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Phase 2- RNU > Week 4 > Flashcards

Week 4 Flashcards

1
Q

Where is fluid in the body?

A

25 litres (63%) intracellular, 12 litres (30%) interstitial tissue, 3 litres plasma (7%)

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2
Q

How is GFR controlled?

A

Sympathetic nervous system causes constriction of the afferent arteriole, angiotensin II causes vasoconstriction of the efferent arteriole. Prostaglandins affect afferent arteriole ?

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3
Q

What is the purpose of fenestrations, and negative charge at the basement membrane of the glomerulus?

A

To prevent proteins from leaving the blood

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4
Q

How does tubular reabsorption occur?

A

Activa transport via channels

Passive transport down concentration or osmotic gradient

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5
Q

What is osmolality?

A

Osmole/unit mass (rather than osmole/unit volume

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6
Q

What hormone acts at the PCT?

A

Angiotensin II has only a minimal effect

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7
Q

What are most channels in the PCT?

A

Sodium - something else co-transporters

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8
Q

How is sodium reabsorbed in the PCT?

A

Na+ in/H+ out pump into basolateral cells, and out by Na+/K+ ATPase

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9
Q

What are the ‘rules’ of the loop of Henle?

A
  1. Thick ascending limb is impermeable to water, but actively transports sodium, potassium and chloride
  2. Thick ascending limb provides the concentration gradient to promote water reabsorption from the thin DLH
  3. Thin descending limb is freely permeable to salt and water
  4. Vasa recta doesn’t wash away the gradient by using countercurrent exchange
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10
Q

What is the important channel in the thick ascending limb?

A

NaKClCl2 channel (channel blocked by loop diuretics)

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11
Q

What is the important channel in the DCT?

A

NCC, blocked by thiazide diuretics

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12
Q

Where does vasopressin (ADH) act?

A

Aquaporin channels in the cortical collecting duct

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13
Q

What is the function of ADH/vasopressin?

A

Water reabsorption for maintenance of intravascular volume

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14
Q

When is aldosterone released?

A

Stimulation by angiotensin II, or hyperkalaemia

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15
Q

How does aldosterone act?

A

Inserts ENaC into cortical collecting duct, resulting in sodium reabsorption and potassium loss (more diuretics (K-sparing) work on these channels)

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16
Q

What are the main channels in the renal tubule?

A

NaK ATPase (PCT), NKCC2 (thick ALH), NCC (DCT), Aquaporin (CCD) and ENaC (CCD)

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17
Q

What is urea?

A

A by-product of amino acid metabolism in the liver (reabsorbed in the inner medullary collecting ducts). It is involved in countercurrent exchange and painting concentration gradient

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18
Q

What is creatinine?

A

Breakdown product of creatinine phosphate (muscle metabolism). It is freely filtered at the glomerulus and not reabsorbed.

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19
Q

What are the different forms of transplant?

A

Autologous (donor and recipient are same individual), syngeneic (donor and recipient are genetically identical), allogeneic (donor and recipient are not genetically identical but are from the same species) and xenogeneic (donor and recipient are from different species)

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20
Q

How is compatibility between donor organs and recipients determined?

A

Blood group compatibility (A with A,O; B with B,O; AB with O, A, B, AB; O with O only) and histocompatibility (a group of genes (found in the major histocompatibility complex on chromosome 6 (HLA genes)) which are associated with the acceptance and rejection of transplanted material from genetically different donors)

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21
Q

How can blood group incompatibility be overcome?

A

Immunoadsorption, plasma exchange and immunosuppression

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22
Q

What would happen if a transplant was incompatible?

A

Hyper-acute rejection of transplanted organ- occurs immediately after connection of blood vessels

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23
Q

What is the structure of HLA class I molecules?

A

Polymorphism located in exons 2 and 3. Peptides are bound in cleft.

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24
Q

What is the function of HLA class I proteins?

A

HLA class I proteins bind peptides derived from intracellular proteins, and display this at the cell surface where they interact with CD8+ T cells

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25
Q

What is the function of HLA class II proteins?

A

HLA class II proteins bind peptides derived from extracellular and cell surface proteins including peptides derived from bacteria. HLA class II proteins then display this to circulating T cells (initiating immune responses)

26
Q

Where are HLA class I molecules found?

A

Expressed on virtually all cells including platelets

27
Q

Where are HLA class II molecules found?

