Genitourinary System Flashcards
What are some causes of metabolic acidosis?
1) Increased acid production
a) Lactic acidosis
- hypoxia
- poort tissue perfusion
- CO or cynaide poisoning
b) Diabetic ketoacidosis (DKA)
- beta-hydroxybutyric and acetoacetic acids
- failure of oxygen delivery to the tissues
2) Decreased acid excretion
a) Renal failure
b) Renal tubular acidosis
- Failure of tubular acid secretion
3) Bicarbonate loss
a) Severe biarrhoea, ileostommy
What would you see in
Acute respiratory alkalosis?
Acute metabolic alkalosis
Acute respiratory acidosis
Acute metabolic acidosis
1) pH
2) bicarbonate
3) pCO2
Normal pH of the body is…
~7.4
Describe the detailed 4-step approach to interpreting acid-base data
- 1) What is the primary diagnosis?
- -Acidaemia/alkalaemia first, then is it primary or acidosis or primary alkalosis? (look at pH)
- -Is the primary disturbance respiratory or metabolic? (look at the pCo2, bicarbonate and Base excess)
- 2) Is the compensation appropriate?
- -Use an acid-base map or use a ‘rule of thumb’ (inappropriate compensation implies a mixed disorder)
- 3) Calculate the anion gap
- -A high anion gap implies metabolic acidosis is present and can determine the diagnosis (+ urine serum anion gap if serum anion gap is normal)
- AG = cations - anions
- AG = (Na+K) - (Cl+ bicarbonate)
- (Normal AG reflects mainly protein anions)
- Increased AG indicates the presence of unmeasured anions
- 4) Calculate the delta anion gap/delta HCO3 ratio
- This helps to identify the presence of a co-existing metabolic acidosis or alkalosis
-
Delta ratio = increased anion gap / decrease [HCO3-]
- Meausred AG - Normal AG
- Normal [HCO3] - measured [HCO3]
- If the delta ratio is lesser than 1 = concurrent with normal AG acidosis
- (e.g. DKA and diarrhoea) (two conditions which result in acidosis)
- If the delta ratio is between 1-2 = pure AG acidosis
- If the delta ratio is greater than 2, it indicates concurrent metabolic alkalosis (e.g. lactic acidosis and vomitting). (one condition which result in acidosis and the other resulting in alkalosis)
Case report:
-42 year old man who is semi-comatosed with seizures
- pH is low
- PO2 is normal
- pCo2 is low
- Bicarbonate is very very low
- Base Excess = -19
Na, K and Cl are normal.
What can we determine from this?
Metabolic acidosis
AG = (140+4) - (102+8) AG = 34 (high)
Ethylene glycol poisoning (dry-freeze) is suspected. Treatment was commenced with an ethanol infusion
What are some causes of normal Anion Gap acidoses (Metabolic acidosis)
Non-renal causes (most common)
-Normal renal acidification by the kidneys but loss of bicarbonate from non-renal causes
1) Diarrhoea
2) GI ureteral connections, ileostomy
3) External loss of pancreatic or biliary secretions
Renal causes
-failure of renal acidification
1) Proximal renal tubular acidosis (type 2 RTA)
2) Hypokalaemic distal renal tubular acidosis (type 1 RTA)
3) Hyperkalaemic distal renal tubular acidosis (type 4 RTA)
4) RTA of chronic kidney disease (failing kidney, but not quite failed)
What is Renal Tubular acidosis (RTA)?
-Defects in acid excretion: urine pH > 5.5 and urine ammonium not increased (inappropriate for metabolic acidosis)
- Proximal (Type 2) or distal (Type 1) types
- Usually hypokalaemia
Why does chronic vomitting cause muscle weakness?
Pathogenesis:
1) Loss of HCl due to vomitting causes alkalosis
2) Hypokalemia is due to
a) alkalosis
b) K+ loss to due to excessive laxative use (in chronic diarrhoea, K+ loss predominates due to the NaK exchange in the colon. In acute diarrhoea, Na+ loss predominates)
3) Hypokalemia causes muscle weakness (hyperpolarises exciatble cells)
What are the boarders of the Inguinal Canal?
