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MRCS Part B > Pathophysiology > Flashcards

Pathophysiology Flashcards

1
Q

Gallstones

1) Types

2) Risk Factors

3) Indications for MRCP

4) Indications for ERCP

A

1) Mixed, Cholesterol, Pigment, Dark Pigment

2) Risk Factors - Age, Female, Pregnancy, Diabetes, Dyslipidaemia, Obesity, Rapid weight loss,

Specifically pigment - Haemolysis, Cirrhosis, Crohn’s/ileal resection

3) Indications for MRCP - Obstructive jaundice, Chronic pancreatitis, Pancreatic congenital abnormalities, Gallstones, Stricture management, HPV malignancy

4) Indications for ERCP -

i) Post operative cholecystectomy for CBD Clearance
ii) Obstructive Jaundice/cholangitis iii) Stent insertion
iv) Biopsy v) SOD dysfunction vi) stricture dilation

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2
Q

1) Indications for cholecystectomy
2) Timing of cholecystectomy
3) Complications of Choleycstectomy

A

1) Indications - Gallstones, Acalculous cholecystitis, gallbladder polyps, porcelain gallbladder
2) Acute Cholecystitis - Early (<7 days ideally within 72 hours- reduced wound infection, hospitalisation, quicker recovery). Early is technically easier due to deterious effects on the local anatomy recognised >72 hours after onset.

Gallstone pancreatitis - Early

Obstructive jaundice after ERCP - elective

Obstructive jaundice no ERCP - early + CBD exploration

3) Complications - Converstion to open/alternatives to cholecystectomy, Liver Bed Bleeding, Bile Duct Injury (A-E. E is major duct and further subclassified using the bismuth classification), Difficult cystic/R hepatic artery bleeding, Bowel Injury, Bile Spillage

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3
Q

1) Goals of perioperative analgaesia
2) “Preventative”
3) Post operative
4) Describe WHO Pain ladder
5) Complications of PCA
6) Pain assessment scales

A

1) Suffering, lenght of stay, recovery, patient satisfaction
2) Fentanyl with induction, LA infiltration of wound, Paracetamol, NSAIDs, Limb Blocks, Transversus Abdominal Plane Block, Epidural analgaesia
3) Post-Operative:

PRN Opioid for “breakthrough pain”

if large open abdominal surgery/thoracic surgery

consider epidural analgaesia (bupivicaine 0.125% 4-10ml/hour)

and if contraindicated then Paracetamol, NSAID + Breakthrough opioid

if NBM status then - IV Paracetamol + IM NSAID + S/C Opioid. Consider use of PCA device (bolus only 1mg morphine with 10 minute lock out)

4) WHO Pain Ladder
i) Paracetamol +/- Adjuvant
ii) Weak opioid + i)
iii) Strong opioid + i)
5) Complications of PCA - trigger for dependency, pruritis, unsteady plasma levels of drug, usual opioid problems,
6) Visual Analog Scales (Faces), Numerical Rating Scales (score pain 1-10)

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4
Q

Describe the main targets of anti-emetics and give some names

A

M1 (muscaranic) - scopolamine, hyoscine

D2 (Dopaminergic) - Domperidone, prochlorperazine

H1 (Histamine) - Promethazine, Cyclizine

5 HT3 (Serotonin) - Ondansetron

NK1 (Substance P) -

GCs - Dexamethasone

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5
Q

1) Purpose of Gastric Acid
2) Gastric Acid secretion phases
3) Gastric acid regulation

A

1) antimicrobial, activate peptides, denature ingested proteins.
2) Cephalic - External stimulus/ thought/ swallowing (Vagus mediated - 30-50% GA secreted)

Gastric - Intragastric food and gastric distension (Local and gastrin mediated - 50-60% secreted

Intestinal - CCK, Somatostatin mediated negative feedback

3) Secreted by parietal cells which receive:

Positive feedback from - Amino acids, vagal activation (acetylcholine), gastric distension, Gastrin (secreted by Antral G cells and act on enterchromaffin cells[ECL] +parietal cells). Cholecystekinin (but functionally negative feedback - see below) Histamines (autocrine and paracrine - released by ECL cells)

Negative feedback from - Somatostatin (released from D cells - release also enhanced by CCK + gastrin) Prostaglandin (autocrine -inhibited by NSAIds)

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6
Q

1) Define DIC

2) Causes of DIC

3) Dx

A

1) Activation of haemostasis –> fibrin deposition + platelet activation + coag factor consumption –> haemorrhage

2) Causes:

Tissue damage, malignancy, Pregnany (abruption, molar, pre-ecclampsia, eclampsia), Infections, Immunological, Toxins, Liver Disease

3) Dx: Low - platelets, fibrinogem High - fibrin degeneration products, APTT, PT, TT

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7
Q

1) Basic stages of haemostasis

2) how are platelets activated

3) Role of platelets in haemostasis

A

1) Vasoconstriction, Platelet activation, coagulation mechanism, fibrinolytic system

2) platelets are activated when exposed collagen/vwf from endothelial cells bind to platelet glycoproteins

3) i) Vasoconstriction (Relase Thromoxane a and serotonin when activates)

ii) Aggregation - (gpIIb/iiia is activated by thromboxane) gpIIb/iiia binds with vwf or fibrinogen. vwf and fibrinogen act as an intermedium between endothelium - platelets + platelet - platelet.

Platelets also interact with thrombin

Formation of platelet Plug

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8
Q

1) Outline coagulation Cascade

A
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9
Q

1) Investigations used to interrogate the coagulation cascade
2) How are platelets produced
3) complications of massive transfusion

A

APTT - intrinsic and common pathway

PT - Extrinsic Pathway

Bleeding Time - Crudely platelet activity

PFA 100 - platelet activity

2) Platelet production occurs in the bonemarrow. precursor cells are megakaryocytes which then fragment into platelets
3) Cx of Mass Tranf. - Hypocalceamia, Hyperkalaemie, thromboycytopenia, Hypothermia, Coag Fact. Deficiency, Fluid overload

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10
Q

Types, mechanisms + presentations of transfusion reactions

A

IMMUNE

i) Pyrexia - due to white cells fragments/ cytokines in blood - fevers, chills, more common with platelets
ii) Alloimunisation - formation of antibodies 2o to repeat transfusions
iii) TRALI - Antibodies/ white cells/ cytokines interact with pulmonary vasculature - low sats, breathlessness, pul oedema
iv) GvHD - Donor lymphocyte proliferation - fever, rash +multi-organ dysfunction in immunologically compromised patients.
v) Urticaria - foreign plasma proteins - urticaria in isolation
vi) Haemolytic - usually ABO incompatability - fever, pain, dark urine, haemodynamic compromise

NONIMMUNE

i) Overload ii) infection iii) Hyperkalaemia
iv) Hypocalcaemia/hypomagnesaeima (Citrate toxicity)

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11
Q

Non-Hodkin Lymphoma

1) Types

2) extra- nodal Sites of predeliction

3) Investigations

4) RFs

5) Tx

A

1) Broadly - HL + NHL (Agressive - Large B Cell, Burkitt’s, T+B lymphoblastic leukaemia/lymphoma, Adult T Cell Lymphoma amongst others. Indolent - Follicular lymphoma, CLL, Splenic marginal cell lymphoma)

2) High prevalence of extra- nodal disease - Skin, testicles, Bone, paraspinal soft tissue, CNS, Kidney, Bone Marrow

3) Investigations -

Bedside - Bloods (LDH, uric acid, abnormal FBC, hypercalcaemia, protein electrophoresis)

FDG Pet/ CT

Lymph node biopsy - Excision biopsy is best, FNAC is more rapidly performed

4) Risk factors:

  • Immunosuppression, Infection (HIV,HTLV, EBV), Autoimmune diseases (SLE, RA, Hashmito’s, Coeliac Disease)

5) Varying regimens but classically

R CHOP - Rituximab, Cyclophosphamide, Doxirubicin, Vincristine, Prednisolone

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12
Q

Hodkin’s Lymphoma

1) Type

2) RFs

3) Classical presentation

4) Investigations

5) Rx

A

B Cells generally speaking

1) Classic- Nodular Sclerosis, Mixed Cellularity, lymphocyte rich, lymphocyte deplete Nodular lymphocyte predominant

2) RFs - Age (Yound adult and older adult), EBV, Other viruses, immunosuppression, smoking, Autoimmune disorders

3) Classical presentation - Constitutional symptoms, lympahdenopathy, mediastinal mass, pruritis

4) Investigations -

Bloods - Hypercalcaemia, FBC abnoramalities, Eosinophilia,

Biopsy - Excision/ FNAC - Reed steenberg cells, CD30 (CD15 commonly seen but absence does not preclude diagnosis)

CT/PET - Staging purposes. Lugano Classification / Ann - Arbor Classification

5) Rx

ABVD - Doxorubicin, Bloemycin, Vinblastine, Dacarbazine

Radiotherapy

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13
Q

1) Histological Features of SCC

2) Criteria for melanoma diagnosis

3) Histological features of melanoma

A

1) Level of differentiation, Perineural invasion, Invasion of absement membrane (by keratinocytes), dysplastic keratinocytes
2) ABCDE - asymmetry, borders, colour, diameter (>6mm), evolution
3) Histological features of melanoma - atypical melanocytes, architectural disorder,

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14
Q

Baroreceptors :

i) Where?
ii) How do they communicate with CNS?
iii) Factors influencing Preload/EDV?

A

i) Present in carotid sinus (dilated segment of ICA

just distal to carotid bifurcation)

ii) via CN IX to the medulla oblongata

iii) EDV is influenced by :

a) Venous Return
b) Venous Blood Pressure (Impaired ventricular contraction, obstruction as in PE)
c) Pumps - Respiratory Pump, Leg Muscle pump

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15
Q

Anticoagulants

1) Classes

2) MOA of Heparin + warfarin

A

1) Vit K Antagonists, Heparins, Antiplatelets, Factor Xa Inhibitors, Factor IIa (thrombin inhibitors)
2) Warfarin - Inhibits Vit K Dependent gamma carboxylation of coag factors II, VII, IX, X, C, S

Heparin - Antithrombin III potentiatior –> inhibits Xa, + IIa (thrombin)

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16
Q

Common Peroneal Nerve

I) Features of CPL Lesion

Deep Peroneal Nerve

i) Origin
ii) Deficit produces?

A

I) Loss of dorsiflexion/foot eversion

Loss of sensation over lateral leg/dorsal foot

Deep Peroneal Nerve (L4-S1)

i) Branch of the common peroneal nerve
ii) Deficit produces:

Motor deficit in anterior compartment (Dorsiflexion)

Sensory deficit in first web space

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17
Q

Shoulder Dislocation

i) How can shoulder’s dislocate

A

i) Anterior - Abduct and externally rotate

Posterior - Adduct and internally rotate

Inferior - Abduct onto onto acromion pushing inferiorly

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18
Q

i) What is a carcinoid tumour?
ii) Common sites of carcinoid tumours
iii) What is meant by carcinoid syndrome
iv) Below what size do they not need furhter investigation
v) Ix

A

i) Carcinoid tumours are well diferrentiatied neuroendrocrine tumours usually in the context of the GI tract.
ii) Ileum>Rectum>Appendix>Colon>Stomach
iii) The syndrome typically refers to metastatic carcinoid tumours as the portal system has been bypassed. the presence of flushing and diarrhoea due to secretion of serotonin + other vasoactive substances being secreted.
iv) Appendix <1cm studies show a low risk of nodal/extra nodal metastases. >1cm the risk increase significantly

Rectum <1cm metastatases are rare. >1cm size associated with mets.

Small intestine and colonic nets all warrant further investigation

v) Ix:

Urinary 5 HIAA + serotonin

Serum serotonin, 5 HIAA, chromogranin A

Imaging - CT, MRI liver, Somatstatin receptor imaging

Endoscopy

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19
Q

Cervical Rib Presentation

A

Vascular - Subclavian artery - thromb./emboli/ Aneurysm

Subclavian vein - thromb.

Cold/Warm Hand

Neurology - Lower trunk Brachial plexus (C8-T1)

Paraesthesia in C8-T1 dermatome.

