Cardiorespiratory 2 Flashcards

Question

Name and explain the mechanism of action of beta blockers

Answer 1

beta blockers e.g. propranolol, atenolol * block beta adrenergic receptors (part of SNS) * causes decrease HR, decrease contractility, decrease systemic vascular resistance (amount of force exerted on circulating blood by the vasculature of the body)

Answer 2

ACE inhibitors e.g. Ramipril, enalapril *inhibit RAAS system; block ACE enzyme which converts angiotensin I--> angiotensin II= lower levels of angiotensin II= vasodilation= decreased BP= prevention of angiotensin II vasoconstriction

Answer 3

calcium channel blockers e.g. amlodipine, verapamil * block voltage-gated calcium channels on cardiac muscle= less Ca2+ enters cell * causes decrease in HR, increase in coronary vasodilation = decrease BP, decrease total peripheral resistance

Answer 4

Statins e.g. atorvastatin *competitive inhibitors of HMG-CoA reductase= reduces cholesterol synthesis (so LDL levels decrease) statins increase the clearance of LDL from the blood n.b. HMG-CoA reductase is the rate-limiting step in cholesterol synthesis

Answer 5

Systemic vascular resistance (SVR), also known as total peripheral resistance (TPR), is the amount of force exerted on circulating blood by the vasculature of the body. Three factors determine the force: the length of the blood vessels in the body, the diameter of the vessels, and the viscosity of the blood within them. Total peripheral resistance is an important concept to understand because it plays a vital role in the establishment and manipulation of blood pressure. This relationship is expressed mathematically as MAP = CO x TPR, where CO stands for cardiac output, and MAP stands for mean arterial pressure.

Answer 6

NO reduces infarct size and endothelial dysfunction NO is an important determinant of basal vascular tone, prevents platelet activation, limits leukocyte adhesion to the endothelium, and regulates myocardial contractility. mechanism: NO activates guanylate cyclase to form cGMP cGMP stimulates dephosphorylation of myosin light chain causes vascular SMC relaxation= Vasodilation= v. effective on coronary arteries!

Answer 7

the thigh or calf pain pain with walking that comes with peripheral arterial disease. PAD is when u have atherosclerotic plaques in peripheral arteries which reduces blood flow to extremities

Answer 8

stable angina (more common) – attacks have a trigger (such as stress or exercise) and stop within a few minutes of resting. unstable angina (more serious) – attacks are more unpredictable (they may not have a trigger) and can continue despite resting.

Answer 9

platelets are produced by megakaryocytes in bone marrow under influence of thrombopoietin (hormone)

Answer 10

a rare disorder in which the blood doesn't doesn't have enough blood-clotting proteins mutation on X chromosome low level or complete absence of coagulation factor VIII or IX Haemophilia A= deficiency of factor VIII Haemophilia B= deficiency of factor IX (rarer) symptoms of haemophilia: -big lumpy bruises -bleeding into muscle + joints particularly knees, elbow, ankles -bleeding for long time after cut - serious internal bleeding into vital organs after insult (deliberate or accidental)

Answer 11

vWD is an autosomal dominant disorder as a result of genetic mutation on chromosome 12 can be passed from either mother or father and therefore child has a 50% chance of being affected carries and protects factor VIII when bleeding occurs Type 1 vWD : 1% of population; reduction in von willebrand antigen + factor FVIII as a result Type 2: von Willebrand factor doesn't work properly + therefore have a low RiCof Type 3: Extremely low levels or complete absence of Von Willebrand antigen, RiCof + factor VIII (most severe type) symptoms; bruising, nose bleeds, heavy period, joint bleeds and muscle bleeds

Answer 12

thrombosis= pathological clot (thrombus) formation within a blood vessel embolism= part of clot breaks off + travels through circulation until obstructed by vessels of smaller diameter

Answer 13

Heparan sulfate is on surface of endothelial cells, These heparin sulphate polysaccharides form projections into the lumen of a vessel. These projections prevent platelet adhesion to intact endothelial membrane= prevents clots. Thrombomodulin binds thrombin which activates the natural anticoagulant, protein C, which reduces clotting. Patients with chronic inflammatory disease have damage to endothelial wall, this reduces amounts of attached heparin + downregulates thrombomodulin= increasing risk of clot formation

Answer 14

Factor V Leiden mutation= causes resistance to activated protein C it is the most common heritable risk factor for DVT/PE (3-8% of ppl w european ancestry carry one copy of Factor V Leiden mutation)

