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PPE > Renal > Flashcards

Renal Flashcards

1
Q

What is the anatomical difference between the left and right gonadal veins?

A
  • Left goes into left renal vein then to ivc

- Right goes straight into IVC

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2
Q

Describe the anatomical relationships between the renal vessels and ureter

A

-Renal vein most superficial, then renal artery then ureters

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3
Q

What is the trigone of the bladder and state its significance

A
  • A triangle area between the two ureter orrifices and the internal urethral meatus.
  • It is a non-distensible area which signals to the spinal cord when stretched
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4
Q

Name the segments of the male urethra

Which segment possesses the most resistance on passage of a catheter?

A
  • Pre-prostatic
  • Prostatic
  • Membranous
  • Spongy
  • Membranous
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5
Q

Give 3 common places a renal stone can get stuck

A
  • Pelviuretic junction (narrowing of the renal pelvis as it transitions into ureter)
  • Pelvic brim
  • Ureteral orrifice
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6
Q

What is the main function of the PCT?

A

-Site of major reabsorbtion of Na, K, bicard, glucose, amino acids and water

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7
Q

Briefly describe the development of the kidney

A
  • First pronephros forms from intermediate mesoderm and develops a duct which extends caudally
  • Mesonephros develops and commandeers pronephrotic duct. Caudal development continues until it makes contact with cloaca and ureteric buds begin to sprout
  • Ureteric buds make contact with metanephric blastema driving development into metanephros which is fuctioning fetal kidney
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8
Q

What is the urogenital ridge?

A

-Area of intermediate mesoderm on the posterior abdominal wall which gives rise to the embryonic kidney and gonads

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9
Q

Describe how the ureteric bud develops into collecting system of the kidney

A

-Makes contact with the metanephric blastema and grows into it by expanding and branching to form the collecting tubules, renal pyramids, major and minor calyx, renal pelvis and ureter

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10
Q

What is renal agenesis and give one physiological cause of this

A
  • Complete absence of a kidney

- Failed interaction of ureteric bud

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11
Q

What is a wilms tumour?

A

-Congenital tumour of the kidney

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12
Q

Describe one possible consequences of duplication defects of the ureteric bud

A

-Incontinence if complete duplicate ureter joins after external urethral sphincter

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13
Q

What is the function of the urorectal septum?

A

-Separates urinary tract from gut tube

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14
Q

What does the urogenital sinus develop into? How is it connected to umbilicus? Describe a pathology which is related to this

A
  • Upper portion of UGS creased bladder and urethra. Lower portion creates lower 2/3 vagina in females and prostate/spongy urethra in males
  • The allantois originally filters liquid waste via umbilicus in exchange with mother and it develops into urachus which is a fibrous remnant of allontois.
  • A patent urachus is failed regression of the patent tube into the medial umbilical ligament. This can lead to urine leaking out through umbilicus
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15
Q

Describe the layers of the renal corpuscle which make the filtration barrier

A
  • Fenestrated capillary endothelium
  • Visceral layer of bowmans capsule
  • Podocytes
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16
Q

What is the juxtaglomerular apparatus made up off and what is its function?

A
  • Macula densa of DCT
  • juxtaglomerular cells of afferent arteriole
  • Extraglomerular mesangial cells
  • Tubuloglomerular feedback -> Detects NaCl conc as a way of interpreting GFR. This results in either prostaglandin and renin secretion if decreased or adenosine secretion if increased leading to vasodilation and RAS activation or vasoconstriction respectively.
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17
Q

How do the collecting ducts form the minor calyx?

A

-Merging collecting ducts form renal pyramids which form renal papillae -> renal calyx

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18
Q

What epithelium lines the bladder and ureters?

