Eng Delhi July 2018

Anatomy: aorto and vena cava

Identify abdominal aorta, name its 3 anterior branches:

Ceiliac, SMA, IMA

Start and end level of abdominal aorta

Starts at the level of T12 as it pierces the diagphram till L4 where it bifurcates into the common iliacs

What structures lies anterior to AA at the level of L1:

Right renal V

Identify IVC and its tributaries

Surface markings of abdominal aorta and structure anterior to it
Just to the left of the midline and ends just above the umbilicus.
Structures ant to it: stomach, pancrease, left renal vein, 3rd part of the duedenum transverse colon,
small bowel

Angiogram of abdominal aorta, show the supply of the gut (imp appendicular A)
Pic of ruptured infrarenal AAA, define aneurysm:
Pathological dilatation in the diameter of an artery due to weakness in the arterieal wall, can be
fusiform or saccular
At what level do tje IVC and aorta pierce the diaphragm:
IVC: T8
Oesophagus: T10
Aorta: T12

Identify azygos vein, what are its tributaries:

Azygos on the right(behind IVC, hemiazgos on the left). Tributaries: hemiazygoes and assessory
hemiazygous, posterior intercostal vein and lumbar veins

Identify the sympathetic trunk, what level of the spinal cord contribute to it:
T1-L2

What communicates the spinal roots and the post ganglionic fibres – gray ramii communicantes

what is a dissecting anuerysm, which layer will seperate:

there is seperation between the inner 2/3 and outer 1/3 of the media. Initiating event: tear in the
intima. Dissection can cause blockage to the blood flow

what is a pseudoanyresm:
when not all the 3 layers of the vessel wall (intima, media and advantitia) are included in the
anyreusm. Collection of blood between the media and adventitia

upper limb

brachial plexus injury: erb’s palsy

C5 will exit between which 2 vertebrae
C4 and C5 (C1 : C1+ skull, C8: C7 +T1, T1: T1+ T2)

Tendon hammer given: show C5 jerk

Biceps + supinator (triceps C7,C8)

Name 3 muscles supplied by musclucutanous, nerve roots:

C5,C6, C7. Brachialis, corachobrachilis, biceps. (skin lat border of forearm: lateral cutanous nerve of
the arm)

External rotators of the arm

Teres minor, infraspinatus, deltoid

Axillary nerve cutanous sensation and muscular supply:

C5, C6 Cut: skin over lower half of deltoid (badge area). Musc: deltoid + teres minor

Critical care: trauma and hemorrhagic shock

Where do we treat such a pt?

Requires resusitation, surgery and post op care in ITU or HDU setting

Pt is in shock, how would you manage circulation?

Get IV access via 2 large bore cannula. Give fluids, in hemorrhagic shock best fluid to give is blood.

How would you monitor response:

Measure Bp and pulse (ideally invasive monitoring), insert a urinary catherer to measure urine
output

CT abdomen shows a liver tear, how would you treat a liver tear
Pathology: testicular CA
35 y/o left groin mass + single palpable testis
What could this be:
An undescended testis with tumour

What is the most common testicular tumour?

Germ cell tumours (95%)

Histology report shows teratoma, reported as T4NX, What does Nx mean?

Cancer in LN cannot be assessed

Name some non seminomatous germ cell tumours of the testis:

Yolk sac tumours, teratoma, choriocarcinoma, embryonal carcinoid, mixed germ cell tumours

Discuss pathology report with family in 3 simple lines

Unfortunatly this is advance form of testicular cancer which has already spread beyond the testes
and is involving the scrotal skin

Where does teratoma spread first?

Para-aortic LN

What is choriocarcinoma, what is its tumour marker

Non seminomatous germ cell tumous: very aggressibe. Tumour marker is B-HCG, they do not
produce AFP

Expect B-HCG name other serological markers?

AFP, LDH

Older age testicular tumour?

Lymphoma (extra-nodal presentation)

Tumour markers:

Seminomas: B HCG rise is small.

