ESA 2 Clinical Conditions Flashcards

Question

Rheumatoid arthritis

Answer 1

Arthritis as a result of an inflammatory response, which causes inflammation of (initially) the synovial membrane, leading to pain when moving the joint. The condition progresses to fibrosis of affected joints, affecting mobility and causing them to seize completely eventually essentially destroying the joint. Not associated with age, and usually starts by affecting one side of the body, but in all types of joints (large and small). Progress can be slowed with steroids, but physiotherapy and lifestyle changes usually necessary Surgery in severe cases can either involve complete joint replacements, joint resurfacing or joint fusion (arthrodesis, this is bad as it stops movement in that joint)

Answer 2

‘Wear and tear’ arthritis as a result of the persistent movement stripping the articular surface (cartilage) from joints. This leads to bone grinding against bone, leading to joints seizing and pain. Usually associated with age as it’s wear and tear, tends to be limited to one class of joints on one side of the body before spreading (such as all MCP joint in right hand). Steroids don’t do much, physiotherapy and lifestyle changes etc are usually much more effective Surgery in severe cases can either involve complete joint replacements, joint resurfacing or joint fusion (arthrodesis, this is bad as it stops movement in that joint)

Answer 3

Gradual loss of muscle mass due to aging. Typical value is 0.5 to 1% loss every year after the age of 50. Differs from cachexia (weight loss) as this is secondary to an underlying pathology ie kwashiorkor . Not always considered a disease or even a symptom, some considering it a normal part of aging. However, it contributes (along with osteoporosis) to an increased risk of mortality/death following a fall/other trauma in the elderly – this is known as frailty syndrome

Answer 4

Pericardial effusion (infection) or haemorrhagic effusion lead to pericardium filling with fluid – heart finds it harder to contract, and will eventually stop. Pericardiocentesis (aspiration of fluid within pericardium) to treat

Answer 5

Infection of pericardium leading to pericardial effusion. Potential cause of tamponade

Answer 6

Rule of thumb, left to right shunt doesn’t cause cyanosis and isn’t as serious, right to left puts deoxygenated blood in systemic circulation so causes cyanosis, more serious Think of the heart like plumbing, imagine the normal setup, visualise the element that’s damaged/added in and work out how you divert blood flow around this/where the blood would go. This makes learning these (and understanding them) a lot easier

Answer 7

Hole in atrial septum that allows communication between atria, left to right shunt due to pressure (blood does pulmonary circuit more than once), huge flow can overload RV and lead to right heart failure

Answer 8

Hole in ventricular septum (usually the membranous portion) that allows communication between the two, left to right shunt due to pressure (blood does pulmonary circuit more than once), pulmonary hypertension due to increased blood passing through, can get so high that the pressure gradient reverses and you get a paradoxical shunt (Eisenmenger syndrome)

Answer 9

PDA stays open after birth, communication between aorta and pulmonary trunk/arteries, blood does pulmonary circuit twice, pulmonary hypertension (similar to VSD)

Answer 10

Fails to close at birth, largely asymptomatic, as it’s so small, but can be a route for venous embolism to join systemic circulation

Answer 11

Constricting of the aorta in the region near the DA, leads to hypoperfusion in vessels distal to this (lower limbs, femoral pulses will be weak), leads to hypertension in vessels before this (aortic arch) in an effort to increase perfusion to lower limbs by the body

Answer 12

4 key defects giving rise to a cyanotic patient, due to the circulation of deoxygenated blood: 1. Ventricular septum misalignment – leads to right ventricular hypertrophy (and therefore hypertension) due to increased difficulty of pumping to pulmonary trunk 2. Pulmonary stenosis – narrowing of pulmonary valve causes hypertension in right ventricle 3. VSD – due to 1 and 2, the pressure in RV exceeds LV, causing a shunt of deoxygenated blood from right to left 4. Over-riding aorta – misaligned aorta takes some blood from RV as well as LV, leading to more deoxygenated blood circulating

Answer 13

Missing/closed tricuspid valve, so no pulmonary circuit formed, only viable if there’s a right to left ASD (necessary to form a complete circuit, possible due to accumulation in RA without filling the RV) and either a VSD of PDA (to allow access to lungs)

Answer 14

Spiral septum doesn’t form correctly, leading to the aorta being connected to RV and pulmonary trunk to LV, now two separate circuits that run parallel instead of one big one, only viable if PDA is open and maintained (completely mixes blood)

Answer 15

LV and ascending aorta undeveloped/absent, LA small, PDA maintained, right ventricle takes over systemic and pulmonary circulation, PDA allows blood into the aorta past the ascending section, maintaining viability. Some communication between LA and RA also needed (ASD)

Answer 16

No pulmonary valve  no access to pulmonary circuit except through PDA

Answer 17

No aortic valve meaningi no access to systemic circulation except through PDA, ASD/VSD often created artificially to stop accumulation in left side of heart

Answer 18

Too much K+ in blood  too much K+ in ECF, so the concentration gradient is less steep, which permanently depolarises the membrane, inactivating some Na+ channels in the pacemaker, and through accommodation of this weak depolarisation you end up with bradycardia, bundle branch blocks and eventual heart failure. ECG features include: Prolonged QRS complex Prolonged PR interval Tented T waves (very similar in shape to a healthy QRS complex)

Answer 19

Too little K+ in blood leading to too little K+ in ECF, so the concentration gradient is more steep, permanently hyperpolarising the membrane, which leads to hyperexcitability of the Na+ channels, less inactivation (this somehow causes a decreased refractory period), leading to tachycardia, then atrial or ventricular fibrillation and eventual cardiac arrest. ECG features include: Enlarged P waves Prolonged PR interval ``` T wave flattening/inversion No Pot (potassium), not tea (T wave)! ```

Answer 20

Appears as a lack of discernable P waves, sometimes with the isoelectric line being disrupted into a ‘wavey baseline’. Not fatal as most filling of the ventricles occurs during diastole, atrial systole isn’t that important

