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Medicine > Urinary case > Flashcards

Urinary case Flashcards

1
Q

Common causes of fluid loss: (4)

A
  • Sweating
  • diarrhoea
  • Hyperventilation
  • Fever
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2
Q

Role of kidneys in fluid/ionic balance:

A
  • Vary water reabsorption to maintain water balance (constant osmolality) and ionic balance
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3
Q

Common symptoms of dehydration:

A
  • extreme thirst
  • lack of urine
  • fatigue
  • dizziness
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4
Q

The role of the kidney:

  • Basic
  • Nephrons
  • Reabsorption
  • Urine composition
A
  • Filter blood plasma
  • Each kidney composed of roughly one million nephrons that filter plasma at the glomerulus
  • As the filtrate passes through the nephron it undergoes reabsorption (95-99%)
  • Urine consists of non-reabsorbed fluid, salts and secreted material
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5
Q

Entire urinary tract composition:

A
  • Kidney, ureters, bladder and urethra
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6
Q

Three layers of glomerular filtration:

A
  1. Capillary endothelium
  2. Basement membrane
  3. Podocyte (epithelial cell fo bowman capsule)
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7
Q

juxtaglomerular apparatus:

A
  • Contains specialised smooth muscle cells (no actin or myosin).. Instead they detect blood speed/pressure and NaCl changes and produce the hormone renin
  • Renin causes an increase in arteriole smooth muscle tone, increasing BP
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8
Q

Hormonal functions of kidney:n(3)

A
  • Renin: Controls blood pressure
  • Active vit.D: calcium balance
  • EPO: Erythrocyte production
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9
Q

Glomerular filtration rate: (GFR)

GFR =

A

GFR = KS(Pgc - Pt) - (Ngc - Nt)

  • KS = filtration co efficient
  • Pgc = hydrostatic pressure (glomerular capillaries)
  • Pt = Hydrostatic pressure (tubule)
  • Ngc = colloid osmotic pressure (glomerular capillaries)
  • Nt = colloid osmotic pressure (tubules)
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10
Q

Glomerular filtration facts (3):

  • Volumes
  • Rate
  • Energy expenditure
A
  • 180 L plasma filtered, 1.5 L of urine produced every 24 hours
  • Normal rate of 90-125ml/min
  • Energy comes from hydrostatic pressure of blood imparted by beating heart, so no energy expenditure required
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11
Q

Glomerular filtrate contains: (3)

A
  • No cells
  • Trace amounts of protein
  • Ions and small organic substances
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12
Q

Factors effecting rate of glomerular filtration of a substance: (3)

A
  • Molecular weight (inversely proportional)
  • Shape: long, thin molecules are filtered more easily
  • Electrical charge: ease of filtering = +&raquo_space; neutral&raquo_space; -
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13
Q

Renal clearance:

  • Definition
  • Equation
A
  • The rate at which a substance is removed from the blood
  • Clearance of substance =
    (Ux X V) / Px
Ux = urine concentration of substance x
V = urine flow rate (ml/min)
Px = plasma conc. of substance x
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14
Q

Control of renal blood flow (RBF) and GFR:

A
  • Systemic blood pressure
  • Renal nervous input
  • Endocrine influences
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15
Q

General properties of proximal tubule: (4)

A
  • Reabsorbs 60-70% of glomerular filtrate
  • Brush border of microvilli: 40X SA increase
  • Reabsorption is isosmotic
  • Stereotyped function (no hormonal control)
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16
Q

Tubular transport of Na+:

  • Mechanism
  • Driven by …..
A
  • Most Na+ reabsorption via secondary active transport in exchange for H+
  • Driven by ionic gradients across apical membrane and ATPase in basolateral
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17
Q

Tubular transport of potassium and calcium:

A
  • Most K+ reabsorption via paracellular route, passively down gradient
  • Ca2+ reabsorption via transcellular and paracellular routes down ionic gradient
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18
Q

Tubular transport of glucose and amino acids:

  • concentration gradient/mechanism
  • apical
  • basolateral
  • Tm
A
  • Both occur against concentration gradient, via secondary active transport (co-transport)
  • Dependant on Na+ gradient on the apical membrane
  • Facilitated diffusion on basolateral
  • When transport maximum (Tm) is reached, excess is secreted in urine)
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19
Q

tubular transport of water:

A
  • Water reabsorption down osmotic gradient
  • Transcellular reabsorption on both membranes due to aquaporins
  • Reabsorption also occurs in loop of hence, distal tubule and collecting duct
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20
Q

Tubular transport of bicarbonate and hydrogen:

  • Combination
  • Breakdown
  • HCO3-
A
  • HCO3- combines with H+ for indirect reabsorption in presence of carbonic anhydrase
  • Once H2CO3 is absorbed CA breaks it down again and H+ is secreted via buffers
  • HCO3- reabsorbed into the blood
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21
Q

Loop of Henle: experimental observations

- Osmotic gradient?

A
  • An osmotic gradient exists in renal medulla
  • Loops of Henle are countercurrent multipliers
  • Longer loops of henle create a larger osmotic gradient
  • parent kidney excretes more concentrated urine
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22
Q

Countercurrent multiplication in the loop of Henle:

A
  • Descending limb: H2O exits the loop of Henle, Increasing the osmotic gradient. Osmolality of 1200
  • Ascending limb: impermeable to water. No water reentry. NaCl is pumped into medulla, diluting the tubular fluid
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23
Q

Urine concentrating mechanism:

A
  • Osmotic gradient established by loop of henle is utilised by the collecting duct
  • majority of water is reabsorbed into the medulla
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24
Q

Distal tubule and regulation of potassium:

  • K+ secretion/reabsorption
  • Aldosterone effects
A
  • K+ is reabsorbed in deficiency and secreted in hyperkalaemic states
  • Aldosterone produced in the adrenal cortex acts on distal nephron to promote K+ secretion and H+ secretion
    (via N+ H+ ATPase)
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25
Q

Osmolality definition:

A
  • Concentration of impermeable solutes per Kg of solute

- Units: osm.kg^-1 solute

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26
Q

Control of body fluid osmolality and water balance

  • Definition
  • Regulation
A
  • Plasma osmolality regulated to prevent cells from swelling or shrinking
  • Regulated by control of water influx (e.g. drinking) and efflux (e.g. urine concentration)
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27
Q 
Plasma osmolality regulation - mechanisms
1- detection
2i) pituitary gland 
2ii) thirst centre 
3
4
A
  1. change in plasma osmolality, detected by osmoreceptors in hypothalamus
  2. Hypothalamus initiates change to:
    i) pituitary gland
    ii) thirst centre
  3. i) release of ADH
    ii) change of thirst response
  4. i) altered urine conc.
    ii) alter water intake
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28
Q

Plasma osmolality general facts:

  • Normal level
  • Control level?
A
  • Normal plasma osmolality (Posm): 290mosmol.kg^-1

- Variation by only 1% activates compensation mechanisms (one of the most tightly controlled homeostatic variables)

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29
Q

Antidiuretic hormone (ADH) increases: (3)

A
  • Water permeability of the collecting duct
  • NaCl reabsorption in the thick ascending limb of the loop of Henle
  • urea permeability in the inner medullary region of collecting duct
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30
Q

Control of ADH secretion:

A
  • Secreted from posterior pituitary
  • ADH is released into the blood by a rise in plasma osmolality of 1% activating hypothalamic neurones
  • Release reduced when osmolality falls
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31
Q

Ion transport: ascending loop of henle

  • Apical
  • Basolaateral
A
  • Apical: Na+/K+/2Cl- transporter

- Basolateral: Na+-pump

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32
Q

ADH: site of action

  • Receptor
  • Stimulates …., generating ….. activating ……
  • Increases ….
A
  • ADH binds to V2 receptors
  • Stimulating AC, generating cAMP, activating protein kinases
  • Increases insertion of water channels (aquaporins)
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33
Q

Diabetes insipidus: (DI)

