Flashcards in Urinary Deck (297):
0
Functions of the urinary system
Regulation of concentrations of key substances in ecf
By virtue of above effecting icf
Excretion of waste products
Endocrine
Metabolism
1
What are the hormones synthesised in the kidneys?
Epo
Renin
Prostaglandins
2
What is the metabolic activity of the kidney?
Activation of vit D
Catabolism of insulin
3
What proportion and amount of body mass is fluid?
60%
42L
4
What proportion and amount of body fluid is ECF
1/3rd
14L
5
What proportion and amount of ECF is plasma?
20%
3L
6
What is the difference between osmolarity and osmolality?
Osmolarity - number of osmoles of solute per litre solvent
Osmolality - number of osmoles of solute per kilogram solvent
7
How much ultrafiltrate is produced by the kidneys each day? Hw much is reabsorbed?
180 L produced
178.5 L reabsorbed
8
What are the vertebral levels of the kidneys?
Left T11-L2
Right T12-L3
9
What are the layers surrounding the kidney from inside out?
Capsul
Perinephric fat
Renal facia (anterior and posterior)
Paranephric fat (posteriorly)
Parietal peritoneum (anteriorly)
10
How does the kidney attach to the diaphragm? What is the consequence for the kidney position?
Via the renal fascia to the diaphragmatic fascia
Moves with respiration
11
How can the renal medulla be subdivided?
Renal pyramids containing nephrons
Renal columns carrying blood flow from hilum to cortex
12
How many major and minor calices are in each kidney
2 or 3 major calices each with 2 or 3 minor calices
13
Which vessel, artery or vein, is anterior as it enters the kidney?
Vein
14
What is the medical consequence of the segmental arteries not anastamosing in the kidney?
Each segment is surgically resectable
15
What are the autonomic nerves to the kidney?
The splanchnic nerves
16
Where do the ureters origionate? What is their abdominal course?
Uretopelvic junction posterior to artery and vein.
Pass down just anterior to the tips of the transverse processes of the spine
17
Where do the ureters enter the pelvis?
By the bifurcation of the common iliac artery (by the sacroiliac joint)
18
What is the course of the ureters in the pelvis?
Turn anteriomedially at the level of the ischial spines
19
How is backflow prevented from bladder to ureters?
They enter obliquely. Increased bladder pressure and constriction of the muscle on voiding close the lumen
20
What is the only thing that passes between the peritoneum and the ureter in males?
The vas defrans
21
Is the ureter anterior or posterior to the uterine artery in females?
Posterior
22
What is the arterial supply of the ureter?
Branches of the renal, gonadal, aorta, common iliac arteries snd internal iliac arteries
Many anastamoses
23
What nerves innervate the ureters?
Where do pain fibres travel?
Adjacent autonomic plexuses
Pain follows sympathetics back to T11 to L1
24
What is the space between the pubic bone and the bladder?
He potential reteropubic space
25
What supports the neck of the bladder?
Puboprostatic ligament (males) and pubovesicular ligament (females)
26
What is the triangle between the ureters and urethra termed?
Trigone
27
What is the arterial supply to the bladder?
Superior and inferior vesicular arteries
28
What are the three stages of urinary development?
Pronephros
Mesonephros
Metanephros
29
When and where does the pronephros form?
What does it do?
In the cervical region creating a duct to the cloaca
Beginning of week 4, regresses after several days
30
Where does the mesonephros develop? What is formed?
Caudal to the pronephros in the intermediate mesoderm.
Excretory tubules appear associated with capillary tufts. As they develop the urogenital ridge is formed
31
What happens to urine produced by the mesonephros?
Drains to the cloaca (not ruptured until week 7) so passes up the alantois into the umbilical cord
32
How does the mesonephros degenerate
Starting cranially even as the caudal end is still developing
33
How does the metanephros form?
Formation of the uteric bud by the mesonephros
Drives development of the metanephric blastema from the surrounding intermediate mesoderm
When the uteric bud contacts the metanephric blastema it branches forming the collecting system up to the collecting ducts of the nephrons
34
How does the metanephros reach its adult position?
What is the consequence?
Ascends from the pelvis
Partely due to cranial movement, partly done by remaining still as the trunk elongates.
Sequential ascending blood supply, usually degenerates but can create accessory vessels either into the hilum or into poles
35
What is renal agenesis?
Uteric bud fails to stimulate metanephric blastema
If bilateral not compatible with life?
36
What is duplication defect of the kidney?
The uteric bud splits forming two collection systems, these can open atopically eg. into the vagina causing incontinance
37
What are the two cyctic kidney diseases? What is different about them?
Multicystic kidney disease is a developmental disease where there is failed recanalisation of the ureter
Polycystic kidney disease is a genetic diaorder that causes renal failure, it has a poor prognosis
38
What is the consequence of failure of the kidneys in utero called? What is it?
Potters sequence:
Oligourea
Oligohydraminos
Hypoplastic lung disease
39
What is the urachus in healthy adult life?
Median umbilical ligament
40
How is the urogenital sinus formed?
Decent of the urorectal septum forms the rectum anteriorly and the urogenital sinus posteriorly
41
What are the three parts of the urogenital sinus? What do they form?