A

-Transitional

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19
Q

Describe the charge on the glomerular basement membrane and state how this helps filtration

A
  • negative charge
  • Repels negatively charged proteins so even if they are small they may not pass through, attracts positively charged proteins so larger ones may pass through
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20
Q

Describe the forces which drive filtration

A
  • Capillary hydrostatic pressure
  • Bowmans capsule hydrostatic pressure
  • Capillary oncotic pressure
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21
Q

Explain how autoregulation of the kidney works?

A

-Within 80-180mmHg range in BP the kidney can control its own perfusion pressure and thus GFR by detecting changes in stretch of smooth muscle. An increase in BP causes an increased delivery of blood to the kidney -> afferent vasoconstriction to reduce blood vol and maintain perfusion pressure and GFR. Decreased BP causes afferent vasodilation maintaining bp and GFR.

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22
Q

Which capillary is wider afferent or efferent? How does efferent constriction effect pressure in the glomerulus?

A
  • Efferent

- Increases hydrostatic pressure

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23
Q

Why is water readily absorbed in the peritubular cappilaries of cortical nephrons?

A

-They have a high oncotic pressure

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24
Q

Describe Na and water resorption in PCT. Which important molecule is co-linked with Na resorption in pct and how?

A
  • NaKATPase sets up Na gradient
  • Na moves down conc gradient across apical membrane
  • Water follows
  • Glucose -> uses the Na gradient to move glucose against its concentration gradient by using SGLTs
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25
Q

In which part of the lumen does secretion of H, K and organic cations occur?

A

-DCT

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26
Q

How do you calculate filtered load?

A

-Plasma conc of substance(mg/ml) x GFR(ml/min) = x mg/min

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27
Q

Why can creatinine be used to calculate GFR? What would be an alternative in a hospital setting? How is GFR calculated?

A
  • Freely filtered, not reabsorbed and not secreted
  • Inulin
  • [urine] x [urine volume]/[plasma]
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28
Q

What is renal clearance?

A

-The volue of plasma which is totally cleared of a substance by the kidneys per unit time

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29
Q

How do you calculate eGFR?

A

-(140-age) x mass(kg) x 1.23(men) or 1.04(women)/serum creatinine

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30
Q

Describe the fluid volume in the different compartments

A

-3L blood
-13L ECF
25L ICF

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31
Q

Why must the kidneys be able to vary their Na excretion?

A

-To match excretion to ingestion to keep plasma volumes steady

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32
Q

Where in the nephron is the most Na reabsorbed?

A

-PCT (67%)

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33
Q

How does water move from the PCT into the vasa racta?

A

-Follows osmotic gradient into tubule cell and then pulled by oncotic gradient of blood and interstitial hydrostatic pressure

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34
Q

What is glomerulotubular balance?

A

-A mechanism to match Na resorption to GFR. As GFR increases Na resorption increase to make sure 67% is always reabsorbed

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35
Q

Describe what happens in the loop of henle in regards to Na and H2O resorption

A
  • Descending limb is water permeable and the increasing electrolyte gradient in the interstitium of the medulla draws water out so by the time in the bottom of the loop there is hyperosmotic filtrate
  • Ascending loop is impermeable to water and in thin ascending limb Na diffuses down its conc gradient into interstitium as it is a hyperosmotic filtrate
  • In thick ascending limb NKCC2 pumps Na into the interstitium to create a hypoosmotic filtrate at the top of the loop
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36
Q

What electrolytes does NKCC2 transport and what other channel is it dependent upon?

A
  • Na, K, Cl, Ca and Mg

- Requires ROMK channels to ensure leakage of K+ back into lumen so it works

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37
Q

Describe Na/H2O resorption in the DCT

A
  • Uses NCCT channels on apical membrane
  • Early DCT is poorly permeable to water and active Na resorption increase hypo-osmolarity
  • NaKATPase pumps Na into interstitium to be reabsorbed
  • Late DCT has ENaC in principle cells
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38
Q

Beside Na, what other electrolytes are controlled in the DCT?