Answer 21

Can be idiopathic, ventricles will occasionally contract without an impulse from the SAN, so initiated by AVN instead. Different place of origin means a different shaped QRS complex, will show up as always wider and sometimes taller in amongst the normal complexes

Answer 22

Genetic or acquired syndrome that leads to abnormal repolarization of the heart, which prolongs the QT interval, allowing a greater chance for re-entry arrhythmias. Particularly more likely to develop torsades de pointes or ventricular tachycardia that will progress into ventricular fibrillation

Answer 23

Associated with prolonged QT interval, particular type of ventricular tachycardia that gives the appearance of winding round the baseline in 3d (despite being on a 2d page) on the ECG. Most episodes are self-resolving within a few seconds but can devolve into ventricular fibrillation

Answer 24

Ventricles no longer able to contract in a coordinated manner, immediate loss of CO and rapid death unless treated. Shows on an ECG as rounded, shallow peaks and then troughs, with no discernable PQRS or T waves/complexes at all. Must be defibrillated

Answer 25

Delay between the contraction of the atria and the ventricles, due to an issue at the atrioventricular node (AVN). Shows as a prolonged PR interval on an ECG

Answer 26

Irregularity of contraction between the atria and the ventricles. The PR interval will get more and more prolonged until the AVN generates its own depolarization, showing as an abnormally shaped QRS complex. This then resets and the same thing is seen again

Answer 27

Complete dissociation between the P and QRS complexes as a result of a complete block between the SAN and AVN. If you measure the RR interval and the PP interval, you will calculate two different heart rates (the RR interval will be slower as its initiated by the less electrically active part of the heart)

Answer 28

Some abnormality occurs that slows/stops the electrical conduction down the left bundle of Purkyne fibers. Shows as abnormally shaped ‘rabbits ears’ QRS complex as the two ventricles depolarize at different rates

Answer 29

Some abnormality occurs that slows/stops the electrical conduction down the right bundle of Purkyne fibers. Shows as abnormally shaped ‘rabbits ears’ QRS complex as the two ventricles depolarize at different rates

Answer 30

Easiest way to differentiate between a right or a left bundle branch block is to check the chest leads and apply the following mnemonic: WiLLiaM MoRRoW If the QRS complex is shaped like a W on the septal leads (closest thing to a right sided view, V1) and an M on the lateral leads (left side of heart, V6), it’s a LBBB If the QRS complex is shaped like an M on the septal leads (closest thing to a right sided view, V1) and a W on the lateral leads (left side of heart, V6), it’s a RBBB

Answer 31

Inability of the blood supply of the heart to match the demand placed on it by the body. Factors that influence either of these are as follows: Supply Coronary flow (determined diastolic BP and coronary resistance) O2 capacity of blood Demand Heart rate Contractility (stroke volume at a given venous pressure) Wall tension (determined by pre-load and afterload) Most likely cause of pathogenesis is a coronary atheroma that causes the lumen of the coronary artery to narrow, increasing coronary resistance (resistance decreases by radius 4 ) and therefore decreasing coronary flow. How badly these arteries are occluded by said atheroma determines the symptoms, and is split into the classifications below

Answer 32

Plaque usually occludes > 70% of the artery lumen, leads to ischaemia of the myocardium not at rest but when demand is increased (can meet the low resting level of demand). Pain is typically ischaemic (central/retrosternal, left sided more than right, crushing or tightening pain) and disappears within 5 minutes of ceasing exertion/with GTN spray

Answer 33

Largely similar to stable angina yet pain appears to crescendo (increase in intensity), doesn’t always go away within 5 minutes. Can appear with no obvious exertion/trigger

Answer 34

NSTEMI: The less severe form of MI, lacking ST elevation on the ECG. Is a result of partial/brief total occlusion of a coronary artery, and so leads to crushing chest pain that isn’t relieved with rest/GTN spray. Autonomic features (sweating, pallor, vomiting etc) are normally present, and the patient may have a sense of impending doom. ECG will be negative but as there has been some necrosis biomarkers will be positive STEMI: The more severe form of MI, showing ST elevation of the ECG at the leads facing the infarct (ie V3 and V4 for anterior). Result of a total occlusion of a coronary artery, and leads to crushing pain that isn’t relieved with rest/GTN spray. Autonomic features, and accompanied with a sense of impending doom. Extensive necrosis of the area of myocardium supplied by the artery, re-opening of the blood supply within two hours is the only way to prevent/minimise necrosis

Answer 35

A cluster of symptoms attributed to occlusion of the coronary arteries, which are described above in the MI section. It is a result of unstable angina, NSTEMI or STEMI, and there are ways to differentiate between the three Treatment of the above varies from type to type but some common things include: Angiography with a view to coronary bypass/stenting (elective procedure in the case unstable angina) Coronary bypass/stenting (emergency surgery in the case of all STEMIs and some NSTEMIs) GTN to increase venodilation to decrease the cardiac output of the heart and therefore demand (angina and unstable angina only, won’t stop occlusion that’s begun in an MI) Long term post infarct medications to reduce either the clotting of the blood or the demand on the heart Blood thinners: warfarin, low weight heparin, aspirin etc Demand reducers: Ca2+ channel blockers, ACE inhibitors, diuretics, beta blockers etc Can also give statins to reduce cholesterol synthesis and therefore (hopefully) the formation of atheromas

Answer 36

Unstable angina No Necrosis ECG changes - ST depression/none Biomarkers - Negative troponin and creatine kinase NSTEMI Some Necrosis ECG changes- ST depression/none Biomarkers - Positive troponin and creatinine kinase STEMI Extensive Necrosis ECG Changes - ST elevations in the leads facing infarct Biomarkers - Positive Troponin and creatinine kinase

