ESA 3 Clinical Conditions Flashcards

Question

Hyperkalaemia Symptoms

Answer 1

``` Heart Predictable ECG changes (LIFE THREATENING) Tented T waves Prolonged PR interval, ST depression QRS widening VF Asystole ``` ``` GI Paralytic ileus (depolarises membrane and leaves Na+ channels inactive  inability of muscular contraction) Acidosis – K+ uptake into cells promotes movement of H+ to ECF ```

Answer 2

IV calcium gluconate – protect the heart Shift K+ into ECF – insulin and dextrose, salbutamol Remove K+ (dialysis) – last resort

Answer 3

Change diuretics, treat DKA etc. Reduce dietary intake Gut resins to bind K+ to inhibit dietary uptake

Answer 4

External balance dysfunction – excessive loss via GI (D and V, bulimia etc.) or renal (loop diuretics, diabetes mellitus or insipidus, high aldosterone e.g. Cushing’s) Internal balance dysfunction – metabolic alkalosis (following vomiting, alkaline tide)

Answer 5

Heart – predictable ECG change Hyperexcitability due to hyperpolarisation Low/absent T waves (no pot, no tea!) GI Paralytic ileus (hyperpolarizes membrane leads to (hyperexcitability leading to inability of muscular contraction) Skeletal muscle – same principle as paralytic ileus leading to muscle weakness Renal – unresponsive to ADH leading to nephrogenic diabetes insipidus

Answer 6

Treat cause (Cushing’s, diuretics etc.) Replace K+ (dietary/IV – BE CAREFUL WITH IV) Consider spironolactone/ACEi with excessive mineralocorticoid activity

Answer 7

Colonization of the urinary tract with bacteria (normally sterile)

Answer 8

Simple/uncomplicated (lower aka cystitis) – woman of reproductive age, most common Complicated (lower aka cystitis) – men, children of both genders, uncommon Pyelonephritis (upper) – inflammation of renal pelvis, can cause AKI/CKD Can lead to septicaemia/septic shock Chronic nephritis

Answer 9

Host Gender (female urethra shorter, shorter distance from perianal area to bladder) Obstruction of collecting system (benign prostatic hyperplasia, tumour, pregnancy, Neurological lesion leading to incomplete emptying therefore stasis and infection Ureteric reflux (angle of ureterovesical junction changes as we enter puberty) leading to ascending bladder infeciton in children Comorbidities – diabetes, CKD, AKI, hypertension, endocarditis etc. Bacteria Fimbrae – epithelial attachment Haemolysins leading to damaged host membranes leading to nutrition K antigen on polysaccharide capsule leading to evasion of macrophages Urease leading to NH3 production for bacterial growth Bacteria that fits most of this is E coli Can also be other enterobacteriacae, enterococci (atypical pathogen, rings alarm bells) or staphylococci

Answer 10

Frequent urination Pyuria (burning/stinging when peeing) Bad smelling urine Cloudy urine Malaise

Answer 11

Fever and chills (shivering) Nausea and vomiting Renal pain SIRS if severe

Answer 12

Urine sample Cloudiness – if it’s cloudy it’s almost always bacteria Nitrite/leukocyte esterase dipstick – bacterial metabolic byproduct and immune response indicate bacteria MCS of urine sample (complicated/pyelonephritis/comorbidities e.g. endocarditis, CKD) WBC/RBC count Culture for pathogens

Answer 13

Conservative – Inc. fluid intake, address comorbidities/underlying conditions Antibiotics Uncomplicated – 3 days trimethoprim (consult trust policy wherever you are) Complicated – 7 days trimethoprim/nitrofurantoin Pyelonephritis – 14 days ciprofloxacin/cefuroxime Can give low dose trimethoprim/nitrofurantoin as prophylaxis for recurrent UTI Chronic nitrofurantoin exposure leading to interstitial lung disease in some people

Answer 14

Stress urinary incontinence (SUI) – urinary incontinence (involuntary passing of urine) in response to exertion (coughing, sneezing etc.). Precipitated by exertion

Answer 15

Childbirth Previous pelvic surgery

Answer 16

Weight/height (obesity lead to Inc. risk of both types of urgency) Abdo exam (exclude palpable bladder for overflow incontinence) Female – external genitalia stress test (get them to cough) Male – prostate exam (hyperplasia)

Answer 17

Urine dipstick (nitrites indicate UTI, haematuria indicate malignancy, proteinuria, glucose indicates osmotic diuresis and overflow incontinence) Frequency and volume chart (urine in and out) Bladder diary (can help to work out SUI vs UUI) Pressure/flow studies (invasive)

Answer 18

General Decrease fluid/caffeine intake Avoid constipation Stop smoking Contained incontinence Indwelling catheter (risk of infection) ‘condom catheter’ – sheath device Incontinence pads Conservative pelvic floor exercises (3x 8 reps a day, every day for 3 months minimum) ``` Pharmacological dulotexine (NorAd/serotonin uptake inhibitor which increases activity of the external urethral sphincter in the filling phase leading to continence) ``` Surgical Female Low tension vaginal tapes – support mid urethra Retropubic suspension procedure – correct position of bladder neck leading to continence Classical fascial sling – use tensor fascia lata/rectus sheath to support urethra and bladder outflow leading to continence Intramural bulking agents – inject substance (fat, collagen etc.) into urethral walls to decrease lumen size leading to increase continence (Temporary measure) Male – artificial urethral sphincter – hydraulic device with control in the scrotum leadign to artificial continence the patient can turn on and off when urinating required

Answer 19

Urinary incontinence preceded/accompanied by urgency

Answer 20

Preceding urgency

Answer 21

General Decrease fluid/caffeine intake Avoid constipation Stop smoking Contained incontinence Indwelling catheter (risk of infection) ‘condom catheter’ – sheath device Incontinence pads Conservative – voiding scale training Void every hour, hold or let it leak in-between Increase duration between voiding by 15 to 30 minutes per week until 2 or 3 hours Pharmacological ``` Cholinergic antagonists (oxybutynin, could theoretically use atropine) Block M3 receptors  detrusor relaxation  less urge to void Nasty side effects from stimulation of other muscarinic ACh receptors e.g. dry eyes, dry mouth, constipation, tachycardia etc. – think exaggerated fight or flight response ``` B3 adrenoceptor agonist (mirabegron) Stimulates B3 adrenoceptors  detrusor relaxation  less urge to void Not many off target side effects ``` Botulinum toxin (Botox) Injected into detrusor and blocks ACh release at M3 receptors leading to loss of detrusor contraction – last resort as semi permanent (min 6 months) ``` Surgical – last resort Sacral nerve neuromodulation Augmentation cystoplasty (bowel used as bladder) Urinary diversion (e.g. send it to GI tract instead)

Answer 22

AKI itself can be defined as the same general thing irrespective of the cause: Clinical syndrome encompassing abrupt decline in GFR, increased [NH3] and [urea], acid/base disturbance and Na+ upset AKI is categorized into stages of severity: 1. Serum creatinine (SCr) >26.5mmol/L or >150% patient’s baseline 2. SCr >200% baseline 3. SCr >354mmol/L (w/acute rise of >44mmol/L in 300% baseline

Answer 23

Renal insult due to hypoperfusion of the kidney

Answer 24

Causes – anything that causes decreased O2 delivery to >50% of kidney parenchyma (so has to be bilateral/patient only has one kidney) Hypovolaemia Systemic vasodilation e.g. septic/anaphylactic shock Left ventricular failure (STEMI, severe valvular disease, cardiac tamponade leading to mechanical shock, tension pneumothorax etc.) Renal artery aneurysm/stenosis/thrombus/embolus Can also have impairment of renal auto regulation Preglomerular vasoconstriction caused by sepsis, NSAID overdose, hypercalcaemia etc. Postglomerular vasodilation caused by ACE inhibitor/AT2 antagonist overdose

Answer 25

Decreased Na+ delivery to macula densa (a result of decreased GFR) causes paracrine prostaglandin release to dilate afferent arteriole In a small GFR change, this is usually enough to correct the defect e.g. minute to Decreased Na+ delivery to macula densa (a result of decreased GFR) causes renin release which eventually leads to angiotensin II release This causes efferent arteriole vasoconstriction, can also correct the defect, more Due to the fact that it is trying to compensate, it is responsive to fluid resuscitation (circulating vol Inc. leading to preload Inc. leading to CO Inc. leading to renal perfusion Inc.)

Answer 26

A result of decompensation following pre-renal AKI that sees the loss of function of the tubular cells Cells of PCT very metabolically active so sensitive to loss of O2, without O2 can’t generate ATP to power Na+/K+ATPase to set up concentration gradient for isosmotic reabsorption Instead, fluid just flows through and out into urine at a constant rate like a sand timer/sieve This means that kidneys can no longer respond to changes in osomolarity so fluid resuscitation can lead to dilutional hyponatraemia So you have to distinguish between pre-renal AKI and ATN to give correct treatment

Answer 27

Ischaemia Nephrotoxins – all drugs considered nephrotoxins until proven otherwise Can also have endogenous nephrotoxins e.g. myoglobin, bilirubin Rhabdomyolysis – huge breakdown of skeletal muscle (trauma) causes huge myoglobin release, which is a nephrotoxin leading to ATN

Answer 28

Any pathological process that actually affects the renal parenchyma Glomerular disease – see nephritic syndromes below Essentially, inflammation/immune response  clogged glomerulus leading to decline in GFR Primary – only affect glomeruli e.g. IgA nephropathy Secondary – part of a wider immune response e.g. Lupus, vasculitis Acute tubulo-interstitial glomerulonephritis – infection (usually) as a consequence of pyelonephritis Can also be toxin induced (nephrotoxic drugs; penicillins, NSAIDs, omeprazole etc.) Other causes – linked by common pathology of endothelial damage leading to microvascular thrombi leading to occlusion of small arteries  microangiopathic haemolytic anaemia leading to dec O2 delivery to renal parenchyma Haemolytic uraemic syndrome – preceded by a bout of infectious diarrhea Malignant (severe) hypertension Pre-eclampsia (hypertension during pregnancy)

Answer 29

Obstruction of the collecting tract Inc. intraluminal pressure leading to backup leading to hydronephrosis thus renal impairment ``` 3 main types Intraluminal – RENAL CALCULI, thrombus, tumour etc. Within wall (usually causes CKD not AKI) – post TB stricture etc. Extrinsic – hyperplastic prostate, tumour, aneurysm (abdo aorta/uterine artery) etc. ``` Almost always causes renal colic and haematuria

Answer 30

Tend to be elderly Hypotensive (BP should be measured as a difference from the norm e.g. an elderly man with angina, hypertension, ACEis and diuretics at 120/80 is essentially hypotensive) Nauseated, lethargic

Answer 31

Hypovolaemic shock – tachycardia, hypotensive, peripheral cyanosis, dec JVP Septic shock – tachycardia, hypotensive, red and warm peripheries, dec cap refill time, rigors, pyrexia

Answer 32

Nephrotoxic drug history Urinary tract infection (see above) Trauma (rhabdomyolysis, particularly in the elderly)

Answer 33

RENAL COLIC – flank pain T11-L3, patient will roll around to try and stop it Anuria Palpable bladder Potentially an enlarged prostate

Answer 34

Urinalysis Nitrites (UTI) Blood and protein (nephritic syndrome leading to renal AKI) Urine biochemistry – pre-renal vs ATN Pre-renal leading to huge ATII release thus high urine osmolarity w/ low [Na+] ATN leading to decompensation and loss of function and thus low urine osmolarity (similar to ECF osmolarity as no reabsorption has taken place) w/ high [Na+] Serum biochemistry – shows immediate concerns/complications In all cases, [urea] and [creatinine] are Inc. Hypocalcaemia (and potentially hyperphosphataemia) Hyponatraemia a result of fluid overload (dilutional) or acute tubular necrosis (pee it all out) Hyperkalaemia – WILL KILL PT IF YOU’RE NOT CAREFUL Imaging USS – query obstruction/no change in pre-renal despite fluid resuscitation (check for stenosis/aneurysm) CXR – assess fluid overload and/or infection (TB, peritonitis etc.) AXR – look for radiopaque stones (USS probably better for this) Renal biopsy – differentiates types of renal AKI when you’re not sure (glomerulonephritis, acute tubular necrosis and acute tubulo-interstitial nephritis show different histology because they’re different parts of the kidney)

Answer 35

Pre-renal – correct the fluid balance (hypovolaemia) and underlying insult (sepsis leading to septic shock) Surgery on renal arteries if needed ATN – supportive of normal body homeostasis Renal – supportive of normal body homeostasis (so carefully monitor fluid intake and treat ion imbalances/acidosis/alkalosis) and treat the specific cause (see below for some common causes of nephritic syndrome) Post-renal – remove blockage Dialysis is a last resort – only indicated in some cases Persistent hyperkalaemia despite treatment (B2 agonists, calcium gluconate, binding resins, insulin and dextrose, discontinue K+ sparing diuretics e.g. amiloride) Fluid overload despite treatment (diuretics, strongest ones are loop diuretics as this is where the most Na+ reabsorption occurs out of all diuretic targets) Metabolic acidosis where supplementary NaHCO3 is contraindicated Dialysable nephrotoxin e.g. antifreeze Severe uraemia (pruritus, pericarditis, dec GCS, nausea and vomiting)

Answer 36

Characterized by >3.5g protein lost through urination in

Answer 37

Presents in adults Focal segmental glomerulosclerosis = scarring in isolated area of glomerulus that leads to Can progress to renal failure, doesn’t respond well to steroids Known to be caused by an immune factor (we just don’t know what this factor is) as filtration dysfunction (generic scar tissue which are not specialized for filtration making them leaky) transplanted kidneys also suffer

Answer 38

Presents in adolescents, worsening proteinuria Minimal change = normal under LM but shows podocyte damage under TEM Unknown pathogenesis but can respond to steroids and not likely to progress to renal failure

Answer 39

Most common in adults Immune deposits in the sub-epithelial space lead to thickened capillary loop lead to leaky membrane leading to proteinuria Follows the rule of 1/3rds (1/3rd get better, 1/3rd show no change (no renal failure) and 1/3rd progress to renal failure) Tends to be associated with lymphoma

Answer 40

Damage to the glomerulus leading to significant haematuria along w/ proteinuria (pores large enough to allow RBCs through) and decreased renal function as a result

Answer 41

