Urinary Flashcards

0
Q

The anatomical position of the prostate

A

Inferior to bladder, superior to the external urethral sphincter. Anterior to the ampulla of the rectum.
The levator ani muscles lie inferolaterally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

The anatomical position of the kidney

A

Retro peritoneal in the the paravertebral channel
Right T12-L3.
Left T11-L2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

The course of the ureters

A

From kidney pelvic inferiorly along psoas major. They cross the pelvic brim by the bifurcation of the common iliac artery. They run along the lateral pelvic wall. At the level of the Ischeal spine they turn obliquely and enter the bladder posteriolaterally. 2cm above the ischeal spine they pass the ovarian artery. Vas deferens found by the volvoureteric junction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

The renal blood supply

A

Renal artery - segmental artery (3) - interlobar arteries- arcuate arteries- interlobular arteries (90 deg) - afferent arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Anatomical position of the bladde

A

Anterior of the pelvic cavity. Posterior to the pubic symphysis and bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Explain the pronephros, Mesonephron and it duct and the metanephros.

A

Pronephros forms in intermediate mesoderm in cervical regions. It’s duct grows caudally and triggers the growth of the mesonephros. Week 4 then regresses
Mesonephros grows caudally week 4 to pronephros, it’s duct grows caudally and joins to the cloaca. Regresses week 8. Mesonephros forms in the urogenital ridge and contains nephrotomes
Urogenital ridge forms on either side from intermediate mesoderm created by the growth of the mesonephros.
The ureteric bud grows from its ducts and joins the metanephric tissue cap. The ureteric bud then stimulates it’s growth. Metanephros is functional from the first trimester

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

The positional changes of the kidney and problems that can occur

A

And the body grows caudally the kidneys rise cranially respectively. The blood supply therefore continually regresses and regrows at different parts of the abdominal aorta known as accessory renal arteries. There is lateral displacement so that the kidneys meet the adrenal glands at a 90 degree angle. The kidneys ascend close to each other and this can result in their fusion and as a result horseshoe kidney which can get trapped under the inferior mesenteric artery. The kidney may also have collateral blood supply.
Grow through arterial fork formed by umbilical arteries but one can fail to do so and so becomes a pelvic kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Formation of the bladder and urethra

A

The urorectal septum (mesoderm) grows and divides the cloaca into the urogenital sinus and the anal canal.
The cranial 2/3rds of the urogenital sinus become the bladder and the bottom parts into the pelvic (urethra) and phalic (spongy urethra).
The primitive bladder grows and absorbs the mesonephric duct so that it enters separately to the ureters (later becomes the vas deferens or regresses.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Ectopic ureteral orifaces/ duplication defects

A

Do not join bladder but join vagina or urethra. From splitting of ureteric bud.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Urachal abnormalities

A

Patent urachus
Uracheal cyst
Presents with BPH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Common fistulae?

A

Exstrophy of bladder- failed reinforcement of cloacal membrane by mesoderm so opens onto abdominal wall.

Hypospadias- defect in folds of urethra so they open onto ventral surface rather than glans of penis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Identify histological structures of the kidney nephron

A

Bowman’s capsule- vascular pole extra glomerular mesangial cells of JA. Urinary pole. Capillaries have fenestrated endotheliums. Podocytes have foot processes making slits. Shared basement membrane
PCT - simple cuboidal with brush boarder
Pars recta (straight part)
Thin AL - simple squamous
Tick AL- cuboidal no bb, with tAL, CD and VR in medulla.
DCT- cuboidal, larger lumen than PCT, more mitochondria
CD- larger lumen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Identify ultra structure of ureters

A

Urothelium

2 layers - circular and longitudinal. Extra layer for final 1/3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Identify ultra structure of bladder

A

Urothelium
LP
3 layers: spiral, longitudinal and circular
Adventitia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe glomerular filtration

A

Through glomerulus, around 20% (filtration fraction GFR/ RPF)
Depends on hydrostatic pressure diff and osmotic pressure (proteins).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe reabsorption in the PCT including OC

A

Basso lateral:
Na pump

Apical:
NHX
Symporters (glucose, aas, vitamins)
Secretion of Organic anion/cation exchangers with H+ (TM) they enter cells via facilitated diffusion and electrical gradient from Na pump at Basolateral membrane..