Answer 15

D-dimer is a fibrin degradation product (small protein fragment released into the blood when a thrombus is degraded by fibrinolysis. BUT, can also increase w inflammation, pregnancy + cancer D-dimer is a blood test that checks for blood-clotting problems; indicates blood clot/DVT/PE *normal D-dimer effectively rules out DVT in those w low likelihood *in those w high likelihood DVT a normal D-dimer is too low to use alone as diagnosis

Answer 16

1) ultrasound of leg +ve ultrasound= proceed with treatment -ve ultrasound= D-dimer 2)D-dimer +ve D-dimer= offer repeat scan in 6 days -ve D-dimer= consider alternative Dx (diagnosis)

Answer 17

international normalised ratio (INR) blood test tells you how long it takes for your blood to clot. A test called the prothrombin time (PT) actually measures how quickly your blood clots. The PT results can be expressed as an INR to standardise the results.

Answer 18

circulatory shock= acute circulatory failure with inadequate or inappropriately distributed tissue perfusion resulting in cellular hypoxia + end-organ damage

Answer 19

Hypoperfusion is a life-threatening condition characterised by poor circulation of blood from heart and lungs to the body's organs.

Answer 20

vasodilation= enhances blood flow to certain areas and reduces SVR (systemic vascular resistance). Occures due to SMC relaxation. Activation of nitric oxide + prostacyclin via cGMP + cAMP. 2ndry messengers cause a decrease in calcium= SMC relaxation vasoconstriction= controlled by SNS. Noradrenaline acts on alpha 1 + 2 receptors to cause vasoconstriction of vessels and SMC contraction. N.b. angiotensin + vasopressin have vasoconstrictive effects

Answer 21

1) initial stage= switch from aerobic to anaerobic metabolism; increase lactic acid; subtle clinical signs 2)compensatory stage= SNS activated; increase catecholamine release, increase cardiac output; vasoconstriction, aldosterone release (urine decrease), heart rate + glucose levels INCREASE 3) progressive stage= body cannot maintain above stage.. decompensation begins,,, electrolyte imbalance, metabolic acidosis, respiratory acidosis, peripheral oedema, irregular tachyarrhytmias, hypotension, pallor, clammy skin, altered level of consciousness 4) refractory stage= irreversible cell damage, impending death

Answer 22

* OBSTRUCTIVE=physical obstruction to vessels entering/leaving the heart *DISTRIBUTIVE=excessive vasodilation, excessive inflammation. Further classified into septic shock, anaphylactic shock, neurogenic shock *CARDIOGENIC= failure of heart to pump blood *HYPOVOLEMIC= due to reduced circulatory volume e.g. from external or internal bleeding, cholera, burns, haemorrhage, post-surgery

Answer 23

* tachycardia + tachypnoea *hypoxia *chest pain *reduced breath sounds on affected side * deviated trachea, AWAY FROM AFFECTED SIDE

Answer 24

- tachycardia -hypotension -distant heart sounds - elevated jugular venous pressure

Answer 25

systolic/diastolic low BP= <80/<60 normal BP= 80-120/60-80 prehypertension= 120-139/80-89 stage 1 hypertension= 140-159/90-99 stage 2 hypertension= 160-180/100-120 stage 3 hypertension= 180+/120+ N.B. U DIAGNOSE BASED ON IF ONE OF THE NUMBERS IS HIGHER THAN NORMAL e.g. if patient has 120/99 then they have stage 1 hypertension as the diastolic reading is high

Answer 26

ARBs bind to and inhibit the angiotensin II type 1 (AT1) receptor and are indicated to treat hypertension, congestive heart failure, and diabetic nephropathy.

Answer 27

natriuretic peptides (NPs)= peptide hormones synthesised by cardiomyocytes Atrial natriuretic peptide (ANP)= from atria B-type natriuretic peptide (BNP)= from ventricles functions of NPs= * decrease renin release= decrease Ang II= decrease aldosterone *increase GFR (by vasodilating afferent arterioles)

Answer 28

caused by rheumatic fever (RF), a systemic infection caused by untreated pharyngeal group A beta haemolytic streptococci infection * rare disease due to penicillin treatment + decreased virulence of bacteria *results in valve thickening and damage carditis is one of RF presentation + can lead to rheumatic heart disease affecting mainly MITRAL valve (but also aortic a bit)

Answer 29

IE/ Infective Endocarditis= is inflammation of endocardium caused by various organisms its often seen in ppl with limited access to healthcare-- those who didnt get antibiotic treatment for infection and it spread to hear *usually present with FEVER and heart murmur +/- emboli/immune complex deposition *other signs= splinter haemorrhages, conjunctival haemorrhage, osler nodes, janeway lesions *causes valve damage + regurgitation due to bacterial vegetations