Most common cause of nephritic syndrome (and commonest type of glomerulonephritis) Presents at age with visible or invisible haematuria Known to have a relationship with mucosal inflammation as IgA protects mucosal surfaces Histological findings are varied, by mesangial proliferation and scarring w/ a positive IgA stain are usually seen Significant proportion leading to CKD and eventual renal failure

Answer 42

One of two common hereditary nephropathies, and the more benign. Thin GBM leads to isolated haematuria, doesn’t really progress to any sort long term renal damage

Answer 43

X linked recessive abnormal collagen IV structure leading to dysfunction of the basement membrane As collagen IV isn’t exclusive to the kidneys, deafness (ear BM dysfunction) also seen Usually progresses to renal failure Exists on a spectrum with thin GBM nephropathy

Answer 44

Aka anti-GBM disease Overnight onset of severe nephritic syndrome due antibody to collagen IV Typically only affects GBM, and not ear (no one knows why) Associated with pulmonary haemorrhage in smokers due to alveolar BM damage (not seen in people with healthy lungs) Can be treated with complete immunosuppression and IgG plasmophoresis if caught early enough

Answer 45

Systemic inflammation of blood vessels (kidney is well vascularized and therefore affected) Blood vessels directly attacked by ANCA (anti-neutrophil cytoplasmic antibody) and neutrophils Histologically appears as segmental necrosis, but can be treated if caught early enough

Answer 46

Carcinoma of the prostate (usually) Risk factors Increased age Ethnicity (black>white>Asian w/ Asian as lowest risk) Family history – BRCA2 gene Why don’t we screen? Won’t improve QOL/life expectancy in a significant amount of patients Prostate specific antigen isn’t specific to prostate cancer, just a general pathology of the prostate Presentation – elderly, haematuria (advanced cases), renal colic – USUALLY ASYMPTOMATIC Bone pain from mets (usually sacrum/hip) Investigation – rectal exam, PSA blood test, bone scan (for mets) and transrectal ultrasound biopsy Treatment – depends the severity of the disease Localised – surveillance (especially elderly, not worth the hassle), radical prostatectomy or radiotherapy (external vs local radioactive beads in rectum) Advanced localized – surveillance, hormones or radiotherapy Metastasised – surgical/medical castration w/ LHRH agonists (overload receptors, shuts down the feedback loop and it stops functioning) which slows growth, bisphosphonates to protect bone and chemo/radiotherapy

Answer 47

Usually a carcinoma Risk factors – smoking, schistosomiasis (only really seen in developing world), occupational exposure to carcinogens (rubber/plastic/oil industry) • Staging – based on TNM but T types are specific of course: • T1 – up to submucosa • T2 – penetrated 50% but

Answer 48

Risk factors – smoking, obesity, dialysis Mets are common Perinephric spread leading to secondary renal tumours Lymphatic spread leading to nodal mets Venous drainage leading to IVC obstruction w/ ‘tumour clot’ Treatment – surveillance, radical nephrectomy Palliative – molecular angiogenesis antagonists e.g. sunitinib

Answer 49

Cancer from the kidney down to the trigone Uncommon, but related to smoking, phenacetin (discontinued painkiller) use and Balkan’s nephropathy (type of familial interstitial nephritis) Leads to hydronephrosis (tumour leading to obstruction) Needs a radical removal of kidney, fat, ureter and part of trigone

Answer 50

Defined as the irreversible and progressive degeneration in renal function over months to years. Universal pathological feature is replacement of renal parenchyma with fibrous scar tissue leading to shrunken, fibrotic kidney that’s no longer specialized for function

Answer 51

Classified into several stages (numbers aren’t that important): GFR based - >90ml/min/1.73m2 is G1 (has to show some underlying pathology etc. polycystic kidney) whilst 30 These two scores combined to give a staging code e.g. G3aA3

Answer 52

DIABETES HYPERTENSION Renal artery sclerosis Infection e.g. chronic pyelonephritis Genetic e.g. Alport’s Obstruction/reflux nephropathy e.g. renal calculi hydronephrosis Idiopathic

Answer 53

CKD has effects spanning several bodily systems Cardiovascular -atherosclerotic plaque formation, hypertension and subsequent cardiac damage (ATII release) and uraemic pericarditis Ca2+ regulation Decrease in tubular function  loss of Ca2+ in filtrate and increased retention of H3PO4- Also, creation of active Vit D decreased (osteomalacia) [Less dietary absorption] Hypocalcaemia causes PTH release and subsequent bone breakdown to generate free Ca2+ (known as osteititis fibrosa cystica) Bone breakdown seen in vertebrae (rugby jersey spine) and terminal phalanges -known as renal osteodystrophy Disarray in Ca2+ metabolism can lead to metastatic/dystrophic calcification (seen in aorta, synovial joints etc.) Bodily pH – acidosis resulting from inability to retain HCO3- – oral NaHCO3 tablets to treat Anaemia – decreased secretion/sensitivity to EPO leading to loss of RBC production Also an element of haematuria in severe cases ``` Some general symptoms also seen: Breathlessness (anaemia) Seizure (uraemia?) Aches and pains (uraemia?) Nausea and vomiting Itching (uraemia) ```

Answer 54

Inulin clearance – give an IV infusion of inulin and because you know its freely filtered and isn’t secreted/reabsorbed you can measure amount in urine and calculate the true GFR ( eGFR – in reality, inulin is expensive and time consuming, so we use the patient’s creatinine levels as a cheap and pretty good approximation Use plasma creatinine and an iPhone app to calculate Importantly, the app adjusts the formula for age (GFR declines w/ age), race (black people have higher muscle mass) and gender (males have higher GFR) Not perfect; only valid for adults, can’t show AKI only CKD and some decline in GFR gives normal creatinine levels (generally>50%)

Answer 55

Context of a Past medical history (PMH )is vital, usually gives the game away Many blood tests available for various causes; immunoglobulin (IgA nephropathy), ANCA (vasculitis/lupus), CRP (infection) etc. Imaging to look for pathology (particularly obstructive/polycystic) USS – hydronephrosis secondary to obstruction CT – renal artery stenosis/aneurysm Nutcracker syndrome is a rare condition where the left renal vein is compressed between the ‘nutcracker arms’ that are the abdominal aorta and the superior mesenteric artery. This venous congestion gives rise to CKD MRI – renal artery stenosis/aneurysm

Answer 56

Modify lifestyle factors – smoking, obesity and lack of exercise Treat comorbidities – mainly diabetes and hypertension Treat underlying pathology if possible Reduce lipid intake/amount (statins) ACEis if proteinuria shown (decrease the amount of this leads to better prognosis and also lowers BP leading to decreased hypertensive damage leads to better prognosis) End of the line – dialysis or renal transplant

Answer 57

Defined as a level of renal function that would cause death without intervention (generally speaking, GFR

Answer 58

symptoms are classified by loss of the kidney’s functions (like an exaggerated version of CKD): Tiredness/fatigue/difficulty sleeping/difficulty concentrating (combination of anaemia and inability to excrete toxins) Volume overload (similar to CHF; raised JVP, SoB, oedema etc.) due to inability to excrete fluid Anaemia (see CKD, same pathology) Bone disease (see CKD, same pathology) Acidosis (see CKD, same pathology) Uraemic symptoms (see CKD) Also results in an increased sensitivity and narrowing of therapeutic index of many drugs due to decreased metabolism and or excretion

Answer 59

Falls under the umbrella term of renal replacement therapy Haemodialysis – uses creation of an arteriovenous fistula (increases blood flow as blood goes artery  vein) to allow a point for withdrawal of 300mls of blood at a time (entire circulatory volume dialysed in theory) This allows for exchange along an extracorporeal circuit that causes diffusion between sterile dialysis fluid and blood (w/ heparin to prevent clotting) across a semi permeable membrane, eliminating toxins within the blood Advantages; less responsibility for own care, 4/7 days off from dialysis, known to be effective in long term Disadvantages; arteriovenous fistulae can be ugly (cosmetic problem, like a bad varicose vein), limits travel, have to keep to specific appointment, can damage CVS due to vol change Contraindications; failed vascular access, heart failure and coagulopathy (last two relative, they’re less likely to kill you than the renal failure) Peritoneal dialysis – uses the peritoneum as the semi-permeable membrane (same guiding principle is the same as haemodialysis). The peritoneum is filled with dialysis fluid and the exchange with the ECF/blood vessels allows for elimination of toxins Two main types, one involves 4-5 bag changes every day, one takes place overnight Advantages; autonomy of care, less fluid/diet/travel restrictions than haemodialysis Disadvantages; no days off, frequent changes, responsibility, indwelling catheter leads to peritonitis, hernia etc. Contraindications; failure of peritoneum (leak, hernia etc.), patient/carer can’t connect bag (elderly), obese/dench (relative contraindication, about peritoneal size to body bulk ratio) Kidney transplant – gold standard for renal replacement therapy. Kidney is plumbed in at iliac fossa rather than normal T11-L2 as it’s easy access to iliac vessels and bladder Types of donor  Deceased after brain death  Decreased after circulatory death  Live donation (usually related but can be altruistic) Advantages; pretty much entirely restores renal function, no repetitive treatment, lower mortality vs dialysis, good long term prognosis >10yrs Disadvantages; risk of operative mortality, limited donor supply (average wait ~3yrs, and have to be matched on blood group and MHC/HLAs), life long immunosuppression leading to infection (and Cushing symptoms if steroid dose high enough), still not a permanent fix Worth noting that elderly patients tend to survive just as long with palliative care for ESRD as they do on haemo/peritoneal dialysis

Answer 60

An increased partial pressure at below sea level leads to diffusion of nitrogen from lungs into blood. If the diver ascends too quickly the rapid change in pressure causes bubble formation (like opening a bottle of coke) and this causes extensive tissue damage and is very painful

Answer 61

A loss of surfactant leads to upsetting of Laplace’s law () as surfactant normally keeps surface tension in small bubbles low. This leads to alveolar collapse due to the pressure difference in different sized alveoli, which reduces surface area for gas exchange and leads to respiratory failure (Type 1 then eventually 2). Commonly occurs in premature babies, and the mum can be given steroid injections to stimulate surfactant generation if anticipated Also occurs as a result of trauma – tricky to treat

Answer 62

CO binds to haemoglobin and forms carboxyhaemoglobin. This variant of Hb can’t bind O2 and so O2 delivery to tissues suffers. If occurs acutely it can kill in sleep (faulty gas boiler for example), but chronic exposure causes headaches, confusion, nausea etc. Needs treating with hyperbaric O2 therapy as in very high concentrations O2 can displace CO and restore function of Hb

Answer 63

Thrombus from a site other than the lungs (common the deep veins of the leg e.g. popliteal) lodges in one of the arteries of the pulmonary tree. This leads to a V/Q mismatch in the section of lung the artery supplies, so the pO2 of the blood leaving that section is low and the pCO2 is high. The hypercapnia causes resp rate to increase. Blood is redirected to healthy lung and the Inc. resp rate meansthe pO2 is normal (Hb is 100% saturated at 13.3kPa) but pCO2 is low. Mixed venous blood (from healthy and infarcted lung) therefore has low pO2 but normal/low pCO2 (Type 1 resp failure, see below) Real danger comes from sudden pulmonary hypertension which can cause mechanical shock due to RV failure in heart

Answer 64

Type 1 | Type 2

Answer 65

pO2 low, pCO2 normal or low. Due to either a diffusion defect or V/Q mismatch Diffusion defect – any factor of Fick’s law affected leading to difficulty of diffusion between capillary blood and alveolar gas As CO2 diffuses 20x more readily than O2 (much higher solubility coefficient) then it’s no surprise pCO2 is relatively unaffected Also, any initial hypercapnia/the hypoxia increases resp rate and excess CO2 is blown off so pCO2 may be lowered Pulmonary oedema – fluid in the alveoli/interstitium, increases diffusion distance Emphysema – decreased compliance of lungs  hyperexpansion  reduced SA for gaseous exchange Pulmonary fibrosis – fibrous deposits between alveolus and capillary BM leading to increased diffusion distance V/Q mimatch – see pulmonary embolism

Answer 66

pO2 low, pCO2 high. A result of ventilation dysfunction leading to an inability to change air and no CO2 removal or O2 delivery. More serious than Type 1. Not easily corrected physiologically as increased respiratory drive won’t remedy the situation (ventilation compromised already) Decreased respiratory effort Narcotics/head injuries/neurological deficit e.g. stroke (anything that impacts ability of respiratory centre) Muscular dysfunction – anywhere from the brain to the NMJ (multiple sclerosis, Duchene’s muscular dystrophy, spinal cord lesion, myasthenia gravis etc.) Chest wall defects (rigid structure makes it harder to move and the lungs harder to inflate) Severe scoliosis/kyphosis (spinal conditions, see ClinicalConditionsESA2) Severe pectum excavatum/carranatum Flail chest (section of ribs detached from thoracic cage by multiple fractures – major trauma) Tension pneumothorax Increased compliance – severe pulmonary fibrosis (IPF, see below) Extremely high airway resistance (such that almost no expiration is possible) Severe life threatening asthma attack Acute exacerbation of late stage COPD (already in Persistent hypoxia w/ CO2 retention)

Answer 67

A reversible airway obstruction

Answer 68

Airway remodeling including Inc. ASM thickness, damaged epithelia/basement membrane as a result of chronic inflammation (TNFa, neutrophils, eosinophils and mast cells) due to a reaction to ordinary stimuli e.g. dust ASM contraction increases airway resistance so less air expired initially (think Poiselle’s law in CVS) Contraction of ASM caused by histamine and prostaglandin release in response to many stimuli (cold temperatures, dust, pet dander etc.)

