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
**What illnesses does Streptococcus Pyogenes Cause** **What virulence factors does strep pyogenes possess** **What systemic complications of streptococcal infections are there (non-invasive)**
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
26
**Different types of prion disease**
Creutzfeld Jacob Disease vCJD Kuru Fatal Familial Insomina Gerstmann- Straussler- Scheinker Syndrome
27
28
What governs interstitial fluid accumulation? Broad causes of oedema
**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)
29
**Respiration:** i) Where is respiration controlled? ii) What is the Hering-Bruer Reflex? iii) Where does CO2 exert its effect on the respiratory system?
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
30
**MOA Dopexamine** **Noradrenaline vs adrenaline therapeutically**
**Adrenergic Agonist -** B2 ( D1 + D2 ) Prevents reuptake of norepinephrine **Adrenaline -** B1 Predominance. Therefore mainly cardiac effects **Noradrenaline -** Alpha agonist - therefore mainly pressor effects
31
**Transplants:** **i) Define a transplant** **ii) What is HLA?**
**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.
32
**Stages of fracture healing:**
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
33
**Common sites of intra-abdominal collection?**
**Morrison's Recess (Hepatorenal)** - Most sensitive in supine patient Paracolic Gutter Between loops of bowel **Pelvis:** Rectovesicular Pouch Pouch Of Douglas
34
**Meckel's Diverticulum?** What is it Associated pathology
**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
35
**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?**
**1st/2nd duodenum -** Gastroduodenal Artery **3rd/4th duodenum -** Pancreaticoduodenal Artery **Lesser curve stomach -** Left Gastric Artery
36
**Bowel Obstruction:** **Large vs Small** X Ray findings Causes Presentation
37
**Decribe cause of pattern of pain in appnendix**
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)
38
**What is the terrible knee injury triad?**
MCL Medial Meniscus ACL
39
**i) Horner's Syndrome Triad** **ii) Causes of Horner's Syndrome**
**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
40
**i) Clinical Features of an orbital blow out fracture?** **ii) Radiological Features of orbital blow out fracture?**
**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
41
**What does the image show - describe pathology**
**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)
42
**What are the causes of Thoracic Outlet Syndrome?** **How do the subclavian artery, vein and brachial plexus relate to the first rib?**
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)
43
**Amylodiosis:** **i) What is amyloidosis** **ii) Histological features** **iii) Types of amyloid protein which sites they favour** **iv) Diagnosis** **v) Rx**
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
44
**Where can isolates of amyloid tissue be found in the body?**
Larynx Urinary Tract Aorta Pituitary Gland Thyroid ( Medullary Cell Carcinoma)
45
**i) Define Aneurym** **ii) Causes** **iii) Size of normal infrarenal aorta vs aneurysmal** **iv) Pathogenesis of AAA** **v) RFs for AAA** **vi) Aneurysm Cx**
**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
46
**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**
**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
47
i) **Define: Aortic Dissection** ## Footnote **ii) Aortic Dissection diseae Ax** **iii) Classifiactions**
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)
48
**i) Causes of Aortic Stenosis** **ii) Pathogenesis of the main variety** **iii) Triad** **iv) Signs** **v) Ix** **vi) Mx** **vii) Causes of IE**
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
49
**Appendicitis:** i) ? Obturator Sign ii) Describe pain seminology iii) Scoring systems iv) Common causes of obstructed lumen v) cx of appendicitis
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
50
**Ascites:** **i) Causes**
**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
51
**Describe starling equation for movement across capillary membrane**
**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
52
**Classify Causes of pitting oedema**
**Increased Hydrostatic Pressure:** Heart Failure, Hypervolaemia, Venous Insufficiency, Pregnancy **Reduced Oncotic Pressure:** Hypoalbuminaemia (nephrotic syndrome, malnutrition, protein losing enteropathy, cirrhosis)
53
**Atherosclerosis:** **i) Definition** **ii) Pathological Process** **iii) RFs**
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
54
**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**
**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
55
**i) Triple Assessment**
**i) Triple Assessment:** Examination Imaging - USS Abdomen / Mammogram Tissue Biopsy - Core Biopsy/FNA
56
**Phylloides Tumour:** **i) Presentation** **ii) Histology** **iii) Treatment**
**i)** **Present -** Large tumours in 40-50s **ii) Histology -** Overgrowth of stromal tissue **iii) Treatment -** WLE / Mastectomy
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**Gynaecomastia** **i) Causes**