Hand wasting

Symptoms worse on raising arm

Adson’s Test

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20
Q

Features of Tetralogy of Fallot

A

i) Overarching Aorta
ii) Right Ventricular Hypertrophy
iii) Pulmonary Valve Stenosis
iv) Ventricular Septum Defect

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21
Q

ECG Changes - Artery Occluded/ Area of tissue damaged

i) II,III, AVF

ii) V3 + V4

iii) V1 + V2

iv) I, aVL, V5 + V6

v) I, aVL, V2-V6

vi) Tall R Wave in V1

A

i) RCA

R Atrium + Posterior Interventricular Septum

ii) Distal LAD

Apical (Anterior)

iii) LAD

Septal (Anterior)

iv) Circumflex Artery

L Atrium + L Ventricle

v) LCA

L Atrium, Ventricle, Anterior IVS

vi) RCA

Posterior IVS

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22
Q

Hip Fracture Classifications - Outline them

A

Garden’s Classification:

I - Incomplete/impacted

II - Complete - non-displaced

III - Partial displacement/angulation

IV - Complete displacement

Pauwell’s Classification: (Angle of fracture)

I - 30 degree

II - 50 degree

III - 70 degree

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23
Q

Nerve Lesions:

i) Complete Sciatic

ii) High Tibial

iii) Common Peroneal Nerve

A

i) Loss of power in leg + Post. Thigh

Loss of sensation to post. thigh and lateral leg

ii) Loss of plantar flexion + inversion.

Loss of sensation to sole of foot

iii) Loss of dorsi flexion + Eversion

Loss of sensation over lat. aspect + dorsum of foot

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24
Q
A
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25
Q

What illnesses does Streptococcus Pyogenes Cause

What virulence factors does strep pyogenes possess

What systemic complications of streptococcal infections are there (non-invasive)

A

Invasive:

Puerperal fever, Nec Fasc, Toxic Shock Syndrome

Non-Invasive:

Pharyngitis, Erysipelas, Impetigo

Virulence Factors:

Streptolysins, Hyaluronidase, Streptokinase

Pyogenic exotoxins - account for toxic shock syndrome

Streptococcal Infections can cause:

Rheumatic Fever, glomerulonephritis, scarlet fever

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26
Q

Different types of prion disease

A

Creutzfeld Jacob Disease

vCJD

Kuru

Fatal Familial Insomina

Gerstmann- Straussler- Scheinker Syndrome

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27
Q
A
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28
Q

What governs interstitial fluid accumulation?

Broad causes of oedema

A

Starling’s Forces:

Capillary Wall permeability

Oncotic Pressure (Large proteinaceous plasma components help retain fluid intrasvascularly)

Hydrostatic Pressure (in other words stasis is the problem)

Oedema:

Increased hydrostatic pressure (congestion)

Oncotic pressure decreasing (loss of protein)

Capillary leaking (Inflammation)

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29
Q

Respiration:

i) Where is respiration controlled?
ii) What is the Hering-Bruer Reflex?
iii) Where does CO2 exert its effect on the respiratory system?

A

i) Medulla by two bodies of neurones (Ventral and Dorsal) receiving multiple inputs and outputs via phrenic nerve. Dorsal neurones initiate inspiration.

Apneustic Centre - Initiates inspiration

Pneumotaix centre - Inhibits inspiration

ii) Inflation of the lungs > 800 ml tidal volumes serving to regulate inspiration.
iii) CO2 - Carotid body and aortic arch receptors

Hydrogen Ions - in the CNS

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30
Q

MOA Dopexamine

Noradrenaline vs adrenaline therapeutically

A

Adrenergic Agonist - B2 ( D1 + D2 )

Prevents reuptake of norepinephrine

Adrenaline - B1 Predominance. Therefore mainly cardiac effects

Noradrenaline - Alpha agonist - therefore mainly pressor effects

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31
Q

Transplants:

i) Define a transplant

ii) What is HLA?

A

i) Transplantation of a tissue from one anatomical region to another

ii) HLA is a genetic loci responsible for displaying - Cell surface recognition antigen.

Class I - presents endogenous cytoplasmic antigen. A, B + C

Class II - presents exogenous antigen. DP, DQ, DR

Both present the antigen (peptide) to immune system ( T Cells ) to stimulate an immune response.

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32
Q

Stages of fracture healing:

A

1) Haematoma Formation - Granulation Tissue
2) new woven bone formation around the bony collar
3) bridging callus formation
4) Fracture site remodelling + formation of haversian system formation

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33
Q

Common sites of intra-abdominal collection?

A

Morrison’s Recess (Hepatorenal) - Most sensitive in supine patient

Paracolic Gutter

Between loops of bowel

Pelvis:

Rectovesicular Pouch

Pouch Of Douglas

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34
Q

Meckel’s Diverticulum?

What is it

Associated pathology

A

Remnant of the vitellointestinal duct - 2inches long, 2% of people, 2 feet from ileocaecal valve

pathology:

  • Appendicitis Mimic
  • Litter’s hernia
  • Bleeding, Perforation, intessusception, obstruction
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35
Q

Erosions in these parts of the UGI system cause bleeding from which artery?

1st 2nd part of duodenum?

3rd or 4th part of duodenum?

Lesser Curve stomach?

A

1st/2nd duodenum - Gastroduodenal Artery

3rd/4th duodenum - Pancreaticoduodenal Artery

Lesser curve stomach - Left Gastric Artery

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36
Q

Bowel Obstruction:

Large vs Small

X Ray findings

Causes

Presentation

A
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37
Q

Decribe cause of pattern of pain in appnendix

A

Central abdominal pain

(appendix initially due to visceral pain fibres enterring the spinal cord at T10 level - same level as umbilical dermatome)

to

Right Iliac Fossa type pain

(Irritation of parietal peritoneum)

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38
Q

What is the terrible knee injury triad?

A

MCL

Medial Meniscus

ACL

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39
Q

i) Horner’s Syndrome Triad

ii) Causes of Horner’s Syndrome

A

i) Miosis, Ptosis, Anhydrosis

ii)

Central - Thalamus, Brainstem, Cervical Cord pathologies (malignancies, stroke, demyelination, haemorrhage, injury)

Pre Ganglionic - Spine roots, Brachial Plexus, Pulmonary Apex, Anterior Neck pathologies ( pancoast tumour, trauma, acquired nerve damage)

Post Ganglionic - Superior Cervical Ganglion, ICA, Base of skull/ carotid canal, Middle ear, cavernous sinus pathologies

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40
Q

i) Clinical Features of an orbital blow out fracture?

ii) Radiological Features of orbital blow out fracture?

A

i) Enopthalmus - Eye being sucked into brain.

Diplopia - Extraocular muscle trapped in fracture

Infraorbital Numbness - Compression of infraorbital n. (V2)

Orbital Emphysema - signals that there is nearby sinus involved in the fracture

ii) Fluid in the sinus, tear drop sign (herniated fat into sinus), Orbital emphysema

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41
Q

What does the image show - describe pathology

A

The RIGHT vertebral artery is catheterised - contrast flows antegrade through the right VA and then we see the basilar artery opacifying and the left VA + SCA opacifying. There is occlusion at R proximal SCA.

Occlusion of the aortic arch proximal to vertebral artery leading to :

  • Retrograde flow through vertebral artery to subclavian artery
  • essentially blood is being ‘stolen’ from the contralateral vertebral artery (/circle of willis)
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42
Q

What are the causes of Thoracic Outlet Syndrome?

How do the subclavian artery, vein and brachial plexus relate to the first rib?

A

Compression of the neurovascular bundle (brachial plexus + Subclavian artery) between the:

i) Anterior and middle scalene muscles
ii) Cervical Rib
iii) 1st Rib
iv) Abhorrent Bands in the thoracic outlet

Subclavian Artery + Brachial PLexus - Overly the first rib in between anterior and middle scalene muscle. (beneath the clavicle)

Subclavian vein - Overly the first rib anterior to the anterior and middle scalene muscle. (beneath clavicle)

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43
Q

Amylodiosis:

i) What is amyloidosis

ii) Histological features

iii) Types of amyloid protein which sites they favour

iv) Diagnosis

v) Rx

A

i) Deposition of abnormal fibrillar proteins in extracellular tissue that cannot be broken down enzymatically
ii) Microscopy - Bright pink hyaline material

Congo red stain - Apple green membranes

iii) AL - Primary - produced by clonal expansion of plasma cells favouring heart, kidney, liver, spleen, peripheral nerves + GI (macroglossia, bleeding), peri orbital purpura

AA - Secondary (RA, IBD, TB, Bronchiectasis, RCC)- Due to inflammatory interleukins stimualting hepatocytes to secrete amyloid precursors. It favours - liver, kidney + spleen

iv) Dx By Isotope scan or more commonly biopsy of rectum/subcut fat/ affected organs
v) Rx - Treatment of MM/ Treatment of inflammatory conditions/ Organ transplant

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44
Q

Where can isolates of amyloid tissue be found in the body?

A

Larynx

Urinary Tract

Aorta

Pituitary Gland

Thyroid ( Medullary Cell Carcinoma)

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45
Q

i) Define Aneurym

ii) Causes

iii) Size of normal infrarenal aorta vs aneurysmal

iv) Pathogenesis of AAA

v) RFs for AAA

vi) Aneurysm Cx

A

i) Aneurysm - Dilation of a blood vessel to 1.5x normal diameter

ii) Causes:

Acquires (Atherosclerotic + traumatic), Infective (Syphilitic), Inflammatory, CTDs

iii) Infrarenal Aorta 2cm = Normal >3cm= Aneurysm

iv) Atherosclerosis –> red. elastic recoil, loss of mechanical integrity + ischaemic changes due to occluded vasa vasorum

v) Age, Smoking, HTN, FH, Cholest., DM, Male

vi) Rupture, Thrombosis, Emboli, Infection, Pressure, Fistula

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46
Q

i) When would AAA be for repair?

ii) When to screen

iii) Which arteries may you have to deal with during procedure?

iv) Complications of EVAR

A

i) >4.5 cm/ Growing >1cm per year/ symptomatic

ii) 3-4 cm - annual

4-5.4 cm - 6 monthly

>5.5 cm - surgeons

iii) Posterior - Lumbar arteries (oversewn)

Laterally - Renal ARteries (Preserved)

Anteriorly - SMA (Reimplanted)

IMA (Reimplanted)

iv) EVAR cx: Endoleak, Mesenteric ischeamia, Renal Failure, Infection, MI, Spinal Ischaemia

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47
Q

i) Define: Aortic Dissection

ii) Aortic Dissection diseae Ax

iii) Classifiactions

A

i) Tear in intima resulting in separation of arterial wall layers

ii) Marfan’s, ED, Osteogenesis Imperfecta

iii) Stanford - A( Proximal) B ( Descending only)

Debakey - I (Arch and descending) II (Ascending)

III (Descending)

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48
Q

i) Causes of Aortic Stenosis

ii) Pathogenesis of the main variety

iii) Triad

iv) Signs

v) Ix

vi) Mx

vii) Causes of IE

A

i) Aortic Valve Calfication

Congenital Aortic Valve

Rhemautic Valve DIsease

Metabolic/Inflammatory - SLE etc.

ii) Calcification is caused by - lipid accumulation, inflammation and calcification

iii) Triad - Syncope, Angina, Dyspnoea

iv) Signs:

Peripheral - Slow rising pulse, Narrow pusle pressure, Heart Failure, Anaemia ( Heyde’s Syndrome)

Precordial - ESM R 2nd ICS PS, Soft S2, LV Heave

v) Ix:

ECG - LVH / Ischaemia

CXR - HF, Calcified valve, Post Stenotic Dilatation

Echo - Valve Assessment, LVH, LVEF

Angiogram - Pre operative assessment / intervention

Cardiac CT / MRI / Exercise testing

vi) Mx:

conservative, Valve replacement, TAVI, Valvuloplasty

vi) Infective Endocarditis - SA, Strep (viridans, B & D), E Coli, Pseudomonas, HACEK organisms

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49
Q

Appendicitis:

i) ? Obturator Sign
ii) Describe pain seminology
iii) Scoring systems
iv) Common causes of obstructed lumen
v) cx of appendicitis

A

i) Pain on hip flexion and internal rotation due to obturator internus rubbing against appendix
ii) Central pain (Lesser Splanchnic Afferents - T10/T11)–> RIF once peritoneal somatic nerves involved
iii) Scoring Systems - Alvarado, Appendicitis Inflammatory Score
iv) Faecolith, tumours, lymphoid, lymphoma intestinal worms
v) Cx - Rupture, Appendiceal mass, Appendix Abscess

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50
Q

Ascites:

i) Causes

A

i) Transudates (<30g protein) Exudates (>30g/L protein)

SAAG:

>1.1g - Portal Hypertension

Cirrhosis, cardiac failure, Budd Chiari Syndrome, Thoracic Duct Obstruction

<1.1g - Non-Portal Hypertension

Hypolabuminaemia (Nephrotic Syndrome, GI protein loss), Peritonitis (bacterial or TB), Peritoneal Carcinomatosis, Pancreatitis

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51
Q

Describe starling equation for movement across capillary membrane

A

Arterial End:

Hydrostatic pressure> Colloid Oncotic pressure

Net movement of fluid out of capillary

Venous End:

Colloid Oncotic Pressure > Hydrostatic Pressure

Net movement into the capillary

Therefore fluid is filtered and then reabsorbed

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52
Q

Classify Causes of pitting oedema

A

Increased Hydrostatic Pressure:

Heart Failure, Hypervolaemia, Venous Insufficiency, Pregnancy

Reduced Oncotic Pressure:

Hypoalbuminaemia (nephrotic syndrome, malnutrition, protein losing enteropathy, cirrhosis)

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53
Q

Atherosclerosis:

i) Definition

ii) Pathological Process

iii) RFs

A

i) Artery wall thickening as a result of fatty materials accumulating
ii) First - Endothelial Insult/Dysfunction Then - Inflammatory cell migration to stabilise forming a lipid core Then- Smooth muscle proliferation to form a fibrous cap
iii) RFs - Age, Smoking, DM, Hypercholesterolaemia, FH

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54
Q

Benign Breast Disease - Demographic , Histology, Presentation

i) Fibroadenoma

ii) Breast Cyst

iii) True Mastalgia (+ management)

iv) Breast Abscess ( Classification, ?bacteria, management )

v) Mondor’s Disease

A

i) Fibroadenoma

Presentation - Defined/Rubbery/Mobile lesions in outter/upper quadrant

Histology - Epithelium/ Stromal tissue proliferation

Demographic - Young women

ii) Breast Cyst

Presentation - Distended/ Involuted Lobules

Histology - Fluid Filled (should not be bloody)

Demographic - Peri-menopausal

iii) True Mastalgia

Presentation - Breast enlargement, pain and nodularity

Demographic - Exaggerated response of breast tissue to hormones

Management - Caffeine, Gammalinoleic Acid, Danazol, Bromocroptine, Tamoxifen

iv) Breast Abscess

Lactational (S. Aureus, S. Epidermydis, Other Staph species) and non lactational

Presentation - Breast feeding, Pain, redness, Heat & Swelling

Mx- Analgaesia, Antibiotics, Cont. Breastfeeding, Drainage

Peri-Ductal Mastitis

Presentation - Young, Smokers, Pain, Discharge, Inflammation

Histology - Inflammation around non dilated sub-areolar ducts

v) Mondor’s Disease

Presentation - Sudden onset pain with tenderness of tissue in cord like shape

HIstology/Pathology - Thrombophlebitis of subcutaneous vein

Mx - NSAIDs

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55
Q

i) Triple Assessment

A

i) Triple Assessment:

Examination

Imaging - USS Abdomen / Mammogram

Tissue Biopsy - Core Biopsy/FNA

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56
Q

Phylloides Tumour:

i) Presentation

ii) Histology

iii) Treatment

A

i) Present - Large tumours in 40-50s

ii) Histology - Overgrowth of stromal tissue

iii) Treatment - WLE / Mastectomy

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57
Q

Gynaecomastia

i) Causes

A

i) Causes:

Physiological - Neonates, Puberty, Elderly

Pathological - Hepatic Failure, Renal Failure, High Prolactin, Testicular Tumours, Kinefelter’s Syndrome

Drug - Anti Dopaminergic, Spironolactone, ACEi. CCBs, Marijuana

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58
Q

Causes of breast discharge

A

i) Physiological - Variations in colour.

Passive discharge .

ii)Duct Ectasia -

Pathology/ Histology- Shortening and dilating of Sub-areolar ducts

Presentation - Mass, Nipple discharge, Nipple Retraction

iii) Intraductal Papilloma -

Presentation - serous/blood stained discharge with lump

iv) Epithelial Hyperplasia

Reddish coloured dicharge

v) Galactorrhoea

Milk Discharge ( Should check prolactin levels)

vi) Cancer

Any lump with discharge should be biopsied

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59
Q

Bladder Cancer:

i) RFs for TCC

ii) RFs for SCC

iii) Other bladder cancers

iv) Ix

v) Surgical Mx

vi) Non- systemic adjuncts

A

i) Smoking, Rubber/Textile Industry Worke, Dyes
ii) Schistosoma Haematobium - African Countries due to chronic inflammation, indwelling catheters, calculi
iii) Adenocarcinomas, Small Cell Carcinoma, Mets
iv) Ix - Ultrasound, Urine Cytology, Cystoscopy + Biopsy, Staging Cross Sectional Imaging
v) Surgical Mx:

TURBT, Partial Cystectomy, Simple Cystectomy, Radical Cystectomy, Pelvic Exenteration

vi) Non Systemic Adjuncts - intravesicular BCG/chemotherapy

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60
Q

Bone Tumors:

i) Benign types

ii) Malignant types

iii) Common bone mets

A

i) Osteochondroma (most common), Enchondroma, giant cell tumour, fibrous dysplasia

ii) 4 types - Multiple Myeloma (most common), Osteosarcoma (second most), Ewing’s Sarcoma, Chondrosarcoma

iii) Breast, Lung, Thyroid, Kidney, Prostate

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61
Q

X Ray appearance:

i) Onion skin appearance & who does it generally effect/presentation characteristics

A

i) Ewing’s Sarcoma (Onion skin relates to successive layers of periosteal development. Periosteal lifting)

  • Children & adolescents
  • Effects axial and perpendicular skeleton. Pelvic tumours have a worse prognosis.
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62
Q
A

Osteosarcoma

- Sunburst appearance

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63
Q

i) Investigations for ?bone tumour

ii) When to operate on a benign bone tumour?

iii) Mx of malignant bone tumours

A

i) Blood - PTH, Ca++, ALP

Imaging - Bone films, MRI, Staging scan of CT, whole body technetium scan

Bone biopsy - Along limb salvage lines so the whole biopsy tract can be removed en block (mitigates tumour seeding)

ii) Surgery - pain, limitation on movement, rapid growth, local effects

iii) Primary - Surgery (Amputation/Limb Salvage) +/- Chemotherapy +/- radiotherapy- Mx in specialist unit

Secondary - Radiation +Chemotherapy + surgery

Fracture prophylaxis - >50% femoral shaft involvement should have Prophylactic IM nail put in - only in carcinoma not in sarcoma

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64
Q

What are the subtypes of surgical resections

A

Intralesional - tumour is cut into during surgery

Marginal Resection - Surgical dissection extends into reactive zone surrounding the malignancy

Wide Local Excision - Surgical dissection remains outside the reactive zone

Radical Excision - Removal of compartments containing the tumour

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65
Q

Clostridium:

i) Types

ii) RFs for C Diff

iii) Most notable complication? and Mx

iv) how does C Diff cause pseudomembrane?

v) What other drugs may increase C Diff Risk?

A

i) Difficile, Tetani, Perfringens, Botulinim

Gram +ve, Anaerobes, Spore producing

ii) Staff, Antibiotics, Elderly

iii) Toxic Megacolon - Acute colonic distesnion, fever, pain and shock

Mx - Resucitate, Decompression (NG+ Flatus), Surgery may be required

iv) Pseudomembrane - Toxin mediated inflammation of the epithelium leads to production of grey/white exudate

Membrane is composed of - neutrophils, bacteria, debris, fibrin and necrotic epithelium

v) PPIs and Beta Agonists are thought to increase the risk through delayed gut transit times (allowing the toxin more time to exert effect)

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66
Q

Abdo X Ray Method

A

Patient details, Film, penetraton, exposure (Lung bases to hernial orifices

Bowel - SB >3cm, LB >6cm, Caecum >9cm

Gas - Biliary, subdiaphragmatic, Rigler’s

Organs - Liver, Spleen, Kidneys, Aorta, Psoas

Bone - Vertebrae, SI joints, Femurs, Inferior Ribs

Other - Any tubes, pessary, FBs, signs of surgery

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67
Q

i) Most common causes of LBO

ii) Most common causes of SBO

A

i) Tumour, adhesions, Diverticular strictures, Sigmoid / caecal volvulus
ii) Adhesions, hernias, Crohn’s, Tumour

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68
Q

Hereditary Polyposis Syndromes:

Names

INheritance Patterns

Cancer Risks

A

Familial Adenomatous Polyposis

- AD mutation of APC (Ch 5)

  • FAP (mandibular osteomas) Gardner’s (osteomas, desmoids, fibromas, lipomas) / Turcot’s (medulloblastoma, GBM)
  • Need flexi sigs/UGI endoscopy every 1-2 years until you see polyps then colonoscopies every 1-2 years with polypectomy of suspicious polyps
  • Subtotal colectomy/ Panproctocolectomy + ileoanal pouch formation are often required
  • Post surgery - UGI endoscopy 3-5 yearly + sigmoidoscopy regularly

Hereditary non Polyposis Coloretal Cancer

- AD mutations in DNA mismatch repair (Ch 2+3)

  • Amsterdam Criteria
  • Colonic + Extra colonic cancer (gynae, pancreatic, gastic, small bowel)

Peutz Jehger

  • AD mutations in STK11 (Ch19)
  • pigmented lesions on face/fingers + hamartamous polyps

Cowden Syndrome

- AD mutations in PTEN (Ch10)

  • Tricholellomas, oral papillomatosis, facial papules
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69
Q

i) Colonic Cancer Classifications

ii) Adenoma - Carcinoma Sequence

iii) Common CRC Metastases

iv) Types of liver resection

A

i) TNM or

Duke’s

A - Muscularis Propria

B - Beyond muscularis propria

C - Nodal involvement sparing highest node (apical)
D - Involvement of apical node/ distal metastasis

ii) Series of mutations resulting in malignancy

First - APC, Then K-RAS/DCC and then p-p3 TS gene

iii) Mets- Liver, Lung, Brain, Bone
iv) Right hemihepatectomy - Counnaud Segment’s 5,6,7,8

Left hemihepatectomy - Counnaud segment’s 2-4

Total Resection

Minor - Wedge, segmental, subsegmental

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70
Q

Layers of the bowel wall

A

Mucosa

Submucosa

Meisner’s Plexus

Muscularis Propriate

Longitudinal Muscle

Auerbach’s Plexus

Circular Muscle

Serosa

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71
Q

Define:

i) Adenocarcinoma

i) Neoplasm

A

i) Cancer of glandular origin

ii) Abnormal mass of tissue with uncoordinated growth, exceeding that of normal tissue that persists after cessation of stimulus

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72
Q

Hepatic Tumours

A

Benign - Haemangioma, Focal nodular hyperplasia, Adenoma

Malignant - Primary ( HCC, Cholangiocarcinoma, Angiosarcoma, hepatoblastoma) Mets.

