Pyuria and what can cause it?
UTI present but can't be cultured for some reason. Can be caused by;
- Patient has already been treated with antibiotics
- Bacteria that are difficult to culture (Chlamydia)
- Due to TB
- Appendicitis
74
How is Pyelonephritis treated?
14 day course of antibiotics with a more potent agent with systemic activity
75
What is an Example of a Loop Diuretic? How does it work?
- Furosemide, Bumetanide
| - Block the NKCC2 (Na-K-2Cl Symporter) preventing the uptake of Na, K + Cl and therefor water
76
What is an example of a Thiazide Diuretic? How does it work?
- Bendroflumethiazide
- Works on the early Distal Convoluted Tubule. Less effective than Loop diuretics + ineffective in treating kidney failure. Work by blocking the Na-Cl symporter
77
What is an example of a K+ Sparing Diuretic and an Aldosterone Antagonist? How do they work?
- Amiloride + Spironolactone
- Both act on the late Distal Convoluted Tubule to reduce sodium channel activity by blocking Aldosterone or directly block ENaC. Both are K+ sparing and can produce life threatening Hyperkalaemia
78
Describe the normal voiding reflex of the bladder
Brain Micturition Centres -> Spinal Micturition Centres -> Parasympathetic neurones (Increase in Parasympathetic innervation via Pelvic Nerve causes the detrusor muscle to contract causing an increase in intravascular pressure). Cerebral cortex makes a conscious decision to urinate reducing the somatic stimulation the the external sphincter.
79
Describe the storage of large volumes of urine
At 400ml afferent neurons begin to signal the need to void the bladder. Brain Continence Centres -> Spinal Continence Centres -> Sympathetic Neurones (Increase in sympathetic stimulation to the bladder via the hypogastric nerve causes the Detrusor to relax + Internal urethral sphincter to contract reducing intravascular pressure). Cerebral cortex makes executive decision not to urinate increasing somatic stimulation to external urethral sphincter
80
What are the 4 types of Incontinence?
- Stress Urinary Incontinence (Involuntary leakage on effort or exertion, sneezing or coughing)
- Urge Urinary Incontinence (Involuntary Leakage accompanied or immediately proceeded by urgency)
- Mixed Urinary Incontinence (Leakage associated with urgency + Exertion, effort, sneezing or coughing)
- Overflow Incontinence (Retention of urine causing bladder to swell, can be low pressure + pain free)
81
What is the specific treatment for Stress Incontinence?
Pelvic floor training
82
What is the specific treatment for Urge urinary incontinence?
Bladder training - Void every hour during the day
83
What surgical management is available for females with Incontinence?
- Low tension vaginal tapes, support mid urethra with polypropylene mesh
- Open retropubic suspension procedure to correct the anatomical position of the proximal urethra
- Classic fascial sling procedure to support urethra and increase bladder outflow resistance
- Intramural bulking agents injected to increase the ability of the urethra to resist abdominal pressure
84
What surgical management is available for males with Incontinence?
- Artificial Urinary Sphincter - Mechanical devise which stimulates the action of a normal sphincter. Problems with Infection, erosion + devise failure
- Male sling procedure - Corrects Stress urinary incontinence which is usually caused by surgery somehow. Experimental using bone tape
85
What is Acute Kidney Injury?
Rapid Deterioration of renal function resulting in inability to maintain fluid, electrolyte + acid-base balance
86
What is Oliguria + Anuria?
```
Oliguria = Less than 500ml of urine a day
Anuria = Less than 100ml of urine a day
```
87
What is Pre-Renal AKI? What can it be caused by?
- Decreased Renal perfusion leading to Acute Tubular Necrosis unless its recognised + treated
- Causes of reduced perfusion include; Reduced effective extra cellular fluid volume (Hypovolaemia, Systemic Vasodilation, Cardiac Failure), Impaired Renal Auto-regulation (Preglomerular Vasoconstriction {Sepsis, NSAIDS, Hypercalcaemia}, Postglomerular {ACE inhibitors, Angiotensin II antagonists})
88
What is Post-Renal AKI? What can it be caused by?
- Indicates an obstruction to urine flow after the urine has left the tubules. Obstruction can occur in the Ureters, Bladder or Urethra
- Obstructions can be classified into; Within the lumen (Calculi, Blood clot, Papillary Necrosis, Tumour of renal pelvis ureter or bladder), Within the Wall (Pelvic Neuromuscular Dysfunction, Megaureter, Neurogenic Bladder, Ureteric Stricture), Pressure from outside (Prostatic Hypertrophy, Malignancy, Aortic Aneurism, Diverticulitis, Accidental Ligation of ureter)
These usually cause CKI rather than AKI
89
What is Intrinsic AKI? What can it be caused by?