**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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**Causes of breast discharge**
**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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**Bladder Cancer:** **i) RFs for TCC** **ii) RFs for SCC** **iii) Other bladder cancers** **iv) Ix** **v) Surgical Mx** **vi) Non- systemic adjuncts**
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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**Bone Tumors:** **i) Benign types** **ii) Malignant types** **iii) Common bone mets**
**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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**X Ray appearance:** **i) Onion skin appearance & who does it generally effect/presentation characteristics**
**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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**Osteosarcoma** **-** Sunburst appearance
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**i) Investigations for ?bone tumour** **ii) When to operate on a benign bone tumour?** **iii) Mx of malignant bone tumours**
**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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**What are the subtypes of surgical resections**
**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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**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?**
**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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**Abdo X Ray Method**
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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**i) Most common causes of LBO** **ii) Most common causes of SBO**
i) Tumour, adhesions, Diverticular strictures, Sigmoid / caecal volvulus ii) Adhesions, hernias, Crohn's, Tumour
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**Hereditary Polyposis Syndromes:** **Names** **INheritance Patterns** **Cancer Risks**
**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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**i) Colonic Cancer Classifications** **ii) Adenoma - Carcinoma Sequence** **iii) Common CRC Metastases** **iv) Types of liver resection**
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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**Layers of the bowel wall**
Mucosa Submucosa Meisner's Plexus Muscularis Propriate Longitudinal Muscle Auerbach's Plexus Circular Muscle Serosa
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# Define: **i) Adenocarcinoma** **i) Neoplasm**
**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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**Hepatic Tumours**
**Benign -** Haemangioma, Focal nodular hyperplasia, Adenoma **Malignant -** Primary ( HCC, Cholangiocarcinoma, Angiosarcoma, hepatoblastoma) **Mets.**
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# Define: **i) Absces** **ii) Pus** **iii) Cyst** **iv) Sinus** **v) Stoma**
**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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# Define: ## Footnote **vi) Aneurysm** **vii) Diverticula**
**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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# Define: ## Footnote **viii) Thrombus** **IX) Clot** **X) Embolus**
**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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# Define: ## Footnote **XI) Necrosis** **XII) Hypersensitivity reactions** **XIII) Polyp**
**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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# Define: ## Footnote **XIV) Hyperplasia** **XV) Hypertrophy** **XVI) Hamartoma** **XVII) Metaplasia** **XVIII) Dysplasia**
**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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**Proportion of thyroid cancers hereditary:** **i) Medullary** **ii) hurthle cell** **iii) Follicular**
**i) Medullary - 25% (MEN 2a/2b. Familial Med. Thyr. Cancer)** **ii) hurthle cell - 7%** **iii) Follicular - 7%**
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**Cytological Classification of thyroid nodules**
Benign Indeterminate Malignant Inadequate Specimen
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**Thyroid Cancer:** **Types**
**Medullary** **Follicular** **Papillary (85%)** **Anaplastic (1%)**
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**What is tertiary hyperparathyroidism**
Development of autonomous PTH secreting nodule in patient with previous secondary hyperparathyroidism
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**Causes of hypoparathyroidism**
Idiopathic/autoimmune Radioidoine treatment Thyroidectomy
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**Primary vs Secondary Hyperalodsteronism**
