Theme 3 lectures - CHatterjee Flashcards
1
Q
Elimination
A
Environment
2
Q
Excretion
A
Body fluid
3
Q
Cortical nephrons [2]
A
Short LOH -> Medulla
Peritubular capillaries
4
Q
Juxtamedullary nephron [2]
A
Deeper into pyramid
Vasa recta
5
Q
Organic acid [3]
A
Uric acid
Antibiotic - penicillin
Diuretic
6
Q
Organic base [2]
A
Creatinine
Procainamide
7
Q
Renal filtration [3]
A
BP
Different diameters
Renal blood flow
8
Q
Glomerular filtration [3]
A
Pores in glomerular cap endothelium
Basement membrane of Bowman’s capsule
Epithelial cells of Bowman’s capsule - Podocytes via filtration slits
9
Q
Two forces filter fluid out
A
Glomerular cap hydrostatic pressure
Bowman’s capsule oncotic pressure (almost zero)
10
Q
Two forces oppose ultrafiltration
A
Glomerular cap oncotic pressure
Bowman’s capsule hydrostatic pressure
11
Q
Filtration pressure
A
(PGC) – (PBS + piGC)
12
Q
Autoregulation of RBF
A
BP 90-200mmHg
Myogenic or metabolic
13
Q
GFR increased by [5]
A
Prostaglandins, ANP, dopamine, NO, kinins
14
Q
GFR decreased by [4]
A
Noradrenaline
(from symp nerves), endothelin, adenosine, ADH
15
Q
Filtration pressure drop = GFR drop [4]
A
Less Na+ enter PT
Macula densa senses change in tubular Na+ levels
Stimulate juxtaglomerular cells to release renin
Ang II generated
16
Q
Na+ co-transported with [2]
A
Sulphate
Phosphate
17
Q
SGLT2 inhibitors
A
Dapagliflozin
Canagliflozin
Empagliflozin
APICAL
18
Q
PAH [4]
A
Non-endoegenous compound
Transported into PT via alpha-ketoglutarate or di/tri carboxylates
Transported out in exchange for another anion
Tubular secretion
19
Q
Thin limb
A
AQP1 and passive TJ movement
Flat cells
20
Q
Thick limb
A
Na+K+2Cl-
21
Q
Cl- and Na+ for K+ in
A
DT (throughout)
22
Q
Na+ for K+ in
A
Late DT and early CD
23
Q
Principal cells
A
Sensitive to aldosterone
Exchange Na+ for K+ in late DT and early CD
24
Q
alpha-Intercalated Cells
A
Secretes acid (H+) via H+/Na+ or H+/K+ exchange, involving ATPase or H+ATPase
Reabsorbs bicarbonate (HCO3-)
25
beta-Intercalated Cells
```
Secrete bicarbonate (HCO3-)
via Pendrin
```
Reabsorbs acid (H+)
26
CD & ADH [3]
Vasopressin V2 receptor
| 10-15min plasma half life Activate intracellular AQP2
27
Nephrogenic - diabetes inspidius
Inability of kidney to respond to ADH
Chlortalidone (diuretic)
Indometacin (anti-inflammatory
28
Neurogenic - diabetes inspidius
Due to lack of ADH production
by the brain
Desmopressin (ADH analogue)
Vasopressin
Carbamezapine (anti-convulsive)
29
SIADH can cause
Hyponatraemia
| Fluid overload
30
ADH
- increased
- decreased
Nicotine
Ether
Morphine
Barbiturates
Alcohol
31
Diuretic use
Reduce circulating volume
| Remove excess fluid
32
Loop diuretic use [6]
Inhibit NaK2Cl in THICK asc LOH
Reduced Na+ reabsorption
Acute pulmonary oedema
Chronic heart failure
Cirrhosis of the liver
Resistant hypertension
Nephrotic syndrome
Acute renal failure
33
Loop diuretic disadvantages [5]
Dehydration
K+ loss leading to low plasma K+ (hypokalaemia)
Metabolic alkalosis (due to H+ loss in urine)
Hypokalaemia can potentiate effects of cardiac glycosides
Deafness (when used with aminoglycoside antibiotics)
34
Thiazide diuretic use
DT to inhibit apical Na+Cl- cotransporter
Hydrochlorothiazide prototype
Hypertension
Oedema
Mild heart failure
35
Thiazide diuretic disadvantages
Plasma K+ depletion (due to urinary K+ loss)
Metabolic alkalosis (due to urinary H+ loss)