A
  • Major site of Ca resorption via Ca channel on apical membrane and NCX on basolateral membrane
  • K secretion through apical K channels (attracted to negative lumen)
  • H+ secreted by a-intercalated cells
  • K+resorption by a-intercalated cells
  • Active Cl- resorption through b-intercalated cells
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39
Q

Where is renin released from? Why?

A
  • Juxtaglomerular cells of JGA
  • Decreased NaCl in DCT detected by macula densa cells of DCT, decreased perfusion pressure and sympathetic stimulation of JGA
  • Stimulates renin release to initiate RAS pathway to increase Na and H2O retention
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40
Q

Where is angiotensinogen made?

A

-Liver

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41
Q

Where is the main site of AgI conversion to AgII?

A

-Lungs

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42
Q

What are the actions of AgII?

A
  • Stimulates SNS
  • Stimulates Aldosterone production
  • Vasoconstriction
  • Direct effects on nephron to increase Na/H2O resorption
  • Stimulates ADH release
  • Stimulates thrist and salt intake
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43
Q

What 4 mechanisms are involved in long term regulation of BP?

A
  • SNS
  • RAAS
  • ADH
  • ANP/BNP
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44
Q

-How does the SNS use the kidney to alter BP?

A

-Causes vasoconstriction of afferent arterioles which decreases flow through the kidney and decreases GFR to decrease Na excretion
-Direct effect on nephron by stimulating NHE and basolateral NaKATPase
-Stimulates JGA to release renin to activate RAS
All together they increase BP

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45
Q

How do the natiuretic peptides function?

A

-Stimulated upon stretch of the atria or ventricles to cause vasodilation of the afferent arteriole to increase blood flow, increase GFR and increase Na excretion

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46
Q

What detects changes in plasma osmolarity? What is the outcome of detecting a increase in osmolarity

A
  • Hypothalamic osmoreceptors in OVLT
  • Stimulates ADH release from posterior pituitary via neural stalk
  • Stimulated thirst
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47
Q

What is the consequence of ADH release? How does it effect the osmolarity of the urine?

A
  • Enters circ and acts on kidney to cause insertion of aquaporin 2 channels into apical membrane of collecting duct which increases the permeability of the collecting duct to water and urea. Also causes vasoconstriction of glomerulus and increases activity of NKCC2
  • Causes the urine to become hyperosmotic
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48
Q

What happens when a decrease in osmolarity is detected?

A

-Removal of AP2 via endocytosis and Na intake stimulated and diuresis occurs producing hypoosmotic urine

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49
Q

What is diabetes insipidus?

A

-Decreased ADH production by the pituitary or acquired kidney insensitivity -> hypernatraemia and hypokalaemia

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50
Q

What is SIADH?

A

-Excessive ADH production from the posterior pituitary or an ectopic source eg small cell lung cancer causes an excessive water resorption leading to dilutional hyponatraemia

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51
Q

What is counter current multiplication?

A
  • A process which creates the descending osmotic gradient within the interstitium of the kidney from cortex to medulla
  • isotonic filtrate enters descending limb which is permeable to water but impearmeable to solutes -> creates a hyperosmotic filtrate in the bottom of the loop as water moves into interstitium
  • The ascending limb is permeable to solutes but not to water and Na diffuses into the interstitium. Most Na diffuses in the bottom of the limb as this is where the greatest gradient between limb and interstitium is. Then as the filtrate moves up the limb it becomes more hypotonic and thus not as much solute diffuses out and therefore the interstitium becomes less hyperosmotic as you move back towards to cortex. By the time the filtrate is at the top of the limb it is actually hypoosmotic
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52
Q

What is the function of the vasa recta?

A

-To maintain the counter current multiplication by flowing adjacent to the nephrons but in the opposite direction. As the vasa recta descends next to the ascending limb the solutes diffuse into the vessel. This causes the blood to become slow moving and hyperosmotic in equilibrium to its surrounding. This allows it to absorb the water from the collecting duct so that it does not dilute the interstitium
As it passes the descending limb the water diffuses into the vessels and the blood becomes isotonic and normal speed by the time it reaches the cortex

53
Q

What is urea recycling?