Upper part - future bladder
Pelvic and phallic part - future urethra
42
Where does the uteric bud open? How does this change during development?
Into the mesonephric duct
As the bladder expands it absorbs this junction and the uteric bud then opens directly into the bladder
43
What is the fate of the mesonephric duct in men?
As the bladder expands its opening is pushed further caudally into the developing prostate
44
What is the renal corpuscle?
The glomerulus within bowmans capsule
45
How does bowmans capsule form?
Blind ended tube of the metanephric blastema contacts and envelopes the glomerulus creating a double layered space with a visceral and parietal layer.
Viceral layer develops into podocytes wrapping around the glomerular capillaries.
46
What does the plasma have to cross to become ultra filtrate in the kidneys?
Fenestrated capillary endothelium
Basement membrane
Filtration slits between podocytes
47
Where is the PCT found? How does it appear in section?
Mainly in the cortex, though does dip into the medulla
Simple ciliated cuboidal
48
What are the four parts of the loop of henle?
Pars recta
Thin descending
Thin ascending
Thick ascending
49
How does the thin limbs of the loop of henle appear histologically?
Simple squamous, no blood cells (distinguish from capillaries), no brush border
50
How does the thick ascending limb of the loop of henle appear?
Simple cuboidal with no brush border
51
How does the dct appear histologically? Where is it found?
In the cortex
A squashed simple cuboidal epithelial tube. No cilia
52
How does the collecting duct appear histologically?
Non ciliated simple cuboidal epithelium. Appears very similar to thick loop of henle but slightly larger and more irregular
53
What are the components of the juxtaglomerular apparatus?
Dct - macular densa cells
Afferent arteriole - juxtaglomerular cells
Between - lacis cells
54
Hw many layers of muscle does the ureter have?
2/3rds bilayered
1/3rd trilayered
55
Where is transitional epithelium found?
Ureters, bladder, proximal urethra
56
What is then structure and function of transitional epithelium?
Stratified cells that are distensible. Covered in umbrella cells that are impermiable even at full stretch.
Function to protect from urine but also prevent tissue fluid entering the hypertonic urine
57
What is the charge on the basement membrane of the renal corpuscle?
Negative
58
Which are filtered more at the renal corpuscle anions or cations?
Cations are filtered more redily ( more end up in ultrafiltrate)
59
What effects filtration rate?
Capillary hydrostatic pressure vs ultrafiltrate hydrostatic pressure and osmotic gradient (outwards due to oncotic pressure)
60
What two methods of autoregulation exist to ensure constant filtration?
Myogenic response (contraction of smooth muscle on stretch)
Tubular glomerular feedback
61
How does tubular glomerular feedback work?
High gfr causes high na+ and cl- at dct
This is detected by macula densa cells causing release of adenosine resulting in afferent arteriole vasoconstriction
Low gfr causes reverse with macula densa releasing prostaglandins dilating afferent arteriole.
62
How is glucose reabsorbed in the pct?
Right the way into the blood please!
Na/k atpase sets up gradient of na+
Glucose and na+ reabsorbed using SGLT2 channels
This moves it against conc gradient into cell
It then moves down conc gradient into ecf then into blood
63
What substances are secreted into the tubule? Why?
Only 20% of plasma filtered therefore secretion necessary if more is needed to be removed
K+
H+
Anions and cations
Drugs (adrenaline, morphine, penicillin)
64
What is normal gfr for males and females?
Males 115-125ml/min
Females 90-100ml/min
65
What is renal plasma flow?
1.1 L/min of blood, 55% plasma thus 605ml/min plasma
66
What is the filtration fraction? How is it calculated?
20%
GFR/renal plasma flow x 100
67
What is clearance in the kidney?
The volume of plasma from which a substance is completely removed by the kidneys/minute
Clearance = ([substance in urine] x urine flow)/[substance in plasma]
68
What properties does a substance need in order to apply its clearance to calculate gfr?
Not secreted or reabsorbed
Filtered freely
Not metabolised in the urine
69
What does egfr account for when measuring serum creatinine?
Age sex mass
70
What is the ideal substance for calculating gfr?
Inulin
71
What is filtered load of a substance?
Plasma concentration x gfr
(amount of substance filtered per minute)
72
What is the transport maximum?
The amount of substance the tubule can reabsorb
73
What is the renal threshold?
The plasma concentration of a substance that will exceed the filtered load that would exceed the renal threshold!
74
Why must the kidneys be able to vary sodium excretion?
To deal with varied dietary absorption
To allow BP control
75
What drives na reabsorption in the kidneys?
What ion comes with it? What is the exception to this rule?
Na/k atpase on basal membrane
Cl but in early pct hco3
76
What is the effect of the early pct reabsorbing hco3- alongside na rather than chlorine?
Increases cholorine tubular concentration allowing paracellular reabsorption
77
Where is most sodium and water reabsorbed? How much?
PCT
65% water
67% sodium
78
What are the sodium channels in the PCT
Which one is under regulation of hormone? Which hormone?
Na/glucose, Na/aa, Na/phosphate, Na/H exchanger
Na/Phosphate under PTH control
79
How do ion channels differ along the PCT?
All present in the first segment
Latter two segments only have Na/H exchanger
80
Why is the reabsorptionin the PCT described as isoosmotic?
