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Esa 3 > Urinary > Flashcards

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

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1
Q

The anatomical position of the kidney

A

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

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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.

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3
Q

The renal blood supply

A

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

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4
Q

Anatomical position of the bladde

A

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

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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

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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

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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.)

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8
Q

Ectopic ureteral orifaces/ duplication defects

A

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

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9
Q

Urachal abnormalities

A

Patent urachus
Uracheal cyst
Presents with BPH

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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.

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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

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12
Q

Identify ultra structure of ureters

A

Urothelium

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

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13
Q

Identify ultra structure of bladder

A

Urothelium
LP
3 layers: spiral, longitudinal and circular
Adventitia

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14
Q

Describe glomerular filtration

A

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

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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..

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16
Q

Describe reabsorption in TAL

A

Apical:
NaKCl2
Rom K (back in)

Basolateral:
NaKATP

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17
Q

Describe reabsorption in DCT

A 
Apical:
Thiazide: Na/ Cl symporter
Ca?
Basolateral:
NaKATP
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18
Q

Reabsorption CD

A

Apical:
ENaC

Basolateral:
Na pump
Aquaporin 2

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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.

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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+

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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%)

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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.

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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
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24
Q

Handling of sodium in PCT

A 
Na/K ATPase
Symporters
NHX
S2/3 - Cl-
3 driving forces for water, osmotic, oncotic, hydrostatic
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25
Q

Glomerulotubular balance and the effect of ECF volume

A

GFR increases normally Na maintained - always 67% but less is reabsorbed

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26
Q

Difference between principal cells and intercalated cells

A

Principle- ENaC, aqua portion 2 variable, K secretion
(More distinct membrane)
Intercalated cells, active reabsorption of Cl-, secrete H+

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27
Q

Describe the regulation of NaCl reabsorption (blood pressure)

A

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.

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28
Q

Describe how the renin- angiotensin system regulates sodium uptake in response to changes in blood pressure

A

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)

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29
Q

Describe the sympathetic control of ADH secretion and the role of the baroreceptor

A

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

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30
Q

Actions of ADH

A

Addition of aquaporin 2 to CD

Increase in NaKCl2

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31
Q

Discuss prostaglandins and NSAIDS

A

Prostaglandins dilate afferent arteriole.
NSAIDs inhibit cycloxygenase and prevent prostaglandin production causing more vasoconstriction decreasing GFR and increasing BP.

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32
Q

Describe essential and secondary hypertension including causes.

A

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

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33
Q

Treating hypertension

A 
Diet, smoking, exercise, alcohol, Na intake.
ACE inhibitors
Ca channel blockers
A1 receptor blockers
Beta blockers
Thiazides diuretics
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34
Q

Regulation of body fluid osmolarity in terms of responses to water deprivation and drinking

A

Deprivation- more reabsorbed to maintain osmolarity and vice versa.
Water to control osmolarity
Na into control vol.

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35
Q

Distinguish the factors that regulate thirst and cause secretion of ADH

A

Stim by hyper osmolarity or hypovolaemia/ hypotension

Detected by osmoreceptors in the organum vasculoum of the laminae terminalis (OVLT).

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36
Q

Key factors of ADH/ thirst stimulation

A

Salt desire opposite of thirst.
Hedanistic appetite and regulatory.
Thirst requires significant change.

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37
Q

Describe the role of ADH and the production of hyper and hypo osmotic urine

A

Aquaporin 2
NaKCl2
Urea

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38
Q

Describe the syndrome of secretion of inappropriate ADH (SIADH) and it’s inappropriate consequences

A

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.

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39
Q

Describe the corticopapillary osmotic gradient

A

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.

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40
Q

Discuss how the kidneys regulate Ca and PO4.

A

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.

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41
Q

Where is ca reabsorbed in the kidney

A

65% PCT
20-25 ascending LOH
10 in DCT under PTH

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42
Q

Discuss the causes, symptoms and management of hypercalcaemia

A

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

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43
Q

Discuss calcium renal stones and their formation

A

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.

