Pathophysiology Flashcards
Gallstones
1) Types
2) Risk Factors
3) Indications for MRCP
4) Indications for ERCP
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
1) Indications for cholecystectomy
2) Timing of cholecystectomy
3) Complications of Choleycstectomy
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
1) Goals of perioperative analgaesia
2) “Preventative”
3) Post operative
4) Describe WHO Pain ladder
5) Complications of PCA
6) Pain assessment scales
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)
Describe the main targets of anti-emetics and give some names
M1 (muscaranic) - scopolamine, hyoscine
D2 (Dopaminergic) - Domperidone, prochlorperazine
H1 (Histamine) - Promethazine, Cyclizine
5 HT3 (Serotonin) - Ondansetron
NK1 (Substance P) -
GCs - Dexamethasone
1) Purpose of Gastric Acid
2) Gastric Acid secretion phases
3) Gastric acid regulation
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)
1) Define DIC
2) Causes of DIC
3) Dx
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
1) Basic stages of haemostasis
2) how are platelets activated
3) Role of platelets in haemostasis
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
1) Outline coagulation Cascade
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1) Investigations used to interrogate the coagulation cascade
2) How are platelets produced
3) complications of massive transfusion
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
Types, mechanisms + presentations of transfusion reactions
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)
Non-Hodkin Lymphoma
1) Types
2) extra- nodal Sites of predeliction
3) Investigations
4) RFs
5) Tx
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
Hodkin’s Lymphoma
1) Type
2) RFs
3) Classical presentation
4) Investigations
5) Rx
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
1) Histological Features of SCC
2) Criteria for melanoma diagnosis
3) Histological features of melanoma
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,
Baroreceptors :
i) Where?
ii) How do they communicate with CNS?
iii) Factors influencing Preload/EDV?
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
Anticoagulants
1) Classes
2) MOA of Heparin + warfarin
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)
Common Peroneal Nerve
I) Features of CPL Lesion
Deep Peroneal Nerve
i) Origin
ii) Deficit produces?
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
Shoulder Dislocation
i) How can shoulder’s dislocate
i) Anterior - Abduct and externally rotate
Posterior - Adduct and internally rotate
Inferior - Abduct onto onto acromion pushing inferiorly
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
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
Cervical Rib Presentation
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
Features of Tetralogy of Fallot
i) Overarching Aorta
ii) Right Ventricular Hypertrophy
iii) Pulmonary Valve Stenosis
iv) Ventricular Septum Defect
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
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
Hip Fracture Classifications - Outline them
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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Nerve Lesions:
i) Complete Sciatic
ii) High Tibial
iii) Common Peroneal Nerve
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
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
Different types of prion disease
Creutzfeld Jacob Disease
vCJD
Kuru
Fatal Familial Insomina
Gerstmann- Straussler- Scheinker Syndrome
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)
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
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
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.
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
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
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
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
Bowel Obstruction:
Large vs Small
X Ray findings
Causes
Presentation
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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)
What is the terrible knee injury triad?
MCL
Medial Meniscus
ACL
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
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
What does the image show - describe pathology
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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)
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)
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
Where can isolates of amyloid tissue be found in the body?
Larynx
Urinary Tract
Aorta
Pituitary Gland
Thyroid ( Medullary Cell Carcinoma)
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
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
i) Define: Aortic Dissection
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)
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
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
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
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
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)
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
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
i) Triple Assessment
i) Triple Assessment:
Examination
Imaging - USS Abdomen / Mammogram
Tissue Biopsy - Core Biopsy/FNA
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
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
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
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
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
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
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
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
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)
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
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
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
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
Layers of the bowel wall
Mucosa
Submucosa
Meisner’s Plexus
Muscularis Propriate
Longitudinal Muscle
Auerbach’s Plexus
Circular Muscle
Serosa
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
Hepatic Tumours
Benign - Haemangioma, Focal nodular hyperplasia, Adenoma
Malignant - Primary ( HCC, Cholangiocarcinoma, Angiosarcoma, hepatoblastoma) Mets.
