anatomy
physiology
mixed 1
mixed 2
pathology
100

What is the order of the structures of the kidney hilum from anterior to posterior?

Renal vein

Renal artery

Renal pelvis/ ureter 

100

What is the anion gap? 

Difference between measured cations and anions

((Na+) + (K+)) - ((HCO3-) + (Cl-))

100
What spinal level do the renal arteries arise from?

L1-L2 IVD

100

Where is renal pain typically referred?

Loin to groin 

100

What is the main difference between nephritic and nephrotic syndrome?

Nephrotic syndrome - proteinuria

Nephritic syndrome - proteinuria + haematuria 

200

Where along the urinary tract are renal stones likely to get caught?

1. PUJ

2. Pelvic brim

3. Intramural part or ureter as it enters the bladder wall. 


200

When would you expect to see acidosis with a normal anion gap?

When the excess acid/ decreased HCO3- is compensated by a measured ion.

- e.g: diarrhoea or renal tubular acidosis

in this, the decreased HCO3- is balanced by an increase in Cl-

(K+Na) - (decreased HCO3 + Increased Cl) = no change in anion gap

200

What transporter is blocked when using thiazide diuretics, and where in the nephron does this take place? 

In the DCT

Apical Na+/Cl- cotransporter is blocked. 

200

What is the innervation of the external urethral sphincter and what spinal levels contribute to this? 

Somatic innervation - pudendal nerve - (S2-S4)

200
What population is primarily affected by minimal change disease?

Children - less common in adults 

300

Which muscles contribute to the TMJ, and there innervation?

Masseter, later pterygoid, medial pterygoid, and temporalis. 

Innervation: CNV3 - trigemnal nerve, mandibular branch

300

What do beta-intercalated cells do in relation to pH control at the kidneys?, and how is this achieved?

Beta-intercalated cells secrete HCO3-, this is done by CO2 (from peritubular capillaries) and OH- (from dissociated H2O). This combines to form HCO3- in the presence of carbonic anhydrase, and are transported into the lumen through an apical Cl-/HCO3- exchanger. 

300

What are the structures of the spermatic cord? 

3 threes

3 arteries - testicular artery (and pampiniform plexus), cremasteric artery, and artery of ductus deferens.

3 nerves - the genital branch of the genitofemoral nerve, sympathetic and parasympathetic. 

3 others - Ductus deferens, remnant of processus vaginalis, lymphatics. 

300

In what pathology would you see onion-like hyperplasia in glomeruli vessels, and explain why it gets this appearance? 

Hyperplastic arteriosclerosis.

From chronic hypertension, endothelial damage results in vascular remodeling where the body continues to add layers of smooth muscle to the tunica media of glomeruli arterioles. 

300

What enzyme converts testosterone to DHT in stromal cells?

5-alpha reductase 

400

Describe the innervation of the tongue

Anterior 2/3 - Fascial nerve (CNVII) - specifically corda tympani for taste, and trigeminal CNV3 - mandibular branch for tough, temp, and pain. 

Posterior 1/3 - glossopharyngeal (CNIX)

400

Explain the ammonia-ammonium buffer system

Glutamine dissociates in the PCT to form ammonium (NH4+). This is trapped in the lumen until the TAL. 

Here it is reabsorbed, and this reabsorption sets up the medullary gradient which favors ammonia (NH3) secretion into the collecting duct lumen.

The NH3 binds to H+ (from alpha-intercalated cells), forming NH4+ to be excreted in the urine. 

This creates more acidic urine. 

400

Infection with what bacteria increases the likelihood of developing a struvite stone, what can these stones be made of, and why does the infection generally occur before the formation of these stones? 

Proteus vulgaris infection, this bacteria results in alkaline urine, which is the environment needed for these stones to form.

Magnesium, ammonium, or phosphate is needed to form these stones.

400

Describe the SNS and PNS control of micturition including names of nerves and spinal levels. 

SNS - innervates the smooth muscle of the internal urethral sphincter.

- T12-L2 (inferior mesenteric ganglion) - becomes superior hypogastric plexus. 

- Sacral splanchnic nerve (T12-L2) 

PNS

- Pelvic splanchnic nerve (S2-S4) - innervates bladder wall smooth muscle. 

All combine to form inferior hypogastric plexus

400
How does a waxy cast form, and what disease would see it in? 

Likley in chronic pyelonephritis, this is a degernerated granular cast, which itself is a degernated cellular cast. 

500

What are the fascia layers of the spermatic cord (superficial to deep)

Dartos muscle and fascia

External spermatic fascia

Cremasteric muscle and fasica

Internal spermatic fascia 

Processus vaginalis (reminant)

Tunica albuginea 

500

How does vasopressin/ ADH contribute to Na+ reabsorption, and where along the nephron does this take place? 

Stimulates Na/K/Cl cotransporter in the TAL

Increases numbers of Na channels in principal cells. 

Inserts aquaporins into the apical membrane in the PCT

500

A patient after a spinal cord injury 12 months ago comes to the emergency with severe urinary retention and undergoes a cystostomy. Where is the lesion likely located in their spinal cord, and explain the neurological reason for their presentation? 

The patient likely has a infrapontine-suprasacral lesion.

The patient is experiencing detrusor overactivity combined with detrusor-sphincter dysynergia (DESD). 

Due to damage in the thoracolumbar region, there is unregulated SNS, so there is a discoordination of contraction and external internal urethral sphincter relaxation. 

Extremely poor bladder emptying ability.  

500

The juxtaglomerular apparatus detects a decrease in NaCl, what do the macula densa cells do, and what does this do to the glomerulus/ nephron.

The macula-densa cell will secrete prostaglandin E, which will stimulate renin release from JG cells (granular cells), which stimulates RAAS, leading to Na+ and water reabsorption in the distal tubule.

The prostaglandins also promote dilation of the afferent arteriole to increase renal blood flow and GFR. 

500
What are the 4 metabolic defects associated with diabetic nephropathy? 

1. RAGE receptor activation on macrophages and endothelial cells from non-enzymatic glycosylation 

2. Excess NADPH reduction from increased glucose in cells, leading to decreased reduced glutathione - leading to oxidative stress and inflammation

3. Protein kinase-C activation intracellularly, leading to increased TGF-beta, leading to increased fibroblasts - increased collagen.

4. Increased deposition of fibronectin and collagen.

All resulting in increased basement membrane thickness

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