Answer 37

Syndrome of symptoms and signs that are a result of the heart being unable to pump enough blood to meet the physiological demands of the body. Caused primarily by IHD, but can have other causes, such as valve disease, chronic arrhythmias etc. One classic sign is a breakdown of the relationship described in Starling’s law – pumping becomes less efficient and so force of contraction no longer corresponds to stretch. Several systems/hormones play a huge part in the exacerbation of heart failure, but the key 4 are: Autonomic nervous system Baroreceptors sense down CO, so inc ANS input to heart Inc CO increases demand on myocardium, damaging it further NorAd stimulates cardiac hypertrophy, and by proxy, myocyte apoptosis and necrosis Renin-angiotension- aldosterone system (RAAS) Drop in BP/renal perfusion releases renin, causing eventual creation of angiotension II (AT2) AT2 causes vasoconstriction (inc TPR  inc BP leading to inc CO leading toinc demand in heart) AT2 increases aldosterone release, so also causes Na+ retention, so inc circulating vol  inc preload Natriuretic hormones Released by inc atrial stretch Oppose the effects of RAAS Promote vasodilation, Na+ loss and inhibit renin/aldosterone release ADH Normally stops water loss when dehydrated and encourages it when hydrated However reverses it in HF, no ADH release leads to no water loss leading to inc circulating vol and inc preload Some systemic changes are also seen: Vasculature – vasoconstriction due to several different factors Skeletal muscle – decreased blood flow due to vasoconstriction  decreased muscle mass/strength, including diaphragm  respiratory issues Renal system – GFR preserved initially, but then deteriorates and so you get too much urea and creatinine in the blood, can be sorted by angiotensin II, but due to this you’re in trouble whether you give ACE inhibitors or not

Answer 38

Left sided Causes Hypertension, IHD, aortic stenosis etc ``` Symptoms Extertional dyspnoea Orthopnoea Paroxysmal nocturnal dyspnoea Can also have tachycardia, cardiomegaly, mitral regurgitation and in late stages, small amounts of pulmonary and peripheral oedema ``` RIght Sided Causes Usually 2ndary to left heart failure (pressure backs all the way up) or ASD/VSD, pulmonary stenosis, chronic lung disease etc Symptoms Raised JVP Pulmonary oedema (worse when laying down) Pitting oedema Ascites due to venous congestion at liver All symptoms relate to build up in venous/pulmonary systems Congestive - Both Combined causes and symptoms

Answer 39

Prevention/modification – smoking, diet (SALT), alcohol, exercise, cholesterol etc Treat underlying factor (if present/treatable) Drug treatment (in order they’d usually be given) – ACE inhibitor and diuretic, beta blockers, spironolactone, digoxin Surgery – Valve replacement (stenosis/regurgitation), pacemaker implantation, revascularisation (IHD), mechanical assist devices, heart transplant

Answer 40

Usually caused by an atheromatous plaque in arteries and thrombus in veins. More common in the lower limbs. Leads to reduced blood flow to or from limb, which can manifest in a number of ways (intermittent claudication is a classic one). Also, the thrombus in a deep vein breaking off and causing a pulmonary embolism is always a big concern. Finally, you can get valve failure in superficial veins, leading to varicose veins (more notes in lower limb MSK summary)

Answer 41

Inadequate perfusion of all tissues throughout the body, leading to widespread ischaemia and death When considering shock, consider the following equations to make life 10x easier: o Mean arterial BP = CO*TPR o CO = Heart rate*Stroke volume o Also remember that Poiseuille’s law states that resistance decreases with radius ^4 (so a small vasodilation = large drop in TPR) Shock is either due to a huge fall in cardiac output (cardiogenic, mechanical or hypovolaemic) or a huge fall in TPR (toxic or anaphylactic)

Answer 42

Arises from within the heart itself. Example causes include a STEMI or a serious arrhythmia (VT or VF). Leads to poor perfusion of coronary arteries and kidneys, exacerbating your problems. Usually find a raised JVP due to blood backing up through the pulmonary system and the right side of the heart as it can’t leave the heart. Patient’s hands will be cold (poor perfusion) and clammy (autonomic nervous system activates when it senses the fall in CO). Result of reduced cardiac output

Answer 43

Failure of the heart to pump due a factor outside that of the heart. Classic two reasons are a cardiac tamponade or a huge pulmonary embolism Tamponade: The pericardium fills so the heart has no space to expand, reducing the pressure in all four chambers. As the blood cannot enter through the venae cavae, your central venous pressure (CVP) raises, but your arterial pressure stays low, as you’re not pumping anything out. Result of reduced stroke volume (electrical activity not altered) Pulmonary embolism: Embolus occludes large pulmonary artery, leading to pulmonary hypertension. This in turn leads to mechanical failure of the right ventricle as it can’t overcome the resistance. The inability of the right side to pump leads to decreased return to the left ventricle, leading to low left ventricle and low arterial pressure. CVP rises as the blood backs up in the venous system. Result of reduced stroke volume (electrical activity not altered)

Answer 44

Reduced blood volume, usually a result of haemorrhage but can be due to diahorrea or fluid loss from burns. Less than 20% blood volume loss can be dealt with by baroreceptor reflex, but anything over 30% starts to show symptoms of hypovolaemic shock. Loss of blood leads to decreased venous return and so decreased CO. The baroreceptors detect this and so increase TPR and cardiac output to try and compensate. However, the increased CO just causes the blood to hose out quicker. The solution is to stop the leak, give IV fluids to re-address blood vol (insert central line and give fluids until your CVP is in a healthy range) and undergo venoconstriction (supports CVP). Body shows some kind of internal transfusion; by increasing TPR you reduce capillary vhydrostatic pressure, and the plasma draws fluid from the interstitium Patient will be tachycardic with a weak and thready pulse, and have cold and clammy hands After a sufficient amount of time, the body decompensates as increased TPR causes tissue ischaemia – local vasodilators released as a response, which causes TPR to drop, and therefore BP plummets, causing multi organ failure Result of both reduced cardiac output and TPR