**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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**i)Causes of cholangiocarcinoma** **ii) Ix for cholangiocarcinoma**
**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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**i) Bacteria commonly found in bile** **ii) Suitable antibiotic cover**
**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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**Necrotising Fascitis:** **i) Clinical Presentation** **ii) underlying pathology** **iii) Types** **Iv) Management of post op wound NF**
**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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**i) Indications for heart transplant** **ii) Donor Criteria**
**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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**i) Grossly what causes GVHD** **ii) Cancers associated with HIV** **iii) Minimising risk when operatiing on HIV +ve patients**
**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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H Pylori ## Footnote **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**
**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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**i) Which Cells produce Gastric Acid?** **ii) What is dumping syndrome**
**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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**i) Risk Factors for Gastric Adenocarcinoma** **ii) Two broad categories of Gastric Adenocarcinoma**
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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**Calcium.** **i) Where are PTH/Calcitonin Produced?** **ii) What does vitamin D do?** **iii) How do surgeons ensure they have removed the parathyroid glands?**
**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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**Types of hypersensitivity reaction**
**+ ?Type V -** Formulation of stimulatory antibodies
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**Type 4 Hypersensitivity Reaction:** **Time-Frame?**
It is a delayed reaction that often takes 48-72 hours to manifest. Caused by T Cells
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**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?**
**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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**Types of immune response to pathogen?**
**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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**i) What are the stages of acute inflammation?** **ii) Some chemical inflammatory mediators** **iii) Difference in inflammatory cells in chronic inflammation**
**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
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# Define: **i) Granuloma** **ii) Granulomatous Inflammation** **iii) Classify Granulomas**
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
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**IBD:** **i) Most commonly quoted pathogenesis** **ii) Extra Intestinal Manifestations**
**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
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**i) Define naevus** **ii) Main Types of Melanoma** **iii) RFs for melanoma**
**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
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**i) Characteristics of Melanoma** **ii) Type of biopsy for suspected melanoma** **iii) Classification and recommended margin**
**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**
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# Define + Locate + Ix/Mx : **i) Branchial Cyst** **ii) Thyroglossal cyst** **iii) Dermoid Cyst** **iv) Sebaceous Cyst**
**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)**
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**i) Define Ludwig's Angina**
**i)** Cellulitis of cervical/floor of mouth soft tissues **usually** secondary to dental infection. - Require resucitation, airway observation/management, antibiotics +/- surgery
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## Footnote **i) Cystic Hygroma - Define + Mx** **ii) Pharyngeal Pouch - Define + Mx**
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
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**What to do when you see neck lump?**
History ENT Exam FNA Imaging
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**Types of necrosis**
**Coagulative** - most common **Caseous -** TB **Liquefactive -** Brain **Gangrenous -** Wet/Dry **Fat** **Necrosis**
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# Define: **i) Necrosis** **ii) Apoptosis** **iii) Outline differences between apoptosis and necrosis**
**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.
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**General spread routes of carcinoma vs sarcoma** **Which thyroid cancer variant spreads haematogenously?**
**Carcinoma -** spreads by lymphatics **Sarcoma -** Spreads haematogenously **Follicular thyroid cancers spread haematogenously**
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**Key differences between benign and malignant neoplasms**
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**Examples of hyperplasia and hypertrophy**
**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
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**Rheumatic Fever:** **i) What is it?** **ii) What type of hypersensitivity reaction?** **iii) Criteria?**
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**
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**i) Diagnosis of infective endocarditis** **ii) Why is it hard to treat?** **iii) What to do pre-op with IE patients?**
**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
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**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**
