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)
where does the common carotid bifurcate
C4- carotid triangle
sympathetics follow the ophthalmic artery (branch of internal carotid) into the eye and innervates
Small smooth muscle portion of the levator palpebrae superioris muscle which opens the eye called the superior tarsal muscle
Pupil- ciliary muscles= pupil dilation
nervous supply to the eye
The levator palpebrae superioris (LPS) is the only muscle involved in raising the superior eyelid- innervated by oculomotor CN III.
A small portion of this muscle contains a collection of smooth muscle fibres – known as the superior tarsal muscle. In contrast to the LPS, the superior tarsal muscle is innervated by the sympathetic nervous system.
Why in Horner’s syndrome, is the ptosis only partial- compared to the more severe ptosis seen in an oculomotor nerve lesion?
Smooth muscle (innervated by sympathetic nerve) part of the Levator Palpebrae Superioris Muscle (LPS), called the superior tarsal muscle, is only a small component LPS, which is innervated by the oculomotor nerve which uses skeletal muscle
therefore if the sympathetic nerve has a lesion then only a small part of the LPS (superior tarsal) will be affected= partial pstosis
full ptosis
If you lose oculomotor nerve (and not sympathetic nerve), you would still get full ptosis due to the smooth muscle (superior tarsal) not being strong enough to open the eye
horners syndrome
Triad of symptoms produced by damage to the sympathetic trunk in the neck:
Partial ptosis (drooping of the upper eyelid) – Due to denervation of the superior tarsal muscle.
Miosis (pupillary constriction) – Due to denervation of the dilator pupillae muscle.
Anhidrosis (absence of sweating) on the ipsilateral side of the face – Due to denervation of the sweat glands.
Horner’s syndrome can represent serious pathology, such as a tumour of the apex of the lung (Pancoast tumour), aortic aneurysm or thryoid carcinoma.
How would the pupil differ in a Horner’s syndrome compared to an oculomotor nerve lesions?
Horners (sympathetic lesion)- constricted pupil (miosis)
- unopposed parasympathetic
Oculomotor lesion (parasympathetic)- dilated pupil (mydriasis)
- unopposed sympathetic
mydriasis in CN III lesion
dilated pupil
interruption to the parasymapthetic innervation (carried by oculuomotor) to the constrictor muscle of the pupil, leaving unopposed sympathetic innervation to dilator muscle of pupil
Causes of Horners syndrome
Patients with apical lung cancer can have sympathetic interference e.g.Pancoast tumour
Patients with anerysms or dissected blood vessels into the neck
Which cranial nerves carry parasympathetic fibres from the brainstem?
Oculomotor
Facial
Glossopharyngeal
Vagus
CNIII isassociated with which nuclei and parasymapthetic ganglion
Edinger westphal
ciliary ganglion (where pre-ganglionic fibre meets the post-ganglionic fibre)
The Edinger–Westphal nucleus
hitchhikes on the oculomotor nevre
innervates the iris sphincter muscle and the ciliary muscle
outline how parasymapthetic nerves get to their target tissues
A
- arise from the brainstem from parasympathetic nculei
- hitchkine on one fo the 4 CNs
- parasymapthetic glanglion
- hicth hike on branches fon CNV
- Ciliary (parasympathetic of the oculomotor nerve)
- Submandibular
- Pterygopalatine
- Otic
- target tissues
target tissues of hitchhiking parasympathetics
Smooth muscle (sphincter pupillae (pupil constrictor) and ciliary muscle (controls lens)
Lacrimal gland
Mucosal gland in nasal/ oral mucos/resp tract
outline CN III oculomotor and parasymapthetic pathway
where is the carotid canal found
within the petroud part of the temporal bone
allows intenral carotid to pass through the base and enter the skull
Carotid triangle borders
superior: posterior border of digastric
medial: superior belly of omohyoid
lateral: medial border of scm
pneumonic for learning 6 branches of the external carotid
some –> superior larygeal artery
ancient —> ascending pharangeal
lover –> lingal?
find–> facial
old–> occipital
positions–> posterior auricular
more–> maxillary
stimulating–> superficial temporal
which arteries combine to provide a dense blood supply to the scalpe (which is one reason why injuries to thesscalp cause excessive beleeding)
posterior auricular, occupital and superficial temporal artery
and
two branches of the internal carotid artery: supra-orbital and supratrochlear
M MA branch of the
maxillary
Drainage of the scalp
Most blood drains away superficially
Some blood from the scalp can drain into areas containing venous blood called Dural venous sinus
Drains via emissary veins through the skull into dural venous sinuses
Risk of infection- meningitis
Budd–Chiari syndrome
occlusion of the hepatic veins that drain the liver by blood clots
classical triad of abdominal pain, ascites, and liver enlargement.