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44
Q

Manifestations of renal stones

A

Asymptomatic
Haematuria
Pain and complications of a blockage in renal tract

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45
Q

Inhibitors of calcium oxalate and calcium phosphate stone formation

A 
Citrate
Pyrophosphate
Magnesium
Glucosaminoglycans (gag)
RNA fragments
Acidic glycoproteins
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46
Q

Management

A

Increase fluids
Restrict oxalate and Na possibly and possibly ca and animal proteins
Referal for surgery

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47
Q

Pathogenesis of UTI

A 
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
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48
Q

Appropriate clinical and laboratory investigations to diagnose UTI

A

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

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49
Q

Appropriate anti microbial treatment and prophylaxis

A 
Trimethoprim, nitroflurotoin
Severe the co-amoxiclav
Most are amoxicillin resistant.
Prophylactic take at night
Increase fluid intake
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50
Q

Summarise the main classes of diuretics and their mechanism of action

A

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.

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51
Q

Theory of rational prescribing of drugs

A

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

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52
Q

The adverse effects of diuretic use and abuse

A

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

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53
Q

The object of diuretic therapy

A

M

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54
Q

What is the normal range for plasma pH?

A

7.38-7.42

55
Q

Clinical effects of acidaemia and alkalaemia

A

Acidaemia- reduced muscle contraction, hyperkalaemia, arrhythmias, reduced glycolysis, reduced hepatic function
Alkaemia- tetany, parasthesia, death

56
Q

Cellular mechanisms of reabsorption of HCO3 in the proximal tubule

A

NaKATPase, NHX, carbonic anhydrase, diffusion.

Aas create ammonium and hCO3 in PCT

57
Q

Cellular mechanisms of H excretion in the distal tubule

A

H pump
H/K X
Active.
Normally not needed

58
Q

Mechanism of buffering H in urine, explain the concept of titratable acid and the role of NH4

A

Minimum pH of urine is 4.5

H+ buffered by PO4 (titratable acid) and ammonia as ammonium

59
Q

Types of UTI

A

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
Q

Describe the interactions between acid base status and plasma K

A

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
Q

Describe the interaction between renal control of acid base balance and control of plasma volume

A

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
Q

Describe the major causes of metabolic acidosis and the role of the anion gap to distinguish

A

Lactic/Ketoacidosisis, loss of HCO3 in kidney.

Anion gap = Na+H - (HCO3+ Cl). Larger if different anion e.g. Lactate

63
Q

Why is the internal balance of K so important?

A

Intracellular lay- acid/base, DNA replication, cell growth, water, enzymes
Resting membrane potential

64
Q

Describe how potassium handling occurs in the various segments of the nephron

A

Pct- passive diffusion 67%
LOH- NaKCC2 20%
DCT cd principle- ENaC K+ secretion 0-20%
DCT CD intercalated - K/H ATPase, 10-12%

65
Q

Effect of aldosterone, ECF k, acid base status and affect on K+

A

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
Q

Describe potassium balance and regualtion of ECF, icf concs.

A

External balance- kidneys
Internal balance- K into/ out of ICF.
Long term vs short term

67
Q

Factors causing K shift inwards

A 
Insulin stim ATPase 
High K ECF
Catecholamines (exercise) stim ATPase
Alkalosis K/H X
Aldosterone
68
Q

Factors causing K shift from icf to ECF

A 
Acidosis,
Low K ECF 
Exercise contraction and net release of K- uptake by non contracting cells
Trauma / cell lysis
Plasma hypersomolarity
69
Q

Effects of K on RMP and heart excitability

A

Hyperkalaemia - depolarised RMP, less active fast Na channels, less excitability
Vice versa

70
Q

Causes of hypokalaemia

A

External balance, low k intake, vomiting, diarrhoea, diuretic drugs or osmotic diuresis, high aldosterone levels
Internal balance - alkalosis

71
Q

Clinical features of hypokalaemia

A

Heart
GI- paralytic ileus
Neuromuscular dysfunction so muscle weakness
Renal- dysfunction of CD, unresponsive to ADH so nephrogenic diabetes