Where is HCG normally found:

It is normally procured by the placenta after implantation

What are the cells seen in choriacarcinoma:

Trophoblast
Extra: investigations
History, examination, testicular US (cystic/ fluid filled mass: unlikely malignant), CT TAP for
metastesis (PET scan post residual disease)

Serum levels of AFP and/or beta-hCG are elevated in 80 to 85 percent of men with
NSGCTs, even when nonmetastatic. By contrast, serum beta-hCG is elevated in less than
20 percent of testicular seminomas, and AFP is not elevated in pure seminomas. A
histological diagnosis is still needed and they are more usefull for disease follow up.

Treatment: surgical orchidectomy via an inguinal approach and retroperitoneal LN dissection

SEMINOMA VERSUS NSGCT — The final pathology analysis is used to stratify testicular
germ cell tumors (GCTs) into seminomas and nonseminomatous germ cell tumors
(NSGCTs). These differ in clinical and biologic behavior.

●Seminomas are more likely to present with localized disease. Approximately 80

percent of men with seminomas present with stage I disease (limited to the testicle),
while 15 percent have stage II disease (limited to retroperitoneal nodes). Fewer than 5
percent of patients have spread beyond the retroperitoneal nodes at presentation.

●Seminomas display relatively indolent growth and a longer natural history, and they
rarely spread via the bloodstream beyond the retroperitoneal lymph nodes to other
areas (eg, liver, lung, bones, or brain). Stage III metastases occur more frequently in
men with NSGCTs.
 ●Seminomas typically do not have marked elevation of serum beta-human chorionic
gonadotropin (beta-hCG) and never have an elevated alpha-fetoprotein (AFP).
Seminoma with an elevated serum AFP is considered a mixed GCT, and these cancers
are treated as NSGCTs. In contrast, beta-hCG and AFP are elevated in the majority of
men with NSGCTs.

●Seminomas are exquisitely sensitive to radiation therapy, while NSGCTs are more
radioresistant

Seminomas 50% of all GCT usually found in older men ; 40 years old, good prognosis, sensitive to RT.

Non seminomas
Yolk sac tumour/ endodermal sinus tumour, most prevelent in prepubertal children. They all have
elevated AFP, they do not produce B-HCG

Embryonal carcinoma: age at presentation 30, rare in pre pubertal males, do not produce AFP

Choriocarcinoma: most aggressive and least common type, widespread hematogenous

dissemination occures early, many present with mets

Teratoma: can be present in prepubertal and adults they contain cell populations from all 3
embryological layers (ectoderm, mesodern and endoderm). In children, teratomas most often
occur before the age of four, are generally seen in their pure form, and behave in a benign
fashion. In adults, teratomas are usually part of a mixed GCT, and they have the potential to
be found at metastatic sites. Elevations in the serum concentration of AFP or beta-hCG
cannot be attributed to teratomatous elements. Rather, elevated tumor markers indicate the
coexistence of other GCT components.

Mixed GCT: 1/3 of all testicular GCTs The average age at diagnosis is approximately 30
years, and they are rare in prepubertal males. Elevations in serum AFP and beta-hCG reflect
some of the components that are present within the tumor.

Polytrauma, blood transfusion and hypersensitivity reaction

Young female, IVDU, hep C +ve. H/o RTA, undergoes splenectomy, only crystilloids given. Blood
picture shows thrombocytopenia, reduced clotting, aneamia, raised PT and aPTT

What explains this blood picture:

DIC (disseminated intravascular coagulation= consumptive coagulopathy) would also be present low
fibrinogen and high levels of FDP and D-dimer

Why else could her clottings factors be low:

Hepatitis with liver failure, dilutionfrom the fluid resus

Causes of DIC?
Sepsis, massive transfusion, acute pancreatitis, major trauma, sever tissue injury (burns and head
injury), pregnancy complication, liver disease
Function of platelet
The plateletes aggregate at the site of endothelial injury and form a platelet plug to prevent further
blood loss. This is later replaced by a fibrin mesh clot

How is it formed
It is formed from precursor megakarocytes from the bone marrow which fragment and give rise to
platletes

Late menifestations of hep C virus

Liver cirrhosis, portal hypertension, liver failure, HCC. Resulting in easy bruising/ bleeding, jaundice,
itching, loss of apitite, nausea, loss of muscle mass

What activates the intrinsic and extrinsic pathway

Intrinsic: surface contact, extrinsic: damaged vessel wall esposing tissue factor

APTT and PT test for which pathways

APTT(activated partial thromboplastin time) : intrinsic, PT: extrinsic (factor VII)

Pt having Hb 8.7, will you transfuse right now?