Answer 30

Aortic stenosis (AS)= obstruction of blood flow during systole = when the aortic valve becomes narrowed, restricting blood flow from the left ventricle (LV) into the aorta during systole. This results in increased afterload and compensatory left ventricular hypertrophy (LVH). causes: - calcification + degeneration (aging) - congenital: bicuspid valve - rheumatic heart disease symptoms: -dyspnoea (increased diastolic pressure in stiff non-compliant LV) -angina (increased o2 demand of hypertrophied LV) -syncope (decreased blood flow to brain) -LVF (contractile failure as ventricle dilates) - sudden death (ventricular arrhythmias signs: -slow rising carotid pulse (pulsus parvus et tardus), heaving nondisplaced apex beat, LV heave+ aortic thrill -S4 +/- ejection click -ejection systolic murmur treatment: -surgical valve repair -transcatheter aortic valve implantation (TAVI)

Answer 31

aortic regurgitation (AR)= occurs when aortic valve does not close completely during diastole, leading to the backflow of blood from the aorta into the left ventricle (LV). AR results in a volume overload in the LV, causing compensatory dilation and, over time, hypertrophy. Chronic AR leads to progressive left ventricular dilation, reduced contractility, and eventually heart failure Causes: Valvular causes/aortic valve leaflet disease: congenital bicuspid aortic valve, rheumatic heart disease, calcific disease, infective endocarditis. Aortic root causes/aortic root dilating disease: Aortic dissection, Marfan syndrome, Ankylosing spondylitis, syphilitic aortitis, or other conditions leading to aortic root dilation. symptoms: -often asymptomatic -dyspnea (contractile failure as ventricle dilates) -angina (increased o2 demand of dilated hypertrophied LV signs: -collapsing pulse -displace hyperdynamic apex beat -corrigan, quinkie,de musset, duroziez signs -early diastolic murmur -systolic murmur - Austin Flint murmur in severe cases treatment: -aortic valve replacement

Answer 32

mitral stenosis (MS)= stenotic mitral valve obstructs blood flow during diastole. LA is met with high resistance leading to enlargement can lead to RVF as a passive consequence of increased left atrial pressure causes: -rheumatic fever -congenital diseases symptoms: -dyspnoea, orthopnea (due to left atrial pressure, poor exercise tolerance) -palpitations signs= -malar flush on face due to cardiac output - purple lips -pre-systolic murmur -low volume pulse

Answer 33

mitral regurgitation (MR)= mitral valve does not close properly during systole, leading to backflow of blood from the left ventricle (LV) into the left atrium (LA). causes: 1. mitral valve leaflet disease= mitral valve prolapse, rheumatic heart disease, infective endocarditis, connective tissue disease, calcified/stenotic mitral valve post surgery 2. subvalvar disease= chordal or papillary muscle rupture (post MI complication), papillary muscle dysfunction 3. functional MR in LV dilatation in DCM (dilated cardiomyopathy)

Answer 34

cranial nerve XI (spinal accessory)

Answer 35

pectoral nerves C5-T1

Answer 36

long thoracic nerve (C5-C7)

Answer 37

intercostal + subcostal nerves (T7-T12)

Answer 38

intercostal nerves (T2-T11)

Answer 39

thoracocentesis (aka pleural tap/needle decompression) * to sample pleural fluid * to avoid damage to intercostal nerves needle is inserted superior to rib *when patient is upright position fluid will accumulate in the costophrenic recess * the 9th mid-axillary line during expiration avoid inferior border of the lung

Answer 40

phrenic nerve (C3,C4,C5) C3,4,5 KEEPS DIAPHRAGM ALIVE

Answer 41

Dilated Cardiomyopathy (DCM) = heart's left ventricle enlarged and weakened= reduced heart function which can lead to heart failure symptoms: fatigue, dyspnea, orthopnea, oedema 'patient cld mistake for weight gain' management; -beta-blockers (control HR) -anti-coagulants (reduce blood clot chance) -diuretics (reduce fluid build up) -ACE inhibitor or ARB (reduce BP) -biventricular pacing implant (control heart rhythm)