A
  • The cortical collecting duct is impermeable to urea meaning it is in high concentration in the medullary CD. When AQP2 channels are inserted into the CD water leaves and the urea in the CD becomes concentrated. This creates a urea gradient and the urea then diffuses out into the interstitium and then into the TAL of LoH to go back into the CD
  • Works as an effective osmole by increasing the osmolarity in the interstitium
54
Q

Describe the proportions of Ca resorption in the kidney

A
  • 65% PCT by paracellular diffusion
  • 25% LoH by NKCC2
  • 10% DCT by PTH
55
Q

How is vitamin D activated?

A

-Passes through liver which does 1st hydroxylation to 25-hydroxycholecalciferol. Then circulates in blood. When PTH is released a1-hydroxylase is activated in the kidney and causes a second hydroxylation to 1,25-dihydroxycholecalciferol which is active vit D

56
Q

What are the actions of active vitamin D?

A
  • Increase bone resorption
  • Increase calcium uptake in gut
  • Stimulate kidneys to increase Ca resorption
57
Q

What are the actions of PTH?

A
  • Stimulate osteoclast activity and slow osteoblast activity
  • Increase Ca and Mg resorption in kidney and decrease PO4 and HCO3 resorption
  • Stimulate a1-hydroxylase activity
58
Q

How is PTH controlled?

A
  • Negative feedback
  • Ca binds to PT cells and inhibits release
  • PO4 binds to PT cells and stimulates release
59
Q

What are the signs of hypercalcaemia?

A
  • Stones, moans, groans and psychiatric overtones

- Renal calyx, fatigue, abdominal pain/constipation, depression/decreased cognitive function

60
Q

Who are renal stones more common in?

A

-Men

61
Q

How do kidney stones form?

A

-Supersaturation of urine with solute and low urine volume caue crystals to form in filtrate ->forms stones

62
Q

Give 3 causes of hyperkalaemia

A
  • Acute kidney injury
  • Metabolic Acidosis
  • Tumour lysis syndrome
  • Tourniquet shock
  • Potassium sparing diuretics eg spironolactone, amiloride
  • Addisons disease
  • Diabetic ketoacidosis
63
Q

Why can DKA cause hyperkalaemia?

A
  • Lack of insulin prevents uptake of K into cells

- Excess H+ in blood exchanged for K+ with cells

64
Q

Give some clinical features of hyperkalaemia

A
  • Arrhythmia/heart block

- Paralytic ileus

65
Q

Describe the ECG changes in hyperkalaemia

A
  • Tall tented T wave
  • Prolonged PR
  • Absent P wave
  • Widened QRS
  • VF
66
Q

How is hyperkalaemia treated?

A
  • IV calcium gluconate
  • Glucose+Insulin IV
  • Beta agonist
67
Q

Give 3 causes of hypokalaemia

A
  • Potassium loosing diuretics
  • Diarrhoea
  • Bulimia
  • Vomiting sickness
  • Diabetes
  • Hyperaldostonaemia
  • Metabolic alkalosis
68
Q

What are the clinical features of hypokalaemia?

A
  • Arrhythmias

- Paralytic ileus

69
Q

What are the effects of increasing and decreasing the extracellular concentration of K?

A
  • Decreasing increases the gradient between ICF and ECF causing more K to leave the cell and hyperpolarisation
  • Increasing ECF decreases the gradient and prevents K leaving bringing the cell closer to threshold
70
Q

What mechanisms shift K from ECF to ICF to keep the internal balance?

A
  • Hyperkalaemia prevents K from leaving the cell
  • Insulin, aldosterone and catecholamines increase activity of NaKATPase
  • Alkalosis shifts K into cells by exchanging it for H+
71
Q

What mechanisms shift K from ICF to ECF to keep the internal balance?