Answer 69

1/11 kids affected (1/12 adults, generational increase due to lifestyle conditions?) Hygiene hypothesis – overuse of cleaning chemicals leads to reduced ‘training’ of immune system on harmless bacteria thus hyperactivity and atopy) Sensitisation to allergens such as smoke, smog, fungal spores, dust etc. through priming of mast cells with IgE Second exposure to the trigger causes IgE activation  histamine release  ASM contraction Other (not allergic) types of asthma: Viral asthma – disappears by ~5 years old Occupational asthma – farmers etc.

Answer 70

History – can make the diagnosis on this ALONE – need two of the following: Expiratory, polyphonic wheeze Dry cough with diurnal variation (worse at night) – induced by exercise Breathlessness (hypoxia leads to peripheral chemoreceptors increase respiratory drive) Chest tightness Variable airflow obstruction (reversed with B2 agonists) Other things to note (increase suspicion but not used to confirm diagnosis): Disturbance to life Other aspects of atopy (hayfever and eczema) Family history (of all atopic diseases) Pets and passive smoke in the house Intolerance to exercise ``` Examination Eczema Lethargy, uncomfortable at rest Below height for age, underweight? ``` Signs of labored breathing: Harrison’s sulcus (indrawing of costal cartilages) Tracheal tug Subcostal recession Obvious use of accessory muscles of inspiration (pec major, scalenes, sternocleidomastoid, serratus anterior etc.) Investigation – diagnostic tools if unsure/monitor progress (particularly PEFR) ``` Primary PEFR – cheap and cheerful, reduced PEFR leads to obstructive airway disease Single breath (vitalograph) spirometry – measure FEV1:FVC (12% Inc.  definitely asthma) ``` Supportive (optional) FENO – patients w/ asthma have high levels of NO due to inflammation – can measure to give an idea of the level of inflammation Skin prick – check sensitivity to common allergens and use to advise lifestyle changes Chest X ray – exclude other differentials (only normally in acute exacerbations) e.g. pneumothorax, bronchitis

Answer 71

Lifestyle – stop exposure to allergens (including passive smoking), exercise, fresh air etc. Pharmacological (note inhalation all about eliminates off target side effects at the doses inhalers are used at) Relievers – stave off acute exacerbations e.g. salbutamol (B2 agonist), ipratropium (Atreovent, M3 antagonist) and aminophylline (Inc. CAMP  Inc. PKA  Inc. SM dilation) Preventers – low dose corticosteroids to suppress immune function locally

Answer 72

Recognition Poor respiratory effort/loud wheeze/silent chest Panicked, agitated, sympathetic features (sweating, dry mouth, dilated pupils, nausea etc.) Altered GCS (cerebral hypoxia) SaO2

Answer 73

A progressive, worsening airway obstruction Umbrella term for two pathologies Chronic bronchitis – mucus hypersecretion and inflammation due to irritation by cigarette smoke Cough chronically productive w/ frequent infections Airway remodeling to Inc. ASM (as with asthma but different cause, result of chronic inflammation instead) Emphysema – pathological destruction of terminal bronchioles and walls between alveoli Inflammatory response to chronic irritation from cigarette smoke causes macrophages to release elastase and other proteolytic enzymes leads to breakdown of elastin Forms large redundant bullae (‘superalveoli’)  collapse on expiration due to loss of supportive tissue leading to obstruction Fick’s law – less SA for diffusion leading to impaired gas exchange Less elastin means less compliance and hyperinflation of lungs Visible as Inc. rib spacing and width of thoracic cavity on CXR – ‘barrel chest’

Answer 74

SMOKING A1-antitrypsin deficiency – hereditary, leads to overactivity of elastase leads to emphysema Seen in young patients usually Pollution (especially common in China) Occupational e.g. coal worker’s pneumoconiosis

Answer 75

Predictable pattern of worsening disease Early stage – productive cough, dyspnoea, tachypnea Middle stage – purse lip breathing (maintain pressure on expiration leads to delay in airway collapse), use of accessory muscles to inspire, barrel chesting Late stage – compensated respiratory acidosis (CO2 retention) Wheeze/reduced breath sounds Peripheral leads to central cyanosis CO2 retention (flapping tremor) Pulmonary hypertension leads to peripheral oedema, raised JVP etc. (cor pulmonale)

Answer 76

Usually pretty confident from the history Single breath spirometry – FEV1:FVC 50% Moderate – FEV1 30% Severe – FEV1

Answer 77

Lifestyle STOP SMOKING Moderate exercise (if MRC allows) Manage other co-morbidities e.g. heart disease ``` Pharmacological B2 agonists (salbutamol) – bronchodilation Leads to systemic effects e.g. tachycardia, tremors etc. if dose too high ``` ``` M3 antagonists (ipratropium/Atrovent) – bronchodilation, more useful than B2 agonists in COPD Side effects akin to sympathetic overload e.g. dry mouth, nausea, tremors, tachycardia, urinary retention ``` Aminophylline (inhibits phosphodiesterase  more CAMP  more PKA  MLCK  bronchodilation) – Inc. respiratory drive and power as well  Low therapeutic window, causes SVT, nausea, seizures etc. w/ overdose Oral corticosteroids – reduce inflammatory pathways  improves chronic bronchitis Nasty side effects >800mg/day Addison’s disease (PAS feedback down regulated so less ACTH release) leads to hypotension when stopped abruptly Diabetes Osteoporosis Weight gain/GI symptoms Mucolytics – thin the mucus lead to easier airway clearance Other interventions Pulmonary rehab – breaks cycle of breathlessness leads to lack of activity leading to weakness and breathlessness etc. 6-12wk MDT led exercise, unsupervised ‘homework’ exercise, nutritional advice, disease education Long term O2 therapy – offered w/ persisting hypoxia (

Answer 78

Acute exacerbation – wary of Type 2 respiratory failure Investigations Pulse ox and ABG Sputum culture, CRP, U and Es, FBC CXR Management Titrated O2 therapy (aim for 88-92% SaO2) Salbutamol, Atrovent and aminophylline High dose steroids (only if confirmed as non-infectious, you’ll kill the pt if you kick their immune system out when they’ve got pneumonia) Non-invasive ventilation Have to be conscious w/ mild resp acidosis (pH7.25)

Answer 79

Ccute inflammation of the middle airways, common in healthy people and nothing sinister in most cases. Usually viral (so no antibiotics). Presents w/ dyspnoea, productive cough, fever, malaise etc. Associated with sinusitis and otitis media due to connections to nasal cavity. Shows a clear CXR as only middle airways affected

Answer 80

Inflammation of the lung alveoli. This impairs gas exchange and causes Type 1 resp failure if unchecked

Answer 81

Where it was acquired – community acquired (discussed in this section) vs hospital acquired Presentation – acute vs chronic (tends to be acute) Organism – bacterial, viral, fungal (PCP, HIV alarm bell) Pathology – lobar pneumonia (most common), bronchopneumonia, interstitial pneumonia etc.

Answer 82

Symptoms Productive cough Fever/malaise/rigors Pleuritic chest pain Nausea/vomiting Signs Pyrexia Tachycardia/tachypnea/cyanosis (all a result of hypoxia) Dullness to percussion/bronchial breathing/pulmonary crackles (alveoli full of exudate)

Answer 83

Bloods: FBC, CRP, U and Es, lactate, MCS Other: Erect CXR (shows as consolidation in the affected lobe – lobar is the most common form), sputum culture ``` CURB65 - a measure of severity of the disease, one point for the following: Confusion Urea >7mmol/L RR>30/min BP 65 ```

Answer 84

dependent on the CURB65 score: >1 – severe pneumonia, need admission to hospital Co-amoxiclav and clarithromycin (cover some atypical pathogens as well) B2 agonists/M3 antagonists may help (particularly in patients with existing asthma) High flow O2 1 or 0 – moderate pneumonia, can be cared for in the community Amoxicillin (probably Streptococcus pneumoniae)

Answer 85

In an ideal world – resolution w/ minimal scarring  return to normal lung function Lung abscess formation leading to rupture and empyema Bronchiectasis (permanent dilation of bronchioles) Septicaemia/meningitis Death due to Type 1 respiratory failure

Answer 86

Inflammation of the lung alveoli. Different from the ‘typical’ pneumonia that are caused by Streptococcus pneumonia and acquired in the community. Several types: Atypical bacterial pathogens – caused by bacteria without a cell wall (Gnegs) so requires antibiotics that are effective for these Examples include Legionella (legionnaire’s disease), Chlamydia etc. Treat with macrolides (clarithromycin) or tetracyclines (doxycycline) Viral – ~10% Adenovirus, respiratory syncytial virus, influenza etc. Tends to be severe, haemorrhages into lung parenchyma so is easily confused with acute Looks like patchy diffuse ground glass on a CXR respiratory distress syndrome (similar symptoms – see earlier) Hospital acquired – any causative agent >48hrs from hospital admission May be on a ventilator already Requires a bronchial lavage to isolate the causative organisms without contamination from the commensals of the URT Co-amoxiclav 1st line, try Tazocin if no improvement More often than not it’s Staph aureus Aspiration – contents of the GI tract end up in the lungs – requires some sort of compromise to epiglottis/larynx as protective mechanisms Common w/ epileptics, stroke victims, alcoholics, drowning victims etc. Tends to viridans Strep and other anaerobes Co-amoxiclav 1st line Immunosuppressive – usually secondary to AIDS/HIV (atypical pneumonia, particularly fungal, is an AIDS defining illness) Common causative agents: PCP, TB, other mycobacteria, Aspergillus, cytomegalovirus etc. Splenectomy puts patient at increased risk of colonization by S. pneumoniae, H. influenzae So immunosuppressive pneumonia but with typical pathogen

Answer 87

Tuberculosis (TB) – bacterial infection of the lungs by (classically) Mycobacterium tuberculosis, can also be M. bovis or other mycobacteria

Answer 88

Mycolic acid coating that gives structural rigidity – but also makes it hard for antibiotics to penetrate so bacteria are very hardy Neither Gneg nor Gpos, uses a ZN stain to characterise it as ‘acid fast’ Non-motile, obligate aerobe (so colonises the upper lobes usually) Transmitted via respiratory droplets but not very infectious (need chronic exposure to actually develop active TB)

Answer 89

Initially phagocytosed by alveolar macrophages – but these can’t destroy it due to the mycolic acid coat Instead drains to a regional lymph node and forms a Ghon focus (local inflammation 1.5cm wide with local lymph node involvement – found in mid and lower zones) Latent vs active Latent TB – Ghon focus contained and usually self heals – bacteria usually stay present in very small numbers (~95%) Can become active TB through just bad luck, but a number of risk factors increase likelihood; immunocompromised, diabetes, kidney disease etc. Active TB – bacteria multiply and this manifests as symptoms of disease Primary – direct progression from initial Ghon focus (~5%) Secondary (5yrs) – re-emergence of bacteria despite initial containment and healing of Ghon focus (~95%) Distinguished by a couple of lab tests (look up) Granulomas formed by active TB Immune granuloma – lymphocytes, Langhaan’s giant cells, epitheliods (differentiated macrophages) and show CENTRAL CASEOUS NECROSIS (differentiates TB granulomas from sarcoidosis) Upper lobes affected as TB is an obligate aerobe – both lung parenchyma and mediastinal lymph nodes involved

Answer 90

Fever and NIGHT SWEATS Occasional pulmonary crackles (usually clear) Anorexia + resultant cachexia Signs of cavitation/fibrosis (reduced air entry, dullness to percussion etc.) ``` Fatigue/malaise Effusion signs (stony dullness to percussion) in some cases ``` Productive cough (sometimes haemoptysis) Dyspnoea

Answer 91

Risk factors to consider from history Migrant to UK (particularly India/rest of Asia) Low socio-economic status (crowding and poor general health) HIV Close contact with relatives with TB

Answer 92

CXR – (usually) apices of lung show patchy consolidation with central cavitation – can be either bilateral or unilateral Sputum analysis – 3x5ml early morning samples Induced sputum or bronchoscopy for those without a productive cough ZN stain and look for acid fast bacteria Sputum culture – considered the gold standard but not usually done (takes 1 to 3 weeks at best) Checking exposure to TB (DOESN’T SHOW ACTIVE TB VS LATENT TB) Mantoux test – intradermal injection of TB protein  large induration (lump) formed if immune system has encountered TB before Subjective to interpretation and affected by other factors – particularly immunosuppression Interferon gamma releasing array (IGRA) – detects antigen specific INF gamma – more objective than Mantoux but more expensive and time consuming

Answer 93

RIPE protocol Rifampicin – interferes with TB’s RNA synthesis Hepatotoxic (contraindicated w/ liver damage) and turns all bodily secretions orange Izoniazid – blocks mycolic acid synthesis leads to breakdown of waxy shell leads to rifampicin able to penetrate Hepatotoxic (contraindicated w/ liver damage) and can cause peripheral neuropathy Pyranzinamide – inhibits ‘trans-translation’ by binding ribosomes Hepatotoxic (most hepatotoxic of entire RIPE protocol) Ethambutol – obstructs formation of cell wall (only in TB I think…) Visual disturbances As side effects are nasty and there are four drugs to take, compliance is always very low, so therapy is directly observed (in person or via video) Take all 4 for at least 2 months, then continue rifampicin and isoniazid until 6 months Cure rate of >90% if correctly adhered to (harmless but warn the patient)

Answer 94

Not the normal pulmonary TB that is susceptible to the RIPE protocol Resistant strains MDR-TB – resistant to rifampicin and isoniazid XDR-TB – resistant to all fluoroquinolones and >1 other of the protocol Both types require differing and more aggressive treatment regimes Miliary TB – TB that is diffuse throughout the body as a result of bacteraemia Lungs always affected as this is how it starts Aggressive and serious symptoms come from other organs e.g. ascites from liver, confusion from meninges etc. Extrapulmonary TB – any site other than the lungs, can be a result of military TB or can be a unique infection (think HIV) Lymphadenitis – usually the cervical lymph nodes  abscess formation GI/peritoneal – adhesions and ascites Bones/joints – usually found in spine TB meningitis – chronic headache, fever, Inc. ICP etc.