  • Description
  • Symptoms
A
  • Lack of action of ADH reduces water reabsorption from CD, quantity that leaves distal tubule will leave body as urine
  • polyuria of dilute urine, excessive thirst
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34
Q 
Causes of diabetes insipidus:
Central DI
- Definition
- Cause 
- Management
A
  • Lack of ADH produced from the posterior pituitary
  • Idiopathic cause or secondarily from head injuries
  • Desmopressin
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35
Q

Causes of diabetes insipidus:
Nephrogenic DI
- Definition
- Aquired Cause

A
  • Kidneys do not respond to ADH
  • Inherited forms: affect expression of ADH V2-receptors or aquaporin proteins
  • Acquired forms resulting from: renal cysts/infection, hypercalcaemia
36
Q

Hypovolaemia:

  • Definition
  • Decreases venous return due to:(2)
A
  • Decrease in blood volume
  • Decreases venous return due to:
  • Decreased cardiac filling in diastole
  • Reduces stroke work, cardiac output and arterial blood pressure
37
Q

Hypervolaemia:
- Definition
- Causes
due to

A
  • An increase in blood volume
  • Increase in venous return due to:
  • Increased cardiac filling in diastole (preload)
  • Increases stroke work, cardiac output and arterial blood pressure
38
Q

How the kidney regulates blood volume: hypovolaemia control

A
  • Senses reduced blood pressure/renal flow
  • Reducing Na+ loss in urine
  • This reduces water lost in urine due to osmotic retention
39
Q 
High pressure sensors for blood volume (kidney): (2) 
- Arterial baroreceptors
Hypovolaemia response
- Juxtaglomerular apparatus
Hypovolaemia response
A
  • Arterial baroreceptors:
    Hypovolaemia: blood pressure falls, baroreceptor reflex increases sympathetic activity to kidneys
  • Juxtaglomerular apparatus:
    Hypovolaemia: blood pressure/renal blood flow decreases, hormonal response reduces Na+ loss in urine, increasing water retention
40
Q

Renal sympathetic nerve action(pressure) (4)

  • Detection
  • SA
  • Reducing ….
  • Restores
A
  • Decrease pressure detected
  • Increased sympathetic activity increases smooth muscle tone of afferent arterioles
  • Reducing GFR, causing less Na+ to be filtered
  • Restores blood volume
41
Q

Renin: blood volume control

  • secretion
  • action
A
  • Secreted by the juxtaglomerular apparatus

- Reduced Na+ excretion at the distal tubule, increasing blood volume

42
Q

Renin-angiotensin-aldosterone (RAAS) system: role

A
  • Controls NaCl levels which effect water reabsorption by the nephron
43
Q

RAAS sytem steps:

  1. Renin action
  2. ACE conversion
  3. Angiotensin II action/effects
A
  1. Renin acts on angiotensinogen (produced by liver) making angiotensin I
  2. Angiotensin I converted to angiotensin II by ACE, primarily in the lung
  3. Angiotensin II stimulates aldosterone release from kidney, ADH release and vasoconstriction
44
Q

Aldosterone:

  • Hormone type and origin
  • Role
A
  • Steroid hormone secreted from zona glomerulosa

- Increases Na+ reabsorption by the nephron

45
Q

Aldosterone action: (4)

  • Initiation
  • Receptor complex stimulates
  • Increases ….. reabsorption via
  • …… uptake enhanced
A
  • Aldosteron binds to receptor.
  • Receptor complex stimulates transcription of apical Na+ channels (ENaC)
  • Increases NaCl reabsorption via principle cells in distal tubule/collecting duct
  • Na+ uptake from lumen is enhanced: Cl- and H2O follow
46
Q

the ureters (Upper urinary tract):

  • Function
  • How??
A
  • Propels urine to the bladder
  • Ureters are lined with smooth muscle. A wave of peristalsis originates in the renal pelvis, passing to the uretero-vesical junction
47
Q

The Uretero-vesical junction

A
  • Ureters penetrate the bladder wall as a non-return valve, as the bladder fills the wall pressure closes the valve.
48
Q