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73
Q

Define:

i) Absces

ii) Pus

iii) Cyst

iv) Sinus

v) Stoma

A

i) Abscess - Collection of a pus walled off and surrounded by granulation/fibrous tissue

ii) Pus - Neutrophils + dead/dying microorganism

iii) Cyst - Abnormal membranous sac (lined by epithelial/endothelial cells)

iv) Sinus - Blind ended tract lined by granulation tissue

v) Stoma - Surgical opening into a hollow viscus

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74
Q

Define:

vi) Aneurysm

vii) Diverticula

A

vi) Aneurysm - An abnormal, permanent dilation of a vessel 1.5x greater than expected diameter

vii) Diverticula - An abnormal outpouching of a hollow viscus into surrounding tissues

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75
Q

Define:

viii) Thrombus

IX) Clot

X) Embolus

A

viii) Thrombus - Solid material formed from blood constituents in flowing blood

IX) Clot - As for thrombus but in stationary blood

X) Embolus - Abnormal mass of undissolved material carrier from one location to another

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76
Q

Define:

XI) Necrosis

XII) Hypersensitivity reactions

XIII) Polyp

A

XI) Necrosis - Abnormal tissue death in life

XII) Hypersensitivity Reaction - Exagerrated host immune response to specified stimulus

XIII) Polyp - Abnormal pedunculated mass of tissue rising from an epithelial surface

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77
Q

Define:

XIV) Hyperplasia

XV) Hypertrophy

XVI) Hamartoma

XVII) Metaplasia

XVIII) Dysplasia

A

XIV) Hyperplasia - Increase in tissue size due to an increase in the number of normal cells

XV) Hypertrophy - Increase in tissue size due to an increase in the size of otherwise normal cells

XVI) Hamartoma - Tumour like malformation composed of disorganised arrangement of tissue found at particular site

XVII) Metaplasia - Reversible replacement of one differentiated cell type with another

XVIII) Dysplasia - Abnormal cell population with increased mitosis and pleimorphism. Doesn’t penetrate BM/metastasise

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78
Q

Proportion of thyroid cancers hereditary:

i) Medullary

ii) hurthle cell

iii) Follicular

A

i) Medullary - 25% (MEN 2a/2b. Familial Med. Thyr. Cancer)

ii) hurthle cell - 7%

iii) Follicular - 7%

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79
Q

Cytological Classification of thyroid nodules

A

Benign

Indeterminate

Malignant

Inadequate Specimen

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80
Q

Thyroid Cancer:

Types

A

Medullary

Follicular

Papillary (85%)

Anaplastic (1%)

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81
Q

What is tertiary hyperparathyroidism

A

Development of autonomous PTH secreting nodule in patient with previous secondary hyperparathyroidism

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82
Q

Causes of hypoparathyroidism

A

Idiopathic/autoimmune

Radioidoine treatment

Thyroidectomy

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83
Q

Primary vs Secondary Hyperalodsteronism

A

Primary - Aldosterone High / Low Renin

Causes - Aldosterone Secreting Adenoma/adrenocortical carcinoma, Adrenal Hyperplasia, Familial

Secondary - Aldosterone High/ High Renin

Causes - Renovascular disease, Renin secreting tumour, Liver cirrhosis

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84
Q

i)Causes of cholangiocarcinoma

ii) Ix for cholangiocarcinoma

A

i) West - PSC (chronic inflammation due to refluxing bile)

Developing - Liver flukes (chronic inflammation due to presence of organisms)

Chronic liver disease, HIV, Congenital Liver Diseases

ii) Imaging - US/ERCP/MRCP

Biopsy - MRCP/ Open biopsy

Bloods - CEA, CA19-9, Obstructive Jaundice

Immunohistochemistry on sample

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85
Q

i) Bacteria commonly found in bile

ii) Suitable antibiotic cover

A

i) Aerobic

Negative - E Coli, Klebsiellus, Proteus, Enterobacter

Positive- Strep Faecalis.

Anaerobic

Clostridium

ii) Broad spectrum antibiotic + Anaerobic cover (Cef + Met / Tazocin)

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86
Q

Necrotising Fascitis:

i) Clinical Presentation

ii) underlying pathology

iii) Types

Iv) Management of post op wound NF

A

i) Pain out of keeping with clinical picture

Violet skin colour (due to necrosis)

Sepsis/Shock

Oedema

ii) Necrotising Fascitis is an infection that spreads quickly in the subcutaneous tissue spreading across fascial planes rather than going deep into the muscles.

iii) A - Polymicrobial

  • S Aureus, Pseudomonas, Coliforms, Bacterioides, Diptheroids

B - Monomicrobial - Strep Pyogenes (GAS)

Clostridium Perfringens (fourniere’s)

iv) A-E

IV Antibiotics / Fluids

Extensive debridement (emergency) with plastics if possible

HDU/ITU

Hyperbaric Oxygen

VAC dressing

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87
Q

i) Indications for heart transplant

ii) Donor Criteria

A

i) NYHA IV Heart Failure (irremediable)

LVEF <14 ml/kg

Deteriorating

<1 year prognosis

No contraindications to transplant in general

ii) Donor Criteria:

<55 years old

Normal ECG

Minimal cardiac risk factors

Macrascopically normal heart at organ recovery stage

and (brainstem death certified, permission from NOK/on organ donor register, ABO compatible, without infectious disease precluding the transplant)

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88
Q

i) Grossly what causes GVHD

ii) Cancers associated with HIV

iii) Minimising risk when operatiing on HIV +ve patients

A

i) Donor T Cells reacting against Host HLA

ii) HIV - Kaposi’s Sarcoma, CNS Lymphoma, Anogenital cancer, Cholangiocarcinoma

iii) HIV Positive Patients:

  • Experienced Surgeons
  • Double Glove, Eyeshield, Impervious Gowns, Disposable anaesthetic circuitry
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89
Q

H Pylori

i) What is H Pylori?

ii) Acid evasive techniques?

iii) How does it cause gastric problems?

iv) How many H Pylori carriers are asymptomatic?

v) Malignancy/Disease associations

vi) Detecting H Pylori

vii) Treatment of H Pylori

A

i) Gram Negative, Spiral shaped bacterium

ii) pH detecting - Has the ability to follow a pH gradient and adhere to neutral epithelial lining

Urease - Secretes urease which converts urea to CO2 + ammonia. Ammonia reacts with H+ to become ammonium thus increasing pH

iii) H Pylori produces - Proteases + Phospholipases + Urease (but problem is ammonia). The three of which cause breakdown of mucous covering in stomach. Leaving the epithelium exposed to gastric acid.

iv) 80%

v) H Pylori can cause (in 1-2% of carriers) - Gastric Adenocarcinomas and Gastric MALTomas

Barrett’s, Duodenal + Gastric Ulcers

vi) Campylobacter Like Organism (CLO Test). This test is dependent on urease prodcution by H Pylori

Culture, Histological Examination, Urease Breath (radiolabelled urea ingestion) Test, Stool Antigen Test, Serum Antibody Test

vii) Triple Therapy:

i) Amoxicillin, Clari, PPI

ii) Metronidazole, Clari, PPI

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90
Q

i) Which Cells produce Gastric Acid?

ii) What is dumping syndrome

A

i) Parietal Cells - Cephalic/Gastric phase of food —> Gastrin secretion by G Cells

—> Histamine (secreted by enterochromaffin cells due to gastrin stimulation) + Gastrin both stimulate parietal cells to produce HCl

PPIs act on parietal cells to prevent HCl production

ii) Dumping Syndrome - Rapid transmission of undigested gastric contents into the small intestine due to pyloric disruption

Phase I - Hyperglycaemia and then reactive hypoglycaemia

Phase II - Hypovolaemia due to fluid shift with a large hyperosmolar load

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91
Q

i) Risk Factors for Gastric Adenocarcinoma

ii) Two broad categories of Gastric Adenocarcinoma

A

i) H Pylori

Excessive Salt

Smoked Fish

Pernicious Anaemia

Family History

Japanese Origin

Men >50 years old

ii) Lauren Classification - Intestinal (resembling intestinal adenocarcinoma) and Diffuse type

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92
Q

Calcium.

i) Where are PTH/Calcitonin Produced?

ii) What does vitamin D do?

iii) How do surgeons ensure they have removed the parathyroid glands?

A

i) PTH - Chief Cells (parathyroid gland)

Calcitonin - Parafollicular C Cells (thyroid gland)

ii) Vitamin D:

1 25 OH D3 - Hydroxylated form. Usually

a) increased intestinal absorption of Ca++
b) increases calcium release from bone
c) decreases calcium excretion from kidney

iii) The specimen is sent for frozen section analysis by pathalogist intraoperatively

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93
Q

Types of hypersensitivity reaction

A

+ ?Type V - Formulation of stimulatory antibodies

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94
Q

Type 4 Hypersensitivity Reaction:

Time-Frame?

A

It is a delayed reaction that often takes 48-72 hours to manifest.

Caused by T Cells

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95
Q

i) 3 Factors contributing to Surgical Infections?

ii) What factors make for favourable closed spaces for infectious organisms?

iii) How does infection spread from one site to another?

A

i) Microorganism

Susceptible Host

Location (poorly perfused/enclosed)

ii) Poor Perfusion, Local Hypoxia

Hypercapnia, Acidosis

Narrow outlet (GB, Ureter)

iii) Spread can be:

a) Haematogenous b) Lymphatic c) Along fat planes

d) Enlargement/local movement

e) Along fascial/subcutaneous planes

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96
Q

Types of immune response to pathogen?

A

Specific Immunity

Recognise specific pathogens/PAMPS:

T Cells - Cell Mediated

B Cells / Plasma Cells - Antibody production –> opsonisation and enhanced killing

Non- Specific Immunity :

Barriers - Skin, Gastric Acid, Lubricant membranes

Phagocytes - Migratory capacity, ingestion, killing/attenuating

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97
Q

i) What are the stages of acute inflammation?

ii) Some chemical inflammatory mediators

iii) Difference in inflammatory cells in chronic inflammation

A

i) 1 - Vasodilation

2 - Increased Vascular Permeability

3 - White cell extravasation

4 - Phagocytosis

5 - Resolution/ Chronicity

ii) Amines- Histamine, Serotonin

Bradykinin, Cytokines, Complement, Coagulation

Arachidonic Acid products (leukotrienes, prostaglandins..)

iii) In chronic inflammation there will be more lymphocytes and macrophages. In more acute inflammation there is a tendency toward neutrophils

98
Q

Define:

i) Granuloma

ii) Granulomatous Inflammation

iii) Classify Granulomas

A

i) A granuloma is a collection of epithelioid macrophages
ii) Chronic inflammation characterised by epithelioid macrophages. Sometimes evidenced are Langhan’s Cells - Multinucleate giant cells

iii) Caseating necrosis is typified by the degradation of tissue into a ‘cheese like substance’

Caseating - TB, Syphilis,

Non - Caseating - Sarcoid, Crohn’s Disease, Leprosy, Rheumatoid Arthritis

99
Q

IBD:

i) Most commonly quoted pathogenesis

ii) Extra Intestinal Manifestations

A

i) Environmental trigger with a genetic susceptibility

ii)

Perianal disease - crohn’s

Eyes - Uveitis, Iritis, conjunctivitis, episcleritis

Mouth- Apthous Ulcers, Angular stomatis (If concurrent iron deficiency), Glossitis (B12 deficiency)

Skin - Erythema Nodosum, pyoderma gangrenosum

Joints - Associated inflammatory arthropathy, Ankylosing Spondylitis/Sacroilitis (Crohn’s)

Biliary - Gallstones (Chron’s), Primary Sclerosing Cholangitis (UC), Cholangiocarcinoma (following on from PSC)

Urinary Tract Calculi

100
Q

i) Define naevus

ii) Main Types of Melanoma

iii) RFs for melanoma

A

i) Naevus - benign proliferation of normal skin constituents

ii) Superficial Spreading Melanoma

Nodular melanoma

Acral Lentiginous

Subungual

Lentigo Malgina Melanoma

Amelanocytic Melanoma

iii) Congenital - Skin Type (Fitzpatrick scale), FH, Presence of lots of naevi, Xeroderma Pigmentosum, Albinism, Giant congenital pigmented naevi

Acquired Sunlight Exposure (radiation in general), Immunosuppresion

101
Q

i) Characteristics of Melanoma

ii) Type of biopsy for suspected melanoma

iii) Classification and recommended margin

A

i) Malingnant proliferation of melanocytes

A symmetry

Irregular B orders

Multiple C olours

D iameter >6mm

E volution (changing

ii) They should undergo excision biopsy with 2mm margin

iii) Breslow Thickness (from stratum granulosum to the deepest point of tumour involvement)

<1mm - 1cm Margin

1-2 mm - 1- 2cm Margin

2-4mm - 1-2cm Margin

>4mm - 2cm Margin

102
Q

Define + Locate + Ix/Mx :

i) Branchial Cyst

ii) Thyroglossal cyst

iii) Dermoid Cyst

iv) Sebaceous Cyst

A

i) Branchial Cyst is stratified squamous epithelium incoorporated into cervical lymphatics (previously thought to be branchial pouch remnant)

Found - Anterior triangle. Anterior to upper 1/3 of SCM

Ix - FNA +/- US guidance. CT/MRI to characterise location

Mx - Excision

ii) Thyroglossal Cyst is a midline swelling that moves superiorly on tongue protrusion. Remnant of thyroglossal duct containing lymph tissue/ thyroid tissue.

Ix - US neck/ Cross-sectional imaging (sometimes patients dont have thyroid gland)

Mx - Sistrunk’s procedure - removal of cyst, duct, and hyoid bone

iii) Dermoid Cyst is an epithelial lined cyst lying deep to skin. Congenital (angles of eyebrows, midlien nose, midline of neck/trunk) or acquired.

Ix - US in congenital to ensure no communication with underlying structure

Mx - Excision

iv) Smooth swellings attached to the skin with a punctum occuring on the scalp,face, neck + trunk

Truly either:

Epidermoid Cyst (epidermis)

Pilar Cyst (hair cells)

103
Q

i) Define Ludwig’s Angina

A

i) Cellulitis of cervical/floor of mouth soft tissues usually secondary to dental infection.