**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**
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**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**
**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)
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**i) Pain history with gastric vs duodenal ulcers** **ii) Cx of PUD** **iii) PUD aetiology**
**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**
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**i) Bilroth Operations** **ii) Vagotomy purpose**
**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
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**i) Polyp Classification** **ii) Polyp complications**
**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
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**Any medications reducing number of polyp in familial polyposis ?**
**Celecocoxib - COX2 NSAID** **Sulindac - A non COX NSAID** Both reduce the numbers and size of polyps
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i) Define: Dysplasia ii) Define: Metastasis
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
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**BPH:** **i) Aetiology** **ii) Symptoms** **iii) Work-up** **iv) Mx** **v) What is PSA?**
**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
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**i) Prostate cancer grading** **ii) Prostate cancer treatment** **iii) Ix** **iv) PSA monitoring post-prostatectomy**
**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
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**TURP Complications**
Bleeding, UTI, Urinary Retention Retrograde ejaculation Urinary incontinence Urethral strictures Erectile Dysfunction TURP Syndrome
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**DDx for Voiding/Storage Sx**
**Bladder Outflow Obstructions** Prostate - BPH/Ca, Urethral Stricture, Urethral sphincter dysynergia **Bladder Dysfunction** Oversensitvity, detrussor overactivity, low detrussor contractility
124
125
**Difference between :** **Staging and Grading**
**Staging -** Assessment of size and spread of tumour **Grading -** Histological assessment of level of cellular differentiation
126
**Complications of ureteric stones**
i) They may not pass ii) Hydroureter + hydronephrosis iii) Infection iv) Haematuria
127
**i) Why do renal calculi form?** **ii) Types and incidence of calculi**
**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
**How are protues mirablis + helicobacter pylori similar?**
Both secrete urease enzyme which cleaves urea to ammonia
129
**Differences between smooth muscle and skeletal muscle**
**Smooth -** Non- Striated Uninucleated Calmodulin (Calcium Binding Protein) Absence of T Tubules **Skeletal-** Striated Multinucleated Troponin (Calcium binding protein) T Tubules
130
**i) Micturition Control** **ii) Spinal injury above T12** **iii) Spinal injury below T12**
**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
**i) Define AKI** **ii) What is dysequilibrium syndrome**
**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
**Side effects associated with:** **i) Tacrolimus** **ii) Cyclosporin** **iii) Azathioprine** **iv) Steroids** **Specific to immunologics**
**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
**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**
**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
**Complications from renal transplant**
**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
**i) Cryptorchidism** - define + associated RFs ## Footnote **ii) Where are undescended testes usually found?** **iii) Mx**
**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
**i) Testicular Cancer Types** **ii) Radiotherapy in testicular cancer** **iii) Where do they tend to metastasise to?** **iv) Lymphatic Drainage**
**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
**Basal Cell Carcinomas** **i) Classical description** **ii) Mx** **iii) What is bowen's disease**
**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
**i) Cytological Features of malignancy** **ii) Histological Features of malignancy** **iii) Pros and Cons of Cytology** **iv) Pros and cons of histology**
**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
**i) Spleen Functions** **ii) Normal Weight/Size** **iii) Splenic Injury Grading** **iv) Indications for splenectomy** **v) Complications of splenectomy** **vi) Which vaccines**
**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
**Causes of splenectomy**
**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
**Duke's Staging**
A - Bowel Wall (**5YS 95%)** B - Through Bowel Wall **(65-75%)** C - Lymph Node Mets (**30-40%)** D - Distant Mets (**5-10%)**
142
**Groin Lump DDx**
**Skin -** Sebaceous Cyst **Subcutaneous -** Lipoma, Lymph Node **Neurovascular -** Saphena Varix, Pseudoaneruysm, Neuroma **Bowel -** Hernia **Other -** Ectopic Testes, Groin Abscess
143
**i) Define: Teratoma** **ii) How is a teratoma linked to gynaecomastia**
**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
**i) Define: Ulcer** **ii) RFs for PUD** **iii) How does h pylori cause ulceration?** **iv)**
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
**Ix of painless haematuria**
**History + Examination + PR** **Urine -** MC&S, Cytology **Bloods -** Hb, Renal Function Testing, PSA **US/TRUS +/- Biopsy** **CT pre/post contrast** **Cystoscopy +/- biopsy**
146