Increased plasma uric acid – gout
Hyperglycaemia (increased blood glucose)
Increased plasma cholesterol (with long-term use)
Male impotence (reversible)
36
eplerenone, spironolactone
Aldosterone antagonists
Spironolactone metabolised to canrenone
Competitive inhibitor of aldosterone
Reduction of protein expression in DT
37
Aldosterone antagonists
eplerenone, spironolactone
38
Non-Aldosterone antagonists
amiloride, triamterene
39
amiloride, triamterene
Non-Aldosterone antagonists
Weak diuretic - act on DT to inhibit Na reabsorption and decrease K+ excretion
Luminal Na+ channel
40
Spironolactone uses [2]
Heart failure
| Oedema
41
Spironolactone disadvantages [5]
Hyperkalaemia (increased plasma K+ levels) – needs to be monitored regularly
Metabolic acidosis (due to increased plasma H+)
GI upsets (peptic ulceration reported)
Gynaecomastia, menstrual disorders, testicular atrophy
Eplerenone produces less unwanted effects than spironolactone
42
Carbonic anhydrase inhibitor
Acetazolamide
Block NaHCO3 reabsorption in PT
Glaucoma (decrease intraoccular p) & epilepsy
Can lead to met acidosis and enhance renal stone formation
43
Mannitol
Osmotic diuretic
Non reabsorbable and excreted 30-60mins
6-8hrs
Increased intercranial p, intraoccular p and acute renal failure
Osmotic p can increase plasma vol = not sued in hypertensive patients
44
Renal failure risk factors [7]
```
Extreme age
Polypharmacy
Specific disease states
Long term analgesia
Transplants
Drug therapy
Patients undergoing imaging procedures
```
45
Clinical assessment [6]
```
Fluid balance
Electrolyte regulation
EPO production
Vitamin D3
Excretion
Acid-base balance
```
46
Electrolyte regulation [4]
Abnormal ECG
Absent P wave
Broad QRS complex
Peaked T wave
47
Bedside Clinical Data [4]
Weight chart
Fluid balance chart
Degree of oedema
Result of urine dipstick testing
48
Modern Imaging Technique [3]
Gamma camera planar scintigraphy
Positron emission tomography (PET)
```
Single photon emission
computerised tomography (SPECT)
```
49
Creatinine increased by [5]
Large muscle mass, dietary intake
(Audley Harrison vs. Audrey Hepburn)
Drugs which interfere with analysis (Jaffe reaction)
e.g. methyldopa, dexamethasone, cephalosporins
• Drugs which inhibit tubular secretion
e.g. cimetidine, trimethoprim, aspirin
Ketoacidosis (affects analysis)
Ethnicity (higher creatine kinase activity in black population)
50
Creatinine decreased by [5]
Reduced muscle mass (e.g. the elderly)
Cachexia / starvation
Immobility
Pregnancy (due to increased plasma volume in the mother)
Severe liver disease (as liver is also a source of creatinine)
51
Drugs which interfere with analysis [3]
Methyldopa, dexamethasone, cephalosporins
52
Drugs which inhibit tubular secretion [3]
Cimetidine, trimethoprim, aspirin
53
Urea increased by [6]
```
High protein diet
Hypercatabolic conditions
e.g. severe infection, burns, hyperthyroidism
Gastrointestinal bleeding
(digested blood is a source of urea)
Muscle injury
Drugs e.g. Glucocorticoids, Tetracycline
Hypovolaemia
```
54
Urea decreased by [4]
Malnutrition
Liver disease
Sickle cell anaemia (due to GFR)
SIADH (syndrome of inappropriate ADH)
55
Freely filtered but not reabsorbed or secreted
Freely filtered and partly or mostly reabsorbed
Freely filtered but fully reabsorbed
Freely filtered, not reabsorbed, fully secreted
INULIN
Electrolyte
Glucose and AA