- Direct injury to the kidney
- Caused by; Acute Tubular Necrosis, Glomerular + Arteriolar Disease, Immune disease affecting glomerulus, Acute Tubule Interstitial Nephritis (Inflammation of kidney Interstitium)
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What are the two types of Acute Tubular Necrosis?
- Severe Acute Ischaemia - Pre-Renal causes, fall in renal perfusion isn't treated quickly it causes tubular necrosis
- Toxic Acute Tubular Necrosis - Nephrotoxins damage epithelial cells lining the tubules + cause cell death and shedding into the lumen. This is much more likely if there is also reduced perfusion. Urine will contain muddy brown casts
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What are the Signs + Symptoms for an AKI?
- Cardiac Failure (Pre-Renal) - Gallop Rhythm, Raised BP, Raised JVP, Pulmonary Oedema
- Sepsis - Pyrexia + Rigors, Vasodilation, Bounding pulse, rapid capillary refill, Hypotension
- Urinary Tract Obstruction - Anuria, Single functioning kidney, Palpable bladder, Pelvic/Abdominal masses, Enlarged prostate
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What investigations would you find with AKI's?
- Serum Biochemistry - Increased Urea, Increased Creatinine (In all causes of AKI), Hyperkalaemia, Hyponatraemia, Hypocalcaemia, Hyperphosphataemia
- ECG Changes in Hyperkalaemia
- Urine Testing - Dipstick (Blood, Proteins + Leucocytes), Microscopy (Pre-Renal [Hyaline casts {Aggregations of Proteins}, -ve for protein + blood in urine], Acute Tubular Necrosis [Muddy Brown Casts {Epithelial cells} -ve for protein + Blood in urine], Glomerulonephritis [RBC casts, +ve for Protein + Blood in urine]
- Imaging - Ultrasound, Chest X-Ray
- Histology - Looked at when Pre + Post Renal has been ruled out
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Whats the Treatment for the different causes of ATI?
- Pre-Renal Failure (Hypovolaemia - Fluid Administration, Heart failure - Diuretics)
- Post-Renal Failure (Urological Intervention to re-establish urine flow)
- Acute Tubular Necrosis (Supportive treatment maintaining good perfusion and avoiding nephrotoxins)
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Whats the most common cause of Macroscopic Haematuria?
IgA Nephropathy
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What is Nephrotic Syndrome? What is the classical triage of symptoms? What can it be caused by?
- Non specific disorder where kidneys are damaged + leak a large amount of protein into the urine.
- Classical symptoms are; Proteinuria (>3.5g/24h), Hypoalbuminaemia (Muehrcke's bands - line in nails), Oedema. Hyperlipidaemia due to loss of HDL's.
- Caused by; Minimal Change Glomerulonephritis, Focal Segmental Glomerulosclerosis, Membranous Glomerulonephritis. Can also be secondary to Diabetes + Amyloidosis
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What is Nephritic Syndrome? What are the classical signs?
- Collection of signs associated with disorders affecting the kidney, characterised by holes in the Podocyte layer large enough for proteins + RBC's to pass through
- Characterised by; Rapid onset, Oliguria, Hypertension, Generalised oedema, Haematuria (smoky brown), Urine contains blood, proteins + RBC casts
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What are the 4 sites of Glomerular Injury?
- Subepithelial - Anything that effects the podocytes/podocyte side of the glomerular basement membrane
- Within Glomerular basement membrane
- Subendothelial - Inside basement membrane
- Mesangial/Paramesangial - Supporting capillary loop
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What is Minimal Change Glomerulonephritis? How does it Present? How is it Treated?
- Under light microscope glomeruli looks perfectly normal, under electron microscope there is obvious damage to podocytes with widening of Fenestration slits
- Presents in childhood with heavy proteinuria or nephrotic syndrome
- Responds well to steroid treatment but may reoccur once treatment has stopped.
Usually no progression to Kidney failure
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What is Focal Segmental Glomerulosclerosis? How does it Present? How is it Treated?
- Podocytes undergo damage + scaring. Focal meaning that it involves
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What is Membranous Glomerulonephritis? What is the prognosis?
- Most common cause of nephrotic syndrome in adults. Results from circulating IgG binding to antigens on podocytes forming immune complexes
- 1/3rd of patients; Get better, Have proteinuria but are fine, progress to renal failure
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What is IgA Nephropathy?