  • Require resucitation, airway observation/management, antibiotics +/- surgery
104
Q

i) Cystic Hygroma - Define + Mx

ii) Pharyngeal Pouch - Define + Mx

A

i) Congenital cystic malformation of lymphatics often occurring in the posterior triangle of the neck

Mx - Aspiration and Sclerotherapy/ Excision (High recurrence rate for either)

ii) True Diverticulum through Killian’s Dehiscence (Weakness between thyropharyngeus and cricopharyngeus). Usual presentation through regurgitation, cough, halitosis in old men.

Ix - Barium Swallow

Mx - Endoscopic Stapling / External Excision

105
Q

What to do when you see neck lump?

A

History

ENT Exam

FNA

Imaging

106
Q

Types of necrosis

A

Coagulative - most common

Caseous - TB

Liquefactive - Brain

Gangrenous - Wet/Dry

Fat Necrosis

107
Q

Define:

i) Necrosis

ii) Apoptosis

iii) Outline differences between apoptosis and necrosis

A

i) Abnormal cell death in life. Always accompanied by inflammation.

ii) Programmed cell death - apoptotic bodies are produced that are phagocytosed. Generally not accompanied by inflammation.

108
Q

General spread routes of carcinoma vs sarcoma

Which thyroid cancer variant spreads haematogenously?

A

Carcinoma - spreads by lymphatics

Sarcoma - Spreads haematogenously

Follicular thyroid cancers spread haematogenously

109
Q

Key differences between benign and malignant neoplasms

A
110
Q

Examples of hyperplasia and hypertrophy

A

Hyperplasia

Physiological - Thyroid in pregnancy, Breast tissue in pregnancy

Pathological - BPH, Adrenals, Parathyroid

Hypertrophy

Physiolgoical - Skeletal muscle, Uterus in pregnancy

Pathological - Cardiomyopathy, Thyroid in grave’s

111
Q

Rheumatic Fever:

i) What is it?

ii) What type of hypersensitivity reaction?

iii) Criteria?

A

i) Systemic immune response to untreated Group A Strep
ii) Type 2 Hypersensitivity - Antibodies produce against antigen
iii) Jone’s Criteria

Major - Joints, Myocarditis, Subcutaenous Nodules, Erythema Marginatum, Sydenham’s Chorea

Minor - CRP, Arthralgia, Fever, ESR, Prolonged PR, Anamnesis, Leukocytosis

For Dx - Positive culture/ ASOT + 2 Major / 1 Major + 2 Minor

112
Q

i) Diagnosis of infective endocarditis

ii) Why is it hard to treat?

iii) What to do pre-op with IE patients?

A

i) 2 Major, 1 Major + 3 Minor, 5 Minor

Major - Blood Cultures

2 Blood Cultures Positive with typical organism

Persistently positive blood cultures

Major - Echo

Evidence on echo of IE

  • Vegatation, abscess, prosthetic valve dehiscence

Minor -

i) Predisposing Factor
ii) Fever >38
iii) Vascular Phenomena - Janeway, Emboli, Pulmonary infarct, Conjunctival Haemorrhage
iv) Immunological phenomena - Osler’s Nodes, Roth Spots, GLomerulonephritis
v) +ve Blood culture
vi) Echo findings

ii) The valves do not have direct blood supply so neither antibiotics/immune system can reach it

iii) -Echo

  • Cardio Review
  • Consider prophylactic antibiotics
113
Q

Acute Pancreatitis

i) Definition

ii) Most important enzyme in the pathogenesis

iii) Which enzymes are released?

iv) When do amylase levels began to decline?

v) Complications

vi) Blood Supply to the pancreas

A

i) Acute pancreatitis reversible inflammatory process of the pancreas that can effect multiple organisms

ii) Activation of trypsinogen –> trypsin. This is thought to begin the activation cascade

iii) Lipases, Proteases, Elastases, Amylase

iv) Levels begin to fall between 24-48 hours after initial insult

v) Complications -

Early - Hypocalacaemia, ARDS, Abdominal Collection, Infection, Shock, Pleural effusion, Coagulopathy, hypercalcaemia, renal failure

Late - Pseudocyst, Chronic Pancreatitis, Malnutrition, Pancreatic Necrosis, Abscess, Haemorrhage, Thrombosis

vi) Superior pancreatoduodenal artery (Branch of the gastroduodenal artery)

Inferior pancreatoduodenal artery (1st Branch of the SMA)

Splenic Artery

114
Q

Parotid Gland:

i) Causes of bilateral parotid gland swelling

ii) Unilateral Parotid Gland Swelling

iii) Are salivary gland stones more common in submandibular or parotid gland?

iv) Sign of malignancy?

v) Post Op Complications of paritodectomy

A

i) Bilateral Parotid Gland:

Local - Sjogren’s, Mumps, Parotitis,

Systemic - TB, Sarcoid, Alcohol, Cushings

Drugs - OCP, Thiouracil, Isoprenaline

ii) Unilateral parotid gland:

Benign - Sialolithiasis, Duct Compression, Neoplasia (Pleomorphic Adenoma + Warthin’s Tumours), Mumps, Parotitis

Malignant - Mucoepidermoid carcinoma, Adenoid Cystic Carcinoma

iii) They are more common in the submandibular gland because the salivary content is more alkaline and mucous containing higher concentrations of calcium and phosphate

  • Parotid Calculi - Small, multiple intraglandular

- Submandibular Calculi - Large, single intraductal

iv) Ipsilateral CNVII Palsy

v) CNVII Palsy, Frey’s Syndrome (auriculotemproal nerve fibers reattaching to cutaneous sweat glands), Salivary Fistula, Greater Auricular Nerve Damage (C2-C3 Nerve Roots)

115
Q

i) Pain history with gastric vs duodenal ulcers

ii) Cx of PUD

iii) PUD aetiology

A

i) Gastric - Pain related to eating

Duodenal - Pain before meals and relieved by eating

ii) Bleeding (DU - GDA)

Perforation

Gastric Outflow Obstruction (scarring/inflammation)

Malignant Transformation

iii) Drugs - NSAIDs, Steroids, Smoking, Alcohol

Infection - H Pylori

Phsyiological stress

116
Q

i) Bilroth Operations

ii) Vagotomy purpose

A

i) Bilroth I - Partial gastrectomy with re-anastamosis

Bilroth II - Partial gastrectomy + duodenal stump + proximal jejunal anastamosis

ii) Vagus nerve usually:

Inhibits Somatostatin

Stimulates Gastric acid, gastrin + histamine release

Vagotomy is useful in preventing peptic acidity related issues

117
Q

i) Polyp Classification

ii) Polyp complications

A

i) Neoplastic - Tubular (most common), Tubulo-villous, Villous (most malignant potential)

Non - Neoplastic - Metaplastic, hamartamous, Inflammatory psuedopolyps (UC)

ii) Malignant transformation, ulceration, bleeding, infection, Hypokalaemia/hypoalbuminaemia, intesusseption

118
Q

Any medications reducing number of polyp in familial polyposis ?

A

Celecocoxib - COX2 NSAID

Sulindac - A non COX NSAID

Both reduce the numbers and size of polyps

119
Q

i) Define: Dysplasia
ii) Define: Metastasis

A

i) Dysplasia - Abnormal cellular development with pre-malignant characteristics such as a abnormal mitosis and pleomorphism but no invasive features (membrane intact)
ii) Metastasis - The survival and growth of cancerous population at a secondary site from original population

120
Q

BPH:

i) Aetiology

ii) Symptoms

iii) Work-up

iv) Mx

v) What is PSA?

A

i) Age, Metabolic, Androgen, Genetic Susceptibility

ii) Storage - Frequency, Urgecy, Nocturia Voiding - Stream, Dribbling,

iii) History/ Exam - + PR + Voiding Diary

IPSS

US/TRUS/MRI/IVU

PSA

Urodynamic studies

iv) Mx:

Lifestyle - bladder training, reduce night time drinking

Medication - Alpha antagonist, 5 a reductase

Surgery - TURP/HOLEP/TULIP, Prostatectomy

v) PSA - Is a glycoprotein enzyme that usually liquefies semen and dissolves cervical mucous

121
Q

i) Prostate cancer grading

ii) Prostate cancer treatment

iii) Ix

iv) PSA monitoring post-prostatectomy

A

i) Gleason Score:

First most common pattern scored 1-5

Second most common pattern scored 1-5

Add them both togethter to give you the overall score

ii) Prostate cancer treatment:

a) Watchful waiting
b) Radiotherapy/ brachytherapy
c) Hormonal therapy - Androgen receptor antagonist (flutamide), LHRH agonists (Goserelin)
d) Orchidectomy, TURP, Radical Prostatectomy +/- chemotherapy

iii) Ix:

History/ Exam/ PR / Spinal Exam

PSA

TRUS + Biopsy/ MRI Prostate

Spinal Imaging

iv) 6 weeks after procedure

6 monthly for first 2 years

Then annually

PSA should be undetectable a week after surgery as the half life is 2-3 days

122
Q

TURP Complications

A

Bleeding, UTI, Urinary Retention

Retrograde ejaculation

Urinary incontinence

Urethral strictures

Erectile Dysfunction

TURP Syndrome

123
Q

DDx for Voiding/Storage Sx

A

Bladder Outflow Obstructions

Prostate - BPH/Ca, Urethral Stricture, Urethral sphincter dysynergia

Bladder Dysfunction

Oversensitvity, detrussor overactivity, low detrussor contractility

124
Q
A
125
Q

Difference between :

Staging and Grading

A

Staging - Assessment of size and spread of tumour

Grading - Histological assessment of level of cellular differentiation

126
Q

Complications of ureteric stones

A

i) They may not pass
ii) Hydroureter + hydronephrosis
iii) Infection
iv) Haematuria

127
Q

i) Why do renal calculi form?

ii) Types and incidence of calculi

A

i) Anatomy - Kidney ariants, VU Reflux

Infection - Proteus (struvite)

Stasis - Atonic bladder, bladder outflow obstruction

Dehydration

Electrolytes- Uric acid cycle abnormalities, Cysteinuria, Hypercalcaemia, Hyperuricaemia

ii) Calcium Oxalate - 75%

Struvite - 15%

Uric Acid - 5%

Cysteine - 2%

128
Q

How are protues mirablis + helicobacter pylori similar?

A

Both secrete urease enzyme which cleaves urea to ammonia

129
Q

Differences between smooth muscle and skeletal muscle

A

Smooth -

Non- Striated

Uninucleated

Calmodulin (Calcium Binding Protein)

Absence of T Tubules

Skeletal-

Striated

Multinucleated

Troponin (Calcium binding protein)

T Tubules

130
Q

i) Micturition Control

ii) Spinal injury above T12

iii) Spinal injury below T12

A

i) Parasympathetic

  • Contracts bladder and relaxes internal sphincter
  • Pelvic Nerve S2-S4

Sympathetic

  • Relaxes bladder and contracts internal sphincter
  • Hypogastric Nerve T12 - L2

External Sphincter - Pudendal Nerve

ii) Above T12 produces a reflex bladder -

Bladder empties as it fills.

No control over external urethral sphincter (constantly relaxed) / no awareness of filling

iii) Below T12 produces an atonic bladder

Detrussor muscle is paralysed and therefore spinal reflex doesn’t work.

