Pathophysiology Flashcards

Question

Hyperparathyroidism

Answer 1

Increased parathyroid levels caused by primary secondary or tertiary causes Primary: high TPH in the setting of high calcium - Adenoma - Parathyroid hyperplasia - Parathyroid caricnoma - familial syndromes Secondary: High PTH in the setting of low PTH - Impaired kidney function impaired production of calcitriol - Inadequate calcium intake or absorption - Vit D deficiency

Answer 2

Disorders of abnormal carbohydrate metabolism characterised by hyperglycaemia - Type 1: Autoimmune destruction of the B cells leading to insulin deficiency - Type 2: Increased insulin resistance at tissues leads to progressive loss of insulin secretion Hyperglycaemia leads to: Microvascular disease - Nephropathy - Neuropathy - Retinopathy Macrovascular disease - PVD - Cardiovascular disease

Answer 3

Stagnation of salivary flow occurs due to dehydration, medications or stricture - Inflammation of the gland or duct, localised injury and bacteria can serve as a nidus for stone formation - Submandibular duct more prone to stones due to long duct running against gravity and with alkaline properties, high mucin and calcium content

Answer 4

Swellings in the neck, due to embryological failure of the branchial clefts to involute during foetal development. - Normally the 2nd arch grows over the 2nd cleft, and the trapped ectoderm dissapears. - 2nd clefts can remain as cyst and is a swelling at the anterior border of SCM, connected via a track to near the palatne tonsil, passing between the internal and external carotid arteries

Answer 5

Remnant cyst of the neck, resulting from the incomplete involution of the thyroglossal tract responsible for the embryological development of the thryoid - Normally, the thyroid develops from the 2nd branchial pouch in week 4 from a diverticulum at the foramen cecum and descends down in the neck, anterior to hyoid bone to its place in the inferior neck. It separates into 2 lobes linked by an isthmus The residual tract dissapears by week 10, with the most distal part of this remaining as the pyramidal lobe - Failure to involute results in either a cyst, tract or sinus, which can result in a midline cyst, swellling or sinus that is prone to infection and has a malignant potential.

Answer 6

False pulsion diverticulum of mucosa and submucosa through Killians triangle, which is a muscle weakness of the posterior wall of the pharyngo-oesophageal junction, where the transverse fibres of cricopharyngeus and oblique fibres of inferior constrictor muscles meet. - Diverticulum develops due to altered upper oesophageal sphincter function, abnormal oesophageal motility or oesophgeal shortening

Answer 7

Gallstones are made up of cholesterol, bilirubin, bile salts, fatty acids and various minerals. Formation of gallstones occurs when there is 3 components - Supersaturation of one of the elements of the above, leading to precipitation of that element into crystal form - Hypokinesis of the gallbladder allowing precipitation of the components - Nucleation of the crystals to form stones, often with mucin serving as a nidus for stone growth

Answer 8

Autoimmune disorder of unknown cause, where auto antibodies are produced against platelet membrane proteins GPIIb/IIIa - Production of antibodies by T helper cells leads to cell-mediated destruction of the cells in the spleen by macrophages, as well as in some other tissues in the body (liver, bone marrow, splenunculi, lymph nodes). - Results in increased clearance of platelets as well as reduced production, leading to clotting impairment

Answer 9

Chronic parenchymal liver injury secondary to diffuse fibrosis and nodular remodeling, which leads to disturbance of liver microcirculation and perfusion - Hepatocellular injury and necrosis - collagen deposition and fibroblast activity - Loss of fenestrations in sinusoidal epithelial cells - Repeated cycle of necrosis, fibrosis and regeneration

Answer 10

Increased pressure within the portal system leading to formation of collateral and port-systemic anastamotic shunting - Initial increase in pressure in portal circulation, most commonly due to cirrhosis (scarring, fibrosis, and increased resistance within liver vessels) - Compensatory dilatation of the splachnic vessels leads to development of collaterals and shunting of up to 90% of flow through portosystemic connections - Gastro-oesophageal - Falciform ligament - Anal canal - Retroperitoneum - Stomal or parastomal