Answer 42

Hypertrophic Cardiomyopathy (HCM) = heart muscle (myocardium) becomes abnormally thick (hypertrophied), particularly affecting the left ventricle. This thickening makes it harder for the heart to pump blood efficiently and can cause problems with the heart's electrical system, leading to arrhythmias. HCM is often genetic (autosomal dominant) and can affect people of any age symptoms; -syncope -angina -palpitations -dyspnea -fatigue -sudden cardiac death upon examination: jerky pulse, double apex beat, systolic thrill @ left sternal edge, harsh ejection systolic murmur management: as u wld treat heart failure

Answer 43

Restrictive cardiomyopathy (RCM)= (least common cardiomyopathy) myocardium has increased stiffness that causes increased pressure in one or both ventricles. This stiffness impairs diastole as myocardium not stretch properly to fill with blood. causes: very variable (e.g. sarcoidosis, cardiac amyloidosis, Loeffler syndrome) but result in: -fibrosis/scarring of endocardium -infiltration of myocardium by abnormal substance - RCM can be genetic w mutations such as mutant troponin I, mutant cardiac desmin, mutant alpha-cardiac actin, mutant beta-MyHC symptoms: -increased JVP -hepatomegaly, ascites -peripheral oedema -fatigue, systemic congestion -palipations + cardiac blocks - maybe S4 heart sound investigations for RCM: - ECG: low voltage QRS complexes, large p wave, AF, AV or bundle branch blocks - CXR= atrial enlargement, pulmonary congestion - management: poor prognosis unless underlying cause can be treated, asses risk for arrhytmia (pacing, antiarrhythmic meds), symptomatic relief of congestion with diuretics

Answer 44

Ventilation (V) refers to the flow of air into and out of the alveoli, while perfusion (Q) refers to the flow of blood to alveolar capillaries.

Answer 45

type 1 resp failure: hypoxemia only PaO2= below 8kPa PaCO2= normal type 2 resp failure: hypoxemia + hypercapnia PaO2= below 8kPa PaCo2= above 6kPa

Answer 46

asthma is a chronic inflammatory condition of airway inflammation leading to reversible bronchospasm, mucus hypersecretion + airway wall inflammation and remodelling if poorly controlled so mechanism is chronic inflammation-> narrowing of airways (bronchocontriction)-> airflow limitation pathology: Th2 (lymphocyte) mediated inflammation via cytokines: * IL-4 + IL-13-> B cell synthesis IgE, mucus production + airway remodelling. * IL-5-> eosinophil activation-> inflammatory products n.b. allergens can activate sensitized mast cells by crosslinking surface-bound IgE molecules to release bronchoconstriction mediators e.g. histamine Peak expiratory flow rate (PEFR) is the volume of air forcefully expelled from the lungs in one quick exhalation FEV1= forced expiratory volume in one second (assesses lung function in patients w asthma)

Answer 47

aerosol inhaler= inhale slow + steady dry powder inhaler (DPI)= inhale quick + deep

Answer 48

Muscarinic vs. Beta-2 Receptors in the Lungs Muscarinic Receptors (M3): Promote bronchoconstriction and mucus secretion, contributing to reduced airflow. Anticholinergic drugs block these M3 receptors to relieve symptoms of bronchospasm in asthma and COPD. drugs used in asthma patients: MUSCARINIC ANTAGONISTS Beta-2 Receptors: Promote bronchodilation and inhibit airway inflammation, enhancing airflow. Beta-2 agonists are used as bronchodilators in the treatment of respiratory conditions like asthma and COPD. drugs used in asthma patients: BETA-2 AGONISTS LABA (Long-Acting Beta-2 Agonist) and LAMA (Long-Acting Muscarinic Antagonist)

Answer 49

MART= maintenance + reliever therapy *patient has 1 inhaler that is both preventer (inhaled steroid) + as-needed reliever (long-acting beta-agonist bronchodilator) (i.e.. no blue inhaler as all in one) can be prescribed 'as needed'= AIR (anti-inflammatory reliever) therapy

Answer 50

salbutamol is a SABA (short acting beta-2 agonist)

Answer 51

COPD management: mild COPD; bronchodilator (1st line) moderate/severe COPD; LABA + LAMA (+ inhaled corticosteroid/ICS if symptoms exacerbated after the LABA/LAMA still) n.b. ICS in COPD= increased risk of pneumonia so BIG CAUTION PRESCRIBING THESE weigh risk-benefit; if the blood eosinophils are high prescribe the ICS