blood supply to the liver
Input
portal vein- low O2 high nutrients (drains superior,middle, splenic vein)
hepatic artery- O2 high
Output
The central veins coalesce into hepatic veins that collect the blood leaving the liver and bring it to the heart (vena cava).
bile leaves the liver via the
common bile duct
the liver is split up into units called
hepatic lobules
6 units of the portal triad surrounding hepatocytes
sinusoids
are low pressure vascular channels that receive blood from terminal branches of the hepatic artery and portal vein at the periphery of lobules and deliver it into central veins. Sinusoids are lined with endothelial cells and flanked by plates of hepatocytes.
sinusoids are populated by
kupffer cells
satellite cells
heptocytes
kupffer cells
macrophages
stellate cells
also known as Ito cells
store vitamin A
during liver cirrhosis, hepatic stellate cells lose their ability to store vitA and differentiate into myofibroblasts
- these synthesise and deposit collagen within the perisinusoidal space - liver fibrosis
why does portal hypertension occur
A
- Due to cirrhosis
- Too much fibrotic tissue
- Not very expansive – needs to be because it drains the whole GI tract
- Too much fibrotic tissue
- If its not very expansive veins entering the liver (from portal venous system) will be compressed
- Increase hydrostatic pressure within portal venous system
oesophagus drainage
upper 2/3- oesophageal vein draining into the superior vena cava
lower 1/3- left gastric vein- drains into the portal vein
why do varices happen in the oesophagus, umbiucus, and anorectal
At the junction where there are veins draining into the main systemic circulation (SVC) (vs portal) is where the pressure builds up–> blood shunts from portal system to the systemic ciruclation via anastomes
- Veins are superficial- therefore become dilatedà easy to rupture
- Significant Haematemesis
what is found in the carotid sheath
common carotid, vagus nerve, internal jugular vein
Umbilical varices
Ligamentum teres (remnant of the left umbilical vein) in adults- usually non functioning in adults
- Can become enlarged
- Caput medusae sign
abdominal muscle
horizontal
- external oblique
- internal oblique
- transverse abdominus
vertical
- rectus abdominus
route of bile out of the liver
- right and left hepatic duct
- common hepatic duct
- common hepatic duct + GB contents= common bile duct
- pancreatic duct secretes into common bile duct
- bile release via the ampulla of vater controlled by the sphincter of oddi into the second part of the duodenum
gall stone
biliary colic- stones in GB press against cystic duct when GB contracts due to CCK
Acute cholecystitis- stone trapped in the cystic duct (Positive Murphy sign)
Ascending cholangitis- stasis due to blockage in CBD
charcots triad and murphys sign
Murphys sign (Acute cholecystitis)
place a hand on right side of the patients stomach and ask them to take a deep breathe in- will push gall bladder down and cause them to take a sharp breathe in pain (wont happen on left hand side)
Charcots triad (ascending cholangitis)
- RUQ pain
- jaundice
- fever
-
breakdown of haem
haemoglobin –> haem and globin
- haem converted to billiverdin –> billirubin
- billirubin conjugated with glucoronic acid in the liver to make it water soluble
- Can travel down to duodenum and stay in the gut –>oxidised to stercobilin
- Can go to the kidney and be excreted as urobilinogen
which type of bilirubin (conjugated or unconjugated) will be raised if cause is post-hepatic
- Conjugated –> water soluble –> goes through blood stream to the kidney (less can go into the bowel)
- More bilirubin excreted by the kidney
- Therefore discolouration of the urine
- Dark urine, pale stools
ALT
AST
ALP
alanine aminotransferase
aspartate aminotransferase
alkaline phosphatase
zones of the liver
- Functional unit of the liver=Acinus
- Region of adjoining liver lobules
- Diamond shape
- Has different zones
- 1- closes to the portal triads
- 2
- 3- nearest to the central vein
Any toxins coming into the liver will affect zone ………. more than zone ……..- closest proximity to blood coming in
Any toxins coming into the liver will affect zone 1 more than zone 3- closest proximity to blood coming in
Zone …… much more likely to be damaged by ischaemia- furthest away from the blood coming in
Zone 3 much more likely to be damaged by ischaemia- furthest away from the blood coming in
Aspartate aminotransferase/ transaminase
- Also found in cardiac (increased troponin) and skeletal muscle (look at increase in CK) and RBC (FBC)
- Chronic liver damage (likely for them both to go up)
what can be measured to confirm raised ALP is of liver origin
Gamma-glutamyl transferase - another enzyme which will confirm if the raised ALP are caused by a damaged or obstructed bile duct as opposed to the bone