Answer 11

Functional disorder of the biliary tree, characterised by chronic biliary type abdominal pain or recurrent pancreatitis caused by dysfunction of the Sphinter of Oddi. 3 types: - Type 1: associated with 4 thigns - abdominal pain, obstructed LFT's, biliary dilatation, delayed GB emptying on functional biliary studies - Type 2: Pain with only 1-2 of above criteria - Type 3: Pain only

Answer 12

Progressive obliterative fibrosis of the intrahepatic and extrahepatic biliary tree, associated with ulcerative colitis in 70% of cases. Complications have 4 c's - Cholangitis - Cirrhosis - Cholangiocarcinoma - Colorectal cancer

Answer 13

2 main types of gastric cancer as classified by the Lauren classification system - Intestinal type. Development is as per the correa hypothesis. Gastritis leads to atrophic gastritis, then with increasing insults to metaplasia and progressive dysplasia to adenocarcinoma. Mutations of p53, KRAS, APC genes all can contribute to carcinogenesis - Diffuse type occurs due to a number of mutations including E-cadherin in CDH1

Answer 14

Arises due to failure of the protective mechanisms of the upper intestinal tract, lower oesophagus and stomach to prevent acid- related damage to the oesophagus. Extent of injury is proportional to the frequency of reflux events, the duration of events and the caustic potency of the reflux fluid. Increased exposure of oesophagus to refluxate - GOJ incompetence - Impaired oesophageal acid clearance Impaired defense against epithelial injury - Pre-epithelial (saliva, oesophageal buffer layer) - Epithelial (tight cell junctions, intra-cellular buffers etc) Affects of inflammation of degree of oesophagitis

Answer 15

Motility disorder of the oesophagus of unknown aetiology which results in progressive neuronal loss of the cells of the Auerbach plexus. Thought to be releated to inflammatory infiltration of the plexus in response to viral infection. Classification is as per the Chicago criteria, which requires hypertonicity of the lower oesophageal sphincter (IRP), and impaired motility int he form of either no contractions (type 1), pan pressurisations (type 2) or disordered contractions or spasm (type 3)

Answer 16

Inflammatory condition of the stomach and duodenum caused by an imbalance of gastric pH content and protective mechanisms of the stomach mucosa Most commonly caused by H. pylori and NSAIDS - H. pylori infection leads to damage of the mucosa, breakdown of protective mucous, hypersecretion of gastric acid and impairement of duodenal bicarb production and cellular function. - NSAIDS cause inhibition of prostaglandin synthesis whihc affects the secretion of gastric acid, the integrity of the mucosal barrier, the amount of bicarb affected and rate of mucosal blood flow.

Answer 17

Syndrome of infective, ulcerative and deformities of the diabetic foot due to complications associated with hyperglycaemia - Neuropathic changes occur due to glucose and lipid induced damage to neurones, leading to reactive oxygen species and proximal axonal damage - Altered sensation and neuronal function causes atrophy and anatomical bony abnormaltiies leading to foot deformities - Deformities and altered sensation and proprioception lead to abnormla pressure distribution causing repetitve stress and trauma - Healing impaired by vascular insufficiency and diabetes, causing ischaemia and necrosis

Answer 18

Acute infection of the dermis and subcutaneous fat. - Most commonly caused by B - hemolytic streptococcus species, though in immunocompromised patients, the pathogens are much more broad - Staph aurues also important, but more common in abscess, and less common in cellulitis.

Answer 19

Chronic inflammatory and degerneative process, affecting the walls of the muscular arteries 1. Endothelial injury - Turbulent flow, trauma, HTM, diabetes with ROS and glycaemic end products 2. Inflammation and formation of fatty streaks within the intima wall - Chemokines and cytokines activate macrophages and SM. Foam cells are macrophages with lipids ingested 3. Plaque formation - Fibrous cap composed of collagen fibres and SM cells. - Necrotic centre filled with foam cells, T cells and cellular debris 4. ECM degradation - Can lead to aneurysmal formation

