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ESA1-4 revision sessions > ESA3 > Flashcards

ESA3 Flashcards

1
Q

Presentation of polycystic disease at

A

Autosomal dominant disease

30-40 years of age with complications of :

  • Hypertension
  • Acute loin pain
  • Haematuria
  • Bilateral palpable kidney
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2
Q

main treatment for polycystic ovary syndrome

A
  • involves controlling BP
    • Medication (ACEi)
    • Low salt diet
  • Dialysis and renal transplant needed if end-stage renal failure develops
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3
Q

In CKD where do cysts develop

A
  • anywhere in the kidney
    • Compress the surrounding parenchyma and impair renal function
  • Also develop cysts in the liver- not as much of a problem
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4
Q

pathological changes in diabetic kidney disease

A
  1. Hyperfiltration/ capillary hypertension
    • Happens before all over changes
  2. Glomerular basement membrane thickening
  3. Mesangial expansion
  4. Podocyte injury
  5. Glomerular sclerosis
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5
Q

why does hyperfiltration occur in early DKD

A
  • 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
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6
Q

first stage of CKD

A

microalbuminuria

GBM thickening and mesangial expansion

30-300 mg/day- Albustix special album pee stick

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7
Q

treatment of DKD

A
  • Tight blood glucose control <48 mmol/mol (6.5%)- MOST IMPORTANT
  • Tight blood pressure control
  • SGLT-2 inhibitors
  • Not smoking
  • Statin therapy
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8
Q

Evidence of hyperfiltration in early DKD

A

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

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9
Q

Q

what is Post obstructive diuresis

A

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

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10
Q

Q

Hydronephrosis

A

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

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11
Q

diagnosis of urothialiasis

A

CT- can see stones

not a function test though

functional test: diuretic renography

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12
Q

brachial plexus injurys

A

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

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13
Q

kernigs vs brudinski sign

A
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14
Q

How can you remember which cranial nerves are to open and close the eyes?

A
  • 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

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15
Q

What are the important branches of the opthalmic nerve (Va)?

A
  • 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

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16
Q

important branches of maxillary

A
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17
Q

What are the important branches of the mandibular nerve (Vc)?

A

- 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
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18
Q

What are the three intracranial branches of the facial nerve and their anatomical course?

A

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

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19
Q

What nerves would need to be damaged to cause a partial and full ptosis?

A

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

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20
Q

sympathetics leave the CNS via

A

thoracolumbar outflow

All sympathetic nerves leaves the CNS from segments T1-L2 ONLY

then enter sympathetic chain

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21
Q

Parasympathetic leave the CSN via

A

Craniosacral outflow

  • Cranial (4 cranial nerves)
  • Sacral (S2-S4)
    • pelvic splanchnics
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22
Q

thoracolumbar t1-T2 (sympathetic innervation to the head and enck) follow

A

routes of blood vessles (hitchhike on the exteranl surface of blood vessels)

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23
Q

outline how thoracolumbar T1/T2 provide sympathetic innervation to the head an enck

A
  • 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
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24
Q

(think of the route of the carotid artery=

A

route of sympathetic nerve)

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25
Q

where does the common carotid bifurcate

A

C4- carotid triangle

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26
Q

sympathetics follow the ophthalmic artery (branch of internal carotid) into the eye and innervates

A

Small smooth muscle portion of the levator palpebrae superioris muscle which opens the eye called the superior tarsal muscle

Pupil- ciliary muscles= pupil dilation

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27
Q

nervous supply to the eye

A

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.

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28
Q

Why in Horner’s syndrome, is the ptosis only partial- compared to the more severe ptosis seen in an oculomotor nerve lesion?

A

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

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29
Q

full ptosis

A

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

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30
Q

horners syndrome

A

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.

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31
Q

How would the pupil differ in a Horner’s syndrome compared to an oculomotor nerve lesions?