Deposition of IgA antibodies in the glomerulus. Classically presents with Haematuria and has a relationship with mucosal infections. Some but not all patients have proteinuria and lots but not all progress to renal failure.
There is no treatment.
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What are the two Hereditary Neuropathies?
- Thin Glomerular Basement Membrane Nephropathy - Thinning of the basement membrane. Patients maintain a normal kidney function throughout life but may present with microscopic Proteinuria + Haematuria
- Alport Syndrome - X-linked disease which causes abnormalities in type IV collagen. Type IV collagen is important in structure of glomerular basement membrane + BM's of the inner ear + eye. Abnormalities in type IV collagen causes gradual scaring of BM in glomerulus. The splitting of the membrane gives a basket weave appearance. This progresses to Renal failure, there is no treatment.
Patients can also suffer from hearing loss + eye abnormalities such as cataracts.
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What is Goodpasture Syndrome?
Relatively uncommon rapidly progressive glomerular nephritis caused by an autoantibody to collagen type IV in the basement membrane (Only of the kidney for some reason), characterised by IgG deposition but no extracellular matrix deposits. Treatable by immunosuppression + Plasmapheresis if caught early enough
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What is the presentation of prostate cancer? How is it Diagnosed? How is it Treated?
- Vast majority are asymptomatic, Urinary symptoms similar to benign prostate enlargement, Bone pain in advanced metastasis, Haematuria in advanced cancers
- Diagnosed with Digital rectal exam, Serum Prostate Specific antigen are used to assess whether or not a biopsy of the prostate is required.
- Lower UT symptoms treated with transurethral resection of prostate
- Localised Prostate cancer: Surveillance if low risk, Radical prostatectomy, Radiotherapy (Low does Brachytherapy)
- Metastatic Prostate Cancer: Hormones (Surgical castration, Medical castration - LHRH agonists)
- Developmental Prostate Cancers: High intensity focused ultrasound, high does Brachytherapy, Primary chemotherapy
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What is the presentation of Bladder Cancer? How is it Diagnosed? What is the treatment?
- Presents with Haematuria, Polyuria + Dysuria
- Diagnosed with a biopsy taken by Cystoscopy
- High Risk Non-muscle invasive Transitional cell carcinoma (Check cystoscopes + Intravascular chemo/immunotherapy). If low risk then just check the cystoscopes
- Muscle invasive Transitional Cell Carcinoma - Potentially curative (Radical Cystectomy or radiotherapy), Palliative - Chemo/Radiotherapy
- Radical Cystectomy - Removal of urinary bladder, piece of ilium may be used to connect ureters to abdomen or reconstruct bladder from small intestine
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What is bad about Renal Cell Carcinomas? How do they present? What is the treatment?
- 30% have metastasis on presentation, these can spread to lymph nodes, up renal vein + vena cava to right atrium.
- Present with: Haematuria, Flank pain, Palpable mass in flank or abdomen. Often asymptomatic
- Treatment: Surveillance, Radical Nephrectomy, Partial Nephrectomy. Palliative treatment includes molecular therapies targeting angiogenesis + Immunotherapy
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Other than Renal Cell Carcinomas what other malignancies can you get of the upper UT?
Upper Tract Transitional Cell Carcinoma
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What is Chronic Kidney Disease? What are the causes for CKD?
- Progressive + Irreversible loss of renal function over a period of months or years. Functional renal tissue is replaced by extra cellular matrix. Means there is progressive loss of both excretory + Hormone functions of the kidney.
- Causes: Immunologic (Glomerulonephritis), Infection (Pyelonephritis), Genetic (Polycystic Kidney Disease, Alport Syndrome), Hypertension + Vascular Disease, Systemic Disease (Diabetes, Myeloma)
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At what point of GFR is Dialysis started?
GFR
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Describe the activation of Vitamin D
Converted into Calcidiol in the Liver, the converted into the Active form Calcitriol in the Kidneys
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What affect can CKD have on other systems of the body?
- CVS - Atherosclerosis, Cardiomyopathy, Pericarditis. These caused by hypertension + changes in blood concentration due to lack of removal of waste products by the kidney.
- Anaemia can be caused due to reduced production or resistance to Erythropoietin
- Renal Bone Disease due to reduced excretion of Phosphate which forms complexes with Calcium reducing effective concentration. Body produces PTH causing breakdown of bone by osteoclasts. Damage to kidney also means less Vit. D is converted to Calcitriol
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Why is Creatinine not a good marker for renal function?
Someone with 40% GFR can have a normal Creatinine level