Fully permeable to water so no change in osmolarity
81
What is the degree of reabsorption of na and water in the loop of henle?
Decending - 10-15% water
Ascending - 25% na
82
How is na reabsorbed in the ascending loop of henle?
In thin limb passive paracellular due to high osmolarity in tubule
In thick limb Na/k atpase driving NKCC2
83
In the thick ascending limb where do the cl- and k+ ions go after reabsorption?
Cl into ecf
K through romk back into tubule
84
What is the character of the fluid found at the top of the ascending limb?
Hypoosmotic
85
What cell type is found in the early DCT?what does it absorb and how?
Tubular cells
Na/KATPase drives Na/Cl synporter with the Cl being extruded basally
86
Where is calcium reabsorption controllable? How?
Tubular cells of Early DCT
NCX on basal membrane allows apical reabsorption from tubule under PTH influence
87
Where is most calcium reabsorbed? Where else?
PCT
Ascending loop by lumen positive potential
88
Explain the principle of glomerulotubular balance
By reabsorbing by percentage rather than amount any increase of decrease in gfr is compensated for
89
How much water and na is reabsorbed in the early dct? What happens to the osmolarity of the filtrate?
5-8% sodium
No water
Becomes more hyposmotic
90
How much sodium and water is reabsorbed in the late dct and cd?
3% sodium
5-25% water depending on adh
91
What are the two cell types in the late dct / cd
Principal cells
Intercalated cells
92
What is the function of principal cells? What are they sensitive too? What is the effect on the lumen?
Na/K atpase sets up na gradient
Enac uniporter for sodium reabsorption
Romk uniporter for K secretion
Sensitive to aldosterone
More na absorption than k secretion so lumen becomes -ve driving the k secretion and Cl reabsorption
93
What are the general functions of the intercalated cells of the dct?
Acid base balance
Active cl reabsorption
94
What systems influence long term blood pressure control?
RAAS
SNS
ADH
ANP
95
What stimulates renin release?
SNS
Low perfusion of afferent arteriole detected by baroreceptors
Low Na/Cl in DCT thus low GFR detected by macula densa
96
Actions of angiotensin II
Stimulates aldosterone release
Vasoconstriction
Increased Na/H in PCT
97
Effect of SNS on BP
Stimulates renin release
Decreases renal bloodflow decreasing GFR
Activates Na/H and Na/KATPase in PCT
98
How does ADH influence blood pressure?
Increased osmolarity or hypovolemia stimulate ADH release resulting in water retention
Also stimulates NKCC2
99
Role of ANP in blood pressure regulation?
Released by atria in response to excessive stretch
Causes vasodilation of afferent arteriole increasing GFR and inhibits Na reabsorption in nephron
100
Why do NSAIDs cause renal failure?
If GFR decreases tubuloglomerular feedback results in prostaglandin release from juxtaglomerular apparatus to dilate afferent arteriole. NSAIDs block the prostaglandin synthesis
101
What are the physiological consequences of HTN?
Increased afterload:
LVH
Myocardial ischemia due to increased demand
Arterial damage (athereosclerosis and weakened vessels):
Aneurysm
Thrombus (Cerebrovascular disease)
Retinopathy
Kidney damage
102
How are changes in osmolarity detected?
How does this occur?
Swelling or shrinkage of hypothalmic osmoreceptors
Surrounding capillaries have fenstrated epithelium exposing the receptor to the plasma osmolarity directly
103
What occurs if plasma osmolarity increases?
Stimulation of osmoreceptors stimulates ADH release and increases thirst.
104
What is the thirst pathway?
Large increased osmolarity or decreased plasma volume increases thirst
Induces drinking behaviour
Immediately pathway is sated - anticipation of water being absorbed once drunk
105
Where is ADH released from?
Posterior pituitary
106
What is the structure of ADH?
Small peptide hormone
107
What are the actions of ADH on the kidney generally?
Vasoconstriction of glomerulus reducing GFR
Increased NKCC2
Activates Gs GPCR on late DCT and CD with increased PKA causing insertion of aquaporin 2 into the apical membrane
108
How does water travel through the basal membrane of the late DT and CD?
Through aquaporin 3 and 4
109
If there is no ADH what happens to urine? Condition?
Large volumes of dilute urine
Diabetes insipitus
110
What takes priority in a case of low blood volume (low BP) and low osmolarity?
The low volume - ADH will be secreted in spite of low osmolarity
111
What is the corticopapillary osmotic gradient? How is it formed?
The gradient of increasing interstitial osmolarity in the interstitium from the top of the cortex (low osmolarity) to the renal papilla (high osmolarity)
- countercurrent multiplying and exchange from the loop of henle and the vasa recta respectively
- recycling of urea
112
How does urea cycling effect the corticopapillary osmotic gradient?
Urea is at high concentration in the collecting duct
It is reabsorbed through aquaporin 2 thus reabsorption increases when ADH is high
It is then reabsorbed into the ascending limb
113
How is a corticopapillary osmotic gradient set up using Na/Cl and water?