Answer 52

Bronchiectasis is a chronic progressive pulmonary disease, characterised by permanent and irreversible DILATION OF BRONCHIAL WALL= produce lots of mucus risk factors: INFLAMMATORY DAMAGE TO AIRWAYS SUCH AS.. -previous severe lower resp tract infection (TB, pneumonia or influenza) -Cystic fibrosis, COPD, asthma + connective tissue disorders e.g. rheumatoid arthritis symptoms: *daily sputum production (large volumes) *chest pain *haemoptysis *cough *dyspnoea *wheeze *crackles during early inspiration *rhinosinusitis diagnosis; HIGH RESOLUTION CT SCAN (HRCT) *sputum culture *CXR *blood o2 * FBC management: -vaccinations (influenza + pneumococcus) - screen for P. aeruginosa then treat if +ve w inhaled antibiotics - AZITHROMYCIN if 3+ exacerbations a year - if absence of sputum culture= commence amoxicillin if penicillin allergy: macrolide - NO ICS n.b. physiotherapy + airway clearance technique!

Answer 53

ICS= inhaled corticosteroids are broad spectrum anti-inflammatory drugs *ICS bind to glucorticoid receptors within airway epithelium *up-regulates anti-inflammatory genes e.g. lipocortin-1 *suppresses pro-inflammatory genes; CXCL8 (IL-8), IL-6, TNF-alpha *reduces eosinophil numbers * inhibits Th2 cytokines (IL-4, IL-5 +IL-13 responsible for IgE production) *prevents airway remodelling + suppress airway hyperactivity

Answer 54

upper respiratory tract: nasal cavity, pharynx + larynx lower respiratory tract: trachea, primary bronchi, lungs

Answer 55

HRV infection of airway epithelial cell -> recognition via toll-like + retinoic acid-inducible gene-1-like (RIG) receptors-> epithelial cells release pro-inflammatory mediators (e.g. TNF-alpha, IFN + CXCL8)-> activation of inflammatory cells e.g. neutrophils

Answer 56

asthma (state of heightened immune + inflammatory response) -> increase cytokine release (e.g. IL-4, IL-5, IL-10, + IL-13) -> increases intracellular adhesion molecule (ICAM-1= major HRV receptor) -> athma patients more susceptible to HRV infection

Answer 57

examples: site of action: blood vessels surrounding nasal sinuses mechanism: alpha1 adrenoreceptor agonists pharmacological effect: VASOCONSTRICTION (if we decrease swelling of blood vessels around sinuses we decrease nasal congestion)

Answer 58

peak flow= max speed of expiration

Answer 59

tidal volume= volume of air move in + out of ur lungs at rest

Answer 60

forced vital capacity= max volume of air forcibly exhaled after taking deep/full breath

Answer 61

inspiratory reserve volume= volume of air u can draw into ur lungs

Answer 62

expiratory reserve volume= volume of air u can expel from ur lungs

Answer 63

residual volume= volume of air that remains in lungs even after max exhalation

Answer 64

the smooth muscle cells (SMC) produce elastic fibres

Answer 65

mesothelium= the epithelium that lines the pleaurae, peritoneum and pericardium

Answer 66

Bronchitis affects the bronchi (larger airways). Bronchiolitis affects your smaller airways (bronchioles). Bronchitis usually affects older children/adults, while bronchiolitis is more common in babies/ young kids <2

Answer 67

- sore throat -cough -fatigue -runny/stuffy nose -fever -body aches -vomiting -diarrhea symptomatic up to 2wk minority: severe illness + require hospital admission (ventilator support)

Answer 68

Consolidation (in lungs)= the state of the lung in which the alveoli (air sacs) are filled with fluid produced by inflamed tissue, as seen in pneumonia

Answer 69

pneumonia is inflammation of the alveoli in either one or both lungs= alveoli become inflamed and fill up with fluid elderly + v young= great risk of mortality *streptococcus pneumoniae = no1 identified bacteria to cause pneumonia symptoms (3-4wk duration) -headache -fever -weakness/muscle aches -sweating -DRY cough -nasal congestion -chills -sore throat diagnosis; -physical exam -full blood count - sputum culture -urine test -PCR -CT scan

Answer 70

CRB65 severity score to assess mortality risk/ whether patient requires hospital admission. 1 point for each feature present: - Confusion -Respiratory rate >30/min - Blood pressure (SBP <90 or DBP <60 mmHg) - age >65 n.b. CRB65= community or CURB65= hospital U NEED TO KNOW WHETHER PATIENT NEEDS TO BE HOSPITALISED FOR PNEUMONIA OR CAN GET BETTER W ANTIBIOTICS ' IN COMMUNITY' (AT HOME)

Answer 71

idiopathic pulmonary fibrosis= unknown cause condition results in scarring/ honeycombing in lung which restricts breathing + o2 exchange symptoms: -dyspnoea -chronic dry cough -finger clubbing -fatigue -weakness -weight loss management: -Prifenidone (Anti-fibrotic agent; mechanism unclear) -Nintedanib (Tyrosine kinase inhibitor= reduces forced vital capacity decline) - antacid therapy (IPF patient with GERD) -oxygen therapy! -pulmonary rehab w physiotherapist!