A
  • Cell lysis
  • Hypokalaemia increases gradient causing an increase in K leaving the cell
  • Acidosis causes H+ to be exchanged for K+
  • Dehydration
72
Q

What is the effect of a high flow rate on K control?

A

-High flow rate keeps K gradient strong meaning more K is lost

73
Q

How does an increase Na delivery to the DCT control K secretion?

A

-Increased Na resorption causes and increased relative negativity in lumen causing more K to be lost

74
Q

What is the normal pH of plasma?

A

-7.35->7.45

75
Q

Why does alkalosis cause hypocalcaemia?

A

-Causes Ca to bind to albumin due to the lack of H+

76
Q

How does the kidney compensate for a respiratory change in pCO2?

A
  • If more pCO2 is blown off and alkalosis occurs the kidney will reduce the reabsorption of HCO3- inorder to compensate for the respiratory alkalosis
  • If there is an increase in pCO2 such as in late COPD then the kidneys will increase bicarb reabsorption and synthesis in order to compensate for the respiratory acidosis
77
Q

How does the kidney synthesise HCO3?

A
  • High metabolising tissue which produces lots of CO2 -> combine with H2O -> H2CO3 -> H+ + HCO3
  • Makes from amino acids like glutamine
78
Q

WHat is the normal ratio of HCO3 to CO2?

A

-20:1

79
Q

How is metabolic acidosis compensated for?

A

-Increase respiratory rate to blow off extra CO2

80
Q

How is matabolic alkalosis compensated for?

A

-Decreased resp rate but compensation limited by decreasing pO2

81
Q

Where is the majority of HCO3 recovered?

A

-PCT via reacting with H+ to form CO2 and H2O. CO2 diffuses into tubule cell

82
Q

Why is it important for HCO3 productions that H+ ions in the DCT are sequestered? What does this?

A
  • In order to drive the forward reaction in the lumen of CO2+H2O
  • HPO4 and NH3
83
Q

What is the minimum pH of urine? When does this occur?

A
  • 4.5

- When all HCO3 has been recovered

84
Q

What is the anion gap? what is it usually? What causes the gap to increase?

A
  • The difference between [Na]+[K+] and [Cl-] +[HCO3-]
  • 10-15mmol/L
  • HCO3 being replaced by other alkalotic ions after HCO3 has been used due to excess acid production eg lactic acid
85
Q

Which groups of people most commony gets UTIs?

A
  • Young women
  • Pregnancy
  • Elderly
86
Q

Give risk factors for a UTI

A
  • Diabetes
  • Neurogenic bladder
  • Obstruction eg BPH or pregnancy
  • Women
87
Q

Give 3 common causative organisms

A
  • E.coli (coliforms)
  • Proteus spp,
  • Enterococcus
  • MRSA in hospitals
88
Q

State the 3 places in which a renal calyx is most likely to get stuck?

A
  • Pelviuretic junction
  • Pelvic brim
  • Uterovesicle junction
89
Q

What are the symptoms of a uti?

A
  • Frequency and urgency (dysuria)
  • Pain
  • Fever
  • Loin pain
90
Q

When do you perform a urine culture in a UTI?

A

-In a complicated case eg male, children, pregnant, ?pyelonephritis

91
Q

Give some differentials of a UTI

A
  • STI
  • Thrush
  • Renal TB
  • Pyelonephritis
92
Q

How are UTIs treated?

A
  • Trimethoprim for 3 days in uncomplicated
  • 7 day course for complicated
  • Pyelonephritis = 14 days of IV ciprofloxacin/gentamicin
93
Q

Describe how voiding of micturition is controlled

A

-Upon filling of the bladder and stretching of the trigone afferent signals are sent to the spinal cord in a reflex arc which signals back to the bladder to empty however there is cortical control over this reflex arc which can inhibit the efferent reflex.