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
Define:
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
Define:
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
Define:
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
Define:
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
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%
Cytological Classification of thyroid nodules
Benign
Indeterminate
Malignant
Inadequate Specimen
Thyroid Cancer:
Types
Medullary
Follicular
Papillary (85%)
Anaplastic (1%)
What is tertiary hyperparathyroidism
Development of autonomous PTH secreting nodule in patient with previous secondary hyperparathyroidism
Causes of hypoparathyroidism
Idiopathic/autoimmune
Radioidoine treatment
Thyroidectomy
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
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
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)
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
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)
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
H Pylori
i) What is H Pylori?
ii) Acid evasive techniques?
iii) How does it cause gastric problems?
iv) How many H Pylori carriers are asymptomatic?
v) Malignancy/Disease associations
vi) Detecting H Pylori
vii) Treatment of H Pylori
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
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
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
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
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
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
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
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
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
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
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
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
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)
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
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
What to do when you see neck lump?
History
ENT Exam
FNA
Imaging
Types of necrosis
Coagulative - most common
Caseous - TB
Liquefactive - Brain
Gangrenous - Wet/Dry
Fat Necrosis
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
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
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
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
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
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)
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
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
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
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
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
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
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
TURP Complications
Bleeding, UTI, Urinary Retention
Retrograde ejaculation
Urinary incontinence
Urethral strictures
Erectile Dysfunction
TURP Syndrome
DDx for Voiding/Storage Sx
Bladder Outflow Obstructions
Prostate - BPH/Ca, Urethral Stricture, Urethral sphincter dysynergia
Bladder Dysfunction
Oversensitvity, detrussor overactivity, low detrussor contractility
Difference between :
Staging and Grading
Staging - Assessment of size and spread of tumour
Grading - Histological assessment of level of cellular differentiation
Complications of ureteric stones
i) They may not pass
ii) Hydroureter + hydronephrosis
iii) Infection
iv) Haematuria
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%
How are protues mirablis + helicobacter pylori similar?
Both secrete urease enzyme which cleaves urea to ammonia
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
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
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
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
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
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
i) Cryptorchidism - define + associated RFs
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)
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
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
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,
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
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
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%)
Groin Lump DDx
Skin - Sebaceous Cyst
Subcutaneous - Lipoma, Lymph Node
Neurovascular - Saphena Varix, Pseudoaneruysm, Neuroma
Bowel - Hernia
Other - Ectopic Testes, Groin Abscess
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)
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.
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
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.
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
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
MOA of PPI
Irreversible blocker of H+/K+ ATPase pump on parietal cells
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
Gastric Cancer Metastasis
Lymphatic - Local lymphatics, Supraclavicular LNs (Virchow’s)
Direct - Omentum, Pancreas, Diaphragm, Duodenum, Colon
Haematogenous - Lung, liver
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
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
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
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
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
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
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)
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)
Describe the clotting cascade
Intrinsic Pathway-
XII -> XI-> IX -> VIII -> common pathway
Extrinsic Pathway-
VII
Common pathway
X -> V -> Thrombin -> Fibrin
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
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
Fever mechanism
Pyrogen –> PGE2 secretion –> acts on hypothalamus which increases “thermal set point” –> Thus causing various thermal regulating factors (shivering, adrenaline secretion, vasoconstriction)
Types of omental tumours
Leiomyosarcomas, Fibrosarcoma, Liposarcoma, Haemangiopericytoma
How are clots degraded
Plasmin is produced by the liver.
It is converted to Plasminogen by:
Urokinase, tissue plasminogen activator
Plasminogen breaks down fibrin
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
Cholangiocarcinoma:
i) Type
ii) Where does it spread
i) Adenocarcinoma
ii) Liver, Stomach, Duodenum + Peritoneum
Common Causes of Post Operative Bloody Diarrhoea
Ischaemic Colitis
Infective Colitis
Pseudomembranous Colitis
Ulceration
FIstulation
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
Crystal Arthropathies
Gout - Uric Acid (Negative birefringence)
Chondrocalcinosis - Calcium Pyrophosphate (Positive birefringence)
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.