Answer 95

Cases notifiable under the public health act to consider finding other symptomatic patients BCG – 70/80% effectiveness in preventing severe childhood TB Very little evidence in preventing adult TB – given to high risk cases only (medical students, yay) Barrier medicine – -ve pressure isolation and PPE (and limit the amount of staff that have to deal with the patient)

Answer 96

SMOKING (90% of cases) Other risk factors but less common: Asbestos (MESOTHELIOMA) Radon – found in the rock in Cornwall Genetics/familial factors Occupational carcinogens – heavy metals generally

Answer 97

Staging – TNM like almost all cancers, but with a few changes T is defined as follows: T1a - 2cm but 3cm but 5cm but 7cm T4 - any N is a bit more precise than just number of lymph nodes involved: N1 – ipsilateral hilar lymph node N2 – ipsilateral mediastinal lymph node N3 – contralateral lymph node (either hilar or mediastinal) M M1 = metastasis

Answer 98

Symptoms (directly resulting from lung damage) ``` None a lot of the time Cough/haemoptysis Dyspnoea Wheezing Hoarse voice (left recurrent Chest pain Recurrent chest infections ``` Local mets symptoms Bloated face (SVC obstruction) Dyspnoea (pleural effusion) Dysphagia (oesophageal compression) Hoarse voice (left recurrent laryngeal nerve damage) Horner’s syndrome (pinprick pupil and drooping eyelid, sympathetic chain damage) ``` Systemic mets symptoms Pathological bone fractures (bone mets) Headaches, double vision (brain mets) Thirst and constipation (hypercalcaemia) Seizures (hyponatraemia) ```

Answer 99

Elevated non pulsatile JVP (SVC obstruction) Clubbing NORMALLY NO SIGNS

Answer 100

Cushing’s (small cell) – no reaction to dexamethasone suppression test SIADH (see urinary section)  dilutional hyponatraemia

Answer 101

Erect CXR Staging CT with or without contrast (thorax and upper abdo, tends to metastasise to liver) PET scan – picks up extra brain mets in 1/20 patients MRI, USS and other tests done as and when the possibility of mets dictate them Biopsy Only done once and on the thing causing the highest staging (e.g. if it’s stage IV you Need to check the malignancy of the tumour – biopsy method depends on the site of the tumour Tumour screen for molecular markers e.g. EGFR mutations Target for treatment in the same way Tamoxifen works for some breast cancer biopsy the distant met)

Answer 102

Oncologist, radiologist, cancer nurse, Macmillan team etc. all come together and analyse patient (w/ extra tests such as spirometry) to come to a decision on their WHO performance status grade: 0 – fully active 1 – restricted by intensive work 2 – up and about (ambulatory) >50% of the time 3 – limited self care, ambulatory 2 WHO grade, actually gives better prognosis than aggressive intervention in these patients Analgesia, patient support, low does radio/chemo etc.

Answer 103

Continued use despite knowledge of negative consequences Craving during abstinence (and other withdrawal symptoms) Failure to stop (average person takes 7 tries to stop smoking) Denial – ‘I’m not addicted I can quit anytime’

Answer 104

Nicotonic ACh receptors stimulated to cause dopamine release, which causes the feeling of satisfaction Like all receptors, Inc. agonist leads to upregulation  larger amount of nicotine to stimulate receptors (Inc. EC50, see M and R)  greater craving Drop in [nicotine] leads to cravings and withdrawal due to decreased dopamine release

Answer 105

Quitting – not realistic for a lot of smokers Healthcare workers second only to family members to convincing people to quit 3As, ask (do you smoke?), advise (why it’s good to stop/bad to continue) and act (refer to NHS stop smoking services) Nicotine replacement therapy – reduces cravings and allows tapering of nicotine addiction instead and are 2x as likely to quit Varenicline – partial NAch receptor agonist leads to reduced withdrawal symptoms but also reduced satisfaction from smoking Harm reduction – much more realistic Cutting down, abstaining for a period of time etc. are harm reduction ``` E-cigs are the newest and most popular harm reduction strategy Vaporize nicotine (route of inhalation makes it more like a cigarette and therefore a better replacement) Toxins are present but in lower numbers (Bronchiolitis obliterans caused by diacetyl (flavouring in popcorn flavoured nicotine cartridges) leads to destruction of bronchioles and thus Type 2 respiratory failure) ``` Long term effects of E-cigs unknown but probably better than actual smoking

Answer 106

An umbrella term for >200 disease processes (usually idiopathic pulmonary fibrosis) that affects the parenchyma between the alveoli

Answer 107

Idiopathic pulmonary fibrosis (IPF) – the most common by far No known cause (duh, idiopathic) Patient usually >80yrs old – 3 year median survival Can be treated with pirfenidine (inhibits growth factors and procollagens) but has bad side effects – 50% of patients come off early due to side effects Asbestosis – caused by asbestos exposure (older patients, retired engineers etc.) Formation of diffuse asbestos plaques Asbestos also leads to mesothelioma, rounded atelectasis and bronchogenic lungcancer, but the thickening of the interstitium is what causes asbestosis Drug induced – many drugs that can cause this (has to be >10yrs) Methotrexate (rheumatoid arthritis/cancer) Bleomycin (lymphoma) Amiodarone (cardiac arrhythmias) Nitrofurantoin (chronic UTI prophylaxis) Not an exhaustive list! Connective tissue disorders – connective tissue within interstitium affected (one facet of a systemic disease) Lupus Scleroderma – autoimmune attack on the connective tissue under the skin Pheumatoid arthritis – autoimmune attack of synovial joints Polymyositis – autoimmune attack of skeletal muscle Sjogren’s syndrome – autoimmune attack of exocrine glands Extrinsic allergic alveolitis Acute (aka farmer’s lung) – immune response to thermophilic actinomyocytes in hay (para-influenzic) Chronic (aka pigeon fancier’s lung) – antigens from pigeons produce chronic immune response leads to granuloma formation in lungs - Shows inspiratory crackles - Shows inspiratory crackles Sarcoidosis – idiopathic granulomatous disease Commonly confused with TB – TB granulomas have central caseous necrosis Can be treated with high dose steroids to dampen immune system (or methotrexate, but this in turn could cause ILD)

Answer 108

Varies widely for each type of ILD, but some always common Older (>60), smokers, previous exposure to respiratory toxins etc. 1 year history of non-productive cough, dyspnoea, cyanosis etc. Tachycardia, tachypnea, reduced SaO2 ‘Velcro’ crackles Signs of cor pulmonale ABG would show pO2 low pCO2 low/normal (most common) or high (late stage) Restrictive spirometry Clubbing

Answer 109

Collection of some type of fluid between the layers of the pleura (visceral and parietal)

Answer 110

Increased production Hydrostatic pressure (LSHF or hypertension) Permeability (sepsis/anaphylaxis/hypertensive damage) Oncotic pressure decrease (cirrhosis) Decreased clearance Lymphatic blockage (tumour/lymphadenitis) Increased venous pressure (RSHF) Transudate vs exudate Exudate - >50% serum protein (30g/L), >60% serum LDH Transudate is below these values Transudate caused by anything that affects Starling’s forces – LSHF, cirrhosis, kwashiorkor, atelectasis, hypertension etc. Exudate caused by something that also brings protein with it – infection, malignancy, pancreatitis, sepsis etc.

Answer 111

Breathlessness w/ unilateral chest expansion Pleuritic chest pain (sharp, knife like and worse on inspiration) Stony dullness to percussion in the lower lobes (when patient is upright) Coarse crackles Dry cough Paroxsymal nocturnal dyspnoea

Answer 112

Haemothorax – blood (either traumatic or iatrogenic, generally speaking) Empyema – pH

Answer 113

Type of fluid needs testing to determine the route cause of the pleural effusion - thoracentesis to acquire fluid Then test appearance, cell count (and type), pH, glucose, LDH, protein and cytology referral Fluid then needs draining completely Also, chemical pleurodesis may be used to cause union of pleura again Rarely, open surgery

Answer 114

Air within the pleural space (normally only contains a small amount of fluid)

Answer 115

Primary – otherwise healthy patient Tend to be lanky, smokers (especially cannabis) Secondary – underlying respiratory pathology e.g. COPD, cancer Iatrogenic – central line etc.

Answer 116

Pleuritic chest pain and dyspnoea Reduced air entry on one side Hyper resonance in affected area of lung

Answer 117

Erect CXR (shows black out where air is in the pleural cavity) Edge of lung now visible against blackout whereas it’s normally flush with the thoracic cage border >2cm is large,

Answer 118

Small (2cm) and any size w/ SOB Simple needle aspiration Chest drain (large primary and all secondary) Chemical pleurodesis – sets the two pleural layers together like glue – only used as a last resort is surgery is contraindicated Surgery – pleurectomy (generally done thorascopically)

Answer 119

Discharge – whenever stable with a primary pneumothorax, kept for at least 24 hours for observation after stable with secondary (increased risk of deterioration) Can’t fly until an outpatient appointment w/ CXR confirms complete resolution >6wks after discharge Diving – completely avoided unless patient has had a bilateral pleurectomy

Answer 120

Huge pneumothorax that is large enough to cause mediastinal deviation and compress the great vessels, leading to circulatory compromise Signs Almost absent chest movement on affected side Hyper resonance to percussion on affected side Tracheal deviation AWAY from the affected side Signs of hypoxia (peripheral cyanosis, confusion, agitation etc.) Early signs of mechanical shock (hypotension, tachycardia etc.) Treatment No time for a chest X ray Emergency needle decompression – large bore cannula into the 2nd intercostal space MCL O2, chest drain and cardiothoracic surgical referral

Answer 121

any disease that distorts the shape of the thoracic cage and/or impacts respiratory function Types Congenital – pectus deformity, scoliosis, kyphosis, muscular dystrophy etc. Acquired – trauma, iatrogenic, ankylosing spondylosis etc. Presentation – to do with the fact that they can’t move as much air Decreased ability to clear secretions through the coughing reflex leads to recurrent infections Sleep disorded breathing (paroxysmal nocturnal dyspnoea) Severe cases cause hypoventilation (Type 2 respiratory failure, pO2 low and pCO2 high)

Answer 122

Inflammation of the appendix due to either lymphoid hyperplasia (infection) or obstruction by hardened stool (fecalith). Irritation and subsequent infection leads to visceral midgut referred pain (periumbilical) but when the appendix becomes so inflamed that irritates the overlying parietal peritoneum it localizes to McBurney’s point (RIF, 1/3rd between ASIS and umbilicus). If it bursts colonic flora get into the peritoneum and cause peritonitis (life threatening) Excised by an appendectomy which uses as a grid iron incision to split the muscle fibers of ext. oblique, int oblique and transversus abdominis

Answer 123

Inflammation of the parotid gland, often by bacteria travelling up Stensen’s duct. Tight fascia means it can’t expand so intense pain and swelling results. High mortality due to the fact the external carotid artery, facial nerve (CNVII) and retromandibular vein travel within the fascia and can become compressed

Answer 124

failure of minute salivary glands to perform their function of destroying pathogenic bacteria leading to bad breath

Answer 125

failure of relaxation of either one of the oesophageal sphincters due to nervous disorganization. Commonly associated with an autoimmune condition e.g. Lupus, but also known to be idiopathic (mechanism is poorly understood). Leads to dysphagia, nausea/vomiting, epigastric pain etc. Can also lead to aspiration pneumonia, particularly from vomit that is aspirated during sleep

Answer 126

Cardiac – retrosternal (extending down left arm, up to neck and jaw), characteristically tightening/crushing Stomach/oesophagus – burning, epigastric (visceral, foregut) Gall bladder – epigastrium (visceral, foregut), RUQ (site of gall bladder) and inferior to right scapula on posterior body wall (body and neck are extraperitoneal), colic (see cholelithiasis) Pancreas – epigastric (visceral, foregut), LUQ (somatic) and radiating to back (T10, retroperitoneal excl tail) Small bowel – umbilicus (visceral, midgut), colic (see bowel obstruction at end of document) Large bowel – suprapubic (visceral, hindgut), colic (see bowel obstruction at end of document) Kidneys Felt in loin (posterior T11-L3, retroperitoneal) Refers to testicles due to the fact the mesonephric duct is converted into the vas deferens in adult males Excruciating, patient rolls around on floor Colic (comes in waves, see renal calculi) Uterus – suprapubic w/ lower lumbosacral Bladder – suprapubic (hindgut derivative) Diaphragm – left shoulder tip (phrenic nerve is C3-5 and so refers to these dermatomes, but ascent blocked on right side by liver apparently…)

Answer 127

hernia = protrusion of an organ through the wall of the cavity in which it normally resides. In inguinal hernias this is related to herniation into/all the way through the inguinal canal. More common in men because canal is wider (carried testes in embryology) Direct – pierces the posterior wall (transversalis fascia) of the inguinal canal at a weak point known as Hesselbach’s triangle (bound by the linea semilunares medially, inferior epigastric vessels superolaterally and inguinal ligament inferiorly). As it involves the conjoint tendon it doesn’t tend to herniate through the superficial ring, meaning no bowel ends up in the scrotum/labia majora Appears medial to the inferior epigastric vessels Indirect – enters through the deep inguinal ring within the posterior wall of the inguinal canal then usually also herniates through the superficial inguinal ring within the anterior wall. Increased lumen of the rings is a congenital defect (usually in men from the descent of the testes). Bowel ends up in the scrotum/labia majora Appears lateral to the inferior epigastric vessels

Answer 128