Answer 72

sarcoidosis= multi-system granulomas; inflammatory disease where immune system goes into overdrive can affect any organ but in lungs v dangerous; sarcoidosis causes granulomas n.b. more common in african descent and northern european descent symptoms: -enlarged lymph nodes -blurred vision -haemoptosis -liver + spleen enlargement -hacking cough -skin rashes; lupus pernio, subcutaneous nodules -joint pain, swelling of knees -heart complications management: -if patient has no symptoms= no treatment - if symptomatic; treat w corticosteroids steroid-sparing alternatives for pulmonary sarcoidosis= methotrexate, folic acid, azathropine, leflunomide, mycophenolate med for refractory sarcoidosis; infliximab

Answer 73

patient critically ill if spO2 is below 85%= risk of hypercapnic resp failure ^u give these patients a non-rebreather mask which is o2 conc of 60-90% when used at a flow rate at 15L/min, Most suitable for trauma + emergency use u need o2 saturation between 94-98% anyone below this needs o2

Answer 74

The 3 factors of Virchow's triad: venous stasis, vascular injury, hypercoagulability

Answer 75

microcytic anaemia= rbc's smaller than normal acronym 'TAILS' T= thalassaemia A= anaemia of chronic disease I= iron deficiency L= lead poisoning S= sideroblastic anaemia

Answer 76

occurs in duodenum + upper/proximal jejunum by ENTEROCYTES eneterocytes have specific transporter proteins which allow them to move iron into cell from gut (apical membrane enterocyte)

Answer 77

* iron-containing food consumed = travels past stomach = chyme * haem gets to apical surface of enterocyte (found in duodenum/proximal jejunum) + is absorbed by haem receptor * within the enterocyte enzyme; haem oxygenase breaks off the iron + leaves enterocyte via FERROPORTIN (iron gate) *this iron is then picked up b y transferrin + is transported around the body n.b. enterocytes can also store iron as ferritin n.b. body has no mechanism for excreting iron!

Answer 78

1) Fe3+ bound transferrin binds transferrin receptor + enters cytosol receptor-mediated endocytosis 2) Fe3+ within endosome released by acidic microenvironment + reduced to Fe2+ 3) the Fe2+ transported to the cytosol via DMT1 4) once in cytosol, Fe2+ can be stored in ferritin, exported by ferroportin (FPN1) or taken up by mitochondria for use in cytochrome enzymes

Answer 79

* excess body iron dangerous-- iron a pro-oxidant causes free radical damage to cells + tissues *body does not have mechanism to excrete excess iron *therefore, iron absorption tightly regulated * hepcidin primary 'master iron regulator'= negative regulater BLOCKS FERROPORTIN= BLOCK IRON EXPORT (n.b. hepcidin is also released in inflammation)

Answer 80

ferritin= major iron storage protein, present in most cells as a iron reserve-- LIVER has highest amount liver also releases ferritin during inflammation (acute phase reactant) clinical relevance= indirect marker of total iron stored in body. Hence, low serum ferritin is diagnostic proof for iron deficiency anaemia

Answer 81

haematopoiesis= formation of blood cellular components erthropoiesis= subtype of haematopoiesis referring to generation of RBCs

Answer 82

erythropoiesis is controlled by peptide hormone ERYTHROPOIETIN (EPO)- produced by kidney interstitial cells around proximal tubules: PERITUBULAR INTERSTITIAL FIBROBLASTS

Answer 83

IF PERSON HAS INFLAMMATION TAKE A TRANSFERRIN RECEPTOR (TfR) CONCENTRATION BLOOD TEST= this will give indication of anaemia as inflammation doesn't effect the TfR concs whereas we know inflammation does affect ferritin levels which is the blood test usually used to diagnose anaemia n.b. the ferritin released during inflammation is usually iron-poor but blood test only measures ferritin level so u cant distinguish between iron poor and iron rich ferritin

Answer 84

PPIs and H2 blocker-induced iron deficiency reduces iron absorption by altering the acidic environment of the gastrointestinal trac