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe reabsorption in TAL

A

Apical:
NaKCl2
Rom K (back in)

Basolateral:
NaKATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe reabsorption in DCT

A
Apical:
Thiazide: Na/ Cl symporter
Ca?
Basolateral:
NaKATP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Reabsorption CD

A

Apical:
ENaC

Basolateral:
Na pump
Aquaporin 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe TGF

A

Increase in GFR = increase in NaCl in DCT
Detected by Macula densa via Nakcl2
Stimulates juxtaglomerular cell to Secrete adenosine to constrict afferent arteriole or prostaglandins to dilate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe secretion

A

Secretion of K so NaKCl2 can work and maintain. Charge.
Secretion of H+ for HCO3 reabsorption
Organic cations/ anions via baso OCT and luminal anti porter with H+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe and calculate clearance, how is it useful

A

The volume of plasma from which a substance has been completely removed
=(urine conc x urine flow)/ plasma conc
Glucose is 0
Inulin is 125 (not secreted or reabsorbed) = GFR
PAH all is secreted so clearance (ml/min) = RPF (90%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How are GFR and clearance related

A

The higher the GFR then the higher the clearance.

Increased by TM- only so much can be reabsorbed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How do the kidneys Handel sodium in order to change ECF volume. Absorption of sodium and H2O in kidney