Bladder empties with overflow incontinence

131
Q

i) Define AKI

ii) What is dysequilibrium syndrome

A

i) AKI

a) Creatinine rise >26 nm/L in 48 hours
b) Creatinine increase 1.5x in 1 week
c) UO <0.5 ml hour for 6 hours

ii) Dysequilibrium Syndrome

Cx of dialysis where rapid changes in serum osmolality lead to cerebral oedema

132
Q

Side effects associated with:

i) Tacrolimus

ii) Cyclosporin

iii) Azathioprine

iv) Steroids

Specific to immunologics

A

i) Tacrolimus - Nephrotoxic, neurotoxic

ii) Cyclosprin - nephrotoxic, gingival hypertrophy, hypertension, hirsutism

iii) Azathioprine - Leukopenia

iv) Steroids -

Skin- Thin, striae, bruising, poor wound healing

Fat - buffalo hump, centripetal obesity, cushing facies

Proximal myopathy

CV - Hypertension, Fluid retention

GI - Pancreatitis, Peptic Ulcers

Endocrine - Diabetes

Bone - Osteoporsis, Avascular necrosis

Immunologics:

Infection - TB reactivation, CMV (Valganciclovir proph.), Pneumocystis Jerovici (co-trimoxazole proph.), JC Virus,

Malignancy - Cutaenous, Kaposis, Lymphoma

133
Q

i) Donor Matching - What do you look for?

ii) Vascular anastamosis in renal tranpslants

iii) What is in renal perfusion/preservation solution?

iv) Immunosuppresion regimen for renal transplants

v) Broad types of rejection

vi) Confirming rejection

A

i) ABO Compatibility

HLA

HLA- A, B & DR are the most important

ii) Donor renal artery/vein transplanted to recipient External iliac artery/vein

iii) Ice cold solution:

impermeable solutes (minimises swelling), pH buffers, free radical scavengers, membrane stabilisers, Adenosine (for ATP)

iv) At time of surgery:

Steroid + One of Alemtuzumab (CD-52) Basiliximab (CD25), Anti thymocyte globulin (CD3)

Afterward:

Triple therapy -

Calcineurin inhibitor (Cyclosporin/Tacrolimus - Blocks IL2 mediated T Cell expansion),

Purine Synthesis INhibitor ( Azathioprin), Prednisonolone

v) Hyperacute - Donor antibodies attack graft. Massive complement activation.

Acute - T Cell mediated within first 100 days. Lymphocyte infiltration

Chronic - B cell mediated chronic vascular/atrophic changes.

vi) Renal Biopsy

134
Q

Complications from renal transplant

A

Rejection - Hyperacute (minutes), Acute (100 days), Chronic

Delayed Function - Reperfusion injury, long cold ischaemic time

Vascular - Anastomatic failure/leak, Torturous vessels, Vascular thrombosis, Vascular Stenosis

Urological - Urine leak, Ureteric stenosis

Infection - Wound, Urine

Lymphocele

135
Q

i) Cryptorchidism - define + associated RFs

ii) Where are undescended testes usually found?

iii) Mx

A

i) Cryptorchidism - Failure of tested to descend from abdomen into scrotum.

Associated with - low birth weight, high pressure abdomen, hormonal abnormalities

RFs - increased risk of testicular malignancy + infertility (orchidopexy reduces the risk but to that of normal background population

ii) Usually found in the inguinal canal. But can be found anywhere along the gubernaculum

iii) Mx - In neonates referral to surgeon after 6 months whereby surgery (orchidopexy) should occur between 6 months - 1 year

If in an adult - Orchidectomy if offered to mitigate testicular cancer risk

iv)

136
Q

i) Testicular Cancer Types

ii) Radiotherapy in testicular cancer

iii) Where do they tend to metastasise to?

iv) Lymphatic Drainage

A

i) Germ Cell Tumours

Seminomas (Most Common, 30-40 yo) (ALP, b-HCG)

Non- Seminomatous Germ Cell Tumours

Non - Germ Cell Tumours

Teratomas (20-30 yo) (B-HCG, AFP, CEA)

Choriocarcinoma ( B HCG)

Yolk Sac Tumours

Embryonal carcinoma

Mixed germ cell tumours

ii) Radiotherapy is useful in seminomas

iii) Tend to metastasise to Lung, Bladder, Colon and Pancreas

iv) Lymphatic drainage of the:

testes - paraortic nodes (therefore incision should be inguinal for cancer operations rather than scrotal so as not to cause tumour seeding to a different lymphatic group)

scrotal skin - inguinal lymph nodes

137
Q

Basal Cell Carcinomas

i) Classical description

ii) Mx

iii) What is bowen’s disease

A

i) Pearly Papule/Nodule with rolled edge

ii) Mx -

Surgical Excision

5 FUC Cream, Imiquimod

iii) SCC in situ - Erythematous slowly growing plaque on skin

138
Q

i) Cytological Features of malignancy

ii) Histological Features of malignancy

iii) Pros and Cons of Cytology

iv) Pros and cons of histology

A

i) Cytological Features

Increased mitotic figures

Abnormal mitoses

Hyperchromatic nuclei (increased DNA)

Pleomorphism

Increased nuclear to cytoplasmatic ratio

ii) Histological Features

Loss of normal tissue architecture

Invasion through BM

Neovascularisation

Necrosis

Haemorrhage

iii) Cytology:

Pros: Quick, Cheaper, Minimally Invasive

Cons: Not as much information, not always sensitive/specific for cancer, Often need to repeat sample obtaining for histology

iv) Histology:

Pros: Allows staging of cancers, Lots of information about tissue

Cons: Longer process (tissue fixing), Invasive, Expensive, Seeding,

139
Q

i) Spleen Functions

ii) Normal Weight/Size

iii) Splenic Injury Grading

iv) Indications for splenectomy

v) Complications of splenectomy

vi) Which vaccines

A

i) 1) Immune response

- Splenic Macrophages present antigens to lymphocytes

  • Filters encapsulated organisms

2) Filter Circulation

  • Filters more old RBCs

3) Storage of platelets

  • Stores 30% of body platelets

4) Neonatal Haematopoiesis

5) Iron Re-utilisation

ii) Weight - 100-200g

Size - 8-13cm

iii) Graded 1-5

1 - Capsular Tear - <1cm

2 - Capsular Tear - 1-3 cm

3 - >3cm involving trabecular vessels

4 - >25% of spleen involving segmental/hilar vessels

5 - Shattered spleen/ Hilar vascular injury

iv) Indications:

Trauma

Hypersplenism - Sickle Cell, HS, HA

Malignancy - Primary splenic / Radical surgery for pancreatic/colonic cancer

v) Complications:

Early - Haemorrhage, Gastric Stasis, Gastric Necrosis, Subphrenic collection, pancreatitis

Late - Thrombocytosis, Infection (encapsulated organisms), Pancreatic fistula

vi) Other than Pen V - Pneumoccocus, haemophillus, Menigitis, Flu

140
Q

Causes of splenectomy

A

Infection - EBV, CMV, TB, Malaria, Kala Azar

Portal hypertension

Haematological - Haemolytic anaemia, SCD, HE, HS Thalassaemia, CML

Systemic - Sarcoid, Rheumatoid arthritis, Gaucher’s Disease

141
Q

Duke’s Staging

A

A - Bowel Wall (5YS 95%)

B - Through Bowel Wall (65-75%)

C - Lymph Node Mets (30-40%)

D - Distant Mets (5-10%)

142
Q

Groin Lump DDx

A

Skin - Sebaceous Cyst

Subcutaneous - Lipoma, Lymph Node

Neurovascular - Saphena Varix, Pseudoaneruysm, Neuroma

Bowel - Hernia

Other - Ectopic Testes, Groin Abscess

143
Q

i) Define: Teratoma

ii) How is a teratoma linked to gynaecomastia

A

i) Tumour able to form tissues from all three cell layers (Ectoderm, Mesoderm, Endoderm)

- Tumour markers B-HCG / AFP

ii) Teratomas/Choriocarcinomas CAN express B-HCG. B HCG can mimic Thyrotrophic Releasing Hormone and therefore cause gynaecomastia (through stimulating prolactin secretion)

144
Q

i) Define: Ulcer

ii) RFs for PUD

iii) How does h pylori cause ulceration?

iv)

A

i) An abnormal discontinuation of a mucous membrane
ii) Drugs - Steroids, NSAIDS, bisphosphonates etc., alcohol, smoking

Infection - H Pylori

Stress, High Vagal Tone

Gastrinoma (ZE syndrome)

Hypercalcaemia (Ca++ stimulates GA secretion)

iii) H Pylori:

H Pylori produces - Proteases + Phospholipases + Urease (but problem is ammonia). The three of which cause breakdown of mucous covering in stomach.

Leaving the epithelium exposed to gastric acid which is hypersecreted due to gastritis cuased by H Pylori.

145
Q

Ix of painless haematuria

A

History + Examination + PR

Urine - MC&S, Cytology

Bloods - Hb, Renal Function Testing, PSA

US/TRUS +/- Biopsy

CT pre/post contrast

Cystoscopy +/- biopsy

146
Q

Renal Cancers

i) Types

ii) what is VHL

iii) Treatment for bladder CIS

iv) Describe ileal conduit

A

i) Renal Cell Carcinoma (most common), Clear Cell, Sarcoma, Rhabdoid renal cell

ii) von Hippel Lindau Syndrome (AD)

  • RCC, Phaeochromocytoma, Pancreatic islet cell tumours, Retinal angiomas, CNS haemangioblastomas

iii) Intravesicular B-HCG First line. This can be given multiple times and patients are followed up with repeat cystoscopies and biopsies

iv) Urine diversion method:

Small ileal portion resected. Distal/Proximal bowel portions anastamosed together.

Ureters anastamosed to this portion of ileum.

One end oversown + the other end brought up as urostomy.

147
Q

Where is b12 absorbed?

A

Terminal ileum:

  • Therefore effected in crohn’s disease/ UC (backwash ileitis)/ Ileal resections

Deficiency can cause:

  • Macrocytic anaemia, peripheral neuropathy, SACD
148
Q

What secretes:

i) Gastric Acid

ii) Gastrin

iii) pepsinogen

iv) mucous

v) what inhibits gastric acid secretion

A

i) Gastric Acid - Parietal Cells

ii) Gastrin - G Cells (antrum)

iii) pepsinogen - Chief cells

iv) mucous - mucous cells

v) GA secretion inhibited by - Indirect inhibiition of scretion through –> Secretin, Cholecystokinin + Somatostatin

149
Q

MOA of PPI

A

Irreversible blocker of H+/K+ ATPase pump on parietal cells

150
Q

i) 1st line imaging for suspected perforation
ii) Mx of bleeding DU

A

i) ERECT CXR

ii) A-E

IV PPI

UGI Endoscopy +/- Injection/ coagulation/ clipping

Surgery - Underrunning of the bleeding artery and perforation

151
Q

Gastric Cancer Metastasis

A

Lymphatic - Local lymphatics, Supraclavicular LNs (Virchow’s)

Direct - Omentum, Pancreas, Diaphragm, Duodenum, Colon

Haematogenous - Lung, liver

152
Q

What is virchow’s triad?

A

Altered Flow - stasis/ turbulence

Altered Constituents - hypercoaguable - infection/platelets/RBCs/drugs

AntithrombinIII/ Protein C/S Deficiency

pregnancy, trauma, surgery

Vessel wall - endothelial injury

153
Q

Thyroid Cancer:

i) Presentation

ii) Classify thyroid tumours

iii) Investigating thyroid masses in clinic

A

i) Neck Lump, Odynophagia, Hoarse voice, lymphadenopathy
ii) Benign - Follicular Adenoma, cysts, nodules

Malignant (primary)-

Papillary Carcinoma, Follicular Adenocarcinoma,

Anaplastic, Medullary (MEN IIA/B),

Lymphoma

Malignant (Secondary) - Direct invasion usually (oesophagus, larynx)

iii) Triple Ax - Examination, Imaging, Biopsy

154
Q

MEN

A

Multiple Endocrine Neoplasia - AD inherited conditions characterised by hyerplasia/neoplasia in various endocrine tissues

MEN1 (Chromosome 11)

Pituatry Adenoma

Pancreatic Islet Tumours

Parathyroid Hyperplasia

MEN2a

Parathyroid Hyperplasia

Phaeochromocytoma

Medullary Thyroid Cancer

MEN2B

Phaeochromocytoma

Medullary Thyroid Cancer

Marfanoid type body habitus

Mucosal Neuromatosis

155
Q

TB

i) What are mycobacterium

ii) Atypical mycobacterium

iii) What is miliary TB?

iv) Diagnosis

A

Mycobacterium Tuberculosis

i) Non-motile, non-sporulating, Weak Gram +ve rods. (Actinomycetales)
ii) Mycobacterium Avium, Mycobacterium bovis, mycobacterium leprae, mycobacterium marinum
iii) Miliary TB - widespread lymphatic + haematogenous spread of TB seen as small 2mm deposits in immunocompromised patients
v) AFB (Ziehl - Neelson Staining), Quantiferon/Elispot

Lowensten-Jensein Culture MEdia

156
Q

i) Define: Tumour Marker

ii) Examples

A

i) Tumour markers are circulating substances found in patients with neoplasm. Not always proportional to tumour burden

ii) CEA - Colonic, Cholangio, Teratoma

Ca19-9 - Pancreatic, Cholangio

CA125 - Ovarian

AFP - HCC, Teratoma

b-HCG - Teratoma, Seminoma

Calcitonin - Medullary Thyroid

PSA- Prostate Adenocarcinoma

Chromogranin/ Urinary 5HIAA - Carcinoid

Placental Alk Phos - Seminoma

157
Q

i) Types of Wound Healing

ii) Types of scarring

A

i) Primary - Re-approximation of wound edges

Secondary - No direct closure allowing for granulation tissue to form over wound (VAC Dressings, Packing with kaltostat)

Tertiary - Delayed primary closure (re-approximation) with initial intentional leaving of wound open

ii) Hypertrophic - Does not extend beyond edges of initial wound

Keloid - Extends beyond edges of initial wound

158
Q

Stages of wound healing (6)

A

1) Haemostasis / Coagulation
2) Inflammation
3) Granulation (Fibroblasts, macrophages, epithelial cells)
4) Angiogenesis
5) Epitheliasation –> Fibroblast proliferation –> Wound contraction (myofibroblasts)
6) Maturation and remodelling (up to 1 year to beyond 1 year)

159
Q

Causes of impaired wound healing

A

Patient - Steroid use, age, diabetes, poor nutrition, hypoxia, other co-morbidities, Drugs

Pathology - Infection, Tumour,

Site - Pressure bearing sites, Radiotherapy,

Wound closure technique (tension on sutures), compromised blood supply (PVD)

160
Q

Describe the clotting cascade

A

Intrinsic Pathway-

XII -> XI-> IX -> VIII -> common pathway

Extrinsic Pathway-

VII

Common pathway

X -> V -> Thrombin -> Fibrin

161
Q

What is FISH

A

FLuorescent in situ hybridisation

  • Cytogenetic method of analysis allowing for the detection of mutagenic DNA
  • With reference to cancers it can help identify types of mutations associated with cancers and there for assess suitability for certain immunological treatments
162
Q

What is CRP

A

Capsular Polysaccharide - Reactive Peptide

Released from the liver in response to IL-6 secreted from macrophages/T Cells.