A

Have a more restricted expression: APCs (dendritic cells, B-cells, macrophages), and on activated T cells (and other activated/disturbed cells)

28
Q

Why is there so much diversity of HLA proteins in an individual?

A

The two classes bind different types of peptides, structural differences affect peptide binding, increases chances that an individual will possess an HLA molecule that will allow initiation of an immune response against a pathogen

29
Q

How is HLA matching used in solid organ transplantation?

A

Kidneys; aim to match HLA-A, B, DR low resolution (to maximise use of available organs), Liver; HLA matching not performed, Cardiothoracic; HLA matching recognised as important but not performed due to logistics. Avoid kidney or cardiothoracic transplant in presence of ‘donor specific antibody’

30
Q

How donor specific antibodies (anti HLA antibodies) formed?

A

Caused by HLA sensitisation via the following routes: pregnancy (mum may produce antibodies against HLA antigens present in child which are inherited from father), blood transfusion, previous transplant, viral infection (cross reactivity)

31
Q

How does a hyper-acute reaction occur?

A

Donor specific antibody bonds to donor endothelial cells expressing alloantigen, resulting in inflammation (cytokine activation), endothelial damage (neutrophils, lytic enzymes) thrombosis and death of organ by ischaemia

32
Q

What is chronic allograft nephropathy?

A

Indolent but progressive form of primarily immunological injury to graft, more slowly compromises organ function than acute rejection

33
Q

How are organs allocated for transplant?

A
  1. Paediatric patients (HLA match), highly sensitised (priority based on waiting time)
  2. Other paediatric patients (HLA match) (priority given based on waiting time)
  3. Adult patients (HLA match), highly sensitised
  4. Other adult patients (HLA match and favourable m/m)
  5. All other eligible patients

Priority for 3,4 and 5 given according to a points score based on waiting time, HLA match and age, age difference, HLA homozygosity and blood group match

34
Q

What are important tests to perform prior to transplant?

A

HLA type patient, HLA type donor, screen patient for presence of preformed HLA alloantiobodies (every three months when patient is on transplant list), crossmatch patient and donor prior to transplant to ensure negative result i.e. no reactions

35
Q

What are important tests to perform post transplant?

A

Recipients continue to be monitored for the presence of donor specific antibodies (many patients will receive more than one transplant)

36
Q

What is the function of the bladder and urethra?

A

Store urine, empty fully and reciprocal contraction/relaxation of bladder/urethra

37
Q

How is the bladder held in the pelvic cavity?

A

Held firmly at bladder neck by puboprostatic or pubovesical ligaments, and median umbilical ligament

38
Q

What is the anatomy of the urethral sphincter?

A

Pre-prostatic sphincter (bladder neck) in men. Functional distal sphincter mechanism: intra-mural striated muscle (small slow twitch fibres, mitochondria/lipid droplets, rich in myosin ATPase), peri-urethral striated muscle (mixture of fast and slow twitch larger fibres)

39
Q

What factors contribute to urethral closure?

A

Muscular occlusion by rhabdosphincter, transmission of abdominal pressure to proximal urethra, mucosal surface tension, anatomical configuration at bladder neck, submucosal vascular plexus, inherent elasticity, urethral length

40
Q

What is the venous drainage of the bladder?

A

Surrounding bladder is a rich plexus of veins, that ultimately empties into the internal iliac veins

41
Q

What is the lymphatic drainage of the bladder?

A

Lympahtics drain into vesicle, external iliac, internal iliac and common iliac nodes

42
Q

Is the bladder intra or extra peritoneal?

A

Superior part is intra-peritoneal, the anterior, inferior and posterior parts are extra-peritoneal

43
Q

What is the afferent innervation of the bladder?

A

Simple nerve endings (sense stretch, filling and pain) in lamina propria/ detrusor. Afferent nerves ascend with parasympathetic neutrons back to the cord and then to pontine and micturition centres. Sympathetic innervation - hypogastric nerve (pain touch and temperature)

44
Q

What is the arterial supply of the bladder?

A

Internal iliac artery, obturator artery and vesical (inferior and superior) arteries. Uterine and vaginal arteries also supply female bladder

45
Q

What is the efferent innervation of the bladder?

A

Sacral pre-ganglionic parasympathetic nuclei in intermediolateral columns of S2, 3 and 4. They run with the pelvic nerves, via the pelvic plexus, to synapse with ganglion cells close to and within the bladder wall. Post-ganglionic axons provide cholinergic excitatory input to detrusor smooth muscle. Noradrenergic terminals also in pelvic ganglia but not in detrusor proper (nerve mediated detrusor inhibitor?)