Answer 85

iron supplements will not correct anaemia inflammation as problem is w iron being absorbed in gut + iron getting out of macrophages, along with depressed erythropoietin release and erythropoiesis caused by inflammatory cytokines= need to treat cause of inflammation

Answer 86

megaloblastic anaemia= is a type of macrocytic anaemia characterized by the presence of abnormally large, immature red blood cells (megaloblasts) in the bone marrow. It is caused by impaired DNA synthesis during erythropoiesis (the process of producing red blood cells) causes development of nucleus to be retarded in relation to cytoplasm *cell division delayed + erythroblasts continue to grow to form megaloblasts which give rise to larger red cells examples: -vitamin b12/folate deficiency -drugs that interfere w DNA synthesis (e.g. some anti-cancer) -some erythroid leukaemias where DNA synthesis is retarded

Answer 87

macronormoblastic erythropoiesis= refers to a pattern of red blood cell production (erythropoiesis) in the bone marrow where the developing red blood cells (normoblasts) are larger than normal but otherwise have typical maturation processes examples -liver disease -alcohol toxicity -some myelodysplastic syndromes

Answer 88

stress erythropoiesis= conditions associated with a high reticulocyte count (reticulocytes are larger than normal RBCs). This high level of erythropoietin leads to an expanded + accelerated erythropoiesis (synthesis of RBCs) examples: -recovery from blood loss due to haemorrhage -recovery from haemolytic anaemia

Answer 89

Folic acid (400μg/day) taken before conception + during 1st 12 wks of pregnancy prevents majority of neural tube defects in babies (e.g spina bifida)

Answer 90

Vitamin b12 is an essential cofactor for DNA synthesis (role in folate metabolism). REQUIRED for normal erythropoiesis and for normal function + development of CNS= MYELINATION. Also required for BCAA (branched chain amino acids)+ FA (fatty acid) metabolism= cofactor methyl malonyl CoA mutase produced by bacteria (NOT plants or animals). Only available from food of animal origin via commensal bacteria/ supplements N.B. vegans must supplement B12 by eating fortified foods daily or taking a B12 supplement daily

Answer 91

- B12 released from food proteins by proteolysis in stomach where binds to haptocorrin -haptocorrin-B12 complex digested by pancreatic proteases in small intestine releasing B12 which then binds intrinsic factor produced by gastric parietal cells -intrinsic factor-B12 complex binds to cubam receptor which mediates uptake of complex by receptor-mediated endocytosis into enterocytes -after lysosomal release in enterocytes, B12 exits via basolateral membrane through MDR1 - binds to transcobalamin in blood + transported around bloodstream -majority of B12 is stored in liver (stores enough B12 requirements for 3-6yrs)

Answer 92

pernicious anaemia is an autoimmune disease where the body make antibodies to parietal cells or IF (intrinsic factor) which destroys and inactivates intrinsic factor =decreased or absent intrinsic factor causes progressive exhaustion of B12 reserves= B12 deficiency diagnosis; u need to order a blood test for these specific antibodies

Answer 93

seen on standard FBC (full blood count) - RDW quantifies degree of anisocytosis (variation in RBC size) why is RDW important? - differentiates types of anaemia -can indicate if someone has more than one e.g. can have both microcytic + macrocytic - used in conjuction w peripheral blood smear example: a patient w both IDA + folate deficiency may have 'normocytic anaemia'= average MCV normal but v high RDW

Answer 94

blood film will show red blood cell fragmentation with both microspherocytes and microdiscocytes, with budding of these round fragments from erythrocytes

Answer 95

hereditary spherocytosis autosomal dominant= causes genetic deficiency in one of the proteins in the red blood cell membrane e.g. spectrin, ankyrin therefore variable clinical features= sometimes picked up by accident main clinical manifestation is splenomegaly + gall stones confirmatory tests: -increased osmotic fragility -reduced EMA dye binding -membrane protein electrophores (SDS-PAGE) -DNA analysis

Answer 96

1. Elliptocytosis: Elliptocytosis is a genetic disorder where red blood cells become elliptical in shape due to defects in proteins like spectrin or ankyrin. Mild cases are asymptomatic, but severe cases can cause hemolytic anemia, jaundice, and may require splenectomy. 2. Ovalocytosis: Ovalocytosis, also known as Southeast Asian ovalocytosis, causes red blood cells to be rigid and oval-shaped due to a mutation in the band 3 protein. Most cases are asymptomatic and may offer protection against malaria, with severe cases rarely requiring treatment. 3. Stomatocytosis: Stomatocytosis is a condition where red blood cells have a "mouth-shaped" central area due to abnormal ion permeability. It can cause hemolytic anemia and jaundice in severe cases, sometimes needing splenectomy. 4. Hereditary Pyropoikilocytosis (HPP): Hereditary pyropoikilocytosis is a rare, severe form of elliptocytosis that makes red blood cells sensitive to heat, causing fragmentation and abnormal shapes. It leads to severe hemolytic anemia from childhood and may require transfusions and splenectomy for management.