A
Absorb more to increase ECF 
Na Vs H20
Proximal tub 67 vs 65
LOH 25 vs ?
DCT 5 vs 0
Cd 3 vs 5-24
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Handling of sodium in PCT
``` Na/K ATPase Symporters NHX S2/3 - Cl- 3 driving forces for water, osmotic, oncotic, hydrostatic ```
25
Glomerulotubular balance and the effect of ECF volume
GFR increases normally Na maintained - always 67% but less is reabsorbed
26
Difference between principal cells and intercalated cells
Principle- ENaC, aqua portion 2 variable, K secretion (More distinct membrane) Intercalated cells, active reabsorption of Cl-, secrete H+
27
Describe the regulation of NaCl reabsorption (blood pressure)
1: RAAS 2: sympathetic- increase CO, decrease TPR, increase RAAS and decrease GFR, NHE in PCT stimulated 3: ADH 4: Atrial natriuretic peptide, released with stretch of atrium, dilates afferent arteriole to increase GFR, decreases Na reabsorption all along tubule.
28
Describe how the renin- angiotensin system regulates sodium uptake in response to changes in blood pressure
Increased by decrease in Na reaching macula densa - sympathetic to juxatoglomerular cells to secrete renin. Reduced perfusion pressure by baroreceptors in afferent arteriole stimulates release. Increased by sympathetic innervation. Renin- angiotensin I - angiotensin II. Increases aldosterone at adrenal cortex (increase ENaC and Na pump) Constricts afferent and efferent arterioles and other vascular SM. Increases NHX Stimulates thirst via ADH release at hypothalamus. Breaks down bradykinin (vasodilator)
29
Describe the sympathetic control of ADH secretion and the role of the baroreceptor
Low pressure- atria, pulmonary circulation and high pressure. Drop in pressure or increase in tonicity increases ADH secretion from posterior pituitary. Baroreceptors to brain stem via vagus nerve which also increases sympathetic nerve activity
30
Actions of ADH
Addition of aquaporin 2 to CD | Increase in NaKCl2
31
Discuss prostaglandins and NSAIDS
Prostaglandins dilate afferent arteriole. NSAIDs inhibit cycloxygenase and prevent prostaglandin production causing more vasoconstriction decreasing GFR and increasing BP.
32
Describe essential and secondary hypertension including causes.
Essential has no cause Secondary does Mild 140-159/90-99 Moderate 160-179/100-109 Severe 180+/110+ Renalvascular disease- low perfusion, baroreceptors increase RAAS. Chronic renal disease Conn's syndrome- aldosterone adenoma Cushings - high cortisol - stim Na reabsorption Pheochromocytoma- secretes adrenaline and noradrenaline
33
Treating hypertension
``` Diet, smoking, exercise, alcohol, Na intake. ACE inhibitors Ca channel blockers A1 receptor blockers Beta blockers Thiazides diuretics ```
34
Regulation of body fluid osmolarity in terms of responses to water deprivation and drinking
Deprivation- more reabsorbed to maintain osmolarity and vice versa. Water to control osmolarity Na into control vol.
35
Distinguish the factors that regulate thirst and cause secretion of ADH
Stim by hyper osmolarity or hypovolaemia/ hypotension | Detected by osmoreceptors in the organum vasculoum of the laminae terminalis (OVLT).
36
Key factors of ADH/ thirst stimulation
Salt desire opposite of thirst. Hedanistic appetite and regulatory. Thirst requires significant change.
37
Describe the role of ADH and the production of hyper and hypo osmotic urine
Aquaporin 2 NaKCl2 Urea
38
Describe the syndrome of secretion of inappropriate ADH (SIADH) and it's inappropriate consequences
Not inhibited by lowering of blood osmolarity Too much water reabsorbed Hyponatraemia- nausea, vomiting, lethargy, headache, appetite loss, irritability, seizures, coma, cramps Treated with ADH receptor antagonists.
39
Describe the corticopapillary osmotic gradient
Osmolarity increases into medullar due to urea and nakCl2/ TAL. Means more water is reabsorbed as medulla up is more conc that tdl and less conc than TAL. Counter current system means that vasa recta is less conc as it descends (next to TAL) so osmolites diffuse into it so it is isoosmotic at the tip of the hairpin, as it ascends it is more conc so h2O that has diffed from tdl diffuses into it.
