Genitourinary System Flashcards

Question

What stimulates release of aldosterone?

Answer 1

Angiotensin II (High NaCl) High Potassium

Answer 2

**_1) Increase sodium and water re-uptake_** * Due to aldosterone binding onto the minteralocorticoid receptor, and therefore the insertion of the ENac channel. This allows sodium to pass through the channel from the tubular lumen back into the body. **_2) Lose more K+_**

Answer 3

Treated by *antagonists to the minerocorticoid receptors.* (**Spironolactone**)

Answer 4

_Increased sodium excretion_ (due to loss of aldosterone-dependent sodium reabsorbtion)

Answer 5

## Footnote **1) Osmolality: Antidiuretic Hormone (ADH)** **2) ECF volume: Renin-angiotension system and Sympathetic Nervous system**

Answer 6

Decreased ECF volume is compensated by _increased renal reaborption of Na+_ When ECF volume increases, there is less reabsorption of Na+ **_Increased Na+ reabsorption_** * -_RAA_ (renin, angiotensin, aldosterone) system * -_Sympathetic nervous system_ * -_ADH_ **_Decrease Na+ reabsorption_** * -_ANP_ * -_Decrease RAA and SNS activity_ * -Domapine * -Prostaglandins

Answer 7

- RAA (renin, angiotensin, aldosterone) system - Sympathetic nervous system - ADH

Answer 8

**_Atrial natriuretic peptide (_**inhibit Na+ reabsorption) -Released from the atria in response to increased filling pressure and increased atrial stretch This _decreases Na+ reabsorption_ in DT and outer medullary CT by blocking ENac and by inhibiting Na, K-ATPase 1) Inhibits release of aldosterone 2) Inhibit renin release 3) Vasodilates afferent arteriole to increase GFR

Answer 9

1) (if change is 1-2%) * -Increased osmolarity * -Sensed by osmoreceptors in the hypothalamus * -Release ADH * -ADH binds to the V2 receptor. * -This leads to aquaporin 2 insertion into the tubular-lumen membrane. 2) (if the dehydration is enough to change the volume ~10%) * -Decreased atrial stretch * -Atrial stretch receptors feedback to the hypothalamus * -Increase in ADH

Answer 10

Greater than 5 (faint = low BP)

Answer 11

Lower than 275 (reabsorb lots of water)

Answer 12

Renal failure = d_ecrease in GFR (glomerular filtration rate)_ Normal = ~100ml/min (A condition in which the kidneys lose the ability to remove waste and balance fluids.) Two main forms: 1) Acute Kidney Injury 2) Chronic Kidney Disease

Answer 13

Normal = ~100ml/min

Answer 14

plasma creatinine **rises** as GFR **falls**

Answer 15

Estimate Glomerular filtration rat using plasma creatinine 1) Weight (muscle mass) 2) Age (again, muscle mass and probably reduction in nephron) 3) Gender (women tend to have less muscle than men) eGFR is inaccurate if muscle mass is unusally high or low (e.g. amputees, body bulders)

Answer 16

1) Acute - acute kidney injury 2) Chronic - chronic kidney disease Both have increased creatinine and decreased GFR

Answer 17

**1) Pre-renal (before kidneys e.g. renal artery)** * -Low BP * -Not enough blood to kidneys (dehydration, septic shock, haemorrhage, cardiogenic shock, severe renal artery stenosis) **2) Renal (kidney)** **3) Post-renal (after kidney e.g. ureter)**

Answer 18

1) High creatinine 2) Potassium: hyperkalaemia 3) Phosphate: high 4) Calcium: may be low

Answer 19

Fix the underlying problem (usually increase BP) 1) Rehydrate 2) Treat bleeding 3) Fix heart 4) Antibiotics for sepsis 5) ICU treatment for persistent low BP (with inotropes)

Answer 20

Acute tubular necrosis (ATN) is a medical condition involving the death of tubular epithelial cells that form the renal tubules of the kidneys. * ATN presents with acute kidney injury (AKI) and is one of the most common causes of AKI. * This makes up the "renal" part of the Acute Kidney Injury - Mainly develops from Pre-renal causes. - Persistant Oliguria and renal failure after correction of underlying pre-renal condition - May take 4-6 weeks to recover. * *_Observe:_** - High creatinine - Low urine output - High potassium

Answer 21

- Maintain normal BP - Treat the underlying problem -If kidneys keep getting worse, put them on dialysis (usually when GFR \<10ml/min)

Answer 22

Inflammation of glomerulus can cause both acute kidney injury as well as chronic kidney disease

Answer 23

Plumbing issues, tips are blocked or squashed 1) Kidney stones 2) Tumour 3) Prostate hypertrophy 4) Urinary retention (cause _Hydronephorsis_ and _hydroureter_)