Answer 20

A spectrum of disease ranging from asymptomatic dilatation of veins to chronic venous insufficiency with complications - Venous hypertension occurs due to increased central pressure, venous obstruction, incompetent balves or inadequate muscle contraction - Loss of valvular competence causes pooling of blood and inflammation of vessel wall and soft tissue deterioration - Endothelial cell dysfunction occurs due to local inflammation, reduced vasoactive mediators and damage to the venous wall and valves - Chronic release of inflammatory mediators lead to trophic skin changes - Increased type 1 collagen, decreased type 3 collagen, degradation of ECM and reduction in SM cell numbers leads to weakening of vessel wall and abnormal venous dilatation - Metalloproteinases break down vessel ECM and leads to abnormal permeability causing oedema - Ulcers occur due to proteolytic enzymes in subcutaneous tissue, which heal poorly due to chronic inflammatory state and oedema. - Hemosiderin deposition occurs due to migration and breakdown of RBC in the tissues, which further causes oxidative stress and contibutes to ulceration - Lipodermatosclerosis occurs due to severe fibrosing paniculitis of the subcutaneous tissue, binding the skin down to the subcutaneous tissue

Answer 21

Chronic progressive fibrotic condition affecting the palmar fascia of the hand, leading to the formation of fibrous cords and nodules and contractures and deformity. - Proliferation of the fibroblasts and deposition of collagen in the fascia leads to initially formation of nodules, and later fibrosis in the palmar fascia causing fibrosis. - Tendons underneath are unaffected.

Answer 22

Chronic inflammatory skin condition affecting the pilosebaceous units of the groin, axilla, perianal, perineal and infra-mammary areas - Inflammation leads to plugging of the hair follicles and keratinocyte proliferation - Follicle rupture and associated inflammatory response with furtehr peri-folliculitis and bacterial infection - Recurrent attacks lead to chronic foreign body granulomatous reaction and abscess, with formation of epithelial tracts.

Answer 23

Chronic inflammatory condition, most commonly of the great toe, caused by growth of the nail plate into the lateral nail folds, leading to recurrent infeciton and inflamamtion - Initial embedding of the spicule into the soft tissue secondary to poor cutting technique, ill fitting shoes and repetetive trauma to the toe - Severe inflammation with oozing and seropurulent discharge - Formation of granulation tissue

Answer 24

Life-threatneing infection of the soft tissues. - Infection with (most commonly) multiple organisms, activation of immune system via PAMP's - cytokines leading to permeability and inflammation - Endo and exotoxins: Hyaluronidase, metalloproteinases lead to destruction of tissue and spread along tissue planes - Activation of coagulation pathway causes microthrombi which further cause necrosis - Anaerobic metabolism of cells causes acidotic tissue - Facultative anaerobes thrive in acidic, necrotic environment - Infection, necrosis and degree of tissue death and destruction leads to systemic SIRS, septic shock, MODS and death

Answer 25

Chronic inflammatory condition of the natal cleft resulting in formation of pits, tracts and abscesses. - Trapping of hair and debris int he natal cleft, which is enveloped within the skin due to suction and friction caused by buttocks - Chronic inflammatory process occurs with foreign body reaction and secondary infection, creating tracts and sinuses with associated abscess cavity

Answer 26

Obstruction of hte gastric outlet leads to a hypochloraemic, hypokalaemic metabolic alkalosis and a paradoxical aciduria - Vomiting of HCl and fluid in the stomach contents leads to loss of HCl. - Na+ is preferentially retained and is exchanged for K+ ions, leading to hypokalaemia - As the dehydration progresses, Na is exchanged for H+ ions in the renal tubules to increase fluid retention, leading to excretion of acid in the urine, despite the metabolic alkalosis

Answer 27

An abnormal connection between 2 epithelialised hollow spaces or organs

Answer 28

Inability of the gastrointestinal tract to maintain nutrient, fluid and electrolyte homeostasis without intravenous or enteral supplementation. Most commonly caused by short gut. Factors contributing to intestinal failure - Length of bowel remaining - Presence of ICV and colon - Loss of ileum altered gastrointetinal motility - Gastric hypersecretion - Mucosal disease in remaining intestine - Altered gut microbiome leading to deconjugatio of bile acids, competition of bacterial absorption of B12, secondary inflammatory response which damages the absorptive surface. 2 main phases of intestinal failure - Hypersecretory phase, characterised by high intestinal fluid losses and metabolic derangement - Adaptation phase, characterised by structural and functional changes in the bowel to improve absorptive capacity.