Occurs along linea alba between xiphoid process and umbilicus – common risk factors are obesity and pregnancy (Inc. intra abdominal pressure  weakness in linea alba) Distinguished from divarication of recti by the fact it doesn’t disappear when laying flat/get worse when abdominal muscles tensed

Answer 129

A hernia through the umbilicus – generally a congenital defect as seen in babies/toddlers Leave alone if not self resolved by >2 years old Can be acquired later on in life through obesity or pregnancy

Answer 130

Herniation into the femoral canal (most medial section of the femoral sheath which is contained itself within the femoral triangle – MSK) Occur more in women than men because the pelvis is wider Relatively small hernia due to the fact there’s not a lot of space until it travels through the great saphenous opening, at which point it may grow larger Prone to incarceration and strangulation because of the pectineal, lacunar and inguinal ligaments

Answer 131

Partial hernia where only the anterior bowel wall protrudes through the abdominal wall (posterior wall still within the abdominal cavity). Prone to strangulation without obstruction (rare, usually obstruction precedes strangulation)

Answer 132

hernia that appears along the linea semilunares, at the point where the posterior rectus sheath ends (intersection with arcuate line) – loss of fibrous sheath makes it an area of weakness

Answer 133

Usually a result of developmental defect, the abdominal viscera herniate into the thoracic cavity Sliding hiatus hernia – gastroeosophageal junction moves through the oesophageal hiatus (T10) along with the cardia of the stomach Rolling hiatus hernia – gastroeosophageal junction remains fixed above the oesophageal hiatus (T10) and a portion of the stomach follows it in

Answer 134

Herniation as a result of abdominal wall weakness due to previous surgery. Probably the most worrying for the NHS. Made worse by obesity/pregnancy

Answer 135

Widening of the linea alba that causes the two opposing sides to oppose each other during muscular contraction and then recede on relaxation. NOT A HERNIA, so just leave it alone/strengthen it with exercises

Answer 136

Usually 270 degrees CCW to put everything where it needs to be Incomplete rotation – only 90 degrees CCW, limbs don’t cross so the cranial limb ends up on the left hand side (entire colon placed on the left instead of framing the abdomen) Reversed rotation – 90 degrees CW, normal disposition apart from the fact that the duodenum is anterior to the transverse colon Both can lead to volvulus leading to interruption of blood supply leading to ischaemia thus loss of gut

Answer 137

Vitelline cyst – fluid filled sac that is anchored to the anterior abdominal wall and the small intestine Risk of volvulus (see above) Vitelline fistula – incomplete obliteration leading to communication between the small intestine and the umbilicus produces faeces externally Risk of infection Meckel’s diverticulum – blind ended outcropping from small intestine, follows the rule of twos: 2% of the population have one 2x as common in men vs women Usually 2ft from the ileo-caecal valve 2 inches long Contains 2 types of ectopic tissue – gastric or pancreatic

Answer 138

Within embryological development, the oesophagus, bile duct and small intestine lose some or all of their patency, relies on recanalization to restore function. If this fails leading to atresia or stenosis Most common in duodenum Can also be caused by vascular accident during development – malrotation, volvulus etc.

Answer 139

Excessive hypertrophy of pyloric sphincter (NOT A FAILURE OF RECANALISATION) Narrows the exit from stomach to duodenum  characteristic projectile vomiting Needs surgery to fix

Answer 140

Failure of fusion of the somatic mesoderm during lateral folding of embryo leading to vertical anterior abdominal wall defect (usually on the right side of the umbilicus) Not covered in amnion, bowel loops normally healthy so good prognosis

Answer 141

Incompletion of physiological herniation during midgut rotation leading to protrusion of bowel through the umbilicus Still covered in amnion (omphalocele is cele’d)

Answer 142

Failure of cloacal rupture, needs surgery to fix

Answer 143

Failure of development of the rectum to the point it reaches the cloaca

Answer 144

chronic presence of gastric acid within the lower third of the oesophagus

Answer 145

Dyspepsia (collection of upper GI symptoms) Heartburn – epigastric, burning pain Persistent cough leading to sore throat Dysphagia (distinguish from odynophagia, a result of oesophageal stricture – long term) Early satiety Nausea

Answer 146

Dysfunction of lower oesophageal sphincter (LOS) – not a true sphincter, so can be change in angle it enters stomach/right crus weakness Delayed gastric emptying (pyloric stenosis?)  Inc. intra gastric pressure  reflux Hiatus hernia Obesity – Inc. intra abdo pressure leading to Inc. intra gastric pressure

Answer 147

Oesophagitis Chronic inflammation and scarring leads to oesophageal stricture Chronic inflammation leading to metaplasia from stratified squamous non keratinised to columnar epithelia – Barrett’s oesophagus Predisposes to oesophageal adenocarcinoma in lower 1/3rd

Answer 148

Inflammation of stomach mucosa Symptoms – often asymptomatic but can present w/ dyspepsia Can also present with bleeding (haematemesis if large bleed) Causes – all acute insults Heavy NSAID use – blocking prostaglandins leading to decreased mucosal blood flow and decreased epithelial renewal thus acid damage to mucosa Alcohol – dissolves mucusa Chemotherapy – attacks rapidly dividing cells such as stomach epithelia Bile reflux from duodenum – not common, alarm bells

Answer 149

Chronic inflammation of stomach mucosa – presentation varies by the cause Helicobacter pylori infestation – similar to acute gastritis (see above) and peptic ulcer (see below) Autoimmune – antibodies raised to parietal cells Pernicious/megaloblastic anaemia (no intrinsic factor  no Vit B12 absorption  defect in RBC synthesis) Glossitis (inflamed tongue) Anorexia/cachexia

Answer 150

Erosion of mucosa and subsequent ulceration of submucosa. A result of Helicobacter pylori formation in most patients Helicobacter as a pathogen Motile, curved bacillus Contains urease that creates NH3  local alkaline cloud  protection from stomach acid Positive chemotaxis to alkaline pH to reach epithelia

Answer 151

Burrows into epithelia Colonises many sites Antrum leading to Inc. gastrin leading to duodenal epithelial metaplasia (CANCER) Body this leads to atrophic effect 1st part of duodenum thus leading to a tendency to bleed more heavily Several mechanisms of damage Cytotoxic compounds leads to direct epithelial insult NH3 levels toxic to epithelia Inflammatory response leading to self injury

Answer 152

Mild – epigastric pain following meals Some say duodenal is worse at night Severe – bleeding (usually leads to malaena as it’s not large enough to cause haematemesis), early satiety (leading to anorexia/cachexia)

Answer 153

Endoscopy – look for inflammation/ulcers/metaplasia of oesophagus Urease breath test – drink urea solution with radiolabelled carbon and measure the radiolabelled CO2 that comes out (shows urea  NH3 + CO2  H pylori present) Chest X ray – perforated ulcer  pneumoperitoneum  visible under diaphragm Haematoocrit – reduced due to bleeding

Answer 154

Conservative Cease insult (alcohol, NSAIDs etc.) Dietary modification – smaller, healthier and more frequent meals No lying down after meals Pharmacological H pylori eradication – clarithromycin and amoxicillin H2 histamine blockers – block receptors on parietal cells  decreased acid production e.g. ranitidine Proton pump inhibitors (PPIs) – block H+ extrusion across apical membrane  Antacids – neutralize excess acid (oral Mg(HCO3)2) decreased acid production e.g. omeprazole Surgical Cauterize bleeding ulcers via endoscopy

Answer 155

Rare gastrin secreting tumour of the pancreas, leads to severe polyulceration

Answer 156

ulceration of the stomach following large physiological insult e.g. burns, sepsis, severe trauma etc. Mechanism unknown but probably decreased mucosal blood flow

Answer 157

Inflammation of lymph nodes within the mesentery proper leads to right iliac fossa pain (commonly confused for appendicitis)

Answer 158

Infestation with and proliferation of Salmonella typhi within the GI tract leads to inflammation and subsequent rupture of Peyer’s patches leading to a GI haemorrhage

Answer 159

Interruption of blood supply to a section of gut  necrosis and dangerous sequelae Causes – systemic hypoperfusion (shock), arterial disease (SMA atherosclerosis), aneurysm (abdominal aortic aneurysm), thrombus/embolus etc. Consequences – if colon is infarcted then it can leak colonic flora  peritonitis leads to death If small section of SI infarcted then can show malabsorption etc. All infarctions pose dangerous risk of infection due to loss of immune protection in that area and stasis (always leads to infection)

Answer 160

Spectrum of progressively worsening liver damage due to high concentrations of alcohol. Encompasses steatosis, acute alcoholic hepatitis and cirrhosis Steatosis – fatty change of liver due to increased alcohol metabolism (alcohol leads to acetaldehyde leads to acetic acid creates NADH as a byproduct, which promotes fat storage) Usually asymptomatic, but a warning sign Reversible in 2 weeks Acute alcoholic hepatitis – can be chronic overexposure or the result of a large binge Toxins badly damage liver, which leads to inflammation Targeted hepatic necrosis occurs Fever, jaundice and tenderness Usually reversible over a few weeks)

Answer 161

Loss of liver function, can be a result of cancer or infection, but tends to be due to cirrhosis (fibrous remodeling leads to loss of function of hepatocytes), which is what is discussed here

Answer 162

Chronic alcohol abuse ``` Paracetamol overdose (leads to NAPQI buildup which is toxic to hepatocytes and glutathione depletion which means liver can’t deal with oxidative stress) Very Acute ``` Untreated, chronic hepatitis B/C Primary biliary cirrhosis – autoimmune obliteration of bile duct leads to absolute obstructive jaundice (bilirubin content so high it’s toxic) Requires a transplant Hereditary haemochromatosis – iron deposition in tissues Gives bronze tint to skin and also attacks pancreas – bronze diabetes Wilson’s disease – deposition of copper in tissues Also affects basal ganglia leading to tremor, dementia A1-antityrpsin deficiency – overactivity of proteases leads to breakdown of liver parenchyma Patient will also have emphysema

Answer 163

Hepatic jaundice Anaemic and bruise easily (liver synthesizes clotting factors) Bone/Ca2+ disorders (liver synthesizes Vit D) Palmar erythema and Dupytren’s contracture – thickening of palmar fascia leads to fixed flexion deformity at MCP and IP joints (no idea why) Liver usually breaks down oestrogen Spider naevi Gynaecomastia in men Portal hypertension – cirrhosis impairs blood flow and hydrostatic pressure backs up throughout the portal venous system. Causes a number of characteristic signs: Ascites and splenomegaly – same principle as pulmonary oedema in RSHF Oesophageal varices – anastomoses between azygous vein and left gastric vein in lower 1/3rd oesophagus dilate due to increased pressure - Dilated, tortuous, rupture easily and hose when they do Haemorrhoids – anastomoses between superior rectal vein and pudendal vein in middle 1/3rd rectum dilate due to increased pressure - Uncomfortable Caput medusae – increased pressure recanalises the umbilical vein leads to dilation of superficial veins of anterior abdominal wall (looks like medusa’s hair and caput is Latin for head)

Answer 164

AST/ALT 2:1 = alcoholic liver disease Inc. clotting time Hyponatraemia and hypoalbuminaemia ALP Inc. Hyperbilirubinaemia (jaundice) Both conjugated and unconjugated

Answer 165

Stop drinking/cease other insult e.g. Hep B Treat symptoms as best you can e.g. spironolactone to try and minimize ascites Carefully manage all drugs (everything is hepatotoxic if your liver function is bad enough)

Answer 166

Severe, acute decompensation of liver function accompanied by hepatic encephalopathy (see below) within 2 months of diagnosis of liver failure Usual liver failure features Also accompanied by hypokalaemia, hypocalcaemia and hypoglycaemia (if you see this, it’s pretty much certain)

Answer 167

Reversible neurological deficit caused by increased NH3 levels Causes Stress – physiological insult to liver e.g. constipation, GI bleeding, sepsis Hypokalaemia – never use non-K+ sparing diuretics (loop/thiazide) with liver failure Signs Liver flap – patient asked to close eyes and extend wrists with arms pronated, won’t be able to hold it steady Constructional apraxia – can’t draw a 5 point star

Answer 168

Aka gallstones | The presence of solid mass with the biliary tree

Answer 169

Female (especially on OCP) Increasing age Obesity Inc. bilirubin levels e.g. haemolytic anaemia

Answer 170

Cholesterol Pigment – Ca2+ and bilirubin Mixed – combination of the two, by far the most common

Answer 171

If only in the gallbladder and not obstructing the neck, relatively asymptomatic If anywhere else in the biliary tree Biliary colic – dull background ache in RUQ that becomes acute and peristaltic after eating (due to CCK release causing the gallbladder to contract and increasing pressure in the biliary tree) Post-hepatic/obstructive jaundice

Answer 172

Cholecystitis – inflammation of the gallbladder due to colonization by pathogen (usually) because stasis leading to infection Oedema leads to mucosal ulceration and exudate formation SIRS and pyrexia, can become septic if left untreated Ascending cholangitis – colonization of the biliary tree by bacteria from the duodenum to the liver and a route into the systemic circulation thus leading to sepsis Characterised by Charcot’s triad: RUQ pain, fever and jaundice Life threatening, must maintain high index of suspicion Biliary-enteric fistula – communication between the duodenum and biliary tree due to erosion as a result of irritation – can lead a gallstone obstructing the ileum leading to bowel obstruction

Answer 173

Surgical – laparoscopic cholecystectomy Non-surgical – ERCP (endoscopic retrograde cholangio-pancreatography)

Answer 174