46
Q

What is the sympathetic motor innervation of the bladder?

A

Pre-ganglionic sympathetic nerve fibres arise from T10-12 and L1-2. These travel in hypogastric nerves and innervate the trigone/blood vessels of the bladder and the smooth muscle of the prostate in men. In females there is sparse innervation of the bladder neck and urethra.

47
Q

Describe the ‘Gating’ theory of bladder control?

A

Afferent input into cord nullified by inhibitory inter-neurones, restricting transmission to pre-ganglionic parasympathetic cell bodies. Within parasympathetic ganglia inhibitory effect of post-ganglionic sympathetic nerves. Effect: post-ganglionic parasympathetic fibres are ‘protected’ from afferent input until the threshold is reached

48
Q

What is the innervation of the urethral sphincter?

A

Dual innervation: pre-ganglionic somatic nerve fibres which innervated striated muscle PLUS parasympathetic nerves from S2-4 from Onuf’s uncle which lies in medial part of anterior horn of spinal cord. These somato-motor nerves run via the perineal branch of the pudendal nerve

49
Q

What is the process of micturition?

A

Spino-bulbar-spinal reflex coordinated in the PMC. It leads to simultaneous detrusor contraction, urethral relaxation and subsequent micturition. Tension receptors relay information via afferents to sacral cord and project to pons to inform brain about state of bladder filling. Positive feedback loop to maintain bladder contraction till bladder empty

50
Q

How does the smooth muscle of the detrusor contract?

A

NMJ transmission- increase in intracellular Ca2+:

  1. Membrane depolarisation- voltage sensitive ion channels- influx of extracellular Ca2+
  2. ACh binds to G-protein-linked (muscarinic) receptors- release Ca2+ from intracellular stores
51
Q

What is autonomic dysreflexia?

A

Spinal cord injury (SCI) T6 or higher Exaggerated sympathetic activity in response to stimulus below level of SCI. Increase BP and decreases HR, causes sweating, flushing above lesion, and vasoconstriction below. Treatment is to remove cause.

52
Q

Where is the Pontine Micturition centre (Barrington’s Nucleus)?

A

Found in the dorsolateral region of the pons

53
Q

From where does the Pontine Micturition centre receive projections?

A

Projections from cortex, cerebellum, brainstem and extrapyramidal system

54
Q

Where do the PMC nuclei send axons?

A

To sacral micturition centre, via lateral columns (both intermediolateral nucleus and Onuf’s nucleus)

55
Q

What is compliance in the context of the bladder?

A

Bladder pressures remain low despite increase in volume

56
Q

What is spinal shock?

A

A period of decreased excitability at and below spinal cord injury

57
Q

Describe the pathophysiology of the upper tract in chronic retention:

A

Combination of diuresis and bladder filling causes upper tract pressures to rise. Once ureters become dilated, co-aptive peristalsis is lost and ureteric drainage becomes dependent gravity. If end void pressure >25cm/H20 deterioration in renal function ensues. HPCR associated with hypertension (50%) and peripheral oedema CCF (20%)

58
Q

What changes occur during a period of chronic obstruction?

A

Reduction GFR, secondary increase in the fractional excretion of solutes and water in an attempt to compensate.

With extremes of dietary intake of salt and water and reduced ability of the nephron to compensate

Salt and water retention are common accompaniments

Clinical features: hypertension, peripheral oedema, heart failure

59
Q

What is post-obstructive diuresis?

A

Refers to marked polyuria (frequent urination) that occurs after relief of bladder obstruction. May be physiological (to excrete retained water and solutes), or pathological (caused by impaired sodium reabsorption or concentrating ability)

60
Q

Why does post-obstructive diuresis occur?

A

Patients with prolonged diuresis are unresponsive to ADH, prolonged impairment of sodium reabsorption, elevated levels of ANP

61
Q

How is post-obstructive diuresis treated and managed?

A

Majority of patients do not need volume replacement. Patients with UO of >200mL/hr for 6 hours need fluid replacement and close observation: aim to replace 1/2 hourly urine output with saline

62
Q

What are the two stages of post-obstructive diuresis?

A

Tubular (0-14 days)- reversal of tubular changes in obstruction- increased fractional excretion of sodium leads to diuresis (maximal at 24 hours)
Glomerular (14 days - 3 months) is gradual and more subtle

Phase 2- RNU (4 decks)

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