Hydronephrosis:

A
  • Urine builds up in the ureters and renal pelvis if urine is not voided properly
49
Q

The lower urinary tract (LUT): Bladder anatomy

  • Bladder dome
  • Trigone
A
  • Bladder dome: most of the bladder, lined by detrusor smooth muscle
  • Trigone: Small region bound by apices of ureteric orifices and the bladder neck
50
Q

The LUT: outflow tract

- Urethra description

A
  • Urethra: a smooth muscle lined tube that is also surrounded by a ring of skeletal muscle (external urethral sphincter)
51
Q

The bladder: filling phase

A
  1. Volume increases by up to 500ml in the normal adult bladder, very small rise in Pdet
  2. No flow (leakage), outflow tract contracted
  3. Sensory bladder nerves signal filling but the brain suppresses voiding
52
Q

Control of voiding: bladder innervation

A
  • Pelvic n. S2-S4
53
Q

Control of voiding: External Urethral Sphincter

A
  • Pudendal nerve S2-S4
54
Q

Control of voiding: Urethra

A
  • Hypogastric nerve T10-L2
55
Q

Bladder filling:

  • Bladder state
  • Urethra
  • External sphincter (EUS)
A
  • relaxed: pelvic nerve activity suppressed
  • Urethra: Sympathetic Hypogastric nerve active
  • EUS: somatic (pudenal) nerve active
56
Q

Voiding phase: (4)

A
  1. Brain makes a decision to void
  2. Bladder wall contracts and Pdetrusor increases
  3. Flow starts, due to rising Pdet and relaxation of outflow muscle tract
  4. Sensation of bladder fullness is reduced, bladder completely empties
57
Q

Bladder voiding:

  • Bladder state
  • Urethra state and EUS state
A
  • Activated: bladder contracts due to pelvic nerve activation
  • Urethra and EUS: relaxed. Pudendal and hypogastric nerves are supressed
58
Q

Renal function tests: Urine (3)

A
  • Observation
  • Dipstick examination
  • Lab tests
59
Q

Renal function tests: blood (5)

A
  • UandE’s
  • osmolality
  • pH
  • Bone profile
  • Full blood count
60
Q

What is used to measure GFR?

A
  • Creatinine
61
Q

Isotonic dehydration:

  • Loss
  • Plasma osmolality
  • Plasma Na+
  • ECV
  • ICV
  • Causes
A
  • Water=salt
  • Normal
  • Normal
  • Decrease
  • Normal
  • Acute diarrhoea
62
Q

Hypertonic dehydration:

  • Loss
  • Plasma osmolality
  • Plasma Na+
  • ECV
  • ICV
  • Causes
A
  • Water > salt loss
  • Increase
  • Increase
  • Decrease
  • Decrease
  • Burn/fever/infection
63
Q

Hypotonic dehydration

  • Loss
  • Plasma osmolality
  • Plasma Na+
  • ECV
  • ICV
  • Causes
A
  • Water < salt
  • Decrease
  • Decrease
  • Decrease
  • Increase
  • Chronic vomiting/diarrhoea
64
Q

pH equation

A

pH = - log [H+]

65
Q

Importance of arterial pH regulation: (3)

A
  • Enzyme structures may be impaired
  • Acidosis can predispose to decreased cardiac contractility (arrhythmias)
  • Effect on other ions (Ca2+ and K+) can lead to abnormal neuromuscular and cardiac fucntions
66
Q

Strong and weak acids:

A
  • Strong acids (HCl): almost completely dissociate when dissolved.
    HCL -> (H+) + Cl-
  • Weak acids: only partially dissociate.
    H2CO3 <=> HCO3- + H+
67
Q

Endogenous acids: volatile acids

  • How is it produced
  • Example
  • Extraction
A
  • An end product of aerobic respiration, Carbonic acid

- Exhaled as CO2

68
Q

Endogenous acids: fixed acids

  • Production
  • Example
  • Extraction
A
  • Produced by catabolism of phospholipids, amino acids and nucleic acids
  • Sulphuric and phosphoric acids
  • Excreted via the kidneys
69
Q