Answer 45

Results from septicaemia (blood poisoning), endotoxins released by circulating bacteria that increase the permeability of blood vessels and also cause systemic vasodilation. This causes TPR to plummet, and so vital organs can no longer be perfused, leading to death. The baroreceptors sense the decreased BP, and so attempt to increase CO and TPR. They can increase CO, but the endotoxins prevent vasoconstriction Patient will have a tachycardic pulse, and their extremities (and all their skin) will be red and warm The hyperperfusion of the peripheral vessels means not enough blood supplies the major organs To treat, you would give adrenaline to counteract the immediate effects (stimulates a1 adrenoceptors) and IV antibiotics Result of a drop in TPR

Answer 46

Severe allergic reaction that results in a massive histamine release (along with other inflammatory mediators such as leukotrines, heparin, IL3, TNF-a, bradykinins etc), causing a huge drop in TPR. The principle of shock is the same as that of toxic shock as the inflammatory mediators override the baroreceptor reflex and keep TPR very low. The mediators may also cause bronchospasm and laryngeal oedema (in fact, the bronchoconstriction is the immediate concern in several cases) Patient will have a tachycardic pulse, and their extremities (and all their skin) will be red and warm The hyperperfusion of the peripheral vessels means not enough blood supplies the major organs Odds are the patient will be carrying an epi-pen, and so you should use this ASAP Patient needs further emergency care such as chlorphenamine (disables the histamine, whilst adrenaline just addresses the drop in TPR) Result of a drop in TPR

Answer 47

Insufficient carriage of O2 within the bloodstream - 1/3 rd of world’s population suffer from this, is a symptom of the underlying aetiologies, of which there are many: Iron deficiency (diet) – most common, just eat an iron poor diet – foods such as red meat, fortified cereals, beans, spinach all good for reversing this – or give iron supplements Iron deficiency (absorption) – diseases that affect GI (for example Chron’s disease) can affect it’s ability to absorb iron, leading to a deficiency within the body Iron deficiency (blood loss) – can be heavy periods (use pill to control), or some GI cancers can cause bleeding into stools. Also, some people can become anaemic in the wake of giving blood, especially if they were borderline beforehand Haemolytic anaemias – any disease that affects function of RBCs (sickle cell, thalassaemias, eliptocytosis etc) will lead to increased breakdown, and body won’t replace at a constant rate, leading to decreased carrying capacity of blood Vitamin deficiencies – B12 and folic acid are both involved in erythrocyte synthesis so a deficiency of these can lead to reduced carrying capacity of blood

Answer 48

Huge breakdown of skeletal muscle leads to release of lots of myoglobin. This plugs renal tubules and causes renal failure

Answer 49

Autosomal recessive - Lack of antitrypsin molecule leads to excess trypsin activation – increased level of elastase release by neutrophils in areas of inflammation leads to excessive breakdown of elastin (destroys alveoli -> emphysema)

Answer 50

Deficiency of hepcidin (Fe2+ storage protein), Fe2+ deposited all over body instead, damages pancreas (bronze diabetes), heart etc – bleed to treat

Answer 51

Microscopic coal dust retained in alveoli and taken up by macrophages, system eventually overwhelmed and immune response causes pulmonary fibrosis, damaging lungs. Reduced air entry -> persistent cough, breathlessness, fainting etc.

Answer 52

Result of serious binge, toxins badly damage liver, formation of Mallory’s hyaline, targeted hepatic necrosis. Fever, jaundice and tenderness. Usually reversible

Answer 53

10/15% of alcoholics. Irreversible severe damage to liver. Shows as micronodules of hepatocytes surrounded by collagen bands. Jaundice, fever, sickness etc. Often fatal.

Answer 54

Streptococcus pneumonae – acuteinflammation causes exudate to accumulate in alveoli, loss of respiratory function. 4 distinct stages: Congestion (day 1-2) – vascular engorgement, some clear exudate deposition into alveoli Red hepatisation (day 3-4) – RBCs leak into exudate, large fibrin deposits formed Grey hepatisation (day 5-7) – RBCs have disintegrated, leading to exudate containing neutrophils and other WBCs to remain, thus appearing grey Resolution (day 8+) – Exudate drained through lymphatics and coughed up, can last up to 3 weeks

Answer 55

Fecaloma (calcified feces) blocks part of appendix, causes inflammation, bacteria colonise. Stays as abscess until wall of appendix ruptures, then can lead to peritonitis and systemic shock

Answer 56

Acute inflammation of the meninges of brain, causing a rise in intracranial pressure, occluding blood vessels supplying brain, leads to brain damage, coning and death. Several causative agents: Neonates – Streptococcus B Children – Neisseria meningitides Adults – Enterovirus – (so viral not bacterial) Elderly – Streptococcus pneumonae

Answer 57

Gallstone causes blockage of bile duct, bacteria can colonise this, causes infection that spreads to liver, is contained as a hepatic abscess. Results in jaundice and steatorrhea (lack of bile emulsifying fat). LFT will show high AST/ALT (hepatocyte lysis)

Answer 58

Autosomal dominant – mutation of C1 esterase inhibitor, means immune system runs out of control, huge generalised oedema throughout body. When affecting airways, leaves you unable to breathe -> death. Family history of death through laryngeal oedema, along with recurrent abdominal pain due to intestinal oedema

Answer 59

Neutrophils unable to form O2- (superoxide) radicals to eliminate phagocytosed pathogens. Instead just take them up by phagocytosis and they stay there, leads to many chronic infections, huge number of granulomas formed

Answer 60

Chronic infection of lungs caused by mycobacterium tuberculosis. Bacterium spread by droplet infection, macrophages phagocytose but can’t destroy due to mycolic acid coating, so forms granulomas, within which the bacteria multiply. Primary area of lung that’s infected known as ghon focus, forms a ghon complex (calcified hilar lymph node) when infection begins to heal. Treat with antibiotics, can lead to pulmonary fibrosis and eventual death. Also can become systemic if left untreated, leading to death due to failure of a system other than respiratory

Answer 61

– Idiopathic granulomatous disease of the lungs, common in young women, characterised by granuloma formation WITHOUT caseous necrosis. Ease symptoms with steroids (differential diagnoses of TB, if you misdiagnose and give steroids, you’ll kill a TB sufferer).