Inflammation of the pancreas as a result of pancreatic enzymes being activated within the pancreas (these contain proteases leading to autodigestion)

Answer 175

GET SMASHED: Gallstones (and gin…) Ethanol Trauma ``` Steroids Mumps Autoimmune Scorpion bite (Trinidad and Tobago only) Hyperlipidaemia ERCP (so iatrogenic) Drugs ``` Useful as GET (1st word) are most common and alcohol is most common overall (get smashed…)

Answer 176

Pain Nausea/vomiting with anorexia Severe so leads to dehydration Ecchymosis (bleeding under the skin) SIRS (can lead to septicaemia) Jaundice (bile salts cant pass through the ampulla of Vater so post hepatic)

Answer 177

Inc. pancreatic amylase Hypocalcaemia Hyperbilirubinaemia (conjugated) and Inc. ALP Hyperglycaemia (impairment of endocrine function)

Answer 178

Differs completely from acute pancreatitis Duct stenosis leads to post-hepatic jaundice Pain Malabsorption (lack of bile salt delivery leads to Steathorrea) Leads to oedema because protein absorption dec leads to hypoalbuminaemia Diabetes (loss of B cells in Islets of Langerhaans)

Answer 179

Inflammation of the diverticuli (outcroppings of weakened large intestinal wall as a result of age/pressure exerted by stools). Become inflamed when colonic flora become trapped in them and start to multiply leading to swelling. If it progresses to abscess formation/rupture can leading to peritonitis

Answer 180

umbrella term for two distinct diseases Chron’s disease and ulcerative colitis

Answer 181

The rapid polymicrobial infection of the mouth and surrounding tissues (facial muscles, connective tissue, hard palate, maxilla, mastoid etc) due to physiological dysfunction Malnutrition, dehydration etc (a disease of the 3rd world) Disfiguring leads to social stigma and shame

Answer 182

Candidiasis = thrush in any location (overgrowth of Candida albicans, a yeast), manifests as white furring in the oral cavity Risk factors include newborns, diabetics, inhaled steroids (preventer inhaler), HIV, antibiotics (elimination of normal protective commensals) etc Treated w/ antifungals

Answer 183

Damage to teeth and gums due to colonization by mouth bacteria as a result of poor oral hygiene Streptococcus mutans (a type of viridans Strep) is most common pathogen Over vigorous brushing to try and remedy leads to gingival damage this is a route into systemic circulation and thus bacterial endocarditis

Answer 184

Laryngoedema as a result of overactivity in response to strep throat/tonsillitis leading to breathing problems and death from Type 2 respiratory failure

Answer 185

Inflammation of the tonsils within the pharynx due to infection (palatine tonsils) leading to dysphagia and odynophagia

Answer 186

An abscess with infected palatine tonsil leading to pharyngeal obstruction leading to breathing difficulty Needs excising and abscess lancing but be careful, lies right next to the internal carotid artery

Answer 187

Thrush of the oesophagus. AIDS DEFINING ILLNESS (shouldn’t be able to breach defences this far down)

Answer 188

Secretory anal gland blocked which leads to stasis and infection by perianal flora (largely the same as colonic flora, always find E coli, Enterococcus faecalis and Lactobacillus) Can progress to anal fistula leading to incontinence

Answer 189

Thrush within and around the vagina. Usually post-antibiotic usage Lactobacillus converts glycogen  lactic acid which keeps vaginal pH low and prevents yeast growth If treated w/ antibiotics that act against Gpos rods (broad spectrum), loss of Lactobacillus leads to raised pH and no inhibition of Candida growth

Answer 190

Cancer of the oesophagus Presentation – progressively worsening dysphagia/weight loss (due to difficulty swallowing) Investigation – endoscopy and biopsy (barium swallow?) Types Squamous cell carcinoma – occurs at any level, no known definitive aetiology Adenocarcinoma – occurs in lower 1/3rd, Barrett’s oesophagus (see GORD) Treatment/prognosis Curative intent – resection, combined chemo/radiotherapy Palliative care – can include canalization of tumour to facilitate swallowing 5% 5yr survival

Answer 191

Cancer of the stomach Presentation Epigastric pain, nausea/vomiting, weight loss, malaise, haematemesis/melena, raised Virchow’s node (left supraclavicular) Investigation – endoscopy and biopsy ``` Pathology Macroscopic – fungates (breaks epithelia), ulcerates and infiltrates Microscopic Intestinal type – glandular formation Diffuse type – signet ring cells ``` Causes Chronic H pylori infestation High smoked/salty food diet (Japan) Treatment/prognosis Early stage – surgical resection, chemotherapy, targeted herceptin Much better prognosis, obviously Late stage – chemotherapy and target Herceptin

Answer 192

Most common gastric cancer Presentation – same as other gastric cancers Investigation – same as other gastric cancers Causes – HIV, chronic immunosuppression or H PYLORI Treatment/prognosis Eradication of H pylori leading to regression of tumour in many patients Chemo/radiotherapy Much better prognosis than normal gastric cancer

Answer 193

Tumour of the ‘pacemaker cells of peristalsis’ Presentation – asymptomatic early on, then same as other gastric cancers Investigation – same as other gastric cancers and check for CD117 marker to confirm it’s a GIST Pathology – wildly unpredictable (varied pleopmorphism, mitotic figures and necrosis) Treatment/prognosis Imatinib – only targets cancer cells due to CD117 marker Surgical resection >80% 5yr

Answer 194

Autosomal dominant failure of tumour suppressor genes  huge amount of adenoma formation, particularly on the colon. Inevitably one of the adenomas  colorectal cancer eventually. Can excise colon as prophylaxis

Answer 195

Cancer of the colon/rectum ``` Presentation Elderly (>60yrs) Fresh blood in stools (haematochezia) Changes in bowel motions Suprapubic (hindgut) pain ``` Investigation – colonoscopy and PR exam Pathology Variation in anatomical site; descending colon are stenotic so can leads to obstruction, but ascending colon are fungating (don’t lead to obstruction) Microscopic; can be adenocarcinoma or can be mucinous/signet cell type Causes – FAP is the big hereditary risk factor Low fibre/high fat diet Other genetic factors e.g. loss of p53 gene Ulcerative colitis Treatment/prognosis Local radiotherapy (via rectum, pelvis too dense to irradiate) Palliative chemotherapy Colectomy Gets worse w/ inc staging, Stage D Duke’s (see MOD 11) is almost always terminal

Answer 196

Carcinoma of the pancreas Presentation Usually presents way too late but some symptoms seen in late stage Back/epigastric pain Post-hepatic jaundice (obstruction of ampulla of Vater) Pain and vomiting (duodenal mets) Malabsorption (steathorrea leas to weight loss) Diabetes (loss of B cells in Islets of Langerhaans) Trousseau’s sign – systemic microthrombophlebitis (very late sign) Investigation – ERCP and biopsy followed by staging CT Pathology Macroscopic – firm pale mass, necrotic, haemorrhagic and cystic Microscopic – 80% are ductal (glands with or without mucin) Causes – chronic pancreatitis (alcohol), smoking etc Treatment/prognosis – worst cancer to get (

Answer 197

Umbrella term for several types of hepatic cancer (can also have liver mets but not covered here) Presentation – hepatic jaundice, RUQ pain, pruritus, nausea/vomiting, weight loss etc Investigation – biopsy Pathology – all types (hepatocellular carcinoma, cholangiocarcinoma, hepatoblastoma etc) have different microscopic appearances Causes – chronic inflammation (alcoholism, hepatitis B/C, drugs etc) ``` Treatment/prognosis Resection of deposits Transplant (early stage disease only, metastases occur quickly) Radiofrequency ablation 10% 5yr ```

Answer 198

blockage of bowel leading to constipation, vomiting and bloating in varying amounts depending on how proximal or distal the obstruction is

Answer 199

Causes – adhesions, strangulated/incarcerated hernias, tumours, infection etc Symptoms – early vomiting, late absolute constipation and minimal distension Colic every 2 to 3 mins Appearance on AXR >3cm wide (wider than a thoracic/early lumbar vertebral body is tall) Central positioning Thin valvulae conniventes visible (cross entire bowel lumen)

Answer 200

Causes – cancer, diverticular disease, incarcerated/strangulated hernia (more common in SI obstruction), volvulus etc Symptoms – late, faeculant vomiting, early absolute constipation and significant distension Colic every 10 to 15 mins Appearance on AXR >6cm wide (>9cm w/ competent ileo-caecal valve) ‘frames’ the small intestine (remember transverse colon hangs down into the pelvis, particularly in women Haustra visible (don’t cross entire bowel lumen)

Answer 201

Twisting of the sigmoid colon around its mesentery  obstruction, ischaemia and possible perforation Shows a coffee bean sign of obstructive bowel from LLQ to RUQ (the loops of dilated bowel sort of look like a coffee bean…)

Answer 202

Inflammation and infection of the peritoneum by bacteria (usually colonic flora) – requires a perforation within the GI tract somewhere so that the colonic flora can leak out Causes Appendicitis leading to ruptured appendix Toxic megacolon leading to rupture Diverticulitis leading to rupture Severe Chron’s leading to complete erosion of intestinal wall leading to fistula Not an exhaustive list! ``` Symptoms SIRS/sepsis Ache across entire abdomen w/ worsening pain Nausea/vomiting Oliguria/anuria ``` Treatment – peritoneal washout and sepsis six (O2, fluids, broad spec antibiotics, catheterize, lactate and blood culture/source control)

Answer 203

Acute inflammation of the stomach and intestines in response to a viral or bacterial infection. Leads to interference with water, salt and sugar absorption within the GI tract so can leading to dehydration. Usually self limiting, and treated by increasing fluid intake and waiting it out. Some notable (common) pathogens include: ``` Norovirus – see I and I key pathogens Campylobacter (direct epithelial damage/immune system damage  loss of function) Salmonella (raw chicken, eggs etc – bacterial multiplication  intestinal inflammation  loss of function) E coli (usually self limiting but 157 strain can be deadly) ```

Answer 204

Gram+ve/-ve: -ve Mechanism(s) of infection: Direct contact with respiratory secretions Patient factors to consider: Age, pathological state (smoking, obesity, diabetes, HIV, chemo), relative time, physiological state, social factors (kissing disease?) Interaction with host: Lives harmlessly in the upper respiratory tract (naso/oropharynx) of 1/10 individuals, but a few individuals are susceptible to this. It colonises and attacks the meninges (the lining of the brain), which causes some of the well known symptoms. It quickly progresses to the blood, causing a non-blanching rash. Due to the extremely potent endotoxin on it’s outer cell membrane, it causes a severe immune overreaction and due to this a drastic fall in TPR, leading rapidly to septic shock, disseminated intravascular coagulopathy, both causing multi organ failure and quickly death. If the meninges become significantly inflamed, the ICP rises to the point the patient cones and death is imminent. How to diagnose: History: Fit and well in last 24 hours, suddenly feeling non-specifically ill (fever, chills). Within next 12 hours neck pain, fever, photophobia, nausea, malaise, abdo pain, severe headache, non-blanching (purperic) rash Examination: Raised temp, tachypnea, tachycardia, low BP, pale cold extremeties Investigation: FBCs, U and Es, BM, LFTs, CRP, clotting studies, ABG, MCS (microscopy, culture, sensitivity), EDTA for PCR Treatment (in meningitis investigations must NOT delay treatment): ``` Supportive High flow O2 Adrenaline (inotropes) Correct fluid balance (IV) Measure urine output Measure lactate Analgesia ``` Specific Blood cultures (consider source control) Broad spectrum antibiotics (ceftriaxone) Duration of illness: Several days, antibiotic wipes out bacteria but this just releases even more endotoxin – gets worse before it gets better Possible sequelae: Septic shock leading to death, respiratory failure, kidney failure, raised ICP leading to coning and death, hearing loss, ischaemia and subsequent coagulative necrosis/dry gangrene of toes/fingers/limbs Prevention: Vaccine available for ACWY and B strains, stop kissing people! At risk individuals ie in close contact with people who show meningitis symptoms given prophylactic antibiotics, particularly those that are immunocompromised

Answer 205

Gram+ve/-ve: +ve Mechanism(s) of infection: Direct contact, is part of the normal flora of the upper respiratory tract but can colonise the lungs under the right conditions if they are not cleared in time Patient factors to consider: Age, pathological state (smoking, obesity, diabetes, HIV, chemo), relative time, calendar time (more common in winter) Interaction with host: Pneumonia occurs when the bacteria colonise the lungs, due to their thick capsule they are not easily phagocytosed. The pus from dead neutrophils quickly accumulates and consolidates in the lungs, producing most of the symptoms in the patient. If left unchecked it may cause bacteraemia and potential meningitis with an atypical pathogen How to diagnose: History: 3 days of dyspnea and malaise, 4 or 5 days of productive yellow sputum Examination: Crackles and bronchial breathing over area of lung, tachypnea, tachycardia, mild hypotension, decreased O2 sats Investigation: CRP, FBCs, U and Es, ABG (things like lactate not needed as you’re dealing with a localised infection) Treatment: Supportive High flow O2 Correct fluid balance (IV, consider inotropes if no change to BP) Nebulised salbutamol Specific Broad spectrum antibiotics Pneumonectomy(?) Duration of illness: 3 weeks after treatment Possible sequelae: Consolidation of lung tissue, possible caseous necrosis of infected lung but then also possible clearance of inflammatory exudate through the lymphatic system. Small chance of passage into the blood and then meningitis/septicaemia may result Prevention: At risk individuals ie those who are immunocompromised and in close contact with those with pneumonia can be given antibiotic prophylaxis

Answer 206