Answer 24

Ultrasound

Answer 25

Gradual decline in renal function Irreversible Once your kidney is scarred, it will never go away. We just try and stop it from getting worse * *_Tests_**: 1) elevated creatinine 2) elevated urea 3) Usually normal urine output

Answer 26

1) elevated creatinine 2) elevated urea 3) Usually normal urine output

Answer 27

1) Water deficit 2) Increase in extracellular _osmolality_ (sensed by osmoreceptors in the hypothalamus) 3) Increase in _ADH secretion_ (posterior pituitary) 4) Increase in _plasma ADH_ 5) Increase in _H2O permeability in distal tubules, collecting ducts_ 6) Increase _H2O reabsorbtion_ 7) Decrease H2O excretion

Answer 28

angiotensin II

Answer 29

1. _increased osmolality_- less than 1% change 2. _decreased volume_- greater than 10% change of the ECF.

Answer 30

ADH (released from posterior pituitary) binds to the V2 receptors (intersititial side) Causes insertion of Aquaporin-2 receptors on the tubular side Causes water comes through the aquaporin-2 and the body reabsorbs water.

Answer 31

**Central and nephrogenic diabetes insipidus** (tasteless urine) _1) Central origin_ (can't produce ADH, due to brain injury or tumour) 2) _Nephrogenic_ (enough ADH but receptor problems- problem to V2 receptor). -Can be diagnosed by measuring levels of _ADH in blood._ If high, they're _nephrogenic_, if low, _central_. -Can also be diagnosed by _giving them ADH_ and seeing if symptoms improve. (Water deprivation test)

Answer 32

Syndrome of inapporpiate ADH secretion -_Plasma ADH levels higher t_han normal for the person's plasma osmolality and volume _-Patient retains water_ inappropriately (has negative free water clearance) -_Plasma osmolarity is significantly lower_ than normal -If patient's water intake is not controlled a hypoosmolal state results with possible dire consequences - SIADH may be caused by _brain injury or tumor,_ by certain _anti-cancer drugs_, and by lung cancer and certain other cancers. - Patients "restricted" from drinking water

Answer 33

Secreted from Granula (JG) cells from the afferent vessels. * In the blood, _renin acts on a protein known as angiotensinogen,_ resulting in the release of angiotensin I. * Angiotensin I is cleaved to form Angiotensin II by ACE enzymes **_Angiotensin II functions_** __1) Increase in _aldosterone_ 2) _vasoconstriction of efferent arteriole_ 3) Increase in _proximal Na+ reabsorption_ 4) Increase in thirst 5) Increase in _ADH release_ 6) _Decrease in RBF, but maintains GFR_ 7) _Decrease in Na+ and H2O excretion_ _8)_ (Can cause vasodilation if they bind to AT2 receptors but we have more AT1 receptors than AT2) **_Factors that promote renin secretion:_** 1) decrease in afferent arteriolar pressure 2) Increase in sympathetic activity 3) Decrease in macula densa NaCl delivery

Answer 34

Angiotensin II functions 1) Increase in _aldosterone_ 2) _vasoconstriction of efferent arteriole_ 3) Increase in _proximal Na+ reabsorption_ 4) _Increase in thirst_ 5) _Increase_ in _ADH release_ 6) _Decrease in RBF, but maintains GFR_ 7) Decrease in Na+ and H2O excretion 8) (Can cause vasodilation if they bind to AT2 receptors but we have more AT1 receptors than AT2)

Answer 35

Block ACE enzyme function Cause decrease in angiotensin II (decrease in vasoconstriction)

Answer 36

**ADH** mainly reabsorbs water **Angiotensin II** drags salt and water follows. Way to correct osmolarity = use ADH Way to correct volume = use angiotensin II

Answer 37

- new balance is achieved. - weight gain due to water retention (in order to maintain constant ECF osmolality). 1) Transient increase in plasma osmolality 2) Increase renal salt excretion (but with a few days lag) 3) Increased thirst (water retained to maintain ECF osmolality proportional to extra salt loaded). 4) Plasma osmolality returns to normal but at the expense of larger ECF volume. 5) Larger ECF volume continues while the high Na+ diet continues. 6) ECF volume returns to normal if less Na+ is ingested or renal Na+ excretion increases (e.g. diuretic). 7) As ECF volume increases, BP increases and renal Na+ loss increases ('pressure natriuresis').

Answer 38

Because the osmolality of the ECF is kept ~constant, the amount of Na+ in the body determines the volume of the ECF. To maintain a constant ECF volume, the amount of Na+ excreted needs to match Na+ input by the diet.