The loop of Henle acts as a countercurrent multiplier - the ascending limb reabsorbs Na into interstitium decreasing filtrate osmolarity and increasing interstitial osmolarity by up to 200momol/l
Water leaves descending limb and is reabsorbed by vasa recta due to high oncotic pressure and counter current exchanger giving it high osmolarity. This concentrates the descending limb fluid
Water from the descending limb moves into the ascending limb, as it is now a higher osmolarity it can have more na reabsorbed concentrating the interstitium further still and so on!
114
What are the actions of PTH?
Increases osteoblasts decreases osteoclasts
Increases DCT reabsorption of calcium
Decreases PCT Pi reabsorption
Activates vitamin d
115
What is the half life of PTH? What causes its release?
4 minutes so can respond quickly to changes in calcium
Released as low calcium increases mRNA transcription and stability
116
Where is PTH produced and degraded?
Chief cells of the parathyroid gland
117
What are the two precursors to vit D? How do they differ?
Cholecalciferol (from light)
Ergocalciferol (from diet)
118
What are the steps of activation of vit d? Where?
Cholecalciferol
LIVER - 25hydroxycholecalciferol
KIDNEY - 1.25dihydroxycholecalciferol (calcitriol)
119
Which step of vit. D synthesis is controlled by pth?
25hydroxyvitd to 1.25dihydroxyvitd
120
What is another name for 1.25dihydroxycholecalciferol?
Calictriole
121
When sufficient calcitriol has been produced where is excess 25.hydroxycholecalciferol diverted too?
24.25dihydroxycholecalcifeole
122
What increases risk of vit d deficiency?
Non-caucasian
Lack of sunlight (indoors, clothes, sunscreen, climate)
Lack of fish oil (ergocalciferol)
Elderly/obese
Cyp450 inducers
123
Actions of calcitriol
Increased gi calcium absorption
Cell differentiation and proliferation
Decreased cell growth
Increase insulin
Decreases renin
124
What is primary hyperparathyroidism?
Biochemical presentation
Adenoma of parathyroid gland
High PTH driving high Ca
125
What is secondary hyperparathyroidism?
Biochemical presentation
Low calcium driving raised PTH to return to normal
Low (uncompensated) or normal (compensated) calcium
High PTH
126
What is malignant hyperparathyroidism?
Release of PTHrP causing high calcium
Calcium very high, PTH low as supressed
127
What is tertiary hyperparathyroidism?
Biochemical presentation?
Long term secondary hyperparathyroidism causing autonomous pth release and thus hypercalcaemia
High pth and high calcium
128
What type of hyperparathyroidism is more likely to be present in raised calcium on investigation of renal calculi. Which one is unlikely?
Primary hyperparathyroidism is likely
Malignant hyperparathyroidism is unlikely
129
What type of hyperparathyroidism is characterised by a rapid onset?
Malignant
130
What are signs and symptoms of hypercalcaemia?
Stones
Moans (constipation)
Grones (depression)
Short QT
HTN
Drowsiness
Polyurea / polydipsia
131
What is the treatment of hypercalceamia?
Underlying condition
Hydration to increase excretion
Loop diuretics
Bisphosphonates
Calcitonin
132
What diuretics can worsten hypercalcemia? Why?
Thiazides
Block na/cl = decreased na reabsorption = low sodium in cells = increased basal NCX = low calcium in cells = increased calcium absorption
133
What are the four most common types of renal calculi?
Calcium (70%)
Magnesium ammonium phosphate
Urate
Cystine
134
What sort of renal calculi is radiolucent
Urate
135
If you have had one renal stone what is your chance of having another?
50%
136
Which gender is more likely to get renal stones?
2:1 males:females
137
What increases risk of renal stones?
Male, dehydrated, previous stone, infection, hypercalcemia/hypercalciurea
Drugs
Loop diuretics - calcium stones
Thiazides - urate stones
138
How do renal calculi present?
Asymptomatic
Haematuria
Pain
139
General treatment options of renal calculi
Surgery
Lithotripsy
Fluid
140
What is used in uric acid stones
Allopurinol
141
What tests in renal calculi?
Blood screen
Urine screen
Radiography
142
What are the effects of alkalaemia?
Increases calciums affinity for albumin lowering serum free calcium. Low free calcium increases NCX, increasing intracellular sodium causing depolarisation - tetany
143
What are the systemic effects of academia
H excreted in exchange for K reabsorption in the kidneys - similar in cells - h taken in extruding k all causing hyperkalaemia.
Damage to enzymes causing decreased muscle contractility, glycolysis and hepatic function
144
What do the kidneys do to compensate or correct pH disturbance. Which type of does the kidney do each for?
Changes HCO3- excretion and creation
Compensates for respiratory
Corrects metabolic
145
What is the general response of the kidney to acidosis?
Recover all filtered HCO3-, secretes H+ and create new HCO3-
146
How does the kidney reabsorb HCO3-?
Secretes H+ through Na/H antiporter
H+HCO3- to CO2 and water
Reabsorb CO2
Recombine with water in cell
excrete H again
NOTE there is no net H+ excretion by this method
147
What is it that triggers bicarbonate reabsorption in the kidneys?
Not just acidosis - what about it and what else!
High CO2 in PCT cells increases H for secretion
Volume depletion increases reabsorption of Na+ thus excretion of H and also increases RAAS and Ang 2 increases NHE
148
Where and how does the kidney make hco3- in acidosis?