94
Q

Describe the muscle of detrusor. What is its innervation? What is the epithelium of the bladder?

A
  • 3 layers of smooth muscle roughly orientated in longitudinal, circular and oblique
  • Innervated bilaterally from T10-L2 by both sympathetic and parasympathetic nerves as well as cortical control over voiding
  • Transitional epithelium
95
Q

What receptors do the symp and parasymp stimulate in the bladder? Which nerve carries these fibres?

A
  • Symp=b3 adrenoreceptors ->hypogastric nerve

- Parasymp = m3 -> S2-S4

96
Q

Which part of the nervous system controls the storing phase of urine? What does activation of this cause?

A
  • Sympathetic neurones and the pontine storage centre in the pons
  • Relaxation of the detrusor and increase in EUS pressure
97
Q

What is the result of a lower motor neurone lesion to the bladder?

A

-Flaccid bladder leading the urinary retention and overflow incontinence

98
Q

What is the result of an upper motor neurone lesion to the bladder?

A
  • Spastic paralysis of the bladder leading to sphincter detrusor dyssynergia -> can lead to hydroureter due to backflow of pressure and AKI
99
Q

What are some risk factors to developing urinary incontinence?

A
  • Child birth
  • Pelvic prolapse
  • Menopause
  • Obesity
  • Cognitive impairment
100
Q

Describe how urinary incontinence can be managed

A
  • Lifestyle modifications such as weight loss, modified fluid intake, timed voiding, avoiding caffiene
  • Indwelling catheter
  • Incontinence pads
  • Pelvic floor muscle contractions
101
Q

What is acute kidney injury?

A

-Significant decline in renal function over hours or days manifesting as an abrupt and sustained increase in serum urea and creatinine, acidosis and water imbalances

102
Q

What are pre-renal causes of AKI? Describe the pathophysiology behind the disease

A
  • Shock
  • Renalvascular compromise eg NSAIDs, ACE I, renal artery stenosis
  • The blood flow and thus GFR are compromised which leads to mass resorption of Na and H2O in order to try and increase GFR
103
Q

Give the main causes of renal AKI. Describe the pathophysiology behind ATN

A
  • Acute tubulonecrosis caused by ischeamia, hypertension, thrombotic thrombocytopenia purpura
  • Interstitial nephritis by drugs (NSAIDs, Abx) and toxins
  • Nephritic syndrome
  • Necrosis does not ensue but cells cannot resorp Na/H2O efficiently, often producing diluted urine
104
Q

Post Renal causes of AKI

Describe the pathophysiology behind the disease

A
  • Stones, neoplasm, stricture, prostate
  • Obstruction must affect both kidneys and causes an increase in intraluminal pressure causing hydronephrosis and decreased renal function
105
Q

What investigations would you do in AKI?

A
  • Bloods -> FBCs, U+Es, LFTs, glucose, Ca, clotting, ESR
  • ABG to look for acidosis, hypoxia and hyperkalaemia
  • urine dip
  • ECG, CXR and renal US
106
Q

What is the main priority in treating AKI?

A

-Blood pressure and electrolyte imbalance

107
Q

Give 3 risk factors for developing AKI

A
  • Advancing age
  • CKD
  • HRH dysfunction
  • Diabetes mellitus
  • Dehydration
  • Critical illness
108
Q

What would be some indications for dialysis?

A
  • Unresponsive hyperkalaemia
  • Unresponsive acidosis
  • Unresponsive fluid overload
  • Signs of uraemia
109
Q

What is nephritic syndrome?

Give some causes

A
  • Damage to the epithelia of the glomerulus leading to haematuria and protein in the urine
  • IgA nephropathy
  • Alports (anti- T4 collagen)
  • Goodpastures (Anti-GBM)
  • Vasculitis
110
Q

What is IgA Nephropathy? When does it commonly present and why?