Answer 62

Tuberculosis Central caseous necrosis in granulomas Can see mycobacterium tuberculosis in granulomas with ZN stain Can culture mycobacterium tuberculosis from tissue sample Sarcoidosis Associated with hypercalcaemia Serum ACE can be elevated

Answer 63

Autoimmune attack on the synovium of joints, leads to granuloma formation, these can then erode the articular surface of the bones and lead to decreased mobility and severe pain. Affects all joints (not wear and tear), common in younger people and smaller joints (metacarpophalangeal first to go – claw hands). Treat with steroids to mediate immune function Forms rheumatoid nodes across the body, clumps of granulomas, indicates a large level of immune response

Answer 64

Varied aetiologies, ones of note include heliobacter pylori irritating the stomach lining, increased use of NSAIDs (aspirin, ibuprofen), these retard mucus defence, allowing acid to erode mucosa and come in contact with submucosa, which impairs function and causes acute pain. Forms ulcers with h pylori, this is an example of chronic inflammation. Treat bacterial infection with antibiotics (and give acid inhibitors at the same time) and the lining will usually heal H. pylori can predispose you to stomach cancer if you’ve had it for a long time

Answer 65

Main symptoms are intermittent abdominal pain, diarrhoea, which is sometimes bloody and weight loss. caused by chronic autoimmune inflammation of the colon, histologically shows crypt abscesses, destruction of mucosa and attack on submucosa. Increases risk of colon cancer, treat using steroids

Answer 66

Autoimmune chronic inflammation of any part of the GI tract (all the way from mouth to anus), leads to abdo pain, diarrhoea (sometimes bloody), and unexplained weight loss. Histologically, many granulomas and cobblestone bowel appearance seen. Common complications include anal lesions and bowel fistulae. Differentiated from colitis by the fact that it’s not restricted to the colon and doesn’t show crypt abscesses. Treat using steroids

Answer 67

Caused by mycobacterium leprae, is a chronic inflammation (producing visible granulomas due to mycolic acid coating) of the epidermis, nerves, eyes and respiratory tract. Leads to neuropathy of epidermis, poor eyesight that leads to eventual loss of extremities due to repeated unnoticed injury. Confirm bacteria with acid-fast test, then treat with appropriate antibiotics

Answer 68

Infectious STD caused by treponema pallidum, occurs in 4 stages: 1. Painless ulcer (acute and chronic inflammation) on genitals 2. As the untreated infection eventually escapes the abscess (>1 month since infection), the body develops a rash, fever, malaise, lethargy, joint pains, raised lymph nodes etc, all signs of a second acute inflammatory response due to the spread to other parts of the body 3. This eventually subdues the syphilis into a latent stage, in which you no longer display symptoms yet are still infected 4. The 4 th stage (tertiary syphilis) begins when the disease causes chronic inflammation in separate areas of the body, such as the brain, liver etc, these chronic inflammations can often lead to death

Answer 69

Autoimmune chronic inflammation which presents with ELK (E = ears/nose/throat, L = lungs, K = kidney), causes huge autoimmune attack on the epithelia of these locations, leading to granuloma formation and fibrosis, can lead to renal and kidney failure if left untreated, treat with steroids to reduce immune function

Answer 70

Vit C deficiency, prolyl hydroxylase can’t convert proline -> hydroxyproline, reduced H bonds, less cross links, weakened structure, “wobbly” collagen. Commonly presents as bleeding gums

Answer 71

Many types which vary depending on which collagen is affected but common feature is inherited defect in collagen gene which leads to hypermobility (more likely to subluxate/dislocate) of joints, stretchy skin, easily bruised, slow healing wounds etc

Answer 72

Disease resulting in type 1 collagen deformity/deficiency, major component in ground substance of bone. Most severe case leads to no conversion of foetal (hyaline) skeleton, incompatible with life. In most cases, repeated fractures lead to bowed long bones, and can be confused with NAI. Blue sclera due to unknown cause, possibly thinning of cornea due to issues with collagen that forms it

Answer 73

X linked dominant - defect in type 4 collagen, leading to major issues with basement membranes of kidney, ear and eye. Leads to nephritis, haematuria and eventual renal failure, along with progressive hearing loss and several varied ocular conditions

Answer 74

Scars that deposit an usually large amount of granulation tissue (mainly consisting of type 3 collagen), so that they extend the boundaries of the original wound (both raised but also extend way past the boundaries of the wound), much more common in darker skinned races than caucasians

Answer 75

Persistent acid reflux can damage the collagen framework of the oesophagus, which leads to scar tissue formation, which is inflexible and due to contraction by myofibroblasts, impacts function, causing dysphagia as primary presenting symptom

Answer 76

After a second or third degree burn, the basal layer of the epidermis is permanently damaged, leading to granulation formation, which, as it’s less flexible (less elastin) than skin, leads to a permanent shortening of the skin. This can occur over a joint, which leads to fixed flexion of the joint. Can be minimised by trying to ensure full extension of the joint for as much time as possible, however this is not always feasible

Answer 77

Autosomal Dominant - Misfolding of fibrillin leading to more elastic connective tissue, so parts of the body will just stretch abnormally when placed under pressure. Very tall, arachnodactyly, death usually around 40 from aortic rupture (arteries too elastic, just snap)

Answer 78

Formation of a thrombus within one of the deep veins of the body, usually in the lower limb. Number of risk factors: Inactivity – post-op, post-partum, long haul flights etc Obesity The pill Heart conditions (reduced cardiac output leading to stagnation of blood, Virchow’s triad) Can be prevented with subcutaneous heparin and TED stockings to reduce likelihood of thrombus formation. Treat with IV heparin/oral warfarin, can break off, migrate to lungs and cause a PE