72
Q

ECG changes in hypokalaemia

A 
(3)
Shallow T wave/ inverted at wave
Prominent U wave(3.5)
ST depression (2)
Wide pr possible
73
Q

Treatment hypokalaemia

A

Treat cause
Oral/ IV K
K sparing diuretics - spironolactone or amiloride if aldosterone

74
Q

Causes hyperkalaemia

A

External
Renal dysfunction e,g. acute/ chronic failure
Mineralcorticoid insufficiency e.g. K sparing or adrenal insufficiency
Internal- cell lysis or acidaemia

75
Q

ECG changes hyperkalaemia

A

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
Q

Treatment of hyperkalaemia

A

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
Q

The innervation of the bladder

A

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
Q

Explain how continence occurs. What drug controls this?

A

Cerebral continence centre - pontine continence centre- sympathetic nuclei in spinal cord- detrusor relaxation
Somatic closes external urethral sphincter
Controlled with B3 agonist Mirabegron

79
Q

Explain how voiding occurs

A

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
Q

Incidence of urinary incontinence

A

SUI most common 50%

Then MUI then UUI and other.

81
Q

Prevalence of UI with age

A

Increases rapidly with age until 50 and then less so.

82
Q

Risk factors associated with urinary incontinence

A

O&G - pregnancy, childbirth, pelvic surgery
Predisposing- race, family predisposition
Promoting- co morbidities, obesity, age high intra abdominal pressure, UTI, drugs, menopause

83
Q

Types of UI

A

SUI - leakage on cough
UUI- sudden urge with accompanies leakage
MixedUI
Overflow- under activity of detrusor

85
Q

Investigation of UI

A

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
Q

Initial management of patient with urinary incontinence

A 
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
Q

Pharmacological management of patients with urinary incontinence

A

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
Q

Surgical management of patients with urinary incontinence

A

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
Q

Examination of UI

A

Height, weight, abdominal exam (palpable bladder), DRE (prostate)- limited neurological examination, female, external genitalia and stress test

96
Q

Pre renal causes of oliguria and AKI

A

Hypovolaemia e.g. Sepsis, heart failure
NSAIDs - constriction
Acei- dilation

97
Q

Renal causes of AKI

A

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
Q

Post renal causes of AKI

A

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
Q

Methods used to investigate AKI

A

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
Q

Management of AKI

A

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
Q

Causes of microscopic Haematuria

A 
Infection
Poly cystic kidneys
Arteriovenous malformations
Kidney/glomerular disease
Renal stones
Renal/bladder tumours
Glomerular disease if microhaematuria with protein or hypertension
102
Q

Causes of macroscopic Haematuria

A

Glomerular disease but often brown and smokey (not clots).
Haemoglobinuria, myoglobin urea, food dyes
Usually painless
IgA nephrology most common

103
Q

Symptoms of proteinuria

A

Frothy urine
Less immunoglobulins so infection
Less oncotic so oedema
Imbalance of coag cascade so risk of thromboemboli

104
Q

Symptoms of nephrotic syndrome

A 
Hypoalbuminaemia
Oedema
Proteinuria >3.5g/24
\+hyperlipidaemia
Often muehrche's bands
May lead to AKf 
Caused by focal segment glomerulosclerosis or membranous cause.
105
Q

Symptoms of nephritic syndrome

A 
Hypertension
Haematuria
Hypoalbuminaemia
Rapid onset
Oliguria
Often occurs in post streptococcal glomerulonephritis in children
Requires renal biopsy for diagnosis
Pores in Podocytes
106
Q

Describe rapidly progressive glomerulonephritis

A

Renal function deteriorates over days. Ureamic emergency.

Renal biopsy required

107
Q

Causes of nephrotic syndrome

A 
Minimal change glomerulonephritis,
Focal segmental glomerulosclerosis
Membranous glomerulonephritis
DM
Amyloidosis
108
Q

Describe minimal change glomerulonephritis

A 
Unknown circulating factor leads to Podocyte damage
Does not normally lead to renal failure 
Child/adolescent 
Responsive to steroids
May recur
109
Q

Describe focal segmental glomerulosclerosis (FSGS)

A 
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
Q

Describe membranous glomerulonephritis

A

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
Q

How does DM cause nephrotic syndrome?