Alpha intercalated cells
H2O and CO2 to H and HCO3-
H actively secreted into lumen in exchange for K (uses ATP)
HCO3- enters ECF
Also secretes NH3 from aa breakdown to buffer H+ in urine to NH4+
149
What buffers H+ in urine, why is this necessary?
Phosphate and ammonia
Prevents damage and maintains concentration gradient
150
How do the kidneys increase H+ secretion? Where from?
H/K exchange in alpha intercalated cells as HCO3- is produced
151
What is the anion gap?
The difference between principle cations (Na+ and K+) and principle anions (HCO3- and Cl-). A high gap means a large number of unusual anions suggesting high acid production (e.g. lactate ions) rather than increased loss of HCO3- (e.g. renal tubular acidosis)
152
How do the kidneys aim to correct or compensate for alkalosis? What may stop this occurring?
Increase HCO3- excretion
But if volumed depleted unable to do this as Na reabsorption also stimulates HCO3- reabsorption
Thus fix by rehydration
153
Why do small changes in the. Balance of K have huge effects on the body?
98% k is in icf thus little change in balance will dramatically shift extracellular concentration
154
How does the body respond to rapid fluctuations in k? Why?
Intracellular buffering
Kidneys cant respond fast enough
155
What is internal k balance
Stabilising ecf K by moving in and out of icf
156
What is external k balance?
Matching excretion to intake
157
What increases K uptake into cells?
Increased ecf K
Hormones (insulin, aldosterone, catacholamines)
Alkalosis (shunt K in for H out)
158
What increases K release from cells?
Low ecf k
Exercise (repolarisation and muscle damage)
Cell lysis (rhabdomyolysis, haemolysis)
Increased ECF osmolarity (relative decreases as water moves out)
Acidosis (K out to allow H in)
159
Where and how in the kidney is K reabsorbed?
PCT - paracellular diffusion
Thick ascending limb - NKCC2
Alpha intercalated cells - K/H antiporter
160
Where and how in the kidney is K secreted?
Principal cells
Apical ROMK
161
How is K reabsorption and secretion controlled in the kidney?
By altering secretion amounts from 15-120%
Responsive to aldosterone
162
What factors cause K secretion in principal cells?
High intracellular K
High intracellular Na (through ENaC) creating electrical gradient with negative luminal and positive cellular potential
163
What increases secretion of k from principal cells?
Increased ecf k activating na/k atpase
Increased na reaching them in lumen
Increased flow in lumen removing secreted k increasing gradient
Increased aldosterone
Alkalosis (stimulates na/k atpase)
164
How does acidosis result in hyperkalaemia?
Increased H/K atpase in alpha intercalated cells
Decreased na/k atpase in principal cells lowering k secretion
165
What can cause hyperkalaemia?
Increased intake (needs renal dysfunction OR IV dose)
Decreased excretion (kidney disease, adrenal disease)
Internal shift (acidosis, cell lysis, exercise)
166
How should hyperK be treated?
Calcium gluconate
Glucose and insulin
Salbutamol
Dialysis
167
Causes of hypokalaemia
Increased loss (diarrhoea, vomiting, diuresis, high aldosterone)
Internal shift (alkalosis, aldosterone, adrenaline)
168
Treatment of hypok
K replacement
Block aldosterone
169
What diseases result in high aldosterone secretion?
Conns syndrome (aldosterone secreting adenoma)
170
What is the lifetime risk of uti in women?
When are they most likely?
50%
Children, sexually active (honeymoon), pregnancy, elderly
171
Risk factors for uti
Short urethra (women)
Obstruction (calculi, prostate, tumour, pregnancy)
Neuro problems (unable to empty bladder fully)
Ureteric reflux (especially children)
172
What adaptations to bacteria aid them in surviving to cause uti
Fimbriae for attachment
Polysaccharide capsule to avoid immune system
Urease production to increase ph
173
How does a lower uti present?
Cystitis
Increased urinary frequency
Mild fever
Dysuria
174
How does an upper uti present
Loin pain
High fiver
175
Who is more at risk of asymptomatic uti?
Elderly
Catheters
176
Define complex uti?
Treatment resistant
Male
Pregnancy
Children
Elderly
Pyleonephritis
177
What urine dip sign is very sensitive for uti? What is very specific?
Leucocyte esterase very sensitive
Nitrites very specific
178
What. Is the negative predictive value of turbidity in urine for uti?
97%
179
When would you culture a uti? What specific test is applied to it?
Complicated uti
Fermenting lactose to dx ecoli
180
What proportion of females with uti symptoms have significant bacteriuria? What may cause this?
50%
Sti urethritis, vaginal infection, mechanical cause, on abx, tb, fastidious organism (complex requirements so hard to grow)
181
When is microscopy of urine indicated?
Kidney disease
Endocarditis
Children under 6
182
What could squames visible on microscopy of urine indicate?
Contaminationn
183
Tx for simple, complex and pylonephritis uti
Simple 3 days
Complex 7 days
Nitrofurantoin or trimethoprim
Pylo 14 days
Ciprofloxacin or ceftrioxone or gentamicin
184
What can be done for frequently reoccurring utis?
