ESA3 Flashcards
Presentation of polycystic disease at
Autosomal dominant disease
30-40 years of age with complications of :
- Hypertension
- Acute loin pain
- Haematuria
- Bilateral palpable kidney
main treatment for polycystic ovary syndrome
- involves controlling BP
- Medication (ACEi)
- Low salt diet
- Dialysis and renal transplant needed if end-stage renal failure develops
In CKD where do cysts develop
- anywhere in the kidney
- Compress the surrounding parenchyma and impair renal function
- Also develop cysts in the liver- not as much of a problem
pathological changes in diabetic kidney disease
- Hyperfiltration/ capillary hypertension
- Happens before all over changes
- Glomerular basement membrane thickening
- Mesangial expansion
- Podocyte injury
- Glomerular sclerosis
why does hyperfiltration occur in early DKD
- Related to hyperglycameia
- Reabsorption of glucose couple with reab of sodium
- More glucose reabsorbed therefore more sodium reabsorbed
- Less sodium left in tubule by DCT
- Macula densa senses reduction in delievery of NaCl
- Activation of RAAS
- Vasodilation of afferent arterial and vasoconstriction of efferent arterial–> hyperfiltration due to increased hydrostatic pressure
- Glomerular hypertension
- Increases GFR
first stage of CKD
microalbuminuria
GBM thickening and mesangial expansion
30-300 mg/day- Albustix special album pee stick
treatment of DKD
- Tight blood glucose control <48 mmol/mol (6.5%)- MOST IMPORTANT
- Tight blood pressure control
- SGLT-2 inhibitors
- Not smoking
- Statin therapy
Evidence of hyperfiltration in early DKD
Evidence of hyperfiltration, big kidneys, raised GFR
Needs to have tight glycaemic control
Albumin and creatinine screening with sensitive dipsticks to test for microproteinuria
ACEi and ARB low level of bp
Q
what is Post obstructive diuresis
A
Following resolution of urinary retention through catheterization
Kidneys can often over diurese–> over filter
Can lead to worsening AKI
Can lose Countercurrent- more water loss
Q
Hydronephrosis
A
Dilation of the renal pelvis and calyces due to obstruction at any point in the urinary tract causing increased pressure and blockage. It can be:
Unilateral
Bilateral
causes
Progressive atrophy of kidney devlops as the back pressure from the obstruction transmitted to the distal part of the nephrone
GFR declines, if bilateral= renal failure
diagnosis of urothialiasis
CT- can see stones
not a function test though
functional test: diuretic renography
brachial plexus injurys
Upper plexus palsy (Erb’s palsy in the OBPI cases) involves C5-C6/C7 roots
- waiters tip
Lower plexus palsy (Klumpke’s palsy) involves C8-T1 roots

kernigs vs brudinski sign

How can you remember which cranial nerves are to open and close the eyes?
- VII Fish Hook: closes by orbicularis oculi
- III Bars Holding Open: opens by levator palpebrae superior
Balance between the two to hold eyelid so if one goes the other wins
What are the important branches of the opthalmic nerve (Va)?
- Frontal: exits front of the orbit as supraorbital and supratrochlear to give sensory supply to forehead (trochlear), upper eyelid, conjuctiva and scalp
- Lacrimal: sensory to lacrimal gland, conjuctiva and upper eyelid
- Nasocilliary: sensory to sinuses, noses and eyes
ALL EXIT THROUGH SUPERIOR ORBITAL FISSURE
important branches of maxillary

What are the important branches of the mandibular nerve (Vc)?
- Inferior alveolar: through bony canal and exits as mental nerve at mental foramen. Sensory to mental protuberance, lower lip and gum. Can be injured in mandible fracture
- Lingual: general sensory from anterior tongue
- Auriculotemporal: general sensory from ear, temple, scalp and TMJ
What are the three intracranial branches of the facial nerve and their anatomical course?
All enter the internal accoustic meatus in the petrous part of temporal bone
Greater Petrosal: Carries PS to the lacrimal and nasal glands and taste from soft pallate through the foramen lacerum
Chorda Tympani: Taste from anterior 2/3rds of tongue and motor to submandibular and sublingual salivary glands. Through petrotympanic fissure
Nerve to Stapedius: Motor to stapedius, dampens down vibrations of loud noises to protect ear
What nerves would need to be damaged to cause a partial and full ptosis?
Occulomotor nerve has a skeletal muscle component, levator palpebrae, and an autonomic component, superior tarsal
Partial: loss of superior tarsal
Full: loss of levator palpebrae
sympathetics leave the CNS via
thoracolumbar outflow
All sympathetic nerves leaves the CNS from segments T1-L2 ONLY
then enter sympathetic chain
Parasympathetic leave the CSN via
Craniosacral outflow
- Cranial (4 cranial nerves)
- Sacral (S2-S4)
- pelvic splanchnics

thoracolumbar t1-T2 (sympathetic innervation to the head and enck) follow
routes of blood vessles (hitchhike on the exteranl surface of blood vessels)
outline how thoracolumbar T1/T2 provide sympathetic innervation to the head an enck
- Superior cervical ganglion most important when thinking of head and neck
- When the pre-ganglionic nerve meets the superior cervical ganglion we meet the cell body of the post-ganglionic sympathetic nerve
- Post ganglionic sympathetic nerve will join the common carotid artery and follow the external carotid artery as it distributes branches across the face and the internal carotid artery as it runs through the base of the skull through the cavernous sinus and a branches into the orbit (think of the route of the carotid artery= route of sympathetic nerve)
- Follows ophthalmic artery (branch of internal carotid) into the eye
- To the smooth muscle of the eyelid
- Pupil
- Follows external carotid to the
- Sweat glands of the forehead
- Sweat glands of face
(think of the route of the carotid artery=
route of sympathetic nerve)




