- *Anterior Wall =**
1) Aponeurosis of External Oblique
2) Internal Oblique (in Lateral 1/3) - *Floor =**
1) Inferior rolled edge of External Oblique aponeurosis (Inguinal Lig.)
2) Lacunar Lig. (Medial) - *Roof =**
1) Fibres of Internal Oblique
2) Transversus Abdominis - *Posterior Wall =**
1) Transversalis Fascia
2) Conjoint Tendon (Medial 1/3)
What is the Hesselbach’s (Inguinal) Triangle?
Site of Direct Heria- pushes through weakened abdominal wall
Corresponds to weak anterior wall (superficial inguinal ring)
Lateral Boarder: Rectus abdominis
Inferior Epigastric artery
Inguinal Ligament
Name the arteries found in the spermatic cord
3 Arteries -
1) Testicular a. (from L2 level Abdominal Aorta)
2) Artery of Vas Deferens (Deferential a.)
3) Cremasteric a.
Name the nerves found in the spermatic cord
1) Genital branch of Genitofemoral n. - (L1-2)
2) Sympathetic nerves (from Testicular plexus)
3) (Ilioinguinal n. - L1) - (DOESN’T actually travel in cord)
A 16 year old NZ European boy presents with severe pain in his left testis associated with some swelling. It started an hour ago and is excruciating. He has otherwise been well in the past.
What is wrong with this patient?
testicular torsion
Spermatic cord twists round, cutting of blood supply (causing Ischaemia)
Surgical EMERGENCY!
Describe the cremasteric reflex
Reflex that indicates whether torsion has occured in the testis
Normal Reflex
- Stroke superior medial thigh
- Stimulates sensory fibres of Femoral branch of Genitofemoral n. & Ilioinguinal n. (L1-2 origins)
- This in turn stimulates motor fibres of Genital Branch of Genitofemoral n.
- Cremaster muscle contracts on Ipsilateral side, raising the testis
If Torsion has occured:
-Reflex not present
-NB: Method is not infallible!
-Ultrasound confirmation = very reliable (Distinguishes torsion from epididymitis by showing lack of blood flow to testis)
-6 hour window of opportunity - chance of saving testis drops significantly after this time
What are Inguinal Hernias?
Inguinal hernias = protrusion of abdominal contents through inguinal canal
2 types: Indirect & Direct
DIRECT: Abdominal contents herniate through weak spot in fascia of posterior wall of Inguinal canal - Hesselbach’s Triangle (don’t travel into the groin)
Direct: **MEDIAL to Inf. Epigastric a.
More older in elderly patients
INDIRECT: Herniation goes through D.I.R. and through ENTIRETY (this is the difference between direct and indirect) of inguinal canal into scrotum Within Spermatic Cord
Indirect: LATERAL to Inf. Epigastric a.
More common in younger patients
How do you differentiate between inguinal or femoral hernia?
1) Inguinal Ligament
- Inguinal: Superior to the inguinal lig (also more common in males)
-Femoral: Inferior to the inguinal lig (more common in females)
2) Pubic tubercle **
- Inguinal: Above and medial
- Femoral: Below and Lateral
How do you differentiate between the 3 hernias?
Q: Is there a Hernia?
Test: Cough impulse & reducibility
A: Positive cough impulse / lump is reducible = Hernia
Q: Is it Femoral or Inguinal?
Test: Find _Pubic Tuberc_le and reference hernia to this point
A: Above & Medial = Inguinal, Below & Lateral = Femoral
Q: If Inguinal, is it direct or indirect? (Without Imaging)
Test: Using your knowledge of the surface anatomy place fingers over D.I.R and have patient cough
A: No Bulge = Indirect
What is Nephrotic Syndrome?
Nephrotic syndrome is often caused by damage to small blood vessels in the kidneys that filter waste and excess water from the blood.