A
  • An abnormal IgA which leads to immune complex formation with IgG which becomes deposited in the mesangium. This leads to infmallatory reaction and glomerular damage causing leakage of protein and RBCs into urine
  • In childhood, associated with mucosal infections due to an increased production og abnormal IgA
111
Q

What is Goodpastures?

A

-Presence of Anti-GBM antibody which attacks type 4 collagen in the kidney and lungs leading to glomerular damage causing nephritic syndrome and pulmonary haemorrhages

112
Q

What is nephrotic syndrome?

Give some causes

A
  • Damage to the podocytes of the glomerulus which leads to increased sized molecules passing into the urinecausing proteinuria. Also characterised by hyperlipidaemia and oedema
  • Minimal change GN
  • Focal Segmental glomerulosclerosis
  • Membranous
  • Diabetes
113
Q

What is minimal change GN?

A

-Common nephrotic syndrome seen in children caused by effacement of the podocytes mediated by the immune system due ot an unknown cause which does not progress to renal failure

114
Q

Why do you get hyperlipidaemia in nephrotic?

A

-Loss of protein means there is a decrease in apoliproteins needed for transport of lipids so they accumulate in the blood

115
Q

What is focal segmental glomerulosclerosis?

A

-Formation of scar tissue in one segment of the glomeruli in one area of the kidney producing nephrotic syndrome due to podocyte damage. no clear underlying cause but does progress to RF

116
Q

What is membranous GN?

A
  • Inflammation and damage to the glomerular basement membrane resulting in increased permeability and nephrotic syndrome. Caused by Anti-podocyte antiboodies forming immune complexes with the podocytes. Results in inflammation and activation of complement leading to destruction of cells.
  • 1/3 remit, 1/3 remain and 1/3 progress to RF
117
Q

What staging system is used in prostate cancer?

A

-Gleesons

118
Q

What is the most common bladder cancer?

A

Transitional cell carcinoma

119
Q

What is chronic kidney disease?

A

-Irreversible and progressive loss of renal function over a period of moths to years. renal parenchyma becomes replaced by ECM leading to fibrosis and scarring

120
Q

What are the common effects of CKD on the body?

A
  • Increased risk of cardiovascular death
  • Increased risk of acidosis
  • Anaemia of chronic disease
  • Alterations in bone morphology due to imbalances in Ca, PO4, PTH and Vit D
121
Q

What are some potential risk factors for CKD?

A
  • Smoking, obesity, lack of exercise
  • Diabetes
  • Hypertension
  • Ace Inhibitors
122
Q

Give some causes of chronic kidney disease

A
  • Immune mediates glomerulonephritis
  • Pyelonephritis
  • Genetics eg PCK
  • Idiopathic
123
Q

How is CKD monitored?

A
  • Proteinuria
  • Serum creatinine
  • GFR
124
Q

What is haemodialysis?

A
  • Blood and dialysate flow in opposite directions to maximise clearance of substances
  • Can be night time at home but often 3xweek in designanted time slot in hospital
125
Q

What is peritoneal dialysis?

A

-Uses peritoneum as a filter via inserting dialysate into pertioneal space. Wasts products cross and then dialysate drained. 4-5x daily of over night

126
Q

What are the advantages/disadvantages of haemodialysis?

A
  • Ad= less responsibilty/days off

- disad=restricted in travel and days off due to inability to miss slot. Food/drink restrictions

127
Q

What are the advantages/disadvantages of peritoneal dialysis?

A
  • Ad=self sufficient, less food/drink restrictions as more frequent filtering
  • Disad= Responsibilty, abdomen distension, storage of dialysate
128
Q

Give some complications of haemodialysis and peritoneal dialysis

A
  • Haemo = increased infection risk, increased risk of thrombosis, cvs instability and systemically unwell due to blood in and out all the time. AV fistulae
  • Peritoneal = peritonitis, leaking, hernias

PPE (15 decks)

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