Misc Flashcards

Question

Factors used in prognostication of NET vs GIST

Answer 1

**NET** * Mitotic count (\<2; 2-20; \>20) * Ki67 (\<3, 3-20; \>20) * Grade (low, moderate, high) based on above 2 * Differentiation (Well vs poorly) **GIST** * Mitotic count (\<5 vs \>50) * tumor size ( \<2cm, 2-10 cm, \>10 cm) * Location (SB worse than stomach * metastatic desease

Answer 2

* **Calories**: 35–40 kcal/kg/day. * **Volume**: 30 ml/kg/day. * **Ratio**: 50% carb; 30% lipid and 20% protein. * **Electrolytes**: Na 1.5 mmol/kg/d; Cl 1.3 mmol/kg/d; K 1 mmol/kg/d;PO4 1 mmol/kg/d; Mg 0.2 mmol/kg/d; * **Trace elements**: Zinc, manganese, Fe — given as multivitamin preparation. * **Essential fatty acids**: 15 g each of arachidonic acid and linoleic acid/day. * Adjust each requirement according to bloods and extent of illness.

Answer 3

1. Assess Immune compatibility (HLA class 1 and II) 2. Assess future risk of organ failure in donor e.g. HTN, DM 3. Assess Function, check both kidneys functioning 4. Assess structure - CTA, assess access 5. Rule out communicable diseases - HIV, CJD, CMV, EBV 6. Rule out malignancy 7. psychosocial support

Answer 4

1. Living donor better than cadeveric donor 2. preservation 1. cooling 2. Wisconsin solution 3. HLA / ABO / other immune comapatibility 4. recipient 1. optimize medical co-morbidieties - e.g DM 2. Immunsuppression

Answer 5

**HYPERACUTE** occurs within minutes due to presence of pre-formed Abs against donor HLA or ABO Ags Rx difficult – can try plasmapheresis & Ig infusion if Dx made early **Acute early rejection** 5/7 (& up to 10 days) after transplant Cell-mediated hypersensitivity involving _CD8 cells_ Manifests as: deterioration in renal fx Ix: Bx Rx: steroids **Acute late rejection** Occurs \>10 days in pts suppressed with prednisone & azathioprine Caused by binding of Ig and complement Manifests as: deterioration in renal fx Ix: Bx Rx: steroids **Chronic / late rejection** Months or years after initial transplant Accumulation of T-cells & macrophages → delayed hypersensitivity Manifests as: deterioration in renal fx Resistant to therapy; graft loss will eventually occur

Answer 6

* Acute liver failure * Cirrhosis with complications (e.g. variceal bleeding). MELD \>15 needed (start assessment once MELD 10) * Liver neoplasm * HCC * Large adenoma * liver based Metabolic diseases with sytemic effects * Wilson * Hemochromatosis * Amyloidosis * Alpha 1 antitrypsin def * Cystic fibrosis

Answer 7

Immunosuppressive drugs **Antimetabolites** – eg Azathioprine, cyclophosphamide inhibit nucleic acid synthesis → limit ability of activated lymphocytes to clonally expand **Corticosteroids**: Anti-inflammatory effect → Suppress T-cell activation (↓ TH1 + 2 cell activation) → ↓ cytokine production (esp IL-2) / chemokines, alter phospholipase A2 activity → ↓ PG, LT, PAF levels Suppress mast cell degranulation ↓ capillary permeability indirectly by inhibiting mast cells and basophils ↓ expression of COX-II and PG synthesis **Calcineurin inhibitor**s – eg Cyclosporine, tacrolimus Inhibit the production & release of IL-2 by TH cells.. & interfere with release of IL-1 by macrophages.. & B cell proliferation I**nhibitors of mammalian target of rapamycin (mTOR**) – eg sirolimus **Polyclonal antithymoblast or antilymphocyte globulin (ALG) & antithymocyte globulin (ATG)** **Monoclonal Ab therapy**

Answer 8

Transplant aptients are at risk of malignancy due to multipe reasons: 1. Immunosuression related 1. decreases the abiltiy of NK and T cells to identify and remove malignancy 2. reduces ability to to fight viral mediated malignancies 2. cancer in native kidney in patients with previous dialysis - unknown mechanism 3. Transmission of occult malignanacy from donor - rare 4. Recurrence of previous malignancy

Answer 9

* Skin * cutaneous SCC * BCC * Melanoma * Merkel cell cancer * Kaposi's scarcoma (HHV 8) * Lymphoma (EBV) * HCC (Hep B/C) * TCC bladder (cyclophosphamide related) * Cervical cancer (HPV) * Anal cancer (HPV) * Kidney cancer - native kidney in patients who have had previous dialysis - unkown mechanism.

Answer 10

MTP is transfusion of 10 units of PRBC in 24 hrs (some experts consider it to be 10 units in 6 hrs). Several scoring systems have been validated, but the critical factor is recognizing that massive transfusion may be needed. It should be activated if the clinicican is concerned about massive transfusion need. ABC (assessment of blood consumption criteria) is 75% sensitive nad 86% specific. 2 of the following needs ot be met: 1. Penetrating injury 2. Posiitve FAST 3. BP \<90 4. Pulse \>120 Hypothermia should be prevented. Tranexemic acid shold be given if within 3 hrs from injury.