PAH
56
Renal disease biomarkers [5]
Kidney injury molecule – 1 (KIM-1) (urine)
Interleukin (IL)-18 (urine)
Fatty-acid binding proteins (FABPs) (urine)
Neutrophil gelatinase-associated lipocalin (NGAL) (plasma & urine)
Cystatin C (plasma)
57
Renal can also branch into
Suprarenal
| Segmental
58
Transcellular transport involves
AQP on apical & basolateral surface
59
ADH
Vasopressin (basal membrane of principal cells)
| AQP2 on apical membrane
60
Central vascular sensors - low p BV receptors [3]
Systemic
Cardiac atria
Pulmonary vasculature
61
Central vascular sensors - high p BV receptors [3]
Carotid sinus
Aortic arch
Renal aff arteriole
62
Renal baroreceptors senses
Decrease perfusion p in aff arteriole
63
Renal Na+ sensors senses
Decrease Na+ in DT
64
SNS supplying JGA senses
Decrease systemic BP
65
Decrease perfusion p in aff arteriole sensed by
Renal baroreceptors
66
Decrease Na+ in DT sensed by
Renal Na+ sensors
67
Decrease systemic BP sensed by
SNS supplying JGA
68
RAAS
Renal baroreceptors & Na+ sensors
69
ANS
Peripheral baroreceptors -> Hypothalamus -> ANS (Haemodynamic and RAAS)
70
ADH
Peripheral baroreceptors -> Hypothalamus -> ADH -> Water reabsopriton increases
71
ADH
Increase plasma osmolality -> Hypothalamus osmoreceptors -> ADH in circ
72
Urine out of the end of the collecting duct [2]
Tubular fluid travels through common collecting duct deep into inner medulla of kidney
Tubular fluid exits collecting duct at tip of renal pyramid - also known as the renal papilla
73
Urine into the renal pelvis and ureter [3]
Minor and major calyces lead to renal pelvis
Fluid stretch renal pelvis SM
Peristaltic contractions at hilus -> bladder
BONUS: the epithelium is impermeable to water and solutes
74
Ureter structure [5]
```
30cm
Transitonal epithelium - impermeable to urine
Inner longitundinal
Outer circular/spiral
Extra longitudinal layer
```
75
Ureter function [3]
Dilation of renal pelvis generates action potential from pacemaker cells in hilum
Peristaltic waves generated – between
1 to 6 per minute…
P NS enhance
76
Peristalsis in ureter [3]
```
Longitudinal m contracts followd by circular m relaxation
Longitudinal relax (forms bolus) and circular muscle pushes against it
```
VERMICULATION
77
Entrance into bladder [3]
Ureter attach to the posterior wall of urinary bladder
Pass through wall at oblique angle 2-3 cm
Slits = ureteral openings (backflow)
78
Urinary bladder structure [4]
Hollow muscular organ - fundus and neck
Outer detrusor muscle layer - longitudinal and circular/spiral m
Inner mucosal layer: Transitional epithelium - rugae (empty = folded) and highly elastic
79
Trigone [2]
Triangular area bounded by openings of ureters and entrance to urethra
acts as a funnel to channel urine towards neck of bladder
80
Internal urethral sphincter [4]
Loop of smooth muscle
Convergence of detrusor muscle
Under involuntary control
Normal tone keeps neck of bladder
and urethra free of urine
81
External urethral sphincter [4]
Circular band of skeletal muscle where urethra passes through urogenital diaphragm
Acts as a valve with resting muscle tone
Under voluntary control
Voluntary relaxation permits micturition
82
Elimination of urine
Females:
Opens via external urethral
orifice located between clitoris and vagina
Males:
Urethra passes through prostrate gland and through uro-genital diaphragm and penis