Answer 29

Intestinal adaptation in small bowel can occur over months - years and involves structural and functional changes to the small bowel Structural - Increased villi length and deepening of crypts - Increased enterocyte numbers - Increased remnant bowel length and dilatation - Increased wet weight of the bowel, protein and DNA content - Increased muscle thickness, circumference and length Functional adaptations - Increased brush border enzyme activity - slowed gut transit - Increased motor activity - Possible changes in gut microbiota

Answer 30

Outpouching of the small bowel, which can be congenital or acquired. - Weakness in the muscle wall where vessels penetrate the mesenteric aspect - altered motility and increased pressures thought to play a role Congenital diverticulae can occur and protrude into the bowel lumen where part of the canal has failed to recannalte during embryological development

Answer 31

Obstruction of the lumen of the small bowel leads to proximal dilatation - Initially get increased contraction, manifest as colicky abdominal pain in the central abdomen due to foregut neural supply - LAter on, the small bowel dilates and becomes filled with fluid, leading to third space losses and hypovolaemia. - Vomiting occurs which leads to further fluid losses, electrolyte imbalance and acid base disturbance - With ongoing distension, impairment of blood supply can occur initially with venous congestion and susbsequent arterial supply, which leads to ischaemia and perforation

Answer 32

Chronic progressive damage to the bowel caused by exposure to radiation, due to a progressive occlusive vasculitis - Damage to the crypt mucosal stem cells from direct radiation damage or vasuclar damage - Infiltration of leukocytes occur with crypt abscess formationa nd ulceration acutely. - Progressive occlusive vasculitis occurs due to foam cell invasion of the intima and hyaline thickening of the arteriolar walls, leading to collagen deposition and fibrosis - Intestinal mucosa becomes inflamed, oedematous, thickened and ischaemic with decreased absorptibe area, leading to impaired absorption, SIBO and altered gut motility

Answer 33

Anatomical disruption and altered gastrointestinal function leads to the nutritional and metabolic complications post-bariatric surgery Malabsorption - Fatty acid malabsorption, leading to diarrhoea, deficiencies in vit ADEK - Impaired absorption of Ca2+ due to preferential binding of calcium to - Impaired B12 absorption due to bypass of intrinsic factor - Decreased iron absorption due to bypass of absoprtion and altered exposure to acidic environment which cleaves iron from proteins - Folate deficiency due to being absorbed in duodenum and proximal jejunum Metabolic - Formation of gallstones due to impaired enterohepatic circulation - Formation of oxalate stones due to preferential binding of calcium to fats, leaving oxalate for absortption in the colonic enterocytes

Answer 34

Abnormal accumulation of interstiail fluid and fibroadipose tissue due to injury, infection or congenital abnormalities of the lymphatic system - Occurs when the lymphatic load exceeds the transport capacity, and results in filtered fluid accumulating in the interstitium - Promotion of adipocytes, and deposition of collagen in the ECM - Presence of protein rich fluid in the interstitial space can trigger inflammation

Answer 35

An acquired systemic coagulopathy which occurs during acute illness or injury due to microvascular thrombi formation and consumption of coagulation factors, leading to bleeding and end-organ damage - Exposure of blood to procoagulants (bacteria, damaged endothelium) - Widespread activaiton of coagulation cascade, causing microvascular thrombus formation, consumption of coagulation facotrs and platelets - Fibrinolysis leads to fibrin degradation products, further inhibiting clot formation and platelet aggregation - End-organ damage occurs due to reduced perfusion, bleeding and or thrombus and altered vascular function - Dysregulated immune system leads to neutrophil extracellular traps which are cytotoxic

Answer 36

Venous thromboembolism is the abnormal formation of clots within the veins of the systemic or pulmonary system, due to presence of abnormal componenet of Virchows triad - Hypercoagulability - Stasis - Endothelial damage