Function - Binds to surface of dead/dying cells to mark them for complement system

163
Q

Fever mechanism

A

Pyrogen –> PGE2 secretion –> acts on hypothalamus which increases “thermal set point” –> Thus causing various thermal regulating factors (shivering, adrenaline secretion, vasoconstriction)

164
Q

Types of omental tumours

A

Leiomyosarcomas, Fibrosarcoma, Liposarcoma, Haemangiopericytoma

165
Q

How are clots degraded

A

Plasmin is produced by the liver.

It is converted to Plasminogen by:

Urokinase, tissue plasminogen activator

Plasminogen breaks down fibrin

166
Q

How do Tyrosine Kinase inhibitors work

A

They are small molecule inhibitors:

Bring about their action by preventing the downstream signalling pathway.

Actions:

  • Allosteric binding of receptor domains
  • Competition for substrate (ATP)
  • Prevent maturation of the kinase domain proteins themselves
167
Q

Adhesive Capsulitis:

i) Presentation

ii) Pathophysiology

iii) Treatment

A

i) presentaiton -

I - freezing phase (insidious reduction in ROM and pain)

II - Frozen phase

ii) Inflammation of joint capsule followed by a chronic inflammatory and fibrotic phase

iii) Conservative - Physiotherapy

Medical - Analgaesia, Anti inflammatories, Intra-articular steroid injections, short term oral steroids

Intervention - External coroporeal shockwave therapy, Joint MUA, Capsule Release, Scalene block

168
Q

Define:

i) Sequestrum

ii) Involucrum

A

i) Sequestrum - Piece of dead bone within alive bone usually in the setting of osteomyelitis

ii) Involucrum - Piece of living bound surrounding dead bone usually in the setting of osteomyelitis

169
Q

Categories of biohazard

A

1- 4 Classification

1- Well known organisms that are not a threat to healthy humans

2- Mild diseases can be caused in healthy humans - Chicken Pox, Influenza

3- Severe/Fatal diseases can be caused in healthy humans but treatment/vaccination exists - TB, anthrax, malaria

4- Severe/Fatal diseases can be caused in healthy humans for which no treatment/vaccine exists - Ebola, Marburg, Mers, Sars, Coronavirus

170
Q

Steps for contact tracing

A

1 Contact Identification

Detailing patient 0s activitities can help elucidate who likely contacts can be (friends, colleagues, healthcare professionals)

2 Contact Listing

Contacts should be contacted:

  • Explained symptamtology
  • High risk may be quarantined
  • preventative measures

3 Contact Follow Up

  • Follow up for symptoms/ testing
171
Q

Serological Tests for TB

A

Interferon Gamma Assays:

  • Whole blood is taken and exposed to various TB Antgiens
  • Quantitative analysis of interferon gamma is conducted —> High levels are sensitive for TB

TB PCR

Antibody Detection Assays:

  • These tests depend on there being an active TB infection whereby anti-TB antibodies are being actively secreted
172
Q

Mechanism of paradoxical aciduria

A

Occurs in the context of metabolic alkalosis:

Hypovolaemia (vomiting, diarrhoea etc) leads to fluid and electrolyte losses.

Activation of RAAS (Hypovolaemia, hyponatraemia).

Increased Na+ Retention and K+ excretion

In the context of hypokalaemia, instead of K+ being excreted, H+ is excreted leading to acidic urine

173
Q

Causes of papilloedema

A

Primary - Idiopathic Intracranial Hypertension

Secondary -

Raised intracranial pressure

Space Occupying Lesion (Tumour, abscess)

Diffuse oedema (Hypoxia, Head injury, Toxins)

Haemorrhage (Sub arachnoid haemorrhage)

Venous sinus thrombosis (Cavernous)

Inflammation - Meningitis, encephalitis

174
Q

Oxygen Dissociation Curve

i) Causes of left shift

ii) Causes of right shift

A

i) Left Shift (INCREASED affinity for O2)

DECREASED - Co2, pH, 2-3 DPG, Temperature

ii) Right Shift (DECREASED affinity for O2)

Increased - CO2, pH, 2-3 DPG, Tempeature

175
Q

Abdominal Compartment Syndrome

i) What mmHg?

ii) Causes?

A

i) >20 mmHg

ii)

Retroperitoneal - AAA rupture, pancreatitis, Retroperitoneal bleeding, Retroperitoneal abscess

Intraperitoneal - Haemorrhage, AAA rupture, Bowel/gastric obstruction/dilation, pneumoperitoneum, abdominal packing, abscess, SIRS

Abdominal Wall - Burns, laparotomy closure under tension, abdominal binders,

Chronic - central obesity, pregnancy, ascites

176
Q

Describe the Hypothalamopituitary Axis

A

Hypothalamus (Blood enters via the superior hypophyseal artery):

Parvicellular neruones secrete neurotrophic hormones in hypothalamus into the superior hypophysealartery which travels in the portal vessels to the pituitary gland:

Gonadotrophin RH, Corticotrophin RH, Thyroid RH, Growth Hormone RH

Pituitary Gland:

Anterior (Adenohypophysis):

TSH, Growth Hormone, Lutenising Hormone, Follicle Stimulating Hormone, Adrenocorticotrphic Hormone, Prolactin

Posterior (Neurohypophysis):

Antidiuretic Hormone, Oxytocin

177
Q

i) Risk factors for nasopharyngeal carcinoma

ii) what type of cancer is it?

iii) What other differentials would you have?

A

i) Male

Age

Salt Cured Food

Eppstein Barr Virus

Family history

Alcohol

Smoking Tobacco

ii) Squamous cell carcinoma

iii) SCC, MALT-oma, Lymphoma, TB, Tonsillitis, Tonsillar Abscess

178
Q

Life span of :

Neutrophil

Lymphocyte

RBC

Platelet

A

Neutrophil - 7 Hours in blood (5 days in tissue)

Lymphocyte - Variable (Days to years)

RBC - 120 days

Platelet - 7-10 days

179
Q

Endometriosis:

i) Locations

ii) Histology

iii) Rx

A

Presence of ectopic endometrial tissue. Adenomyosis is the presence of endometrial tissue in the myometrium

RFs - FH, Early Menarche, Dysmenorrhoea, Menorrhagia,

i) Locations - Ovaries, Broad ligament, uterosacral ligament, colon, bladder

ii) Histology - Endometrial glands and stromal elements

iii) Rx - COCP, GnRH Analogue, Danazol

Surgery - Conservative / Radical

180
Q

Causes of obstructive jaundice

A

Intrahepatic

  • Hepatitis - Viral, Alcoholl, Drug Induced,
  • Cirrhosis
  • Drug induced stasis
  • PBC/ PSC
  • Malignancy
  • Infections

Extrahepatic

  • Malignancy
  • Stricture
  • Stone
  • SOD Dysfunction
  • Infections / Abscess (Histoplasma, Ascaris, Flukes)
  • PBC/PSC
181
Q

Enteroehepatic receycling

i) Method

ii) Why is it important

iii) What is bilirubin conjugated to?

A

i) Bile acids are secreted by the liver into the bile ducts and stored in the gallbladder. Secreted in bursts throughout the day in concjunction with mealtimes.

They are then re-absorbed by enterocytes in the terminal ileum enterring the portal circulation for re-secretion into the duodenum.

ii) - The liver is only capable of synthesising 3g of bile acids a day. Through cycline 24g of bile acids a day are excreted into the liver to cope with the 100g of fat the average person consumes.

- Downstream effects of bile acids (beyond the ileum) can contribute to steattorhoea, impaired water and electrolyte absorption

  • Important in absorption of fat soluble vitamins

iii) Conjugated to Glucoronic Acid by Glucoronyltransferase in the liver

182
Q

Explain the signs of obstructive jaundice

A

Icterus - Elevated conjugated bilirubin in blood deposits extracellularly.

Pale Stools - Conjugated bilirubin does not enter the intestine. Usually when it does it is broken down by bacteria to stercobilin which gives the stools their brown colour.

Dark Urine - Conjugated bilirubin accumulates in the blood and is excreted through the urine thus making it dark.

Itching - Bile Acids/Salts or Opioid release

183
Q

i) How do bile acid aid fat absorption?

ii) How much bile is produced a day?

A

i) Form Micelles - Hydrophilic layer outside and hydrophobic centre where the lipid is contained.

Provides a large surface area for the action of lipases

ii) 400-800ml

184
Q

i) What is a pseudoaneurysm?

ii) Management

A

i) A false aneurysm where an artery has been punctured:

  • Incomplete haemostatic plug
  • Extravasation of blood outside of artery leading to capsule formation

ii) Management:

Non - Surgical - Ultrasound guided compression, Endovascular Embolisation, Endovasular stenting

Surgical - Repair of artery +/- Bovine Patch closure

185
Q

Cholangiocarcinoma:

i) Type

ii) Where does it spread

A

i) Adenocarcinoma

ii) Liver, Stomach, Duodenum + Peritoneum

186
Q

Common Causes of Post Operative Bloody Diarrhoea

A

Ischaemic Colitis

Infective Colitis

Pseudomembranous Colitis

Ulceration

FIstulation

187
Q

Wet vs Dry Gangreen

A

Wet Gangrene - presence of bacteria in necrotic tissue -> high propensity for systemic spread

  • Venous Cause
  • Worse prognosis
  • unclear line of demarcation
  • commonly in bowel

Dry Gangrene - Purely caused by ischaemia to tissue

  • Arterial Cause
  • Better prognosis
  • Clear line of demarcation
  • commonly in limbs
188
Q

Crystal Arthropathies

A

Gout - Uric Acid (Negative birefringence)

Chondrocalcinosis - Calcium Pyrophosphate (Positive birefringence)

189
Q

Broadly outline pancreatic development

A

Pancreatic Development

The pancreas is formed from two buds from the foregut.

It is endodermal in origin

Ventral + Dorsal Pancreatic Buds join together to form the pancreas.

190
Q

What is TNF?

A

TNF is a pro-inflammatory cytokine released by macrophages involved in the acute phase response:

Induces phagocytosis

Chemoattractant for neutrophils

amongst other functions

191
Q

WHere is the vertebral venous plexus?

Why is it important?

A

Vertebral Venous Plexus - Is in the extradural space

Importance :

  • Provides alternative routes of venous drainage when there is Jugular/ IVC Compression
192
Q

What leads to cyst development in ADPKD?