40
Discuss how the kidneys regulate Ca and PO4.
Vitamin D - short half life ask converted to 25 Hydroxy/ calciferol. Converted to calcitriol by 1 alpha hydroxylase stim by PTH and inhibited by PO4. Stim osteoblasts to stim osteoclast precursor cells to mature, increases gut absorption and kidney reabsorption (also PO4). PTH stimulates osteoclasts, kidney reabsorption at DCT of ca and mg amd decreases PO4.
41
Where is ca reabsorbed in the kidney
65% PCT 20-25 ascending LOH 10 in DCT under PTH
42
Discuss the causes, symptoms and management of hypercalcaemia
Causes: Primary hyperparathyroidism- parathyroid tumour Haematological malignancy or non producing PTrH. CVS: arrhythmias, shortened QT, enhanced sensitivity to digoxin General: depression, coma, fatigue GI: anorexia, poly uria, poly dipsia, constipation Nephrocalcinosis General management. Hydrate, loop diuretics to increase Ca excretion. Specific measures- bisphosphonates, calcitonin Treat underlying condition
43
Discuss calcium renal stones and their formation
Factors: Low urine Hypercalcuria High oxalate consumption. Organic matrix Formation: Supersaturation with respect to calcium oxalate Ionic strength decreases risk e.g. Na, k, Cl PH affects- lower pH enhances urinary citrate, but It favours uria acid stone formation.
44
Manifestations of renal stones
Asymptomatic Haematuria Pain and complications of a blockage in renal tract
45
Inhibitors of calcium oxalate and calcium phosphate stone formation
``` Citrate Pyrophosphate Magnesium Glucosaminoglycans (gag) RNA fragments Acidic glycoproteins ```
46
Management
Increase fluids Restrict oxalate and Na possibly and possibly ca and animal proteins Referal for surgery
47
Pathogenesis of UTI
``` Bacteria travels up urethra in between micturition. E. coli and pseudomonas aeruginosa. Use pili to adhere. Urease for protection from urea. Ecoli has k antigen to protect from host defense. Haemolysins damage cell membranes. May be coag neg staph on hospital Patient factors: Short urethra Blockage e.g. BPH, renal stone Diabetes- glucosuria Incomplete emptying- neurological Ureteric reflux ```
48
Appropriate clinical and laboratory investigations to diagnose UTI
Simple- urine dipsitic- nitrates and leukocyte esterase. If both positive give 3 days antibiotics Complex (not a women or recurrent)- look for cause e.g. Imaging, midstream culture (msc), bacterial count over 105 cfu/ml (colony forming units) then significant. Look at turbidity, Haematuria, proteinuria. Possibly microscopy. Antibiotic testing. 5 days antibiotics, treat underlying condition. If pyelonephritis or systemic then 10-14 days treatment. Sterile pyuria- antibiotics, STI, TB, appendicitis
49
Appropriate anti microbial treatment and prophylaxis
``` Trimethoprim, nitroflurotoin Severe the co-amoxiclav Most are amoxicillin resistant. Prophylactic take at night Increase fluid intake ```
50
Summarise the main classes of diuretics and their mechanism of action
Loop diuretics- nakcc2, inhibit Ca absorption, more volume so less Na absorption distally. Furosemide Thiazide- Na/Cl symporter, increases ca absorption. K sparing e.g. Bendroflumethiazide. ENaC blockers - k sparing e.g. Amiloride Aldosterone inhibiting - not as potent e.g. Spironolactone. Osmotic diuretics - cannot be reabsorbed, increase osmolarity so less Na reabsorbed and h2O. Also draws h20 out of cells into ECF Carbonic anhydrase inhibitors, less H+ so less NHX so more Na excreted. PCT. Not potent as other means e.g. Cl.
51
Theory of rational prescribing of drugs
Spironolactone first as K sparing. Loop diuretics very potent e.g, heart failure or cirrhosis after spirono. Hypertension then thiazides as it has vasodilator effects. Conns syndrome then spironolactone
52
The adverse effects of diuretic use and abuse
Hyperkalaemia/ hypokalaemia depending if K sparing or not. Hyperkalaemia particularly dangerous if on m supplements, ace inhibitors or renal impairment. Stim raas (increase I'm vol) which also leads to hypokalaemia (aldosterone) Carbonic anhydrase can cause acidosis but good for treatment of glaucoma. Thiazides and loop diuretics can cause high uric acid levels which leads to gout, glucose intolerance and increased LDLs. Thiazides cause erectile dysfunction All can cause hyponatraemia