**Renal Cancers** **i) Types** **ii) what is VHL** **iii) Treatment for bladder CIS** **iv) Describe ileal conduit**
**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
**Where is b12 absorbed?**
**Terminal ileum:** - Therefore effected in crohn's disease/ UC (backwash ileitis)/ Ileal resections Deficiency can cause: - Macrocytic anaemia, peripheral neuropathy, SACD
148
**What secretes:** **i) Gastric Acid** **ii) Gastrin** **iii) pepsinogen** **iv) mucous** **v) what inhibits gastric acid secretion**
**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
**MOA of PPI**
Irreversible blocker of **H+/K+ ATPase** **pump** on parietal cells
150
i) 1st line imaging for suspected perforation ii) Mx of bleeding DU
**i) ERECT CXR** **ii) A-E** **IV PPI** **UGI Endoscopy +/-** Injection/ coagulation/ clipping **Surgery -** Underrunning of the bleeding artery and perforation
151
**Gastric Cancer Metastasis**
**Lymphatic -** Local lymphatics, Supraclavicular LNs (Virchow's) **Direct -** Omentum, Pancreas, Diaphragm, Duodenum, Colon **Haematogenous -** Lung, liver
152
**What is virchow's triad?**
**Altered Flow** - stasis/ turbulence **Altered Constituents** - hypercoaguable - infection/platelets/RBCs/drugs AntithrombinIII/ Protein C/S Deficiency pregnancy, trauma, surgery **Vessel wall** - endothelial injury
153
**Thyroid Cancer:** **i) Presentation** **ii) Classify thyroid tumours** **iii) Investigating thyroid masses in clinic**
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
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**MEN**
**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
**TB** **i) What are mycobacterium** **ii) Atypical mycobacterium** **iii) What is miliary TB?** **iv) Diagnosis**
**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
**i) Define: Tumour Marker** **ii) Examples**
**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
**i) Types of Wound Healing** **ii) Types of scarring**
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
**Stages of wound healing (6)**
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
**Causes of impaired wound healing**
**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
**Describe the clotting cascade**
**Intrinsic Pathway-** XII -\> XI-\> IX -\> VIII -\> common pathway **Extrinsic Pathway-** VII **Common pathway** X -\> V -\> Thrombin -\> Fibrin
161
**What is FISH**
**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
**What is CRP**
**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**
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**Fever mechanism**
Pyrogen --\> PGE2 secretion --\> acts on hypothalamus which increases "thermal set point" --\> Thus causing various thermal regulating factors (shivering, adrenaline secretion, vasoconstriction)
164
**Types of omental tumours**
Leiomyosarcomas, Fibrosarcoma, Liposarcoma, Haemangiopericytoma
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**How are clots degraded**
**Plasmin** is produced by the **liver**. It is **converted** to **Plasminogen** by: Urokinase, tissue plasminogen activator **Plasminogen** breaks down fibrin
166
**How do Tyrosine Kinase inhibitors work**
**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
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**Adhesive Capsulitis:** **i) Presentation** **ii) Pathophysiology** **iii) Treatment**
**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
# Define: **i) Sequestrum** **ii) Involucrum**
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
**Categories of biohazard**
**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
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**Steps for contact tracing**
**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
**Serological Tests for TB**
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
**Mechanism of paradoxical aciduria**
**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
**Causes of papilloedema**
**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
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**Oxygen Dissociation Curve** **i) Causes of left shift** **ii) Causes of right shift**
**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
**Abdominal Compartment Syndrome** **i) What mmHg?** **ii) Causes?**
**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
**Describe the Hypothalamopituitary Axis**
**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
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**i) Risk factors for nasopharyngeal carcinoma** **ii) what type of cancer is it?** **iii) What other differentials would you have?**
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**
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**Life span of :** **Neutrophil** **Lymphocyte** **RBC** **Platelet**
**Neutrophil - 7 Hours in blood (5 days in tissue)** **Lymphocyte - Variable (Days to years)** **RBC - 120 days** **Platelet - 7-10 days**
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**Endometriosis:** **i) Locations** **ii) Histology** **iii) Rx**
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
**Causes of obstructive jaundice**
**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
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**Enteroehepatic receycling** **i) Method** **ii) Why is it important** **iii)** **What is bilirubin conjugated to?**