Answer 79

Embolism (usually originates from the deep veins of the lower limb) that migrates to the pulmonary arteries, occluding these vessels and leading to respiratory symptoms. >60% reduction in lung function is always fatal. PEs can be major (shortness of breath, blood in sputum) or minor (shortness of breath or asymptomatic). Treat with clot busters (ie streptokinase). Can cause death through a few means: Right sided heart failure due to severe pulmonary hypertension Mechanical shock due to severely decreased preload of the left heart Critical hypoxaemia due to the ischaemia of a huge part of the lung (if it’s this bad, the effects on the heart will probably kill you first)

Answer 80

Bubble of air that becomes trapped in a blood vessel, can be a result of care provider error (cannulation etc), barotrauma (diver holds breath as they come up rapidly, bursting the alveoli), or decompression sickness (the bends, nitrogen as opposed to just air). If it gets into the heart (over 150ml air) it’s fatal, but will occlude any artery small enough – risk of stroke, ischaemic limb etc. Treat with hyperbaric chamber (bring to high pressure to dissolve the air then let the pressure down slowly)

Answer 81

Embolism as a result of a long bone breaking, releasing yellow marrow into the bloodstream. Carries the same risks as other embolisms, not easily treated, wait for the body to remove the fat, fix the bone ASAP

Answer 82

Recessive X Linked – No/reduced factor VIII production -> blood can’t clot as well (factor Xa production down 50%). Treat with recombinant factor VIII, avoid thrombolytics/blood thinners.

Answer 83

Widespread overactivation of the clotting cascade, which leads to the formation of many thrombi, can lead to multiple organ damage and eventual death. Also consumes platelets and clotting factors, making clotting at sites where it’s actually required less likely. Can treat to a limited extent with platelet transfusion to prevent haemorrhage

Answer 84

Lack of thrombocytes (platelets) in blood, as a result of either decreased production (folic acid deficiency, cancer of bone, infection etc) or increased destruction (usually a result of an autoimmune condition). Can however be caused by some medications (ie methotrexate). Treat underlying cause or give platelet transfusion

Answer 85

Excessive clotting throughout the body as a result of various genetic disorders, leading to overactivation of the clotting cascade, but not as severe as disseminated intravascular coagulation. Increased risk of DVT

Answer 86

Embolism as a result of a traumatic birth, where amniotic fluid finds it’s way into blood vessels through the female reproductive system. Same risks as other embolisms. Treatment is supportive as the amniotic fluid cannot be removed, the body must dissolve/remove it

Answer 87

Death of bowel due to occlusion of one of the mesenteric arteries (superior or inferior). Usually due to a thrombus coming from the left side of heart, which is a result of a L to R shunt (such as an ASD/VSD). Can also be due to atherosclerosis

Answer 88

Death of myocardium as a result of ischaemia, due to an occluded coronary artery. Usually a result of atherosclerosis but can be due to thrombosis as well. Prognosis is very poor as cardiac muscle has no regenerative capacity, what is dead is dead. Treat with a coronary bypass and/or stenting to open a narrowed coronary artery

Answer 89

Colloquially known as a ‘mini stroke’, is a result of cerebral ischaemia, but is not deprived of oxygen enough to leave permanent damage. Symptoms reside within 24 hours, therefore known as transient

Answer 90

Atheroma in arteries of the leg leads to reduced capacity to perfuse distal lower limb. Manifests as intermediate claudication first, but then progresses to constant ischaemic pain, and eventually ends up as dry gangrene as blood supply is completely lost

Answer 91

Long term atheroma causes weakening and therefore stretching of abdominal aorta, which leads to permanent dilation, sometimes clinically silent until it ruptures, at which point you get a colossal haemorrhage and almost definitely die. Can be seen as a pulsatile mass the abdomen if it’s sufficiently large. Usually left alone until the aorta’s lumen gets bigger than 4cm, at which point it’s operated on

Answer 92

Disorders of some aspect of the LDL mechanism that means that LDLs cannot be uptaken into cells, instead they are left in blood, which leads to this. Deposited at atheroma sites, tendons (tendon xanthoma), skin (xanthelasma) and cornea (corneal arcus)

Answer 93

Sharp chest pain that is elicited upon exertion due to the narrowed coronary arteries being able to meet the demands of the heart at rest but not during exercise. Disappears upto 10 minutes after excerise ceased (if it takes longer than this, start thinking MI)

Answer 94

Inability of the heart to supply the needs of the body ie cannot pump enough blood. Many contributing factors but a major one is atherosclerosis, leading to ischaemic heart disease as the heart cannot get enough blood

Answer 95

Cerebral infarction, either as a result of an embolism or atherosclerosis. Causes a very wide range of syptoms, usually on one side of the body FAST Face – one side will droop Arms – won’t be able to hold one in the air Speech – speech will slur due to paralysis of muscles involved in speech/muscles around mouth

Answer 96

Impaired blood flow to the colon, can be idiopathic but can also be caused by atherosclerosis of either mesenteric artery. Leads to malabsorption, abdominal pain and can progress to an infarction, which will require a section of bowel to be removed

Answer 97

Peripheral vascular disease that specifically affects the abdominal aorta at the point that it bifurcates into the common iliac arteries. Leads to a triad of symptoms in men: claudication in buttocks and thigh, weak/absent femoral pulses and impotence. Treat with stenting to re-open the artery

Answer 98

Relapsing/recurring inflammatory skin condition characterised by a rash that commonly is found in the skin creases. Usually triggered by exposure to a specific allergen. In MOD terms it is a result of excessive hyperplasia, leading to psoriasis like areas of scaling (chronic only, other forms of eczema have different pathophysiologies)

Answer 99

Extreme overproduction of skin cells (genetic link), which leads to an excessive deposition of keratinocytes at the stratum corneum, manifests as painful red ‘scaling’ of the skin. In MOD terms is an example of pathological hyperplasia

Answer 100

Hypothyroidism 2ndary to iodine deficiency – hyperplasia of thyroid gland to compensate for inefficiency (DIT/MIT require a source of dietary iodine to be synthesised successfully, which are then combined into T3 or T4). Pathological hyperplasia

Answer 101

Example of pathological hypertrophy, compensatory mechanism by the heart to try and overcome hypertension/aortic stenosis/aortic regurgitation (increased afterload/aortic pressure requires a stronger force of contraction). Decreased compliance from thicker muscle leads to impaired contraction past a certain point If the hypertrophy is slight and a result of extreme aerobic exercise, then it can be beneficial for short bursts of time ie. During a sprint

Answer 102

Enlargement of the prostate, leads to pressing on the urethra, so problems with voiding bladder. Largely a result of age NOTE, it is named hypertrophy as that is how surgeons describe it, but at a cellular level it is actually benign prostatic hyperplasia!