53
The object of diuretic therapy
M
54
What is the normal range for plasma pH?
7.38-7.42
55
Clinical effects of acidaemia and alkalaemia
Acidaemia- reduced muscle contraction, hyperkalaemia, arrhythmias, reduced glycolysis, reduced hepatic function Alkaemia- tetany, parasthesia, death
56
Cellular mechanisms of reabsorption of HCO3 in the proximal tubule
NaKATPase, NHX, carbonic anhydrase, diffusion. | Aas create ammonium and hCO3 in PCT
57
Cellular mechanisms of H excretion in the distal tubule
H pump H/K X Active. Normally not needed
58
Mechanism of buffering H in urine, explain the concept of titratable acid and the role of NH4
Minimum pH of urine is 4.5 | H+ buffered by PO4 (titratable acid) and ammonia as ammonium
59
Types of UTI
Lower UTI Bacterial cystitis- dysuria, polyuria, Haematuria, suprapubic pain Abacterial cystitis- no bacteruria, honeymoon cystitis, trauma, fastidous organisms, STI, non infective inflammation, Prostatitis- fever dysuria, perineal and low back pain- prostate Upper UTI- acute pyelonephritis, with fever and loin pain Chronic interstitial nephritis, renal impairment following chronic inflammation. Asymptomatic covert bacteruria only important in children and pregnancy
60
Describe the interactions between acid base status and plasma K
Hyperkalaemia acidosis due to favoring extracellular H+ movement so less H+ excretion Hypokalaemia alkalosis due to intracellular pH acidic favoring HCO3 reuptake and H+ excretion
61
Describe the interaction between renal control of acid base balance and control of plasma volume
Volume comes first. E.g. Vomiting- hypovolaemic and alkalosis. Na uptake increase so NHX and Na/HCO3 adds to alkalosis. Give fluids and it will sort itself out.
62
Describe the major causes of metabolic acidosis and the role of the anion gap to distinguish
Lactic/Ketoacidosisis, loss of HCO3 in kidney. | Anion gap = Na+H - (HCO3+ Cl). Larger if different anion e.g. Lactate
63
Why is the internal balance of K so important?
Intracellular lay- acid/base, DNA replication, cell growth, water, enzymes Resting membrane potential
64
Describe how potassium handling occurs in the various segments of the nephron
Pct- passive diffusion 67% LOH- NaKCC2 20% DCT cd principle- ENaC K+ secretion 0-20% DCT CD intercalated - K/H ATPase, 10-12%
65
Effect of aldosterone, ECF k, acid base status and affect on K+
Aldosterone- increases Na/K ATPase ECF k - stimulates aldosterone secretion and K secretion in principle cells as higher K intracellularly Acidaemia decreases K in principles decreasing secretion and vice versa.
66
Describe potassium balance and regualtion of ECF, icf concs.
External balance- kidneys Internal balance- K into/ out of ICF. Long term vs short term
67
Factors causing K shift inwards
``` Insulin stim ATPase High K ECF Catecholamines (exercise) stim ATPase Alkalosis K/H X Aldosterone ```
68
Factors causing K shift from icf to ECF
``` Acidosis, Low K ECF Exercise contraction and net release of K- uptake by non contracting cells Trauma / cell lysis Plasma hypersomolarity ```
69
Effects of K on RMP and heart excitability
Hyperkalaemia - depolarised RMP, less active fast Na channels, less excitability Vice versa
70
Causes of hypokalaemia
External balance, low k intake, vomiting, diarrhoea, diuretic drugs or osmotic diuresis, high aldosterone levels Internal balance - alkalosis
71
Clinical features of hypokalaemia
Heart GI- paralytic ileus Neuromuscular dysfunction so muscle weakness Renal- dysfunction of CD, unresponsive to ADH so nephrogenic diabetes
72
ECG changes in hypokalaemia
``` (3) Shallow T wave/ inverted at wave Prominent U wave(3.5) ST depression (2) Wide pr possible ```
73
Treatment hypokalaemia
Treat cause Oral/ IV K K sparing diuretics - spironolactone or amiloride if aldosterone
74
Causes hyperkalaemia
External Renal dysfunction e,g. acute/ chronic failure Mineralcorticoid insufficiency e.g. K sparing or adrenal insufficiency Internal- cell lysis or acidaemia