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
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
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 +
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
Insulin effects
Increases GLUT4 Mediated glucose uptake
Glycogen Sythesis
Fatty Acid Synthesis
Protein Synthesis
What is sign of Hertoghe?
Loss of lateral third eyebrow in hypothyroidism
Management of pituitary tumours?
Observe
DA (cabergoline, bromicriptine) - If Prolactin Secreting
Octreotide - If GH producing
Surgery - Transphenoidal
Types of Knot
Square Knot
Surgeon’s Knot
Granny Knot
Variants of sciatic nerve
Usually - Inferior to piriformis
Sometimes:
Through Piriformis
Upper and lower portion go around priiformis
What is a baker’s cyst?
Often related to degnerative disease of the knee.
Accumulation of synovial fluid in the gatrocnemio- semimembranosus bursa
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
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.
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
Complications of resuscitation with IV Fluids?
Volume Overload
Hyperchloraemic Metabolic Acidosis
Hypokalaemia
Hypocalcaemia
Dilution Coagulopathy
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)
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
i) Perforated PU - Mx options?
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
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
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
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
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
Functions of Calcium
i) Muscle Contraction
ii) Pre-Synaptic Neurotransmitter Release
iii) Cardiac Myocytes
iv) Bone Mineralisation
v) Coagulation
Definition of false localising sign
In the context of neurology are signs that are distant from the expected anatomical locus.
Calculate Sensitivity / Specificity
Sensitivity :
True Postive / (True Positive + False Negative)
Specificity:
True Negative / (True Negative + False Positive)
Define: Pleomorphism
Pleomorphism refers to the variability in cell: Size, Shape, Staining of cells and their nuclei
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
Causes of carpal Tunnel Syndrome
Endocrine - Diabetic Mononeuropathy, Hypothyroidism, Acromegaly
Systemic - pregnancy, Oedema
Bone - Lunate dislocation, Colles Fracture
Causes of chronic rectal bleeding
Infectious - Amoebiasis, Intestinal SPirochetosis, Bacilliary Dystnery
Diverticulosis (right sided)
Angiodysplasia
Inflammatory - Inflammatory Bowel Disease
Malignancy
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
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
Risk factors for hypertrophic / keloid scarring?
Site - Mandible, Posterior neck, sternum, earlobe
Trauma
Infection
High Tension Areas
Keloid - Ethnicity
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),
What are pleural plaques?
Deposits of collagen and fibrosis that may/may not be calcified.
Associated with Chronic Asbesos exposure
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.
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
Causes of positive trendelenberg test
SGN Palsy/ Damage
Hip Fracture
Gluteual muscle weakness
Radiculopathy/ Disc Herniation
Hip Dislocation
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
RFs for oesophageal cancer:
SCC
Adenocarinoma
SCC: Tobbaco, Alcohol, Genetic, Nitrosamine, Achlasia, HPV, radiation
ADC: Barret’s, GORD, Tobacco, FH, H Pylori
Sciatic Nerve Surface Anatomy
Midway between the greater trochanter and the ischial tuberosity under the cover of gluteus maximus
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
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.
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
Where else might you find parathyroid glands?
Thymus (also from 3rd pharyngeal arch)
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
Why erythema surrounding skin cancers?
Neoangiogenesis
Reactive Capillary Formation
Immune cells - lymphocytes causing local vasodilation
Echo findings in endocarditis
Vegitation
Dehiscence of prosthetic valves
Regurgitation
how does EBV cause lymphoma
EBV infects B Lymphocytes –> Can cause mutations within lymphocytes leading to loss of function/gain of function mutations
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
Pott’s Fracture
Trimalleolar Fracture
Pott’s Fracture - Bimalleolar Fracture
Trimalleolar Fracture - Bimalleolus + Posterior Distal Tibia
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.
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