Answer 103

Observed metaplasia of the epithelium of the oesophagus (strat squamous  simple columnar) due to chronic acid reflux as this better resists the acid’s damaging effects. Clinical significance is that it is very strongly associated with oesophageal adenocarcinoma, an aggressive cancer

Answer 104

Example of metaplasia, conversion of connective tissue inside muscle into bone as a response to fracture healing. More likely in a younger person who doesn’t let their fracture heal properly before bearing weight on it again

Answer 105

Imbalance of oestrogen vs progesterone (oestrogen > progesterone) causes uncontrolled proliferation of the endometrial lining. Can predispose to cancer (more divisions = more chance of cancer developing)

Answer 106

Wastage of muscles due to lack of usage, can be reversed with proper usage again

Answer 107

Loss of bone density (wastage) due to lack of usage of bone (no stress on bone means reduced osteoblast function, so less deposition of new bone), example of atrophy

Answer 108

Malignant bowel cancer, higher chance of developing if you have ulcerative colitis. Can cause severe symptoms by growing large enough to cause a bowel obstruction. Five year survival: 65%

Answer 109

Aka uterine fibroids. Benign tumour that arises from the smooth muscle (myometrium) of the uterus. Can cause heavy/painful menstruation, painful sex and increased urinary frequency. Common cause for elective hysterectomy

Answer 110

Malignant bone cancer. Aggressive, likely to metastasise and forms osteoid (uncalcified bone precursor), so makes a pathological fracture more likely. Occurs most commonly in children and the elderly. 5 year survival: 68%

Answer 111

Usually benign tumour that contains normal derivatives of more than one germ layer (found in ovaries in this case). May contain anything from muscle tissue and teeth to skin and hair. Normally asymptomatic but can predispose to ovarian torsion (which will cause referred abdominal/pelvic pain)

Answer 112

Rare type of benign ovarian neoplasm that contains mainly thyroid tissue. May produce excess T3/4 and cause hyperthyroidism

Answer 113

Malignant cancer of the lymphocyte progenitor cells that leads to overproduction of B lymphocytes (usually), depositing these immature and therefore useless cells into the bloodstream, crowding out both the red and white blood cells. This eventually leads to anaemia and potentially fatal infections. If the ZAP-70 marker is present, average survival 8 years. If ZAP-70 negative, >25 year survival rate

Answer 114

Malignant cancer of plasma cells (terminally differentiated B cells that produce antibodies). Crowds out the blood much like leukaemia, but bone lesions and subsequent hypercalcaemia (released into blood following bone damage) also present. Antibody known as paraprotein also produced, which can lead to kidney damage. 5 year survival = 45%

Answer 115

Benign tumour composed of adipose tissue. Soft to touch, mobile and generally harmless (ie asymptomatic, don’t metastasise as they are benign)

Answer 116

Malignant tumour of the testicle. One of the most treatable and curable malignant cancers, survival rates over 95%

Answer 117

Malignant tumour of the endothelial lining of vessels (can either be lymphatic or circulatory systems. Location permits rapid metastasis so poor prognosis

Answer 118

Can be either benign or malignant, depending on the grade of the tumour, with benign ones being able to progress into malignant ones eventually. Tumour of the astrocytes, (large type of glial cells that make up the blood-brain barrier). Can occur in most parts of CNS. Prognosis good if early stage and able to be removed surgically, otherwise very poor. Cause unknown

Answer 119

Rare and aggressive (rapidly metastasizing) cancer of the melanocytes (pigment cells) in the skin. More common in Caucasians (less melanin = less protection), especially those that live in sunny climates (strong link with excessive UV exposure). Prognosis good if it hasn’t penetrated the basement membrane, bad otherwise. Five-year survival: 91%

Answer 120

Slow growing neuroendocrine tumour, that appear malignant MICROSCOPICALLY but behave in a benign fashion (carcinoid literally means carcinoma like). Usually found in the gut or lung. Can lead to excess production of serotonin, which causes carcinoid syndrome, characterized by flushing, wheezing, diarrhea, abdominal cramps and peripheral oedema.

Answer 121

Aka pancreatic cancer. Malignant cancer of the exocrine portion of the pancreas that leads to weight loss, jaundice, abdominal pain etc (ie non-specific symptoms). As symptoms are non-specific it is generally metastasized by the time a confirmed diagnosis is made

Answer 122

Benign tumour of one of the parathyroid glands, which cans an overproduction of PTH, leading to both hypercalcaemia and phosphate deficiency. This can lead to pathological fractures (due to reduced bone density), kidney stones, abdominal pain and depression (bones, stones, moans and groans). Treat with a parathyroidectomy

Answer 123

Aka pulmonary carcinoma. Common symptoms include haemoptysis (coughing up blood), chest pain, weight loss and shortness of breath. One of the big 4 that causes up to 54% of all cancer diagnoses. Due to the fact that it is very common and also very deadly, it is the UK’s biggest killer out of all cancers. Can metastasize through blood (to the whole body) or the pleural cavity (to other parts of the lung). Very strong link with smoking. Five year survival rate: 17%

Answer 124

Second most common type of skin cancer, behind basal call carcinoma. Malignant, and more aggressive than BCC. Chronic sun exposure is the most common environmental factor linked to this cancer, common on sun exposed parts (calves, arms, face and neck)