Answer 37

Transplant rejection is the immune-related failure of the transplanted graft. there are 3 main processes or types of rejection Hyper acute rejection: Occurs wihtin 24 hours - Due to preformed antibodies to the graft HLA or blood group antigens - Results in activation of cytokines, coagulation pathways and acute inflammation leading to microthrombi and acute infarction of the graft Acute rejection - weeks - months - Mostly T cell mediated, but can involve B cells and Antibodies - Presentation of graft antigens on APC's leads to activation of CD4 and CD8 T cells. - Recruitment of NK cells and B cells causes inflammation of the graft in the form of arteritis, tubulitis and interstial inflammation, with T cell infiltrate in the BM. - T cell disease treated with: steroids, ATG, monoclonal antibody and adjusting immunosuppressants - B cell disease treated with plasmaphoresis, IVIG, monoclonal antibodies, steroids and adjusting baseline immunosuppressants Chronic rejection - months - years - B cell mediated - Leads to chronic progressive fibrosis of the interstitium, tubular atrophy and CD4 staining of the peritubular capillaries - Difficult to treat

Answer 38

Clinical manifestations resulting from systemic consequences of muscle injury and rhabdomyolysis, leading to AKI and death - Crush injury causes venous obstruction and in combination with ischaemia of tissue leads to accumulation of potassium, phosphate, lactate, myoglobin and toxic metabolites in the tissues - Injury and buildup of above components leads to membrane dysfunction, oedema and swelling - In the extremity, this can lead to compartment syndrome and further muscle death - On release of the compression, reperfusion injury adds to damage, and release of toxic metabolites can lead to arrhythmias, renal failure, SIRS, MODS and death

Answer 39

Burns cause damage through both local and systemic effects. Local response according to Jackson's model of burns (Zone of coagulation, zone of stasis, zone of hyperaemia) Systemic response occurs with burns > 20% TBSA. - Body moves between ebbs (decreased CO due to volume loss, reduced TPR causing show, end organ injury) and flows (hypermetabolic phase with SIRS response) - Vasodilatation causes increased permeability of vessels, leading to albumin loss and intravascular hypovolaemia - Hypermstabolic state occurs due to cortisol, catecholamines and glucagon, leading to muscle breakdown - Hypothermia occurs due to vasodilatation and skin loss - Immunosuppression due to loss of immune and physical barrier of the skin - ARDS due to damage to endothelium and alveolar epithelium

Answer 40

The inability of the cardiovascular system to adequately perfuse tissues to meet metabolic demands, due to inadequate blood volume. - Bleeding or ECF volume loss leads to hypovolaemia - Impaired perfusion leads to decreased oxygen and nutrient delivery, resulting in anaerobic metabolism and lactate production, with damage to end-organ tissues Compensation occurs - Compensatory vasoconstriction and increased total peripheral resistance acts to restore circulating pressures - Tachycardia acts to increase cardiac output in the face of inadequate circulating volumes - Vasopressin, and angiotensin:renin:aldosterone axis activated to retain Na and fluid Decompensation occurs - If no intervention to restore circulating volume, compensatory mechanisms are overwhelmed and circulatory collapse occurs

Answer 41

The pathophysiology of trauma has 2 main phases Ebb phase: Due to acute severe shock, characterised by oxygen consumption and enzyme activity - Hypovolaemia leads to decreased tissue perfusion causing release of catecholamines - Tissue damage releases inflammatory mediators which activate inflammatory response and SIRS response - Free-radicals produced which Flow phase - Hormonal mediators such as sympathetic system, cortisol, ADH and aldosterone leads to increased fluid conservation via sodium retention - Hyperdynamic state stimulated by inflammation - Increased metabolic requirements lead to catabolic state

Answer 42

Formation of an aneurysm is a multifactorila process, involving embryological factors, histological changes and hemodynamic stresssors - Embryology: Development of infrarenal aorta from mesodermal somites have decreased collagen and decreased number and thickness of elastic lamellae - Inflammation occurs, which leads to production of cytokines, which degrade collagen, elastin and ECM matrix proteins - Increased hyperdynamic stress leads to dilatation of the weakened wall.