Gram+ve/-ve: -ve Mechanism(s) of infection: Ingestion of contaminated food or direct spread from perforated bowel Patient factors to consider: Age, pathological state (smoking, obesity, diabetes, HIV, chemo), relative time Interaction with host: Can either colonise the GI tract (harmful strain) and this causes gastroenteritis (this is considered below), or it directly exits from the bowel after a perforation/surgery, which can lead to peritonitis How to diagnose (a very serious case of gastroenteritis/peritonitis, mild cases will self medicate at home): History: Ingested food between 1 to 8 days ago, after a few days nausea, diahorrea, vomiting, fever, malaise, muscle weakness, stomach cramps, chills Examination: Tender abdomen, raised temperature, may be some changes to BP, HR and resps Investigation: (as only severe cases present to hospital, these investigations should be performed) MCS, FBC, U and Es, lactate, LFTs, CRP Treatment: Supportivec IV fluids (consider inotropes) High flow O2 Specific Broad spectrum antibiotics Source control might be needed in peritonitis (debridement) Duration of illness: Will resolve after a few days of illness, especially if antibiotics are administered Possible sequelae: Restoration to physiological state most likely, in peritonitis there could be some organ damage (particularly liver), septic shock or death Prevention: Don’t share belongings/cook with people who have gastroenteritis (for 48 hours after diahorrea and vomiting stop), disinfect food prep areas regularly

Answer 207

Gram+ve/-ve: +ve bacillus Mechanism(s) of infection: Appears as an opportunistic infection when the normal microbiota of the gut is eliminated by antibiotics (ceftriaxone) for an unrelated infection (the flora that are removed usually outcompete the C diff, which is a normal albeit minor component of gut flora) Patient factors to consider: Age, pathological state, previous admission, physiological state, relative time Interaction with host: Exotoxin A causes inflammation that leads to the intracellular spaces widening (due to the excessive release of histamine), whilst exotoxin B exits through these gaps and kills the healthy cells of the host (both contribute to disease) How to diagnose: History: 2 days of severe diarrhoea, rarely vomiting, abdo discomfort, previous antibiotic treatment Examination: Generalised tenderness over the abdomen (particularly umbilicus), BP down slightly, slightly tachy Investigation: FBCs, CRP, U and Es, serum creatinine (calculate eGFR), stool sample, haematocrit (will be down in dehydration) Treatment: Supportive IV fluid bolus ORT Specific Faecal transplant Metronidazole Discontinue causative antibiotics Duration of illness: 7 to 10 days Possible sequelae: Severe diarrhoea can lead to acute renal failure and cognitive impairment in severe dehydration, perforated/toxic megacolon leading to peritonitis and septic shock Prevention: Isolation, responsible prescribing, good barrier medicine (throw away gowns/gloves, wash hands thoroughly)

Answer 208

Gram+ve/-ve: -ve rod Mechanism(s) of infection: Faecal-oral transmission (contaminated food and water) Patient factors to consider: The standard ones (age, pathological state, relative time – incubation period) along with calendar time (how long since they got back?) Interaction with host: Enters GI tract and hits SI, where it interacts with Peyer’s patches (part of the RE system) – adheres with fimbriae. If lysis occurs, it will release endotoxins. Also, secrets invasin to allow intracellular growth. Eventually enters the blood through the Peyer’s patches, causing bacteraemia, which rarely advances to sepsis How to diagnose: History: Incubation period of 7 to 14 days so become unwell soon after returning from country of origin. Travel to Sub-Saharan Africa or Asia. Slowly increasing intensity of fever, headaches, abdominal tenderness, constipation and dry cough Examination: Fever (severe ie >40C), relative bradycardia for disease state (these two combined are known as Faget’s sign), hepatosplenomegaly Investigation: FBCs, MCS, stool culture, LFTs, U and Es, CRP Treatment: Supportive Oral rehydration therapy Antipyrexials (paracetamol) Pain relief (paracetamol) Specific Ceftriaxone or azithromycin Duration of illness: Generally 4 weeks Possible sequelae: Normally resolves with no long term complications if ORT and antibiotics are administered, but if left untreated may progress to intestinal haemorrhage, intestinal perforation, encephalitis, metastatic abscesses (endocarditis) etc Prevention: Food and water hygiene increase ie proper hand washing, those who are sick don’t prepare food, vaccine (high risk travellers) and chlorinate water

Answer 209

Gram+ve/-ve: -ve rods Mechanism(s) of infection: Aerosolisation of water and soil infected with the bacteria. Held in reservoirs with amoebae in water (even water such as that circulating in vapour in air conditioning systems) Patient factors to consider: Normal ones (age, pathological state, relative time), particularly concerned about co-morbidities ie HIV Interaction with host: Undergoes phagocytosis but inhibits formation of phagolysosome, so instead multiply within the macrophage until it bursts (so both depletes WBC count and uses this to bolster its own numbers) How to diagnose: History: Fever, shortness of breath, productive cough Examination: Tachypnea, high grade fever, bibasal crepitations of lungs, SpO2 of

Answer 210

Gram+ve/-ve: +ve cocci in chains Mechanism(s) of infection: Normal commensal in the oral cavity, however if the oral mucosa is breached it can become an important factor in tooth decay (inoculation) and spread to the CVS (haematogenous spread) Patient factors to consider: Age, pathological state (immunocompromised), relative time, physiological state (dental hygiene and phobia of dentists in particular) Interaction with host: Initially colonises the tooth surface, where it converts ingested sucrose into lactic acid, which lowers the pH of the tooth enamel and leaves it vulnerable to breakdown. After this, if the oral mucosa is breached by this low pH or any kind of abrasion (eg. vigorous brushing) then the bacteria have a route into systemic circulation. This causes harmless bacteraemia, but they can get stuck on the heart valves due to turbulent flow, which leads to them colonising these as a ‘vegetation’ – this is infective endocarditis How to diagnose (infective endocarditis due to viridans Strep): History: Poor access to dental care, systemic response (fever, chills etc) for 6 weeks at least, lack of energy, breathlessness, toothache, anorexia, cahexia Examination: Poor dentition/dental abscess, heart murmur, tachypnea, possible tachycardia, possible hypotension (slight), peripheral oedema (due to decreased CO reducing hydrostatic pressure) Investigation: FBC, CRP, U and Es, MCS, echocardiogram, ECG, serum creatinine Treatment: Supportive Measure urine output (if U and E elevated) O2 to address tachypnea Specific Replace defective valve in surgery Penicillin and gentamicin Duration of illness: When the antibiotics are given and the valve removed, the defect is correct, so depends on the wait for surgery (~3 weeks?) Possible sequelae: Heart failure (left or right depends on the valve that is defective, if tricuspid or pulmonary then right, if mitral or aortic then left), valvular dysfunction (stenosis or regurgitation), cardiogenic shock Prevention: Good dental hygiene (dentist every 6 months)

Answer 211

Gram+ve/-ve: +ve cocci in clusters Mechanism(s) of infection: Inoculation onto prosthetic surfaces during surgery Patient factors to consider: Age, pathological state (in particularly their presenting surgical complaint), relative time (how long has the graft been in?) Interaction with host: Usually a commensal as a part of the normal skin flora. It can form biofilms on surgical equipment that bypasses the primary defences of the innate immune system (intubation bypasses mucociliary escalator, catheters bypass periodic flushing etc), and so has a route to cause local infection. If biofilms are sheared off this can provide a route into systemic circulation and cause extremely rapid sepsis and shock. Can also cause rejection of prosthetics such as artificial knees or hip replacements if It infiltrates at the time of surgery. How to diagnose: History: Pain in site of implant/prosthesis (eg hip) and unsteadiness on the affected joint (eg hip again). Can also have tenderness at site of insertion of line etc (central venous lines are the most common) Examination: Malaise, fever, possible myalgia, reduced power in affected limb (if joint replacement), infection tends to be localised so SIRS symptoms tend to be absent Investigation: FBC, MCS, CRP, U and Es, swab pus if present Treatment: Supportive Manage symptoms such as fever Physiotherapy for affected joint Replace prosthesis to restore normal function (after antibiotics have worked) Specific Surgical exploration of infected joint, possibleremoval of the prosthesis Extensive antibiotic regime (flucloxacillin, switch to vancomycin/doxycycline if MRSA detected – minimum of 14 days) Removal of infected line Duration of illness: When treated properly, infection is removed after 2 weeks normally, but obviously the joint dysfunction will still remain until a new prosthesis is fitted Possible sequelae: If lines are not removed + infection not cleared, it may progress to septicaemia, septic shock and death due to multi organ failure Prevention: Silver coated IV lines (act as antibacterial agent), good ANTT used when inserting cannulas, sterile surgical environment when performing joint operations, antibiotic prophylaxis when anaesthetised (co-amoxiclav 1.2g IV)

Answer 212

Gram+ve/-ve: Gneg bacillus (rods) Mechanism(s) of infection: Inhalation of bacteria which then begin to colonise the respiratory tract/lungs (Can also enter through other routes at other sites eg up urethra in cystitis) Patient factors to consider: Age, pathological state (CF!!!), relative time, physiological state (how are they managing their condition?), social factors (do they smoke?) Interaction with host: Opportunistic pathogen that requires a disease state to take hold eg. HIV, CF, neutropenia etc. Is a facultative anaerobe, which is essential when it is trapped in the sputum of a CF sufferer (low O2 diffusion). Enters through the URT, where it begins to colonise the brochi, leading to bronchopneumonia. Blocks eukaryotic protein synthesis leading to oncosis. Has a mucopolysaccharide capsule that makes it hard to phagocytose, so even more disastrous for immunocompromised eg neutropenic How to diagnose: History: Presents in a similar fashion to regular pneumonia eg productive cough (very dry mucus), fever and SOB. Obviously are known to have CF Examination: Tachycardic, tachypnic, cyanotic, dullness to percussion, pulmonary crackles etc Investigation: FBC, U and Es, CRP, lactate, MCS Treatment: Supportive High flow O2 Ventilation if needed Nebulised salbutamol Specific Tobamycin (IV or inhalation, not absorbed from GI) Duration of illness: Normal pneumonia is 3 weeks after treatment, but due to impaired lung function/clearance may be much more Possible sequelae: Significant cause of mortality within CF sufferers, can cause worsening of existing fibrosis Prevention: Don’t let CF sufferers meet (risk of cross infection), pulmonary physiotherapy, prophylactic antibiotics

Answer 213

Gram+ve/-ve: G+ve coccus Mechanism(s) of infection: Invasion (break of mucosa), inhalation, ingestion etc Patient factors to consider: Age, pathological state (are they immunocompromised eg neutropenic) Interaction with host: Has a number of important virulence factors (but here are the first 3 I found): Coagulase – converts fibrinogen to fibrin, forming a micro clot around the bacteria that protects it from phagocytosis Hyaluronidase – breaks down hyaluronic acid (key component of ground substance in connective tissue) which leads to ability of bacteria to break down barriers and spread DNA ribonuclease – breaks down host DNA How to diagnose: History: Staphylococcus typically forms skin lesions in people who are immunocompromised, such as impetigo, boils, abscesses etc. History of these before (severe, persistent, unusual and recurrent) w/ recent new formation Examination: Evidence of large lesion, if it’s lead to sepsis can expect SIRS eg tachypnea, tachycardia, hypotension Investigation: Swab wound and culture, MCS, CRP, FBC, U and E, serology (antibodies) Treatment: Supportive If septic needs the sepsis six (see Neisseria meningitidis) Speicifc Antibiotics Drain abscess Duration of illness: Time the lesion takes to resolve depends on the severity of it, some small cuts cleared in a few days, but large abscesses can take weeks to heal by secondary intention Possible sequelae: Chronic abscess formation, scar tissue formation, resolution, sepsis Prevention: Hand washing technique, decontaminating cooking surfaces etc

Answer 214

Capsid structure: Icosahedral Enveloped: Non-enveloped DNA/RNA: ssRNA Mechanism(s) of infection: Directly from person to person, or indirectly from contimated water or food (extremely contagious) Patient factors to consider: Age, calendar time, pathological state (diabetes, HIV, cancer treatment) Interaction with host: Multiplies within the small intestine and irritates the lining of the GI tract, causing vomiting, nausea etc (gastroenteritis) How to diagnose: History: Vomiting under 2 days after first exposure, diarrhoea, usually in contact with someone with the virus, classic symptoms of dehydration (sunken eyes, dry hair, pale, reduced urine output, headache, tiredness, dry lips etc) Examination: Usually wouldn’t examine the patient as those with norovirus are advised to stay at home, but would expect abdominal tenderness along with dec BP and inc HR if the dehydration got very bad Investigation: U and Es, PCR of virus, FBCs Treatment: Supportive IV fluid bolus ORT Specific None Duration of illness: 72 hours generally (self limiting) Possible sequelae: Very unlikely to cause death, especially if fluid balance is restored, most patients make a full recovery Prevention: Barrier medicine, wash everything patients come in contact with (with bleach), wash hands thoroughly after any contact etc

Answer 215