Answer 39

1) Filter out blood and remove waste 2) Blood pressure/volume regulation 3) pH balance 4) Electrolyte balance

Answer 40

RK sits behind and below rib 12 LK sits behind and below rib 11/12 (higher because no liver) Located posteriorly in abdomen (retroperitoneally) Sitting on top of Psoas and quadratus lumborum in the abdominal cavity.

Answer 41

Ureters exit kidney at L1 (Transpyloric plane)

Answer 42

Abdominal aorta

Answer 43

* *Renal Arteries (lateral @L1/2)** - anterior & posterior branches - (into segmental branches) **Right Renal artery is longer than Left (pass IVC)** **_Runs posterior to IVC_**

Answer 44

L. renal runs under the SMA at the L1 plane (note _compression of left renal_ with _aneurism of either SMA or Aorta_) Runs Anterior to Aorta, Under SMA & Posterior to Splenic v./Body of Pancreas

Answer 45

Leave the kidneys at @L1 Extend vertically down from hilum on surface of Psoas muscle Crosses Bifurcation of Common Iliac Artery Passes on lateral wall of Pelvis (Ilium) towards the Ischial Spine Enters Bladder on inferior surface at the Trigone

Answer 46

1) _Junction of the ureters and the renal pelvis_ (Pelvic-ureteric junction PUJ). \* * \*Most common sites of renal calculus obstruction 2) Where ureters cross the _pelvic brim_ 3) As they enter the _wall of the bladder_ (UVJ/VUJ). \*

Answer 47

4 Distinct regions: 1) Pre-Prostatic 2) Prostatic Widest part - many ducts emptying in 3) Membranous Thinnest part - Through deep perineal pouch 4) Spongy Through Corpus Spongiosum

Answer 48

Bernhardt-Roth Syndrome (Meralgia parasthetica) - numbness of outer thigh due to compression of the nerve as it passes under the Inguinal lig. - Many causes (e.g. seat belts, exercise, tight clothing)

Answer 49

Hyponatremia is a condition that occurs when the level of sodium in your blood is abnormally low. When this happens, your body's water levels rise, and your cells begin to swell.

Answer 50

1) Proximal tubule reabsorbs 2/3 of filtered water, Na+ and Cl-, and 90% of HCO3-. and 100% of glucose. Na+ coupled transport dominates. Filtrate remains at 300 mOsm (as water follows the Na+). pH drops only slightly as most H+'s are used to reabsorb HCO3-. Some new HCO3-made from glutamine. --------------------- 2) Loop of Henle. Thick ascending limb pumps out NaCl but water cannot follow. Countercurrent multiplier established by short loops in outer medulla (300-600 mOsm gradient). In long loops, when ADH is high: NaCl moves from tip and ascending thin limb into inner medulla by osmosis, urea is deposited in inner medulla by collecting duct. Inner medulla gradient established (600-1200 mOsm) and draws water from descending thin limb and collecting duct to concentrate the urine. --------------------- 3) Early distal convoluted tubule: impermeable to water. More NaCl absorbed (blocked by thiazide diuretics eg Furosemide). Urea becomes concentrated. --------------------- 4) Late distal convoluted tubule, connecting tubule and cortical collecting duct, what happens depends on ADH. Absence of ADH: No aquaporins inserted, tubule is impermeable to water. NaCl continues to be reabsorbed by ENaC (target of K+ sparing diuretics). Urine stays dilute. Presence of ADH: tubule becomes water permeable. Urine concentrated (300 mOsm). Intercalated cells secrete H+ (some used to reabsorb HCO3 - some freely excreted (pH balance). --------------------- 5) Medullary collecting duct: what happens depends on ADH. Absence of ADH: No aquaporins inserted, tubule is impermeable to water. NaCl continues to be reabsorbed. Urine stays dilute. Presence of ADH: tubule becomes water permeable and more urea permeable. Urea deposited into medullary interstitium. NaCl moves osmotically from long thin loops to interstitium. Urine becomes concentrated (max 1200 mOsm). Intercalated cells secrete H+ (some used to reabsorb HCO3 - some freely excreted (pH balance). pH can drop to 4.5. Additional H+ excreted by NH4 + 'diffusion trapping'.

Answer 51

Decrease blood flow Decreased glomerular hydrostatic pressure Decreased GFR

Answer 52

Increases blood flow Increase glomerular hydrostatic pressure Increase GFR

Answer 53

Moderate vasoconstriction Increase glomerular hydrostatic pressure Increased GFR

Answer 54

**_Extrinsic mechanisms_** 1) _Renin-angiotensin II:_ constriction of the efferent arteriole - increase GFR) 2) _Arterial natriuretic peptide ANP and BNP_: dilation of the afferent arteriole- increase GFR) 3) _Sympathetic nervous system:_ constriction of the afferent arteriole - decrease GFR - important in shock **_Intrinsic mechanisms_** _1) Myogenic:_ increased arterial pressure stretches the afferent arteriole inducing it to constrict: offsets pressure increase and keeps GFR stable _2) Tubuloglomerular feedback_: macula densa cells monitor NaCl levels in in distal tubule, if high they signal to the afferent arteriole to constrict (decrease GFR to return it to the stable setpoint).