Answer 43

Maintained by a complex endocrine feedback loop involving the parathyroid glands, gut, kidneys and bones - Low calcium in the blood causes activation of Parathyroid glands, which produce increased PTH release PTH acts on: -Bone to increase osteoclastic activity of bone leading to resorption and release of calcium and phostphate into the blood stream. - Gut cells to increase calcium reabsorption and phosphate reabsorption - Kidneys to increase calcium reabsorption and reduces phosphate excretion - Kidneys to increase activation of 1,25, Dihydroxyvitamin D3, which then acts on the gut to increase calcium absorption and phosphate absorption Negative

Answer 44

Inflammatory condition of the thyroid caused by autoimmune antibodies to thyroid peroxidase and thyrogubiln. - Leads to infiltraiton with CD4 helper T celles, causing initial inflammation and hyperthyroid state, followed by fibrosis and hypothyroidism

Answer 45

Autosomal dominant inherited mutation of calcium sensing receptor. - Leads to inappropriate release of parathyroid hormone in regards to calcium levels - Causes hypercalcaemia with inappropriately low urine calcium due to inappropriate PTH secretion

Answer 46

Aldosterone is a mineralocorticoid secreted by the adrenal cortext - Acts on renal tubule cells to increase Na+ reabsoprtion and increase K+ excretion. - Leads to fluid reabsorption and hypokalaemia

Answer 47

Potentially life-threatening metabolic complication of reintroduction of nutrients after a period of starvation or severe malnutrition, characterised by electrolyte and fluid shifts. - During period of starvation, levels of PO4, K, Na and Mg are depleted, particularly phosphate to make ATP from fats and protein - Reintroduction of food leads to insulin production, which triggers uptake of phosphate, potassium and magnesium into the cell to replenish intracellular stoes. - Leads to low extracellular phosphate and potassium, leading to inability to produce ATP, tissue hypoxia and damage of cells resulting in: Peripheral oedema and CHF, rhabdo, seizures, hemolysis, resp insufficiency

Answer 48

- Increase in counter-regulatory hormones such as cortisol, Adr, glucagon and inflammatory cytokines - Increase in daily energy and nitrogen requirements - Preferential oxidation of lipids - Insulin resistance and glucose intolerance - Incrased gluconeogenesis and protein catabolism - Fluid retention and hypoalbuminaemia - Consequential effectS: impaired immune function, delayed wound healing, atrophy of smooth and skeletal muscle, impaired cardiac and respiratory function, increased post-op morbidity and mortality

Answer 49

Impaired occulosympathetic pathway, leading to ptosis, myosis and anhidrosis. - Caused by central, pregangionic or post ganglionic lesions affecting the sympathetic fibres supplying the Mullers muscle, the iris dilator and the fibres supplying the facial skin and glands

Answer 50

3 main factors contributing to the formation of gallstones - Hypomotility of the gallbladder - Super-saturation and precipitation of crystals of cholesterol - Enucleation. Mucin provides a nidus for precipitated crystals to accumulate and form stones

Answer 51

H pylori is a gram negative flagellated rod with multiple virulence factors which allow it to exist in the gastric mucosa - Flagella - Urease - CagA and VacA cytotoxins - Polysaccharides and adhesion molecules - Proteinase, mucinase, lipase - Reduces bicarb secretion by duodenal cells - Causes metaplastic changes of duodenum which allow it to be invaded

Answer 52

- Restriction of amount of oral intake - Malabsorption - Altered hormonal signalling (Increased GLP1,GLP2 production, leading to increased satiety) - Decreased hunger signalling - Altered vagal signalling leading to decreased Ghrelin, meal sizes and food preferences

Answer 53

Complication of gastrectomy caused by a high solute load entering into the small bowel . Early: Delivery of a high solute and high carbohydrate load into the small bowel leads to rapid osmotic shifts of fluid into the small bowel, causing distension and activation of vasoactive peptides, leading to crampy abdominal pain, palpitations, flushing, dizziness LAte: Delivery of carbohydrate load leads to insulin release and overshoot, which causes a rebound hypoglcaemia and catecholamine release. Symptoms include neuroglycopenic symptoms - fatigue, lethargy, weak, nausea, vomiting, coma