**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
**Explain the signs of obstructive jaundice**
**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
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**i) How do bile acid aid fat absorption?** **ii) How much bile is produced a day?**
**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**
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**i) What is a pseudoaneurysm?** **ii) Management**
**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
**Cholangiocarcinoma:** **i) Type** **ii) Where does it spread**
**i) Adenocarcinoma** **ii)** Liver, Stomach, Duodenum + Peritoneum
186
**Common Causes of Post Operative Bloody Diarrhoea**
Ischaemic Colitis Infective Colitis Pseudomembranous Colitis Ulceration FIstulation
187
**Wet vs Dry Gangreen**
**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
**Crystal Arthropathies**
**Gout - Uric Acid** (Negative birefringence) **Chondrocalcinosis** **- Calcium Pyrophosphate** (Positive birefringence)
189
**Broadly outline pancreatic development**
**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
**What is TNF?**
TNF is a pro-inflammatory cytokine released by macrophages involved in the acute phase response: Induces phagocytosis Chemoattractant for neutrophils amongst other functions
191
**WHere is the vertebral venous plexus?** **Why is it important?**
**Vertebral Venous Plexus -** Is in the extradural space **Importance :** - Provides alternative routes of venous drainage when there is Jugular/ IVC Compression
192
**What leads to cyst development in ADPKD?**
**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
**Grossly describe phagocytosis**
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
**Insulin effects**
Increases GLUT4 Mediated glucose uptake Glycogen Sythesis Fatty Acid Synthesis Protein Synthesis
195
**What is sign of Hertoghe?**
Loss of lateral third eyebrow in hypothyroidism
196
**Management of pituitary tumours?**
**Observe** **DA (cabergoline, bromicriptine) -** If Prolactin Secreting **Octreotide** - If GH producing **Surgery -** Transphenoidal
197
**Types of Knot**
Square Knot Surgeon's Knot Granny Knot
198
**Variants of sciatic nerve**
**Usually -** Inferior to piriformis **Sometimes:** Through Piriformis Upper and lower portion go around priiformis
199
**What is a baker's cyst?**
Often related to degnerative disease of the knee. Accumulation of synovial fluid in the gatrocnemio- semimembranosus bursa
200
**What is a choriocarcinoma?**
**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
**Stages of heamatoma resolutsion**
**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
**What is group and save / Cross Match**
**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
**Complications of resuscitation with IV Fluids?**
**Volume Overload** **Hyperchloraemic Metabolic Acidosis** **Hypokalaemia** **Hypocalcaemia** **Dilution Coagulopathy**
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**What is the borrman classification for gastric cancer?**
**Type I :** Polypoid or Fungating **Type II :** Ulcerated with elevated edges **Type III :** Ulcerated with infiltration at edges **Type IV :** Diffuse (linitis plastica)
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**TNM Classification**
**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
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**i) Perforated PU - Mx options?** ## Footnote **iii) Definitive Ulcer Surgery**
**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
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**How do the 'caine' local anaesthetics work?**
They're intraneuronal sodium channel blockers therefore preventing propagation of action potentials thus interfering with pain signal transmission
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**Hypothermia** **Causes** **Complications - intraoperative / postoperative**
**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
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**i) Genes associated with familial melanoma** **ii) How does UV light cause cancer?**
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
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**WHy do B12 and FOlate deficiency lead to macrocytic anaemia?**
There is an inhibition of DNA synthesis --\> Arresting of maturation of the RBCS This leads to larger RBCs as they are not completely mature
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**Functions of Calcium**
i) Muscle Contraction ii) Pre-Synaptic Neurotransmitter Release iii) Cardiac Myocytes iv) Bone Mineralisation v) Coagulation
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**Definition of false localising sign**
**In the context of neurology are signs that are distant from the expected anatomical locus.**
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**Calculate Sensitivity / Specificity**
**Sensitivity :** **True Postive / (True Positive + False Negative)** **Specificity:** **True Negative / (True Negative + False Positive)**
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**Define: Pleomorphism**
**Pleomorphism refers to the variability in cell: Size, Shape, Staining of cells and their nuclei**
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**Complications of immobility**
