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

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

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