A

Horners (sympathetic lesion)- constricted pupil (miosis)

  • unopposed parasympathetic

Oculomotor lesion (parasympathetic)- dilated pupil (mydriasis)

  • unopposed sympathetic
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32
Q

mydriasis in CN III lesion

A

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

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33
Q

Causes of Horners syndrome

A

Patients with apical lung cancer can have sympathetic interference e.g.Pancoast tumour

Patients with anerysms or dissected blood vessels into the neck

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34
Q

Which cranial nerves carry parasympathetic fibres from the brainstem?

A

Oculomotor

Facial

Glossopharyngeal

Vagus

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35
Q

CNIII isassociated with which nuclei and parasymapthetic ganglion

A

Edinger westphal

ciliary ganglion (where pre-ganglionic fibre meets the post-ganglionic fibre)

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36
Q

The Edinger–Westphal nucleus

A

hitchhikes on the oculomotor nevre

innervates the iris sphincter muscle and the ciliary muscle

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37
Q

outline how parasymapthetic nerves get to their target tissues

A

A
  • arise from the brainstem from parasympathetic nculei
  • hitchkine on one fo the 4 CNs
  • parasymapthetic glanglion
  • hicth hike on branches fon CNV
  1. Ciliary (parasympathetic of the oculomotor nerve)
  2. Submandibular
  3. Pterygopalatine
  4. Otic
  5. target tissues
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38
Q

target tissues of hitchhiking parasympathetics

A

Smooth muscle (sphincter pupillae (pupil constrictor) and ciliary muscle (controls lens)

Lacrimal gland

Mucosal gland in nasal/ oral mucos/resp tract

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39
Q

outline CN III oculomotor and parasymapthetic pathway

A
40
Q

where is the carotid canal found

A

within the petroud part of the temporal bone

allows intenral carotid to pass through the base and enter the skull

41
Q

Carotid triangle borders

A

superior: posterior border of digastric
medial: superior belly of omohyoid
lateral: medial border of scm

42
Q

pneumonic for learning 6 branches of the external carotid

A

some –> superior larygeal artery

ancient —> ascending pharangeal

lover –> lingal?

find–> facial

old–> occipital

positions–> posterior auricular

more–> maxillary

stimulating–> superficial temporal

43
Q

which arteries combine to provide a dense blood supply to the scalpe (which is one reason why injuries to thesscalp cause excessive beleeding)

A

posterior auricular, occupital and superficial temporal artery

and

two branches of the internal carotid artery: supra-orbital and supratrochlear

44
Q

M MA branch of the

A

maxillary

45
Q

Drainage of the scalp

A

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

46
Q

Budd–Chiari syndrome

A

occlusion of the hepatic veins that drain the liver by blood clots

classical triad of abdominal pain, ascites, and liver enlargement.

47
Q

blood supply to the liver

A

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).

48
Q

bile leaves the liver via the

A

common bile duct

49
Q

the liver is split up into units called

A

hepatic lobules

6 units of the portal triad surrounding hepatocytes

50
Q

sinusoids

A

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.

51
Q

sinusoids are populated by

A

kupffer cells

satellite cells

heptocytes

52
Q

kupffer cells

A

macrophages

53
Q

stellate cells

A

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
54
Q

why does portal hypertension occur

A

A

  • Due to cirrhosis
    • Too much fibrotic tissue
      • Not very expansive – needs to be because it drains the whole GI tract
  • If its not very expansive veins entering the liver (from portal venous system) will be compressed
    • Increase hydrostatic pressure within portal venous system
55
Q

oesophagus drainage

A

upper 2/3- oesophageal vein draining into the superior vena cava

lower 1/3- left gastric vein- drains into the portal vein

56
Q

why do varices happen in the oesophagus, umbiucus, and anorectal

A

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
57
Q

what is found in the carotid sheath

A

common carotid, vagus nerve, internal jugular vein

58
Q

Umbilical varices

A

Ligamentum teres (remnant of the left umbilical vein) in adults- usually non functioning in adults