75
ECG changes hyperkalaemia
6.5- 7 tall peaked T 8 prolonged P-R interval, tall T, st segment depression 9 no P wave widened QRS 10 VF.
76
Treatment of hyperkalaemia
Acute - reduce k effect on heart with IV calcium gluconate Insulin and glucose Dialysis ``` Long term Dialysis Oral k binding resins in the gut Reduce intake Treat cause ```
77
The innervation of the bladder
Sympathetic innervation to detrusor muscle (B3) to relax and a1 to the urethra to contract (T10-L2) hypogastric nerve. Parasympathetic to contract detrusor (M3) via the pelvic nerve S2-4. Somatic innervation to the external sphincter via the pudendal nerve S2-4 and nicotinic receptor Also a sensory nerve- bladder, spinal cord, thalamus/pons- cerebral cortex.
78
Explain how continence occurs. What drug controls this?
Cerebral continence centre - pontine continence centre- sympathetic nuclei in spinal cord- detrusor relaxation Somatic closes external urethral sphincter Controlled with B3 agonist Mirabegron
79
Explain how voiding occurs
When bladder around 400ml Sensory innervation fires more rapidly. Micturition regions in cerebral- pons- sacral levels of ps - bladder to contract. External sphincter opens via somatic nerve
80
Incidence of urinary incontinence
SUI most common 50% | Then MUI then UUI and other.
81
Prevalence of UI with age
Increases rapidly with age until 50 and then less so.
82
Risk factors associated with urinary incontinence
O&G - pregnancy, childbirth, pelvic surgery Predisposing- race, family predisposition Promoting- co morbidities, obesity, age high intra abdominal pressure, UTI, drugs, menopause
83
Types of UI
SUI - leakage on cough UUI- sudden urge with accompanies leakage MixedUI Overflow- under activity of detrusor
85
Investigation of UI
Urine dipstick- UTI, haem, glycosuria, protein Non invasive urodynamics- frequency volume chart, drink and void, bladder diary, post micturition residual volume Invasive urodynamics- flow and pressure, in anal canal and bladder to find bladder pressure Pad tests - urine weight Cystoscopy- look for tumour
86
Initial management of patient with urinary incontinence
``` Drink less Stop smoking- cough Less caffeine UUI Avoid constipation Bladder training- scheduling Pharmacological Surgical Pelvic floor muscle trainingkndwelling catheter, sheath device or incontinence pads Weight loss ```
87
Pharmacological management of patients with urinary incontinence
Anticholinergic - oxybutynin but non specific so side effects B3 agonist- Mirabegron Botulism toxin to inhibit ACh release ŵith UUI Duloxetine- not recommended, noradrenaline and serotonin uptake inhibitor increasing external urethral sphincter
88
Surgical management of patients with urinary incontinence
Women permanent: Sling (adds resistance uses fascia lata or Rectus fascia) Retro public suspension proceedure (improve support and urethral positioning Low tension vaginal tapes (minimally invasive and supports urethra) Temporary: Bulking agents e.g. Collagen and silicone to increase urethral resistance Male: Sling Artificial urinary sphincter Also for UUI: Augmentation cystoplasty (bowel) Urinary divergence
95
Examination of UI
Height, weight, abdominal exam (palpable bladder), DRE (prostate)- limited neurological examination, female, external genitalia and stress test
96
Pre renal causes of oliguria and AKI
Hypovolaemia e.g. Sepsis, heart failure NSAIDs - constriction Acei- dilation
97
Renal causes of AKI
Renal artery/ vein occlusion, intra renal vascular/. Intrarenal obstruction Glomerulonephritis primary or secondary e.g. Vasculitis, wegners granulomatosis, SLE (systemic lupus erythromatosus) Ischemic ATN (from prerenal) Toxin ATN- drugs e.g. Gentamicin,urate, bilirubin, endotoxins, x ray contrast Interstitial disease- acute pyelonephritis or toxin induced Rhabdomyolysis Malignant hypertension Pre eclampsia
98
Post renal causes of AKI
Obstruction Lumen- calculi, blood clot, papillary necrosis, tumour Wall- congenital e.g. Megaureter, neurogenic bladder, ureteric stricture (CKD) Pressure- BPH, Diverticulitis, tumour, aortic anneurysm, ligation of ureter
99
Methods used to investigate AKI