A

Germ Line Mutation in PKD1/PKD2:

  • Regulates the morphology of epithelial cells
  • In PKD renal tubular cells replicate until they form sac
  • The sac fills with transepithelial secretions (Water / NaCl)

Secondary changes are seen in the kidney:

Fibrosis of the interstitium, THickening of the basement membrane, macrophage infiltration, Neovascularisation

leading to a bleeding propensity +

193
Q

Grossly describe phagocytosis

A

Pathogen is detected by immune cells (neutrophils via PAMP):

Neutrophils/Macrophages/ Monocytes encoutnering these pathogens bind them via recognising certain receptors (Mannose)

–> Phagocytosed and undergo apoptosis (release of granules that breakdown the microorganism in a cotnrolled manner –> Then cell fragmentation in a controlled manner)

–> These then begin to signal through cytokines to attract more immune cells (dendritic cells, neutroophils, monocytes)

—> Complement, CRP and other factors are involved in the phagocytosis of other

Dendritic Cells -> APCs. BRidge between innate and adaptive immunity

194
Q

Insulin effects

A

Increases GLUT4 Mediated glucose uptake

Glycogen Sythesis

Fatty Acid Synthesis

Protein Synthesis

195
Q

What is sign of Hertoghe?

A

Loss of lateral third eyebrow in hypothyroidism

196
Q

Management of pituitary tumours?

A

Observe

DA (cabergoline, bromicriptine) - If Prolactin Secreting

Octreotide - If GH producing

Surgery - Transphenoidal

197
Q

Types of Knot

A

Square Knot

Surgeon’s Knot

Granny Knot

198
Q

Variants of sciatic nerve

A

Usually - Inferior to piriformis

Sometimes:

Through Piriformis

Upper and lower portion go around priiformis

199
Q

What is a baker’s cyst?

A

Often related to degnerative disease of the knee.

Accumulation of synovial fluid in the gatrocnemio- semimembranosus bursa

200
Q

What is a choriocarcinoma?

A

Tumour usualy seen in women originating from the placenta (rarely testicle).

Trophoblastic tumour consisting of syncitotrophoblasts and expressing B HCg.

High Cure Rate in placenta - Treatment with methotrexate

Terrible cure rate when found in the testes

201
Q

Stages of heamatoma resolutsion

A

Hyperacute - Oxygenated Blood

Acute - Platelet plugging/aggregation stable. Blood is deoxyhemoglobin/mmethemoglobin

Subacute - Red Cell Lysis + expansion due to water being drawn in

Chronic - Phagoyctic Phase. White cell migration occurs and phagocytosis of lysed red cells etc.

202
Q

What is group and save / Cross Match

A

Group and Save:

Confirmation of patients blood group and presence of antibodies in their serum

Crossmatch:

Performed when issuing blood where a small amount of patient serum is mixed with the donor red cells to check for comaptibility

203
Q

Complications of resuscitation with IV Fluids?

A

Volume Overload

Hyperchloraemic Metabolic Acidosis

Hypokalaemia

Hypocalcaemia

Dilution Coagulopathy

204
Q

What is the borrman classification for gastric cancer?

A

Type I : Polypoid or Fungating

Type II : Ulcerated with elevated edges

Type III : Ulcerated with infiltration at edges

Type IV : Diffuse (linitis plastica)

205
Q

TNM Classification

A

Tumour

T0- No tumour

Tis - Carcinoma in situ

T1 - Invades mucosa/submucosa

T2 - Invades Musclaris Propria

T3 - Through Muscularis Propria

T4 - Invades Local structures

Nodes

N0 - No LN involvmenet

N1 - LN Involvement

Metastases

M0 - No Mets

M1 - Distant Mets

206
Q

i) Perforated PU - Mx options?

iii) Definitive Ulcer Surgery

A

i) Gastric Ulcer

Conservative - If barium swallow no evidence of contrast extravasation/not peritonitic than can watch and wait

Oversewing of Ulcer

ii) Duodenal Ulcer

Graham Patch repair

Modified Grahm Patch Repair

Cellen Jone’s Repair

iii) Definitive Ulcer Surgery:

If patient is stable - Vagotomy + Antrectomy

  • Highly Selective Vagotomy
  • Truncal Vagotomy + Pyloroplasty

- Excision of ulcer + Frozen Section + Bilroth Procedure

207
Q

How do the ‘caine’ local anaesthetics work?

A

They’re intraneuronal sodium channel blockers therefore preventing propagation of action potentials thus interfering with pain signal transmission

208
Q

Hypothermia

Causes

Complications - intraoperative / postoperative

A

Causes:

Preoperative Hypothermia

Co-Morbidities

Combined General + Local Anaesthetic

Long Operative time

Poor Cardiac Function

Complications:

  • Altered tissue perfusion ( due to increased affinity for oxygen) –> Impaired wound healing, Organ ischaemia

Platelet Dysfunction

Coagulopathy

Peripheral Vasoconstriction

Arrhyhthmias

Low Cardiac Output

ALtered Enzyme Function

Altered Drug Metabolism

209
Q

i) Genes associated with familial melanoma

ii) How does UV light cause cancer?

A

i) CDKN2A (p16 TS Gene)

CDK4 (Oncogene)

ii) Most data is correlatory:

UVB - thought to be the culprit leading to gain / loss of function mutations associated with melanocyte/keratinocyte proliferation

210
Q

WHy do B12 and FOlate deficiency lead to macrocytic anaemia?

A

There is an inhibition of DNA synthesis –> Arresting of maturation of the RBCS

This leads to larger RBCs as they are not completely mature

211
Q

Functions of Calcium

A

i) Muscle Contraction
ii) Pre-Synaptic Neurotransmitter Release
iii) Cardiac Myocytes
iv) Bone Mineralisation
v) Coagulation

212
Q

Definition of false localising sign

A

In the context of neurology are signs that are distant from the expected anatomical locus.

213
Q

Calculate Sensitivity / Specificity

A

Sensitivity :

True Postive / (True Positive + False Negative)

Specificity:

True Negative / (True Negative + False Positive)

214
Q

Define: Pleomorphism

A

Pleomorphism refers to the variability in cell: Size, Shape, Staining of cells and their nuclei

215
Q

Complications of immobility

A

Disuse Atrophy of Muscles

Disuse Osteoporosis (Reduced mechanical stress leads to osteoclast mediated bone resorption)

Flexion Contractures

Pressure Sores

Increased risk of other infections

Reduced muscle mass/ Increased fat

216
Q

Causes of carpal Tunnel Syndrome

A

Endocrine - Diabetic Mononeuropathy, Hypothyroidism, Acromegaly

Systemic - pregnancy, Oedema

Bone - Lunate dislocation, Colles Fracture

217
Q

Causes of chronic rectal bleeding

A

Infectious - Amoebiasis, Intestinal SPirochetosis, Bacilliary Dystnery

Diverticulosis (right sided)

Angiodysplasia

Inflammatory - Inflammatory Bowel Disease

Malignancy

218
Q

Vicryl - What is it? What is it made from? When is it absorbed?

Benefits of braided over non braided

A

Vicryl:

Synthetic, Braided, Absorbable

Polyglycolic Acid

Approximately 60 days

Benefit of braided:

  • Good knots, Good Handling
  • Soft and pliable
  • Good tensile strength

Disadvantages:

  • Tissue Trauma
  • Infection risk
219
Q

i) Synthetic Nonabsorbable Monofilament Sutures

ii) LA with + without adrenaline

A

i) Prolene, Nylon

ii) With:

  • Improves length of time of action
  • Permits a larger dose to be used if warranted (reduced toxicity)
  • Reduced bleeding

Without:

  • Extremities
  • May be dangerous if CVD, HTN
  • May be dangerous if injected into a blood vessel directly
220
Q

Risk factors for hypertrophic / keloid scarring?

A

Site - Mandible, Posterior neck, sternum, earlobe

Trauma

Infection

High Tension Areas

Keloid - Ethnicity

221
Q

Causes of post transplant lymphoproliferative disease

A

Immunosuppression leading to CMV/EBV infection in patients who have had solid organ transplants

Mx - Reduce Immunpsuppresion, IVIG, Monoclonal Antibodies against B Cells (Rituximab),

222
Q

What are pleural plaques?

A

Deposits of collagen and fibrosis that may/may not be calcified.

Associated with Chronic Asbesos exposure

223
Q

Causes of gastric outlet obstruction

Metabolic abnormality

Why are they hyponatraemic?

A

Benign - Peptic Ulcer Disease

Crohn’s Disease

Polyps

Pyloric Stenosis

Pancreatic Pseudocyst

Bezaor

Diabetic Gastroparesis

Malignant -

Pancreatic Cancer

Gastric Cancer

Cholangiocarcinoma

Hypokalaemic Hypochloraemic Metabolic Alkalosis

Hyponatraemic secondary to ADH secretion leading to water retention.

224
Q

Pancreas:

Embryology (again)

Ductal Drainage

Which parts retropertioneal

A

Embyology. Proliferation of teh ventral and doral panreatic bud + the duodenal bud (endodermal origin)

Ductal Drainage:

Major Pancreatic Duct - body,, tail + part of head

Accessory Pancreatic Duct - Part of head and uncus

Tail + uncinate are intraperitoineal. Rest is retropertioneal

225
Q

Causes of positive trendelenberg test

A

SGN Palsy/ Damage

Hip Fracture

Gluteual muscle weakness

Radiculopathy/ Disc Herniation

Hip Dislocation

226
Q

i) Structure at risk in supracondylar femur fracture

ii) Causes of mass in popliteal fossa

A

i) Popliteal Artery (Deepest structure)

ii)

Popliteal Vein Varicosity

popliteal Artery Aneurysm

Baker’s Cyst - Other tendon related bursas

Neuroma

227
Q

RFs for oesophageal cancer:

SCC

Adenocarinoma

A

SCC: Tobbaco, Alcohol, Genetic, Nitrosamine, Achlasia, HPV, radiation

ADC: Barret’s, GORD, Tobacco, FH, H Pylori

228
Q

Sciatic Nerve Surface Anatomy

A

Midway between the greater trochanter and the ischial tuberosity under the cover of gluteus maximus

229
Q

How do glucocorticoids mediate effects?

A

Cytoplasmic Glucocorticoid Receptor:

On binding to steroid it enters the nucleus and causes gene transcription at many points which brings about the many and varied effects of steroids

230
Q

How does urinary alkalanisation work in the context of rhabdomyolysis?

A

Attempts to alkalanise the urine to help prevent the formation of casts and damage to tubules.

231
Q

What does lymph drain?

What does lymph system do?

A

Lymphatic Vessels drain the interstitial fluid to regional lymph nodes.

Lymph:

Absorbs fat

Adaptive Immune system - recognising foreign antigens and help stimulating a clonal resposne to the antigen to clear it

232
Q

Where else might you find parathyroid glands?

A

Thymus (also from 3rd pharyngeal arch)

233
Q

What is in the vertebral canal beneath L1?

Importance of the venous plexus from question above?

A

CSF, FIlum Terminale, Cauda Equina, Paravertebral venous plexus

Paravertebral venous plexus:

  • Important as a route of metastasis
  • Site of collateralisation in IVC Obstruction
234
Q

Why erythema surrounding skin cancers?

A

Neoangiogenesis

Reactive Capillary Formation

Immune cells - lymphocytes causing local vasodilation

235
Q

Echo findings in endocarditis

A

Vegitation

Dehiscence of prosthetic valves

Regurgitation

236
Q

how does EBV cause lymphoma

A

EBV infects B Lymphocytes –> Can cause mutations within lymphocytes leading to loss of function/gain of function mutations

237
Q

What is the coeloemic metaplasia thoery

A

Respect to Endometriosis

Coleoemic epithelium lines abdominal organs and in embryogenesis is the precursor to endometrium.

It is thought that this can undergo metaplasia and become endometrial tissue

238
Q

Pott’s Fracture

Trimalleolar Fracture

A

Pott’s Fracture - Bimalleolar Fracture

Trimalleolar Fracture - Bimalleolus + Posterior Distal Tibia

239
Q

Phases of fracture healing

A

Haemorrhage + Stabilisation

Granulation - Inflammatory Cells phagocytose blood and dead bone

Callus/ Woven bone Formation - Proliferation of osteocytes and osteoblasts from osteoid progenitor cells in a haphazard manner. Angiogenesis also occurs

Lamellar Bone formation and fracture remodelling - Occurs over a long period of time in response to shear stress and load.

240
Q

Sickle Cell Disease

Genetics

Mx

Surgicl Mx

A

Genetics - Chr 11. AR mutatuion in gene encoding Beta Haemoglobin

1x Trait

2x Diseae

Mx - Genetic Counselling, Keep hydrated, Pain killers when having crises, Prophylactic antibioitcs (Hyposlplenism)

Surgical Problems:

Avascular Necrosis

Gallstones

MRCS Part B (11 decks)

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