More than three a year, prophylactic nitrofuritoin or trimethoprim
185
Which uti patients need imaging?
Children
Suspicion of problem with posterior urethral valve (men)
Suspicion of vesicouteric reflux (women)
186
What is the somatic, sympathetic and parasympathetic innervation to the bladder?
Som - pudendal
Symp - hypogastric nerve
Para - pelvic nerve
187
What does parasympathetic stimulation to the bladder do on a cellular level?
Stimulates M3 Ach receptors causing activation of GalphaQ to IP3 and DAG causing detrusor muscle contraction
188
What does sympathetic stimulation to the bladder do on a cellular level?
Detrusor muscle
Stimulates Beta3 receptors triggering GalphaS resulting in K efflux and hyperpolarisation thus muscle relaxation
Internal sphincter
Stimulates Alpha1 receptors triggering GalphaQ resulting in IP3 and DAG thus contraction and sphincter closure
189
What are the two phases of the bladder?
Storage
Voiding
190
What is the reflex involved in storing urine?
Low levels of stretch stimulate pelvic afferents
These activate the spinal continence centre
1) causing pudendal to close sphincter
2) causing hypogastric to stimulate detrusor relaxation and internal sphincter contraction
191
How can higher centers influence urinary storage?
Cerebral storage centre activates pontine storage centre which bilaterally activates the spine continence centre to activate the pudendal nerve closing the external sphincter.
192
What is the effect of detrusor relaxation during bladder filling?
Very little change in pressure
193
How does the micturition reflex occur?
Stretch of bladder detected by pelvic afferents, triggers stimulation of parasympathetic pelvic nerve and inhibition of the pudendal and sympathetic hypogastric nerve. This promotes voiding.
194
How do higher centres influence micturition?
Also recieve afferents informing them of stretch.
Cerebral micturition centre stimulates pontine micturition centre which in turn causes the increased parasympathetic and decreases symp and somatic. If urination not desirable can consciously activate storage centres promoting contraction of the external sphincter.
195
What would happen to the bladder in a spine injury above S2?
Lack of conscious control
On filling sacral spine reflex will cause detrusor contraction but lack of stimulation from pontine micturition centre will mean:
1) incomplete voiding
2) dyssynergia - external sphincter will not relax in time with contraction causing retention
196
What would happen to the voiding of the bladder in a sacral or peripheral nerve damage?
Flaccid bladder - overfilling with overflow incontinence
197
4 types of incontinance
Stress (SUI) - leakage on effort, sneezing, cough, exertion
Urge (UUI) - leakage preceded by urgency
Mixed (MUI) - SUI and UUI
Overflow (OUI) - dribbling of urine secondary to LMNL
198
What is overactive bladder syndrome?
Polyuria, nocturia and urge +/- UUI
199
What are non modifiable risk factors for incontinance?
Family hx
Anatomical abnomalities
Neurological abnormalities
Age
200
Modifiable risk factors for incontience
Drugs, uti, chronic cough, obesity, preggo, childbirth, pelvic surgery, dementia
201
Examinations in incontinent patients?
Bmi
Abdo
DRE
Vaginal
Urine dipstick
Frequency volume chart/diary
202
Advanced investigations for incontinace
Invasive urodynamics
Pad test
Cystoscopy
203
SUI management
Stop smoking (decrease cough)
Pelvic floor training
Duloxetine (NA/5HT reuptake inhibitor)
Vaginal tape
Fascial sling
Intermurial bulking
204
UUI Management
Decrease caffine
Scheduled voiding with gradual increase in duration over months
Anticholinergics e.g. Oxybutynin
Beta 3 agonists
Botulinum toxin
Sacral nerve neuromodualtion
Urinary diversion into a bag
205
Management of overflow incontinance
Treat compression
Avoid constipation
206
Ways of mitigating incontinance?
Catheters
Sheaths
Incopads
207
What is AKI?
Clinical syndrome causing acute decline in GFR over days to weeks
208
Diagnostic criteria of AKI
Raise in serum creatining greater than 26.5mmol/l in 48 hrs or 1.5x baseline in 7 days
Maybe low urine volume (<0.5ml/kg/hr) for 6 hours
209
What can AKI cause?
Changes to ecf volume
Electrolyte abnormalities
Ph abnormalities
210
What is the in hospital incidence of. AKI
5%
211
Cause of prerenal AKI
Decreased renal perfusion
- volume depletion, chf, systemic vasodilation, preglomerular vasoconstriction (NSAID), postglomerular vasodilation (ACEi/ARB)
212
What is the effect of pre renal aki on sodium excretion?
Active reabsorption of na and h2o thus fractional na excretion less than 1%
213
Treatment of pre renal aki
Fluids
Underlying cause
Stop offending meds
214
What different pathologies can cause renal aki?
ATN
Glomulonephritis
Interstitial disease
Intrarenal obstruction
215
Causes of ATN
Sepsis
Nephrotoxins
Ischemia
Continum from pre renal AKI
216
What effect does ATN have?
Damage to tubular cells impaired salt and water reuptake with expulsion of excess water.