Answer 54

Clinical syndrome caused by overgrowth of bacteria in the small bowel due to stasis, altered acidity of bowel contents, lack of local immunoglobulins or disruption of normal bowel anatomy. Overgrowth of bacteria leads to: - Deconjugation of bile salts and fat malabsorption, with ADEK deficiencies - Altered calcium and oxalate metabolism - Vit B12 binding and malabsorption - Catabolsim and fermentationof carbs and protein causing malabsorption and gas production

Answer 55

Constellation of symptoms associated with metastatic or extra-gastrointestinal well-differentiated neuroendocrine tumours. Neuroendocrine tumours release vasoactive amines such as serotonin, bradykinin, histamine and kallikrenin, which have effects of flushing, diarrhoea, wheeze, tachycardia and can cause valvular heart lesions. When produced by gastrointestinal tumours, the products are broken down and inactivated in the liver, however in liver lesions or lung lesions, these can exert their effects and symptoms occur

Answer 56

- Apotosisi of tubular cells - Obstruction of collecting tubules with casts and necrotic cells - Imparied filtration and reabsorption - Back leak of filtered tubular fluid across the damaged epithelium causing increased intratubular pressure - Inflammation of interstitium - Endothelial injury causing microvascular flow disruption and extending ATN

Answer 57

Rare aggressive neuroendocrine tumour of the skin - Unknown cell lineage (? keratinocyte vs epidermal stem cell vs fibroblast) - 2 pathways: virus pathway, or non-virus pathway Virus positive pathway - Polyomavirus integrates into the host genome and produces 2 oncogenes - small T antigen and large T antigen, which initiates tumourigenesis and inhibits tumour suppressor genes, leading to uncontrolled proliferation Virus negative pathway - UV damage causes multiple mutations with loss of function Histology shows: Small round blue undifferentiated cells, with high mitotic figures, scant cytoplasm, apoptosis, necrosis and IHC staining for neurofilament, CK20, CK7 and TTF1

Answer 58

Acute dilatation of the colon in the absence of a mechanical cause for obstruction - Unknown cause, but thought to be due to autonomic dysfunction of the nerves of the distal colon, leading to acute atonia, and upstream dilatation - Can be caused by an inciting event, such as electrolyte disturbance, medicaitons (anticholinergics, opiates, steroids) or post-operatively after joint replacement or cardiac surgery - Increased risk in those who are institutionalised

Answer 59

- Autosomal dominant disease causing impaired production spectrin, which is a RBC cytoskeleton protein - Spherocytes get trapped in the reticuloendothelial system and destroyed by spleen

Answer 60

Due to senna-containing laxatives, which have anthraquinones. - Leads to breakdown of enterocytes and phagocytosis by macrophages - Releases lipofuscin pigment, which discolours hte mucosa brown - Treated by cessation of laxatives, which will resolve the discolouration within a year

Answer 61

Chronic inflammatory condition affecting the pilosebaceous unit. - Plugging of the pilonsebaceous unit due to rubbing of skin or clothing on intertiginous areas - Keratin plugging leads to obstruction and rupture of the glands, leading to inflammation, secondary infection and abscesses - Repeated infection and chronic inflamamtion leads to foregin body granulomatous reaction, and formation of epithelialised tracts and sinuses Graded by the Hurley grading system - Grade 1: Abscess, no tracts - Grade 2: Mild disease with widely separated areas - GRade 3: Severe disease with multiple tracts, sinuses and scarring

Answer 62

Electrocautery is an energy device that we use to surgery to control bleeding and dissect tissues. - Generator provides a current is delivered to the patient via a handheld electrode - Current passes through the tissues to a return electrode, which has a large surface area that dissapates the energy - The current then returns to the generator to complete the circuit. - Waveform generation can vary depending on desired effect: Coag function delivers short bursts of current, whilst cut delivers a continuous waveform. Electrocautery works by: - Spasm of vessel walls - Denaturation of proteins - Dessication of tissues - Vessel trombosis

Pathophysiology Flashcards

(87 cards)