No unless there was a large and sudden Hg drop and the pt is symptomatic

What test to do before transfusion:

Cross match (indirect Coombs test to check for ABX in the doner’s blood against the pt’s blood

After transfusion there is heomolysis , what reaction is this?

Acute hemolytic reaction due to ABO incompatability. Type II hypersensitive reactions involve antibody-
mediated destruction of cells. This type of reaction is best seen by blood-transfusion reactions, in which host
antibodies react with foreign antigens on the incompatible transfused blood cells and mediate destruction of these
cells.

Splenectomy pt, why should he receive vaccination?

There is an increase risk of infection with encapsulated organism: S. Pneumonia, H. Influenza, N.
meningitiidis

Pt recieves penicillin and he experiances an inflammatory reaction, what type of reaction is this?
Type 1 hypersensitivity reaction (anaphylaxis)

Name another type of hypersensitovity reaction + mechanism?

Asthma. Contact with antigen causes an AB Anrespons with IgE mediated release of histamin from
mast cells resulting in activation of the immune system and bronchospasm, increase mucous
production

Stages in bone healing:

Hematoma formation, fibrocartilaginous callus formation, bony callus formation, bone remodelling
(inflammation, repair, remodelling)
Steps in hemostasis:
Vasoconstriction, platelte plug formation, clot formation. Platelet plug (1ry hemostasis) forms at the
site of injury. Platelets accumulate at the site with the aid of vWF. The coagulation cascade is
activated which leads to the formation of fibrin mesh around the platelte plug to keep it in place
( 2nd coagulation)

Examinations

Peripheral arterial disease + ulcer

Resp exam of pt with COPD (pre op)
Pre, intra and post op managment. Choice of aneasthesia

Pre op: advised to stop smoking at least 6 weeks prior to operation, review by resp physician for
optimazation for surgery, perform lung spirometry

Intra op: use regional aneasthesia when possible, avoid drugs that can lower the resp drive

Post op: chest phsyio : lung expansion exercises. Ensure adequate analgesia (e.g epidural analgesia),
early mobilization, avoid high conc of oxygens, not to lower the resp drive, cont. Previous treatment

Post op
Cranial nerves exam: bitemporal hemianopia

Differential: a pituitory mass compressing the optic chiasm, craniopharyngioma, Rathke’s cleft cyst,
meningomas
Investigations
Check for signs of acromegally, hypo/hyperthyroidism, galactorea
Blood test: horms secreted by the pit: ACTH, TFT, prolactin, GH, LH, FSH
Imaging: MRI with gadelinium (pituitory lesions), CT craniopharygoma/ meningoma: better visualised

How will you manage:

Pituitory resection via a trans sphinoidal approach

Critical care

Scenaria given: polytrauma – GCS poor but no evidance of head injury. Right side decreased breath
sounds, abdomen distended. Hypotensive and tachycardic

How will you manage step wise:

A: is the pt speaking ? need for geudel or LMA
B: check SpO2, is percussio n note dull / resonnate ? need for chest drian esp if pneumothorex
C: fluid resus with permissive hypotension. In polytrauma ideal fluid is blood
D: check pupils, glucose, any lateralizing signs

If stable 2nd survey

What are the advantages and disadvantages of a full body CT:

Advantage: assessment of the whole body in a relatively short time, can help priorities injuries for
surgery and identify any possible missed trauma

Disadvantage: involves a lot of radiation, not ideal for the unstable pt, contrast is nephrotoxic,
expensive

What test will yoo do to check the abdomen:

FAST scan

After giving crysalloids and bloods, what would you consider giving next?
FFP and platelets