217
Examples of endogenous nephrotoxins
Bilirubin
Myoglobin
Urate
218
Examples of exogenous nephrotoxins
Xray contrast
Nsaids
Animoglycosides
Lithium
Antifreeze
Weedkiller
219
What can cause a low fractional excretion of sodium that isn't pre renal AKI.
Glomerulonephritis
Early rhabdomyolitis
Hypercalcemia
Vasoconstrictive drugs (e.g. NA)
Hepatorenal syndrome
Contrast nephropathy
220
Signs that an AKI is. Prerenal?
Postural hypotension
Low JVP
Sepsis/CHF
Rapid weak pulse
Low CVP
221
Why does ATN cause decreased GFR and thus fluid overload if aggressively resuscitated
Increased sodium - tubularglomerular feedback - afferent constriction
Back leak of filtrate in pct
Obstruction of tubule by debris from dying tubular cells
222
What can cause tubulointersitial nephritis?
Pyleonephritis
Toxins
223
What causes post renal AKI?
Obstruction if bilateral or effecting a sole functioning kidney
224
Examples of. Obstruction causing post renal aki
Luminal - calculi, blood clots,
Wall - neuromuscular dysfunction, neurogenic bladder, stricture
External - tumour, prostate, AAA, ligation
BLOCKED CATHETER
225
Tests in AKI?
Dipstick
Culture
Microscopy
Biochemistry (U+E, FENa+)
Imaging in post renal or non refractory prerenal/renal
CVP and CXR if risk of fluid overload
Histology in renal if not clear ATN
226
When would dialysis be considered in AKI?
HyperK not responsive to medical tx
Non refractory metabolic acidosis
Fluid overload not refractory to diuretics
Dialysable nephrotoxin (eg aspirin OD)
Uremia
227
Signs of uremia
Pericarditis
Lowered GCS
N+V
228
What different dysfunctions can renal disease present with?
Excretion - hyperK, fluid overload, acidosis
Glomerular - proteinuria, haematuria
Tubular - nocturia, polyuria, glycosuria
Hormonal - osteomalacia, anaemia, htn
229
Causes of microscopic haematuria
Uti
Polycystic kidneys
Renal stones
Tumours
AV malformations
Glomerular disease
230
At what age should all haematuria cases receive a cystoscopy?
>45
231
Differentiate haematuria from glomerular disease and lower urinary tract
Glomerular - smoky brown +\- protein, painless
LUT - red, clots, pain, no protein
232
Non blood causes of red/brown urine
Myoglobinuria
Beetroot
233
At what point in GFR do CKD symptoms present?
<30ml/min
234
Presentation of proteinuria
Frothy urine
Oedema due to low oncotic pressure
Infection due to low plasma immunoglobulin
Thrombus risk due to imbalanced coagulation factors
235
Types of protienuria
Glomerular - increased permiability
Tubular - decreased reabsorption of filtered small proteins
Overflow - filtration of small proteins above transport maximum
236
Cause of overflow proteinuria
Multiple myeloma
237
What is nephrotic syndrome. How does it feed back on itself? What random thing does it cause?
Proteinuria with oedema 2ndry to hypoalbuminia
Decreases circulating volume increases RAAS increases sodium retention, increases oedema
High cholesterol
238
What is nephritic syndrome?
Rapid onset oligouria, low GFR, HTN, oedema, haematuria, normal albumin.
239
How can the renal capsule result inpathology?
Blockage
Leakage
240
What 4 points of the glomerulus are vulnerable to damage?
Subepithelial
Basement membrane
Subendothelial
Mesangial
241
Glomerular causes of nephrotic syndrome
Minimal change glomerulonephritis
Membranous glomerulonephtitis
Diabetes mellitus
242
Age distribution of minimal change glomerulonephritis?
Treatment?
Consequence of this
Most common nephrotic syndrome in children
Very good response to steroids
Treat and if responds no need to biopsy
243
Changes of minimal change glomerulonephritis on biopsy?
None to light microscopy
On electron loss of podocyte foot processes
244
Prognosis of minimal change glomerulonephritis?
Responds well to steroids. May progress to renal focal segmental glomerulosclerosis and renal failure. If so often returns post transplantation.
245
What is the commonest adult glomerular nephrotic syndrome?
What causes it?
Membranous glomerulonephritis
Immune complexes forming and damaging subepithelial layer - autoimmune or secondary to SLE or plasmodium malariae
246
How does membranous glomerulonephritis appear histologically?
What is the treatment?
Masses of immunoglobulin deposition
Immunosuppressants
247
How does diabetes cause glomerular disease?
Microvascular glomeruli disease causing progressive proteinuria
Basement membrane thickens
Podocytes detach
Scarring and nodules form
248
Primary causes of nephritic syndrome
IgA nephropathy
Thin glomerular basement membrane disease
Alports syndrome
Goodpastures syndrome
249
When does IgA nephropathy tend to occur?
What does it cause?
Post mucosal infection
Immune complex deposition in mesangium
Haematuria
250
What is the prognosis of IgA nephropathy?
Progression to renal failure with transplant as the only option
251
What is the prognosis of thin glomerular basement membrane disease?
Benign
252
What is alports syndrome?
X linked inherited disease causing split basement membrane
Progresses to renal failure
253
What is goodpastures syndrome?