  • Can become enlarged
  • Caput medusae sign
59
Q

abdominal muscle

A

horizontal

  • external oblique
  • internal oblique
  • transverse abdominus

vertical

  • rectus abdominus
60
Q

route of bile out of the liver

A
  1. right and left hepatic duct
  2. common hepatic duct
  3. common hepatic duct + GB contents= common bile duct
  4. pancreatic duct secretes into common bile duct
  5. bile release via the ampulla of vater controlled by the sphincter of oddi into the second part of the duodenum
61
Q

gall stone

A

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

62
Q

charcots triad and murphys sign

A

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

-

63
Q

breakdown of haem

A

haemoglobin –> haem and globin

  1. haem converted to billiverdin –> billirubin
  2. 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
64
Q

which type of bilirubin (conjugated or unconjugated) will be raised if cause is post-hepatic

A
  • 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
65
Q

ALT

AST

ALP

A

alanine aminotransferase

aspartate aminotransferase

alkaline phosphatase

66
Q

zones of the liver

A
  • 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
67
Q

Any toxins coming into the liver will affect zone ………. more than zone ……..- closest proximity to blood coming in

A

Any toxins coming into the liver will affect zone 1 more than zone 3- closest proximity to blood coming in

68
Q

Zone …… much more likely to be damaged by ischaemia- furthest away from the blood coming in

A

Zone 3 much more likely to be damaged by ischaemia- furthest away from the blood coming in

69
Q

Aspartate aminotransferase/ transaminase

A
  • 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)
70
Q

what can be measured to confirm raised ALP is of liver origin

A

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

71
Q

describe how saliva is produced

A
  1. 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
  2. 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
  3. Producing a hypotonic solution near the end of the duct (removal of ions >secretion)
72
Q

The amount of modification (more or less hypotonic)by the ductal cells depends on how quickly the saliva is moving through the ductal system

A

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

73
Q

more secretion of HCO3- when

A

active saliva production

74
Q

common incision sites

A
75
Q

how would smalll bowel obstruction look on CT

A

3cm or more= distended small bowel

central position of bowel

plica circulares clear- lines across hole of bowel

76
Q

how would a large bowel obstruction look on a CT

A
  • more peripheral
  • can seehuastra which doesnt go the whole way across
  • 3/6/9 rule
77
Q

in patients where there is an appropriate reticulocyte response what is expected

A

LDH released when RBC breakdown

78
Q

sickle cells vs thalassaemia

A

thalassaemia

reduced or absent expression of structurally normal chain

sickle cell

abnormality of the chains themselves

79
Q

Thalassaemias

A

are autosomal recessive, inherited diseases resulting from the reduced rate of synthesis of normal α- or β- globin chains.

80
Q

sickle cell anaemia

A

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.

81
Q

Q

Cleft lip and palate

A

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

82
Q

fracture healing

A
  1. haematoma formation- haematoma converted to granulation tissue
  2. soft callous- deposition of collagen and fibrocartilage (granulation tissue –> soft callus)
  3. hard callous- osteoblast deposit bony collar around fracture while ossification occurs
  4. remodelling- osteoclasts and spongy bone –> compact bone

harry saw hard rock

83
Q

neck of femur fracture and avascular necrosis

A

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

84
Q

NOF fracture

A

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.

85
Q

NOF presentation

A
  • Short/ externally rotated
  • Due to muscles contracting and pulling gluteal and quad
86
Q

intracapsular vs extracapsular

A
87
Q

what is at risk with a distal humerus at risk

A

medial nerve and brachial artery–> think of the cubital fossa

88
Q

FOOSH

A

scaphoid fracture

distal radius

89
Q

high ulnar nerve vs low ulnar nerve

A

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’.

90
Q

“hand of benediction” which is caused by

A

proximal (at elbow level) median nerve damage.

cant put hand in fist

91
Q

ulnar claw

A

ulnar nerve damage causing paralysis of the lumbricals.

cant straighten all fingures from fist but can make fist

92
Q

the long bone

A
93
Q

types of ossification

A

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
94
Q

presentation of anteiror dislocation (95%)

A
  • They present with an externally rotated and abducted
  • Pain, deformity, loss of function
95
Q

presentation of posterior dislocation

A

They present with an internally rotated and adducted arm. There is also squaring of the shoulder and a prominent coracoid process.

  • light bulb sign

ESA1-4 revision sessions (17 decks)

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