1) >3.5g/day urinary protein
2) Low serum albumin
3) Oedema (due to the loss of albumin which reduces oncotic pressure and results in aggregation of fluid in the interstitial space)
4) Frothy urine
5) Hypercholesterolaemia
6) Blood clots
7) Renal function may be normal or impaired (GFR)
What is the difference between Nephritic and Nephrotic syndrome?
Nephrotic ( o = odemia)
Nephritic = acute kidney injury
What are the root values of Sciatic Nerve?
L4-S3
What causes the rectum to be bent?
What is the significance of this?
Puborectalis from the Pubococcygeus part of the Levator Ani
Levator Ani is innervated by:
- pundendal nerve (S2-4)
- nerve to levator ani (S3-4)
If this is damaged, you lose the ability to control your bowel movements
What is Guevedoces? (DHT syndrome)
Condition characterised by lack of Androgen DHT (5α-Dihydrogen Testosterone) during development
- 5α-Reductase deficiency (5a-reductase converts testosterone to DHT)
- DHT = 2-3x more potent androgen than testosterone
Males born with female primary sexual characteristics (i.e. no/underdeveloped penis - genitally ambiguous)
Sex = Male but Gender = Female due to lack of conspicuous male genitalia
Puberty: Raised androgen sex hormones may result in radical virilisation and development of Male genitalia
- Choice about whether they want to adopt the male gender identity or remain female
If the right renal artery becomes abnormally constricted, what will happen to renin secretion by the right kidney and the left kidney?
Also state what would happen to the BP
Right: Decrease flow, so Renin secretion will increase (constrict)
Left: May see increased flow because BP goes up (because of the increase in renin secretion by the right side). Renin secretion will decrease
Overall: Acute increase in renin. Will hit the rest of the body. B_P will go up._
What stimulates release of aldosterone?
Angiotensin II (High NaCl)
High Potassium
What is the consequence of aldosterone activity?
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+
What is Hyperaldosteronism treated by?
Treated by antagonists to the minerocorticoid receptors. (Spironolactone)
If you lose the function of your adrenal glands. What would you observe in the tubular secretion patterns?
Increased sodium excretion (due to loss of aldosterone-dependent sodium reabsorbtion)
What are the mediators of
1) osmolality
2) extracellular fluid volume
1) Osmolality: Antidiuretic Hormone (ADH)
2) ECF volume: Renin-angiotension system and Sympathetic Nervous system
How is decreased ECF volume compensated for?
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
Name 3 things that increases sodium reabsorption
- RAA (renin, angiotensin, aldosterone) system
- Sympathetic nervous system
- ADH
What does ANP do?
What does it result in?
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
What happens during dehydration?
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
If someone has Syndrome of inappropriate antidiuretic hormone secretion (SIADH)…
1) What would you expect ADH levels to be in this patient (provided normal ADH levels can range from 1-5 picograms per milimeter)
Greater than 5
(faint = low BP)
If someone has Syndrome of inappropriate antidiuretic hormone secretion (SIADH)…
What would expect the osmolality levels in this patient to be? (provided normal range between 275-295 mm/kg)
Lower than 275 (reabsorb lots of water)
What is kidney failure?
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
What is the normal glomerula filtration rate?
Normal = ~100ml/min
Plasma creatinine ______ as GFR _____
plasma creatinine rises as GFR falls
What is eGFR?
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)
Describe the surface anatomy of kidneys
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.
Describe the arterial supply to the kidneys
- *Renal Arteries (lateral @L1/2)**
- anterior & posterior branches
- (into segmental branches)
Right Renal artery is longer than Left (pass IVC)
Runs posterior to IVC
How does the L.renal vein run?
What is the significance of this?
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
Where are the 3 possible constrictions of the ureter?
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). *
Name the regions in the male urethra
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
What is absorbed at different parts of the nephron?
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’.
Describe when the Renin-angiotension mechanism is activated and desribe how it works
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
What % of things are reabsorbed in the proximal tubule?
~66% water and inorganic ions (Na+, Cl-, K+ etc.)
~100% glucose and amino acids
~90% of bicarbonate (filtrate becomes acidified)
What sets up the Na+ gradient in the medulla in the short loop of nephrons? (describe the channels involved)
- 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