Answer 11

**Box 1** * PRC x2 * FFP x 2 * *give tranexemic acid if within 3 hrs of trauma* * *check FBC, Coag, ABG, K and Ca* **Box 2** * PRC x 4 * FFP x 4 * Cryo x 3 **Box 3** * PRC x 4 * FFP x 4 * Platelets x 1 (if needed - i.e. platelet count \<75) * *check FBC, Coag, ABG, K and Ca -. continue checking every 30 mins* *Box 2 and 3 keeps cycling* ***Other factors: correct if*** INR \>1.5 --\> FFP 4 U fibrinogen \<1g/dl --\> Cryo x 3 Platelets \<75 --\> platelet x 1 ionized Ca \<1 --\> give calcium 10 mls **Rationale for the above regime:** * 1:1:1 for red cells, plasma and platelets * FFP takes time to thaw hence only 2 units in box 1 * Platelets drops last, often dosen't drop to low levels and scarce hence platelets are given last and only if platelet count \<75

Answer 12

Keloids represent an abnormal tissue resopnse to trauma secondary to exagerrated fibroblast and collagen formation. **Management** *_Prevention_* * limit scars * silicone gel sheet dressing * try to make incisions in cosmetically less sensitive areas *_Treatment_* * Intralesional triamcenalone (40mg) or 5FU * Cryo * Radiation * Re-excise

Answer 13

Pathogenesis of unkown but associated with proliferation of myofibroblasts causing contaction along with deposition of collagen. ultimately leads to contracture. Can be idiopathic, alc, liver disease, vibration tool use. Treatment may be: * Non-operative * Physiotherapy * Local injections of Triamcinolone * Irradiation * Operative * Fasciotomy * Z-plasty * Full thickness excision with grafting * Amputation of non-functional finger

Answer 14

HEMOSTATIS * 5-10 mins * platelet clot * fibrin mesh iNFLAMMATION * up to 3 days * recruitment of inflammatory cells EPITHLIALIZATION * up to 2 days * epithelial migrate along fibrin mesh up to dermis level FIBROPLASIA * 3-10 DAYS * fibroblast recruitment * collagen synthesis * contracture * Angiogenesis MATURATION * strength reaches 80% by 6 months * Collagen crosslinking, remodelling and wound contracture,

Answer 15

The pathophysiology of atherosclerosis can be described in a histological step-wise fashion; 1.Fatty streaks •Focal thickening of the intima with accumulation of lipid-laden macrophages (foam cells) and extracellular matrix 2.Fibrous cap •Lesion becomes a well defined lipid core with a fibrous cap 3.Vasa-vasorum •Eventually the vasa-vasorum from nearby adventitia in-grows to supply to lesion, weakening the walls and causing remodelling 4.Fibrous plaque •Smooth muscle hypertrophy and consolidation of the deep lipid core characterises the fibrous plaque, which may have a relatively thin surface, vulnerable to rupture 5.Intra-plaque haemorrhage •Plaque neovascularization results in spontaneous haemorrhage and subsequent rupture and thrombo-embolism.

Answer 16

●Poor tissue perfusion due to tension or ischemia at the anastomosis ●Presence of foreign material, such as staples or nonabsorbable suture ●Excess acid exposure in the gastric pouch due to gastrogastric fistulas ●Nonsteroidal anti-inflammatory drug use ●Helicobacter pylori infection ●Smoking treatment - * PPI 6 weeks * sucralfate * h pylori * smoking cessation perforation treatement- * stable - revise gastro jej * unstable - graham patch, drain and feeding tube

Answer 17

three principal sites: 1. A mesenteric defect at the jejunojejunostomy 2. A space between the transverse mesocolon and Roux-limb mesentery (ie, Petersen's defect) 3. A defect in the transverse mesocolon in patients with a retrocolic Roux-limb

Answer 18

**Prevent secondary brain damage by preserving CPP** * intubate GCS \<9 * Prevent seizures * stop anticoagulation * ICP monitoring * Prevent hypoxia * Maintain PaCo2 \<30 * Nurse head end up * Hypertonic saline/ Mannitol * ventriculostomy/ decompressive craniectomy

Answer 19

Patients with NF-1 have a mutation in the Neurofibronin Gene on Chromosome 17q. This is a tumour suppressor gene and mutations lead to unchecked RAS activity. Diagnosis - must have 2 or more of the following criteria: (CAFESPOTS Fhx) * Cafe-au-lait spots (6) * Axillary or inguinal freckling * Fibromatous lesions (2) * Eye signs (Lisch spots) * Skeletel abnormalities; sphenoid dysplasia, bowing of tibia * Phaechromocytomas * Optic Tract gliomas * Family history of NF-1

Answer 20

Virulence factors may be classified into those that promote adhesion, those that promote immune evasion, those that promote spread, and those that have toxic effects. **Adhesion factors:** •Vibrio cholera, H pylori, and Streptococcus pyogenes all have adhesion molecules **Immune evasion:** •Encapsulated bacteria; Neisseria, Haemophilus, Streptococci, E. coli, Klebsiella **Facilitate spread:** * Hyaluronidase elaborated by Staphylococcus aureus, Streptococcus pyogenes, and Clostridium perfringens * DNAase by staph aureus * Protease and collagenase by clostridium perfringens **Toxins:** * Alpha toxin by staph aureus and clostridium * Super-toxins by Staph and Strep that cross-link and hyper-activate lymphocytes causing massive cytokine release * Endotoxins on the surface of gram-negative e. coli