Function Na excretion = (urineNa/ plasmaNa)/(urineCr/plasmaCr) x100 BP Dehydration- HR, cool extremities, mucous membranes, dry axillae, increased skin turgor. pH Electrolytes Osmolarity Sepsis? Abdo exam- obstruction? Rectal exam, blood in catheter? Urinalysis- blood, protein, leukocytes Urine microscopy - red cell cast the. Glomerulo nephritis Imaging Renal biopsy after post and pre and ruled out CXR for fluid overload +\- infection Signs of cardiac failure, sepsis or UTI
100
Management of AKI
Volume overload- give fluids Hyperkalaemia- calcium gluconate Acidosis- protein restrict, bicarbonate Dialysis especially if ureamic- pericarditis, intractable N/V, reduced consciousness Supportive for ATN Post renal failure- urological intervention TPR e-establish urine flow
101
Causes of microscopic Haematuria
``` Infection Poly cystic kidneys Arteriovenous malformations Kidney/glomerular disease Renal stones Renal/bladder tumours Glomerular disease if microhaematuria with protein or hypertension ```
102
Causes of macroscopic Haematuria
Glomerular disease but often brown and smokey (not clots). Haemoglobinuria, myoglobin urea, food dyes Usually painless IgA nephrology most common
103
Symptoms of proteinuria
Frothy urine Less immunoglobulins so infection Less oncotic so oedema Imbalance of coag cascade so risk of thromboemboli
104
Symptoms of nephrotic syndrome
``` Hypoalbuminaemia Oedema Proteinuria >3.5g/24 +hyperlipidaemia Often muehrche's bands May lead to AKf Caused by focal segment glomerulosclerosis or membranous cause. ```
105
Symptoms of nephritic syndrome
``` Hypertension Haematuria Hypoalbuminaemia Rapid onset Oliguria Often occurs in post streptococcal glomerulonephritis in children Requires renal biopsy for diagnosis Pores in Podocytes ```
106
Describe rapidly progressive glomerulonephritis
Renal function deteriorates over days. Ureamic emergency. | Renal biopsy required
107
Causes of nephrotic syndrome
``` Minimal change glomerulonephritis, Focal segmental glomerulosclerosis Membranous glomerulonephritis DM Amyloidosis ```
108
Describe minimal change glomerulonephritis
``` Unknown circulating factor leads to Podocyte damage Does not normally lead to renal failure Child/adolescent Responsive to steroids May recur ```
109
Describe focal segmental glomerulosclerosis (FSGS)
``` Other end of spectrum from minimal change. Circulating factor unknown Causes scarring, fibrosis Less responsive to steroids Progressive to renal failure Recur in transplant ```
110
Describe membranous glomerulonephritis
IgG immune complexes in BM deposited Commonest cause of nephrotic Rule of thirds- third have KF Autoimmune or secondary to SLE, lymphoma or malaria
111
How does DM cause nephrotic syndrome?
Thickening of BM Micro vascular disease Mesangial sclerosis Progressive to renal failure
112
Causes of nephritic syndrome
IgA nephropathy Hereditary nephropathies Goodpasture syndrome (anti GBM) Vasculitis
113
Describe IgA nephropathy
``` IgA in mesangium leading to damage and scarring Associated with mucosal infections Commenest GN Often causes renal failure Any age Very variable ```
114
Describe hereditary nephropathies
``` Thin GBM nephropathy Benign familial nephropathy Isolated Haematuria (blood is normal) Alport: X linked Abnormal collagen 4 Deafness Abnormal GBM Progressive to renal failure ```
115
Describe goodpasture syndrome (anti-GBM)
Antibody (IgG) targeting collagen IV Rapidly progressive Acute onset of severe nephritic syndrome Treated with immune suppression and plasmapheresis Rare Association with smokers and pulmonary haemorrhage
116
Describe vasculitis
Associated with anti neutrophil cytoplasmic antibody (ANCA) treatable if early Segmental necrosis Urgent biopsy needed Inflammation destroys blood vessels
117
Risk factors prostate cancer
Age- >80 75% Fam history Black>white> Asian BRCA2 gene mutation
118
Screening prostate cancer
Not recommended as overdiagnosis Often PSA raised in other things e.g. BPH, infection, inflammation. False pos and negs.
119
Clinical presentation prostate cancer
Asymptomatic Urinary symptoms e.g. Overactivity Bone pain from mets Haematuria (advanced)