A

Thickening of BM
Micro vascular disease
Mesangial sclerosis
Progressive to renal failure

112
Q

Causes of nephritic syndrome

A

IgA nephropathy
Hereditary nephropathies
Goodpasture syndrome (anti GBM)
Vasculitis

113
Q

Describe IgA nephropathy

A 
IgA in mesangium leading to damage and scarring
Associated with mucosal infections
Commenest GN
Often causes renal failure
Any age
Very variable
114
Q

Describe hereditary nephropathies

A 
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
Q

Describe goodpasture syndrome (anti-GBM)

A

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
Q

Describe vasculitis

A

Associated with anti neutrophil cytoplasmic antibody (ANCA) treatable if early
Segmental necrosis
Urgent biopsy needed
Inflammation destroys blood vessels

117
Q

Risk factors prostate cancer

A

Age- >80 75%
Fam history
Black>white> Asian
BRCA2 gene mutation

118
Q

Screening prostate cancer

A

Not recommended as overdiagnosis
Often PSA raised in other things e.g. BPH, infection, inflammation.
False pos and negs.

119
Q

Clinical presentation prostate cancer

A

Asymptomatic
Urinary symptoms e.g. Overactivity
Bone pain from mets
Haematuria (advanced)

120
Q

Diagnosis/ investigation prostate cancer

A

DRE
Serum PSA
TRUS- transracial ultrasound - guided biopsy of prostate

121
Q

Treatment of prostate cancer

A

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
Q

Risk factors bladder cancer

A 
Age
Males
90 TCC
Smoking x4
Occupational e.g. Rubbers, plastics, painters, hairdressers
Schistosomiasis
123
Q

Treatment bladder cancer

A

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
Q

Staging and grading of bladder cancer

A

TNM

Normal stuff e.g. Mitosis, cytoplasm

125
Q

Renal cell carcinoma aetiology, investigations and treatment

A

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
Q

TCC risk factors, investigation and treatment

A 
Smoking, phenacetin (fever and pain)
Ultrasound
Ct
Retrograde pyelogram
Ureteroscopy
Treatment nephro-ureterectomy- kidney fat, cuff of bladder, ureter.
127
Q

Main causes of chronic kidney disease

A 
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
Q

Risk factors for chronic kidney failure

A

N

129
Q

Define CKD

A

Progressive and irreversible loss of kidney function from months to years

130
Q

Classification of CKD

A

Stages 1-5 based on GFR
1 >90
5 <15

131
Q

Ways in which CKD can affect the CVD system

A 
Increase in Na and h2O
Acidosis
Atherosclerosis
Cardiomyopathy
Pericarditis
132
Q

Ways in which CKD can affect the haemopoitic system

A

Anaemia- low erythropoietin

133
Q

Ways in which CKD can affect the Musculocutaneous system

A

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
Q

Other effects of CKD

A 
Neuropathy
Seizures
Coma
Tiredness
Breathlessness
Restless legs
Sleep probs
Aches and pains
NV
Itching
Chest pain
135
Q

Investigating CKD

A

GFR via inulin (in theory too expensive and time) or 24hr creatine clearence.
eGFR ethnicity gender and age

136
Q

Conservative management of CKD

A 
Lifestyle - smoking, obesity, exercise 
Treat diabetes 
Treat BP
Ace inhibitors
Lower lipids e.g. Statin 
Monitor
137
Q

When is dialysis needed

A

Typically GFR <10

Ureamic, hyperkalaemia, pericarditis, acidosis

138
Q

Describe haemodyalysis

A

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
Q

Describe peritoneal dialysis

A 
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
Q

Describe renal transplant

A 
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
Q

Sensory innervation of kidneys?

A

T10-11

142
Q

Blood supply of the ureters

A

3 parts:
1 renal arteries
2- common iliac, abdominal aorta and gonadal
3 - internal iliac arteries and everything else

143
Q

Innervation of ureters

A

Sensory T12-L2

Esa 3 (5 decks)

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