ALP can be high in children that are growing quickly/ also malignancy of bone
describe how saliva is produced
- Acinus is where the saliva is produced
- Isotonic with plasma
- Isotonic solution passes out of the acinus due to myoacinus epithelial cells which contract the acinus to move saliva into the duct
- Once in the ductal region , ductal cells use transporters to move Na+ and Cl- out of the solution and K+ and HCO3- into the solution
- Producing a hypotonic solution near the end of the duct (removal of ions >secretion)
The amount of modification (more or less hypotonic)by the ductal cells depends on how quickly the saliva is moving through the ductal system
Basal level- most hypotonic solution
When eating the solution moves through much quicker, less contact with ductal cells- smallest change to the tonicity of the isotonic solution (more secretion of HCO3- when active saliva production
more secretion of HCO3- when
active saliva production
common incision sites
how would smalll bowel obstruction look on CT
3cm or more= distended small bowel
central position of bowel
plica circulares clear- lines across hole of bowel
how would a large bowel obstruction look on a CT
- more peripheral
- can seehuastra which doesnt go the whole way across
- 3/6/9 rule
in patients where there is an appropriate reticulocyte response what is expected
LDH released when RBC breakdown
sickle cells vs thalassaemia
thalassaemia
reduced or absent expression of structurally normal chain
sickle cell
abnormality of the chains themselves
Thalassaemias
are autosomal recessive, inherited diseases resulting from the reduced rate of synthesis of normal α- or β- globin chains.
sickle cell anaemia
However, in sickle cells disease, when deoxygenated the defective haemoglobin S (HbS - haemoglobin specific to sickle cell disease) polymerises causing deformation of the cell, losing its biconcave structure and becoming ‘sickle’ (or crescent moon) shaped.
This irregular shape causes the sickle cells to become stuck in blood vessels, impairing the flow of blood to certain areas of the body. Furthermore, the cells are quite fragile so easily break down or are removed by the spleen, leading to a haemolytic anaemia.
Q
Cleft lip and palate
A
Lateral cleft lip
Failure of fusion of medial nasal prominence and maxillary prominence
Cleft lip and cleft palate
Combined with failure of palatal shelves to meet in midline
fracture healing
- haematoma formation- haematoma converted to granulation tissue
- soft callous- deposition of collagen and fibrocartilage (granulation tissue –> soft callus)
- hard callous- osteoblast deposit bony collar around fracture while ossification occurs
- remodelling- osteoclasts and spongy bone –> compact bone
harry saw hard rock
neck of femur fracture and avascular necrosis
femoral head supplied by medial circumflex femoral artery
disruption to this artery causes avascular necrosis (even if the hip is fixed).
Patients with a displaced intra-capsular fracture therefore require joint replacement (arthroplasty), rather than fixation.
Intracapsular fracture
NOF fracture
The neck of the femur connects the head of the femur to the shaft.
Neck of femur fractures can be divided into two categories – intracapsular and extracapsular.
NOF presentation
- Short/ externally rotated
- Due to muscles contracting and pulling gluteal and quad
intracapsular vs extracapsular
what is at risk with a distal humerus at risk
medial nerve and brachial artery–> think of the cubital fossa
FOOSH
scaphoid fracture
distal radius
high ulnar nerve vs low ulnar nerve
It is important to differentiate this from the appearance of the hand in a high ulnar nerve injury
Unexpectedly, the appearance of the low ulnar claw is more severe than the appearance of the high ulnar claw. This is because with a high ulnar nerve injury, the innervation to flexor digitorum profundus is destroyed, meaning the fingers cannot flex as much as they can in a low ulnar nerve injury, when this muscle is spared. This is called the ‘Ulnar paradox’.
“hand of benediction” which is caused by
proximal (at elbow level) median nerve damage.
cant put hand in fist
ulnar claw
ulnar nerve damage causing paralysis of the lumbricals.
cant straighten all fingures from fist but can make fist
the long bone
types of ossification
intramembranous and endochondral.
intramembranous the skull
- bones develop from fibrous membrane
- flat bones: skull and clavical
endochondral
- bone replaces hyaline cartilage mould
- most of the skeleton
presentation of anteiror dislocation (95%)
- They present with an externally rotated and abducted
- Pain, deformity, loss of function
presentation of posterior dislocation
They present with an internally rotated and adducted arm. There is also squaring of the shoulder and a prominent coracoid process.
- light bulb sign