Rapidly progressing nephritic syndrome with autoantibodies against basment membrane
Treatable with immunosupression and plasmaphoresis if caught early
254
What is. Goodpastures syndrome associated with?
Pulmonary haemorrhage in smokes
255
What is a secondary cause of nephritic syndrome? What marker will be raised?
Vasculitis e.g. Wegners
Antineurtophil cytoplasmic antibody ANCA
256
What is the epidemiology of prostate cancer?
Most common male cancer
Second most common cause of male cancer death
257
What is the prognosis of prostate cancer?
Most people diagnosed are unlikely to die of the cancer
258
What increases the risk of prostate cancer?
Age
Family history
Black ethnicity
259
Why is the fact that prostate cancer incidence increases with age problematic?
Urinary symptoms and benign enlargement also increase with age so harder to detect
260
What can cause a raised prostate specific antigen? What does this mean for screening?
Malignant cancer
Prostatic hypertrophy
Benign cancer
Prostatic inflammation
Massive overdiagnosis
261
What are the risks involved with prostate cancer treatment?
1/3 risk LUT symptoms
1/3 risk erectile dysfunction
5% risk incontinence
262
What is the prevalence of prostate cancer in 80 year old males
80%!
263
What are symptoms of prostate cancer?
Asymptomatic
Bladder overactivity
Metastatic bone pain
Urinary tract obstruction
Uncommonly weight loss and haematuria
264
What investigations are warranted in diagnosing prostate cancer (two routes)
DRE and PSA - transrectal ultrasound guided biopsy
LUT symptoms - TURP
265
How is prostate cancer graded?
Gleason grade - two numbers
First - grade of the most common area of the biopsy
Second - grade of the least differentiated area that is not the first
266
What treatments are available for prostate cancer?
Surveillance
Radical prostatectomy
Radiotherapy (external or brachytherapy)
267
What hormone treatment is used in metastatic prostate cancer?what complication does this have?
Surgical or chemical castration to reduce testosterone (as cancer is testosterone sensitive)
Flare - initial surge in testosterone
268
What non hormonal treatments are available for metastistied prostate cancer?
Targeted radio and chemo therapy for the bone mets
Bisphosphonates
269
What is the normal type of bladder cancer?
Transitional cell carcinoma
270
What are risk factors for bladder cancer?
Smoking
Occupational exposure to rubber, plastic, oil
Schistosomiasis causing metaplasia
271
How are bladder tumours staged?
Superficial (most)
In situ
Invading muscle
272
How are superficial bladder tumours treated?
Transureathral resection of bladder tumour
273
Hw are bladder tumours that have invaded muscle treated?
Radical cystectomy
Palliative
274
Risks for renal cell carcinoma
Smoking
Obesity
Dialysis
275
How can renal tumours spread?
Perinephric
Lymph nodes
Into IVC to right atrium
276
How can upper tract transitional cell carcinomas spread?
Pelvis to bladder NOT reverse usually due to urine. Flow
277
How are renal cell carcinomas treated
Radical or partial nephrectomy
278
How are upper tract transitional cell carcinomas treated
Nephrouterectomy (kidney, fat, ureter, cuff of bladder)
279
What is ckd
Irreversible and sometimes progresive loss of renal function over months to years
280
Cuases of ckd
Glomerulonephritis
Pyelonephritis
Obstruction
Htn
Vascular disease
Dm
281
How is ckd. Detected?
Opportunistic testing of at risk groups
282
How id ckd graded?
g1-G5 based on GFR
A1-A3 based on protein:creatinin ratio in urine
283
What. Grade of ckd is kidney failure?
G5
284
What. Is the main cause of death in CKD
Cvd
285
What does proteinuria mead diagnostically in ckd?
Increased risk of need of dialysis
286
When should a biopsy be performed in ckd?
Normal sized kidney with no obvious diagnosis
287
Complications of CKD
Acidosis
Anaemia
Bone disorders.
Non bone calcification
Cvd
288
What are the bone disorders of ckd?
Osteomalacia due to low active vit d thus low calcium absorption
Ostitis fibrosa cystica due to high PTH resulting in areas of reabsorbed bone replaced with fibrous cysts
289
Benefits and costs of haemodialysis
Benefits - others to talk to, low responsibility, days off
Costs - disruption to life, see others get ill, time consuming, high diet restrictions, high fluid restrictions, large number of meds
290
Contraindications and side effects of haemodialysis
Contraindications - failed vascular access, heart failure (relative - can it cope with extra 300ml)
Complications - infection of central line, thrombus at fistual, steal syndrome, cvs instability, bleeding
291
Benefits and costs of peritoneal dialysis
Benefits - convinience, independence, low diet and fluid reatrictions, initially better renal preservation
Costs - high responsibility, frequent bag changes or on every night
292
Contraindications and complications of peritoneal dialysis
Contraindications - adhesions, hernias, extensive abdo surgery, unable to do at home by pt or carer
Complications - peritonitis, infection, leaks into scrotum, hernia, failure of ultrafiltration due to scarring
293
When is the largest risk post kidney transplant?
3 months
294
What are the risks post kidney transplant?
Infection
Cancer
HTN
295
What type of donor provides best chance?
What is ave. life expectancy
Related live
12 years
296