Answer 55

One of the extrinsic mechanisms 1) Low GFR 2) Less NaCl passes the macular densa cells in the JGA 3) Paracrin signals released 4) JG cells release **Renin** 5) **angiotensin II** produced 6a) constriction of *efferent arteriole* _7a) Increase GFR_ 6b) **Aldosterone** released 7b) *Increase Na+* uptake from distal nephron _8b) Increase blood volume_

Answer 56

~66% water and inorganic ions (Na+, Cl-, K+ etc.) ~100% glucose and amino acids ~90% of bicarbonate (filtrate becomes acidified)

Answer 57

Either hereditary or acquired results from an impaired ability of the proximal tubule to _reabsorb HCO3-, Pi, amino acids, glucose and low-MW proteins_ resulting in increased urinary excretion of these solutes.

Answer 58

* NKCC2 and Na/K ATPase mediates Na+ transfer to ECF * (Pumps Na+ and 2xCl- and K+ into the cell.) * ROMK channel recycles some fo the K+ * Tight junctions are water-tight * ECF becomes hypertonic ('single effect'). * NKCC2 is the target of the diuretic Furosemide

Answer 59

NKCC2 is the target of the diuretic Furosemide

Answer 60

The Na/Cl transporter is blocked by thiazide diuretics

Answer 61

Na/Cl transporter (in the arly distal convoluted tuubule)

Answer 62

Mutation in the Na/Cl transporter (in the early distal convoluted tubule) This results in Na+ and Cl- wasting, hyperaldosteronism and resultant hypokalemic metabolic alkalosis. Patients are hypo-calciuric and hypomagnesemic.

Answer 63

1) Principal cells (red) 2) Intercalated cells (green)

Answer 64

Found in the distal convoluted tubule, connecting tubule and collecting duct. Principal cells reabsorb Na+ and secrete K+ (K+ increases in the urine) Absorbed via the Electrogenic Sodium Channel (ENaC) - Reabsorption of Na+ makes lumen electronengative, which drives the K+ secretion. - More lumenal Na+ present, the more K+ secreted - This is important because if the Na/Cl is blocked in the early distal convoluted tubule using thiazide, there's going to be more Na+ uptake by the principal cells, and more K+ will be secreted - This can cause hypokalemia, which can cause ventricular arrhthmias -This channel is the target of Potassium-sparing diuretics e.g. amiloride

Answer 65

ENaC channels Electrogenic sodium channel (in collecting duct/principal cell)

Answer 66

Found in the prinicpal cells - Reabsorption of Na+ makes lumen electronengative, which drives the K+ secretion. - _More lumenal Na+ present, the more K+ secreted_ - This is important because if the Na/Cl is blocked in the early distal convoluted tubule using thiazide, there's going to be more Na+ uptake by the principal cells, and more K+ will be secreted - This can cause hypokalemia, which can cause ventricular arrhthmias - This channel is the target of Potassium-sparing diuretics e.g. amiloride

Answer 67

Mutation that causes increase in number of ENaC. Too much NaCl is reabsorbed, leading to increased ECF volume and hypertension.

Answer 68

_Aldosterone stimulates Na+ reabsorption and K+ secretio_n by gene expression changes: Up-regulates activators that open ENaC channels AND induces more ENaC and Na/K ATPase (more K+ is secreted) _Spirolactone (weak K+ sparing diuretic) blocks aldosterone_

Answer 69

Aldosterone

Answer 70

Found in the distal convoluted tubule, connecting tubule and collecting duct 1) Important for acid-base balance and K+ absorption 2) Usually secrete H+ (H+ ATPase and H+/K+ ATPase) 3) Some H+ aer used to reabsorb HCO3- 4) Some H+ can be freely secreted (generates NEW HCO3-) 5) Some are just lost (way of losing acidity)

Answer 71

This depends on the level of anti-diuretic hormone (ADH) aka Arginine Vasopressin (AVP) Binds to V2 receptor which activates cAMP ADH causes aquaporin water channels to be inserted into the apical membrane Now water gets reabsorbed rather than excreted into the urine (tube fluid can be 300mOsm) In the absence of ADH, water remains in the tubule lumen Response to ADH is rapid (vesicles rapidly inserted or re-internalised)

Answer 72

High ADH-\> high water reabsorption -\> concentration urine Low ADH -\> low water reabssorption -\> dilute urine

Genitourinary System Flashcards

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