Capsid structure: Icosahedral Enveloped: No DNA/RNA: dsDNA Mechanism(s) of infection: Droplet infection, direct contact, faecal-oral transmission Interaction with host: Enters through the respiratory route normally, may either colonise the pharynx and upper airways to cause an URTI (with conjunctivitis if it travels up the nasolacrimal duct or if they sneeze and rub their eyes), or down the oesophagus to colonise the GI tract and cause gastroenteritis How to diagnose: History: ~3 day history of pain in pharynx, cough, sinus pain (in some cases), temperature, malaise etc Examination: Red, inflamed pharynx. Enlarged tonsils, lymphadenitis (in neck) etc Investigation: Temperature Treatment: Supportive Mild pain relief eg paracetamol Increase fluid intake Specific Only with potentially lethal strain 14 – antivirals Supportive management in most cases, only one strain (14) is potentially lethal. In this case you would give antivirals but other than that, bedrest, paracetamol and up fluid intake Duration of illness: Usually self limiting and resolves after a week Possible sequelae: Almost always resolves, but can lead to epiglottitis (dysphagia and aspiration of food common so life threatening) or quinsy (see GI, clinical conditions ESA 3) Prevention: Spreads by droplet infection so stay away from those showing symptoms, avoid enclosed spaces

Answer 216

Capsid structure: Circular Enveloped: Yes DNA/RNA: non-sense ssRNA Mechanism(s) of infection: Droplet infection Patient factors to consider: The usual factors (age, pathological state and relative time), along with calendar time (flu season is winter) Interaction with host: Droplets inhaled into the respiratory tract, where the virus begins to enter the cells of the upper respiratory tract. Virulence is determined by the levels of haemagglutinin and neuraminidase expressed on the outer envelope of the virus (these determine the strain of virus depending on their type of toxins ie H1N1). Haemagglutinin helps facilitate the entrance of the virus into a cell by binding the envelope to the CSM (the virus can only affect the URT because the enzymes to cleave haemaggulutinin to its active form are only present there – exception is H5N1 which is diffuse across the whole lung). Neuraminidase cleaves glycoproteins to allow viral release from a cell following replication. Cytokine overreaction is the cause for most of the symptoms How to diagnose: History: Fever, aches and pains, dry cough, malaise, myalgia (beginning a day or two agp) Examination: Fever, tachypnea, maybe tachycardia Investigation: FBC, U and Es, CRP, sputum culture, AP chest X ray, nasal swab w/PCR, MCS Treatment: Supportive Pain relief Antipyrexials (if slight fever leave it, its good for you!) Specific Neuraminidase inhibitor (Oseltamivir aka Tamiflu) Antivirals (acyclovir) Duration of illness: Normally 1 week Possible sequelae: Chest infection, sinusitis, in VERY severe cases can get meningitis Prevention: Flu vaccine (changes every year as virus tends to mutate) and good hygiene (hands, cooking surfaces etc)

Answer 217

Linnaean name: Human Immunodeficiency Virus Capsid structure: Roughly circular Enveloped: Yes DNA/RNA: ssRNA (sense) Mechanism(s) of infection: Spread through bodily fluids (vaginal fluid, semen, blood, breast milk and pre-ejaculate), so can occur through unprotected sex, sharing of needles, vertical transmission (in-utero) or from medical proceedures (organ donation, blood transfusion etc) Patient factors to consider: Age, relative time, pathological state (especially cancer, and any infections have the potential to be life-threatening), sexuality (more common in MSM), physiological state (intravenous drug use) Interaction with host: Enters the bloodstream, then infects the CD4+ T cells (along with other cells of the immune system), where the ssRNA is converted to DNA by reverse transcriptase and inserted into the genome of the T cells. Following this, it is transcribed and translated, which eventually results in budding of immature viral proteins (and genetic material), and they exit by causing lysis of the T cell. Eventually, a viral protease cuts the proteins, which converts it into an active virus, with ssRNA genetic material again. As this happens over and over the number of CD4+ T cells declines, which leads to a loss of the cell mediated (active) immune system. As this progresses, infections the body would be able to fight off with a healthy immune system take hold. These are known as ‘AIDS defining infections’, the key ones are as follows: Opportunistic oral candida albicans – oral thrush, occurs as a direct result of lack of immunity Extrapulmonary mycobacterium tuberculosis (eg brain) Pneumocystis pneumonia/PCP (caused by Pneumocystis jerovecii, an opportunistic yeast like fungi) Kaposi’s sarcoma (rare tumour of the skin caused by infection with HHV8 (human herpes virus 8), an opportunistic virus) How to diagnose: History: Acute HIV infection (~3 weeks) is a flu like illness so malaise, lethargy, fever, muscle aches, headache, nausea and vomiting etc. Following this, you would expect AIDS defining illnesses as it progresses through stages of HIV eventually to AIDS, along with persistent weight loss, lymph node enlargement, chronic fatigue etc Examination: All manner of findings depending on the type of AIDS defining illness (upper lobes dull to percussion in TB, crackling in lower lobes in PCP) Investigation: HIV antigen/antibody screen, FBC (checking CD4+ count) Treatment: Supportive Treat the AIDS defining illness Specific CD4+ count checked on a regular basis and action taken if it falls below a certain level (500 Stage II – mild, CD4+

Answer 218

Capsid structure: Icosahedral Enveloped: Yes DNA/RNA: dsDNA non-sense Mechanism(s) of infection: Spread through bodily fluids (vaginal fluid, semen, blood, breast milk and pre-ejaculate), so can occur through unprotected sex, sharing of needles, vertical transmission (in-utero) or from medical proceedures (organ donation, blood transfusion etc) Patient factors to consider: Age, pathological state (HIV, cancer etc), physiological state (IV drug use), relative time Interaction with host: Enters the bloodstream and replicates within hepatocytes, which leads to host damage by inflammation when the active immune system recognises the viral molecules (cytotoxic T lymphocytes) How to diagnose: History: Fatigue, abdominal pain, anorexia, nausea, vomiting, arthralgia, malaise, myalgia etc. Can develop anywhere from 1 to 5 months after initial infection (previous history of unprotected sex/intravenous drug use to be expected) Examination: Hepatomegaly, jaundice (particularly of the sclera) Investigation: FBC, U and Es, CRP, LFTs, Hep B serology, PCR (to search for Hep B DNA) Treatment: Supportive Nothing specific, just treat symptoms as and when they occur (paracetamol for fever and pain etc) Hepatitis B serology (assesses state of infection/immune response) Specific Vaccinate if you catch it early enough (ie if you know they’ve been exposed within 24 hours of it happening) Peginterferon-alfa-2a to stimulate immune system to destroy virus Antiretroviral drugs (in chronic infection) Duration of illness: Tends to self-resolve after 6 months, but can persist chronically. Can use Hep B serology to work out the progress of the clearance of the virus: HBsAg – surface antigen, virus recognised, first to appear HBeAg – e-antigen, signals highly infectious period, symptoms at this point IgM – core antibody (can’t detect core antigen) – first antibody to appear, immune system is mounting challenge) HBeAb – e-antibody, signals end of infectious period and viral inactivity (immune system is winning) HBsAb – surface antibody, last antibody to appear, virus is cleared and patient has recovered IgG – core antibody – persists for life Possible sequelae: If HBsAg persists for 6 months, then patient has chronic Hep B. 25% of chronic cases result in cirrhosis and 5% result in hepatocellular carcinoma. Most patients make a full recovery Prevention: Vaccinate (need to check HBsAb levels, needs to >10 for adequate protection and >100 for long-term protection), avoid infected person’s bodily fluids, use PPE with patients

Answer 219

Capsid structure: Icosahedral Enveloped: Yes DNA/RNA: ssRNA (sense) Mechanism(s) of infection: Blood to blood contact (primarily), classic spread of infection is sharing of needles in intravenous drug users. Blood transfusions prior to 1991 are at risk (couldn’t detect until 1991). Possibly spread by unprotected sexual contact (unknown) Patient factors to consider: Age, pathological state (HIV, cancer etc), physiological state (IV drug use), relative time Interaction with host: Travels to the liver and replicates within hepatocytes, but does not usually cause symptoms How to diagnose: History: Most patients will be asymptomatic, but in ~20% of patients you may see fatigue, nausea, anorexia, dark urine and RUQ abdo pain Examination: RUQ abdominal pain, possibly hepatomegaly Investigation: FBC, U and Es, LFTs, CRP, Hep C antibody test, PCR Treatment: ``` Supportive Lifestyle changes Stop drinking and smoking Eating a healthy diet Regular exercise ``` Specific Pegylated interferon (stimulates immune system) Ribavirin (antiviral, stops replication) Duration of illness: May resolve spontaneously, but 80% of patients go on to develop some kind of chronic infection that persists for years Possible sequelae: Can lead to cirrhosis due to chronic liver damage, liver failure (requiring a transplant) or liver cancer (which is almost always fatal) Prevention: Harm reduction strategies (giving clean needles to IV drug users, ensuring proper screening of all blood products), PPE when dealing with patients etc

Answer 220

Capsid structure: Icosahedral Enveloped: Yes DNA/RNA: dsDNA Mechanism(s) of infection: Inhalation of virons that are expelled from the lungs of infected person (very contagious). Can also have direct contact with blisters/shingles Patient factors to consider: Age (childhood disease is almost a rite of passage), pathological state (immunocompromised) Interaction with host: Normal adaptive immune response (presentation of Class I MHCs activating CD8+ T cells  cytotoxic T cells) followed by lifelong persistence of IgG antibodies, conferring lifelong immunity. Varicella zoster lies dormant in dorsal ganglion of sensory nerves. Reactivation leads to rash that’s known as Shingles How to diagnose: (Shingles in the context of the immunocompromised patient) History: Previous exposure and case of chickenpox (almost always in childhood). Sudden appearance of rash that usually roughly corresponds to a dermatome. Some type of immunocompromise Examination: Red, raised rash at a localised area of the body Investigation: Varicella zoster IgG serology (sometimes, diagnosis usually made on history alone) Treatment: Supportive Pain relief Anti itching cream Specific None Duration of illness: Heals within two to four weeks Possible sequelae: Resolution (by far the most common), can lead to chronic nerve pain in a small number of patients Prevention: Not really preventable, apart from treating any cause of immunocompromise that is modifiable (obviously chemotherapy isn’t as destroying the cancer is more important

Answer 221

Mechanism(s) of infection: Ubiquitious within the normal air (spores always present), inhaled constantly by a patient. Only causes disease in people with immunocompromise (immune system very good at clearing fungal moulds before they become dangerous) – opportunistic Patient factors to consider: Key one is pathological state (immunocompromised eg chronic granulomatous disease) Interaction with host: Cleared by mucociliary escalator/internalised by alveolar macrophages in most patients (healthy). In those that have a phagocyte deficiency eg CGD, a switch to hyphae and active multiplication is seen in the alveoli/alveolar epithelium How to diagnose: History: At least a week (can be chronic) long hx of SOB, productive cough, fatigue, weight loss etc Examination: Tachypnea, tachycardia, hypotension, cyanotic, wheeze etc Investigation: FBC, U and E, CRP, erect CXR, CT thorax, MCS, sputum culture Treatment: Supportive High flow O2 Pain relief Anti-pyrexials Specific Antifungals Colony stimulating factors (some cases only) Duration of illness: Can be resolved in a few weeks, but many cases progress to chronic disease Possible sequelae: Resolution, progression to chronic pulmonary aspergillosis, death Prevention: Avoid areas where Aspergillus spores are abundant eg rotting plants, soil, compost. Air purifiers in the home (but ver expensive)

Answer 222

Mechanism(s) of infection: Vector spread by the female Anopheles mosquito (travels in their saliva, and is ingested from human’s blood) Patient factors to consider: Normal ones (age, pathological state and relative time – incubation period) along with calendar time (how long they’ve been back) Interaction with host: Enters host by being ejected from the salivary glands of the Anopheles mosquito, entering the bloodstream, where it then travels to the liver, colonising that until it matures and re-enters systemic circulation. Here it invades RBCs and uses Hb as a nutrient until oncosis of the RBC occurs through the intracellular multiplication of the protazoa. This leads to haemolytic anaemia How to diagnose: History: Fever, chills and sweats, cycling so they occur on the 3rd or 4th day, dry cough, headache, nausea and vomiting and myalgia. Recently returned from an area where malaria is endemic (ie Sub-Saharan Africa) Examination: Unremarkable save for splenomegaly Investigation: Three blood smears, FBC, U and Es, LFTs, BM, coagulation studies, head CT (if headache) Treatment: Supportive Antipyrexials Anti-emetic if needed Pain relief Specific Species dependant (falciparum is most common but other types exist): Falciparum – quinine or armitemisin Vivax, ovale or malariae - chloroquine Duration of illness: N/A Possible sequelae: Usually leads to haemolytic anaemia, can progress to cerebral malaria and therefore lead to coning. Also, jaundice, acute renal failure, shock, pulmonary oedema and of course death. Can cause stillbirth in pregnant women A – Assess of risk of patient (pregnant women!!) and area they’re travelling to B – bite prevention: DEET, nets, longs o’clock C – Chemoprophylaxis (antimalarials), resistance is specific to geographical locations ie doxycycline is suitable in Sub-Sahaan Africa

ESA 3 Clinical Conditions Flashcards

(249 cards)