120
Diagnosis/ investigation prostate cancer
DRE Serum PSA TRUS- transracial ultrasound - guided biopsy of prostate
121
Treatment of prostate cancer
Surveillance Radiotherapy Radical prostatectomy - open, laparoscopic or robotic. New: HIFU (high intensity focused ultrasound) Primary cryotherapy High dose rate brachytherapy or external beam Mets: Hormones e.g. GnRH agonist or surgical castration Palliative- single dose radio therapy Bisphosphonates- zoledronic acid and chemotherapy If locally advanced then hormones, surveillance and radiotherapy. BPH via transurethral resection
122
Risk factors bladder cancer
``` Age Males 90 TCC Smoking x4 Occupational e.g. Rubbers, plastics, painters, hairdressers Schistosomiasis ```
123
Treatment bladder cancer
Transurethral resection bladder tumour Chemotherapy- intravesical instillation of mitomycin C Immunotherapy (intra vesicular) for high risk non muscle invasive. Muscle invasive - chemo and radical cystectomy or radio Cystectomy them ileal conduit (belly button) or in younger people reconstruction from bowel
124
Staging and grading of bladder cancer
TNM | Normal stuff e.g. Mitosis, cytoplasm
125
Renal cell carcinoma aetiology, investigations and treatment
Smoking, obesity dialysis. May spread peri tubular, IVC/LA, lymphatics Ultrasound or CT Radical/partial nephrectomy, surveillance, for mets then molecular therapies against angiogenesis
126
TCC risk factors, investigation and treatment
``` Smoking, phenacetin (fever and pain) Ultrasound Ct Retrograde pyelogram Ureteroscopy Treatment nephro-ureterectomy- kidney fat, cuff of bladder, ureter. ```
127
Main causes of chronic kidney disease
``` Infection e.g. Pyelonephritis Immune e.g. Glomerulonephritis Genetic e.g. Poly cystic kidney disease, Alport syndrome Obstruction and reflux nephropathy Hypersension Systemic e.g. Diabetes, myeloma Vascular Risk factors: Proteinuria Hypercalcaemia ```
128
Risk factors for chronic kidney failure
N
129
Define CKD
Progressive and irreversible loss of kidney function from months to years
130
Classification of CKD
Stages 1-5 based on GFR 1 >90 5 <15
131
Ways in which CKD can affect the CVD system
``` Increase in Na and h2O Acidosis Atherosclerosis Cardiomyopathy Pericarditis ```
132
Ways in which CKD can affect the haemopoitic system
Anaemia- low erythropoietin
133
Ways in which CKD can affect the Musculocutaneous system
Bone- renal bone disease Less VitD- osteomalacia Less GFT so more po4 so less Ca (complex) so more PTH so osteitis fibrosa cystica Extra articular calcification
134
Other effects of CKD
``` Neuropathy Seizures Coma Tiredness Breathlessness Restless legs Sleep probs Aches and pains NV Itching Chest pain ```
135
Investigating CKD
GFR via inulin (in theory too expensive and time) or 24hr creatine clearence. eGFR ethnicity gender and age
136
Conservative management of CKD
``` Lifestyle - smoking, obesity, exercise Treat diabetes Treat BP Ace inhibitors Lower lipids e.g. Statin Monitor ```
137
When is dialysis needed
Typically GFR <10 | Ureamic, hyperkalaemia, pericarditis, acidosis
138
Describe haemodyalysis
3x a week for 4 hours Modified diet low in K and PO4 so no potatoes Risk of infection Requires arterial/venous fistula which requires surgery. Lead to ischemia and swelling. Catheter cause stenosis Home dialyse but need to live with someone Anti coag and pump needed in machine Countercurrent system with purified water Effective but expensive
139
Describe peritoneal dialysis
``` Tube into peritoneum 5x a day or overnight High risk of infection High risk of adhesions and GI risk Less cvs risk Most effective initially Leaks may occur ```
140
Describe renal transplant
``` Gold standard From linpvint, cadavas or non heart beating donors or after brain death Placed in iliac fossa Cheap Long term survival Limited supply Op risks Life long immunosuppression Progressive CKD ```
141
Sensory innervation of kidneys?
T10-11
142
Blood supply of the ureters
3 parts: 1 renal arteries 2- common iliac, abdominal aorta and gonadal 3 - internal iliac arteries and everything else
143
Innervation of ureters
Sensory T12-L2