Endogenous acids:

  • Gastric cells
  • Pancreatic cells
A
  • Secrete HCl into the lumen and HCO3- into the venous blood (alkaline tide)
  • Secrete HCO3- into lumen and H+ into venous blood
70
Q

Buffers:

  • Definition
  • Effect on pH
  • Buffer composition
A
  • A substance that resists the change in pH by absorbing (or releasing) H+ ions the an acid (or base) is added
  • pH still changes, but magnitude is reduced
  • Consists of a weak acid and its conjugate base
71
Q

Henderson Hasselbach equation:

A

pH proportional to

[HCO3-] / PaCO2

71
Q

Henderson Hasselbach equation:

A

pH proportional to

[HCO3-] / PaCO2

72
Q

PaCO2 equation =

A

Rate of CO2 production/ Rate of CO2 removal

73
Q

Reabsorption of filtered bicarbonate:

A
  • Filtered at the glomerulus, 99.9% is reabsorbed

- Pathological rise of 40mmol/L will exceed reabsorption mechanism, lost in urine

74
Q

Reabsorption of Filtered bicarbonate is increased by: (3)

  • ECF
  • R-A-A
  • PaCO2
A

1- ECF volume contraction directly
2- activation of R-A-A system. Angiotensin II stimulates Na-H exchanger in the PCT
3- Increased PaCO2 provides more CO2 for conversion to HCO3-

75
Q

Acid-base disturbances: Acidosis

  • Cause
  • Effect
A
  • Cause: pathological rise in [H+] and a fall in arterial pH+
  • Effect: Acidaemia
76
Q

Acid-base disturbances:

A
  • Cause: Pathological fall in [H+]

- Effect: rise in pH (alkalaemia)

77
Q

Acid-base disturbances: terminology

  • Respiratory
  • Metabolic
  • Simple
  • Mixed
  • Compensation:
A
  • Respiratory: Pathological change in PaCO2
  • Metabolic: pathological change in [HCO3-]
  • Simple: only one disorder
  • Mixed: multiple AB disorders
  • Compensation: physiological change to return pH to 7.4
78
Q

Potassium balance:
1- Shift of K+ into ICF:
2- Shift of K+ out of ICF:

A

1- Hyperkalaemia

2-Hypokalaemia

79
Q

Nitrogen balance:

  • Definition
  • Healthy adults
A
  • The balance between loss and gain of nitrogen

- Have a net zero nitrogen balance

80
Q

Amino acid metabolism:

  • Transport
  • Liver role
A
  • Broken down inside cells then transported to the liver as alanine or glutamine
  • Here they are broken down and excreted as urea
81
Q

Amino acid conversion to glutamine:

  • Transaminase reactions
  • Glutamine synthesis
  • Transport
  • Conversion
  • Deamination
A
  • Transaminase reactions in muscles convert amino acids to glutamate
  • Glutamine synthase converts glutamate to glutamine
  • Glutamine transported in blood to the liver
  • Glutamine converted to glutamate, releasing NH4+
  • Glutamate is deaminated inside liver mitochondria, releasing NH4+ and regenerating alpha-ketoglutarate (reactant)
82
Q

Urea cycle:

A
  • ATP, CO2, NH4+ and fumarate are consumed
  • Produces fumarate
  • Committed step: CO2 and NH4+ combined via 2 ATP
83
Q

Glucogenic amino acids:

A
  • Donate carbon skeletons to form pyruvate or CAC intermediates
84
Q

Ketogenic amino acids:

A
  • Donate carbon skeletons to form acetyl CoA and thus ketone bodies (enters CAC)
85
Q

Marasmus and kwashiorkor:

A
  • Marasmus: lack of protein and energy (starvation)

- Kwashiorkor: lack of protein

86
Q

PKU defect:

A
  • Defect in the gene for Phe Hydroxylase stops the conversion of Phe to tyrosine
  • [Tyr] reduced, [neurotransmitters] reduced

Medicine (18 decks)

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