Answer 125

Malignant yet not aggressive, rarely metastasizes or kills. 30% of Caucasians will develop during their lifetime. Causes significant damage to facial structures as it commonly occurs on face or neck

Answer 126

Most gastric cancers are gastric carcinomas (ie developing from the endothelial lining of the stomach). Commonly caused by infection from h. pylori. Hypothesised that chronic inflammation from h. pylori predisposes the individual to cancer. Symptoms are non-specific and often confused with indigestion/gastro-oesophagal reflux disease, which leads to misdiagnosis and time for the cancer to metastasise. Five year survival rate: 28%

Answer 127

Type of lymphoma focusing on the destruction of B lymphocytes. Strong association with the Epstein-Barr virus, which accounts for the disease’s high prevalence within equatorial Africa

Answer 128

Hereditary condition characterized by numerous polyps, which may turn cancerous if untreated. Due to a hereditary error in the APC gene, which is a tumour suppressor gene that interacts with e-cadherin

Answer 129

Cancer of the cells of the retina that has a strong hereditary element. Very common in children, and involves a mutation in the RB gene that usually acts as a tumour suppressor. As all germline cells have one faulty allele, you only need one more mutation ‘hit’ to start developing cancer

Answer 130

Genetic defect that leads to the inability to perform excision DNA repair, which leaves cells incredibly vulnerable to UV damage. Makes patients with this much more likely to develop malignant melanoma, or any other type of skin cancer

Answer 131

Autosomal dominant baseline mutation that leads to problems with mismatch repair. Makes patients incredibly likely to develop colon cancer

Answer 132

Was the basis of realizing the relationship between carcinogens and cancer. Strongly associated with exposure to 2-napthylamine, which was a dye used in industry. Proved that cancer can take decades to develop after exposure, that there was a dose-response relationship and that different carcinogens can target specific organs

Answer 133

Primary cancer of the liver (not a metastasis) is very rare, but can be caused by Hep B/C acting as indirect carcinogens. The chronic inflammation and resulting high cell turnover that Hep B/C cause makes a mutation more likely just by chance, and then makes that mutation be promoted/proliferated quicker. Remission can be monitored by the presence of a- fetoprotein in the blood

Answer 134

Almost never seen without exposure to asbestos decades before – is cancer of the mesothelium (ie pleura) that surrounds your lungs. Asbestos acts a complete carcinogen (is essentially crushed silicate rocks) and so both initiates and promotes mesothelioma

Answer 135

Cancer of connective tissue (usually in skin but can be anywhere) due to infection with human herpesvirus 8. Human herpesvirus 8 cannot usually infect an immunologically healthy person, and is seen very commonly in HIV positive patients. This essentially means that HIV acts as a once-removed indirect carcinogen, as it lower immunological defenses to allow an indirect carcinogen to cause cancer

Answer 136

Cancer of the cervix. Caused by infection by the HPV virus (at least 99% of cases have an association with this virus). Huge steps taken in the UK to combat it, including regular smear screening and HPV vaccination. Is a good example of a cancer for which the staging is important.. T stages for TNM staging is as follows: 1 – <2cm 2 – 2 to 5cm 3 - >5cm 4 – Spread to wall/muscle/become inflamed

Answer 137

Cancer of the breast. One of the big 4 (along with prostate, bowel and lung) that make up 54% of all cancer diagnoses. Very good example of a cancer for which the clinical grading as well as staging is important. Can respond to hormone targeted therapy as tumours of the breast are normally oestrogen sensitive. The Bloom-Richardson scale is used to grade the differentiation of the tumour: Grade 1 – Presence of tubules Grade 2 – Mitoses Grade 3 – Nuclear pleomorphism

Answer 138

Cancer of the prostate. One of the big 4 that causes up to 54% of all cancer diagnoses in the UK. Has a reasonable survival rate. Good example of a cancer that uses tumour markers for both signposting cancer and checking remission. However, the issue is that prostate specific antigen isn’t specific to cancer, just disorder of the prostate

Answer 139

Cancer of the testes or surrounding tissue. Good example of a cancer that uses tumour markers (beta-HCG) to check remission. Thanks to the invention of cisplatin and the relative ease with which a testicle can be removed, it has the highest five year survival rate of any cancer in the UK, at well over 90%

Answer 140

Type of lymphoma focusing on the destruction of lymphocytes. Presence of the Reed-Sternberg cell (large, moth eaten multinucleate) confirms that it is Hodgkin’s instead of non- Hodgkins (such as Burkitt’s). Uses the Ann-Arbor classification system: Stage I: One lymph node group Stage II: Multiple lymph node groups confined to one side of the diaphragm Stage III: Multiple lymph node groups either side of the diaphragm Stage IV: Extralymphatic involvement (ie liver, lungs)

Answer 141

Serious but uncommon cancer. Not usually caught until it has metastasized so has a very poor prognosis (3 rd most deadly in the UK at an incidence of 15%). Symptoms include difficulting swallowing, weight loss, persistent cough etc

Answer 142

Specific type of leukaemia in which there is a huge overproduction of all white blood cells (as myeloids are progenitors), and this causes a reduction in RBC and platelet counts. Leads to anaemia, inability to clot blood and vulnerability to fatal infections. Results from the formation of a philidelphia chromosome (from a t9:22) that creates a new oncogenic fusion protein. Imatnib can inhibit this protein, giving a good prognosis. Five year survival rate is 90%

Answer 143

Cancer of the ovaries. Good example of a cancer in which you can use tumour markers to monitor the remission of a cancer, as it has CA-125 as a specific marker

Answer 144

Aka uterus or uterine cancer. Risk of this can be increased by the long-term use of tamoxifen, which is a hormone therapy for breast cancer. Risk can also be lowered however by the long-term use of the contraceptive pill

Answer 145

Specific type of cancer of the lungs. Noted for the fact it commonly releases PTHrp (parathyroid related protein), which can cause hypercalcaemia as it mimics PTH, also leads to osteoporosis as the bone is broken down to release the calcium

ESA 2 Clinical Conditions Flashcards

(169 cards)