**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**
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**Causes of carpal Tunnel Syndrome**
**Endocrine -** Diabetic Mononeuropathy, Hypothyroidism, Acromegaly **Systemic -** pregnancy**,** Oedema **Bone -** Lunate dislocation, Colles Fracture
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**Causes of chronic rectal bleeding**
**Infectious** - Amoebiasis, Intestinal SPirochetosis, Bacilliary Dystnery **Diverticulosis (right sided)** **Angiodysplasia** **Inflammatory -** Inflammatory Bowel Disease **Malignancy**
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**Vicryl - What is it? What is it made from? When is it absorbed?** **Benefits of braided over non braided**
**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
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**i) Synthetic Nonabsorbable Monofilament Sutures** **ii)** **LA with + without adrenaline**
**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
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**Risk factors for hypertrophic / keloid scarring?**
**Site -** Mandible, Posterior neck, sternum, earlobe **Trauma** **Infection** **High Tension Areas** **Keloid - Ethnicity**
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**Causes of post transplant lymphoproliferative disease**
**Immunosuppression** leading to CMV/EBV infection in patients who have had solid organ transplants **Mx -** Reduce Immunpsuppresion, IVIG, Monoclonal Antibodies against B Cells (Rituximab),
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**What are pleural plaques?**
**Deposits of collagen and fibrosis** that **may/may not** be **calcified.** **Associated with Chronic Asbesos exposure**
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**Causes of gastric outlet obstruction** **Metabolic abnormality** **Why are they hyponatraemic?**
**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.
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**Pancreas:** **Embryology (again)** **Ductal Drainage** **Which parts retropertioneal**
**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**
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**Causes of positive trendelenberg test**
**SGN Palsy/ Damage** ## Footnote **Hip Fracture** **Gluteual muscle weakness** **Radiculopathy/ Disc Herniation** **Hip Dislocation**
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**i) Structure at risk in supracondylar femur fracture** **ii) Causes of mass in popliteal fossa**
i) Popliteal Artery (Deepest structure) ii) **Popliteal Vein Varicosity** **popliteal Artery Aneurysm** **Baker's Cyst - Other tendon related bursas** **Neuroma**
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**RFs for oesophageal cancer:** **SCC** **Adenocarinoma**
**SCC:** Tobbaco, Alcohol, Genetic, Nitrosamine, Achlasia, HPV, radiation **ADC:** Barret's, GORD, Tobacco, FH, H Pylori
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**Sciatic Nerve Surface Anatomy**
Midway between the greater trochanter and the ischial tuberosity under the cover of gluteus maximus
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**How do glucocorticoids mediate effects?**
**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
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**How does urinary alkalanisation work in the context of rhabdomyolysis?**
**Attempts to alkalanise the urine to help prevent the formation of casts and damage to tubules.**
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**What does lymph drain?** **What does lymph system do?**
**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
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**Where else might you find parathyroid glands?**
**Thymus** (also from 3rd pharyngeal arch)
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**What is in the vertebral canal beneath L1?** **Importance of the venous plexus from question above?**
**CSF, FIlum Terminale, Cauda Equina, Paravertebral venous plexus** **Paravertebral venous plexus:** - Important as a route of metastasis - Site of collateralisation in IVC Obstruction
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**Why erythema surrounding skin cancers?**
Neoangiogenesis Reactive Capillary Formation Immune cells - lymphocytes causing local vasodilation
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**Echo findings in endocarditis**
Vegitation Dehiscence of prosthetic valves Regurgitation
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**how does EBV cause lymphoma**
EBV infects B Lymphocytes --\> Can cause mutations within lymphocytes leading to loss of function/gain of function mutations
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**What is the coeloemic metaplasia thoery**
**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
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**Pott's Fracture** **Trimalleolar Fracture**
**Pott's** **Fracture -** Bimalleolar Fracture **Trimalleolar Fracture -** Bimalleolus + Posterior Distal Tibia
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**Phases of fracture healing**
**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.
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**Sickle Cell Disease** **Genetics** **Mx** **Surgicl Mx**
**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