Answer 97

- haemoglobin molecule is a tetramer consisting of 2 pairs of similar polypeptide chains called globin chains - to each of the 4 chains is attached heme which is a complex iron in ferrous form + protoporphyrin -the major (96%) type of Hb present in adults is called HbA and it has * 2 alpha globin chains and * 2 beta globin chains

Answer 98

treatment of AIHA: -folic acid supplementation -transfusion -immunosuppression- steroids, rituximab, MMF -splenectomy

Answer 99

detoxyfying compound cytochrome p450: regenerates epithelium of small airways when damaged

Answer 100

Non-Small Cell Lung Cancer (NSCLC) = 85-90% lung cancers -squamous cell (smoking) -adenocarcinoma (women + non-smokers) -large cell carcinoma Small Cell Carcinoma (smoking) 10% lung cancers -adenocarcinoma (non-smokers + radon exposure) -rare tumours (carcinoid) <5%

Answer 101

-cough -dyspnoea -wheezing -haemoptysis -lung infection -chest/shoulder pain -weight loss -lethargy -malaise (vague sense of feeling mentally/physically unwell)

Answer 102

* pancoast tumours cause severe pain going down arm and thenar wasting of hand ! make sure u dont miss *causes HORNER SYNDROME (SPAM) pathology; the pancoast tumour presses on the cervical sympathetic chain (stellate ganglion) . This loss of sympathetic innervation leads to ptosis due to action levator palpebrae superioris muscle not being helped by Muller's muscle, Miosis from unopposed sympathetic action on pupillary sphincter muscle. Anhidrosis because of lost sympathetic stimulation to sweat glands

Answer 103

Muller's muscle and levator palpibrae superioris keep eye open. Muller's muscle has sympathetic innervation. Levator palpibrae superioris is innervated by CN III occulomotor n. Horner's is a sympathetic injury hence it only effects Muller's muscle NOT levator palpibrae

Answer 104

REGIONAL METASTASES: -bloated face (SVC obstruction) -hoarseness (left recurrent laryngeal nerve palsy) -dysphagia (oesophageal compression) -chest pain (parietal pleura involvement) -dyspnoea (anaemia, pleural or pericardial effusions) DISTANT METASTASES: -bone pain/fractures -CNS symptoms (headache, double vision, confusion, altered personality) -spinal cord compression ; MED EMERGENCY; (back pain, limb weakness, urinary or faecal incontinence)

Answer 105

chest pain thats worse on inspiration/ deep breathing

Answer 106

more common in countries closer to equator lymphatic filariasis is a tropical disease where roundworm/nematode infection block lymphatic drainage (vector is mosquito)

Answer 107

Chylothorax= build up of lymph (CHYL) caused by rupture of thoracic duct= build up of chyl in pleural space

Answer 108

left venous angle of subclavian vein

Answer 109

lymphedema

Answer 110

normal pH of arterial blood= 7.35-7.45 normal pH of venous blood= 7.31-7.41

Answer 111

acidaemia= state when arterial blood pH <7.35 acidosis= process leading to the acidaemia processes that lead to acidaemia; METABOLIC: -increased acid ingestion/toxins -increased acid production e.g. diabetic ketoacidosis, sepsis w high lactate levels -decreased acid excretion e.g. renal disease -renal and/or GI bicarbonate losses e.g. renal disease, diarrhoea RESPIRATORY: (increased co2 levels) -COPD -hypoventilation from drug overdose -CNS trauma -neuromuscular disorders e.g. Duchenne's -spinal deformities e.g. kyphoscoliosis

Answer 112

alkalaemia= state when arterial blood pH >7.45 alkalosis= is process leading to the alkalaemia processes that lead to alkalaemia: METABOLIC: -increased proton loss e.g.GI loss of hydrogen ions from vomiting or NG tube -increased loss of protons from kidney -decreased protons in plasma secondary to shift intracellularly e.g. hypokalemia as potassium ions move out of cells, hydrogen ions move into the intracellular space to maintain electrical neutrality RESPIRATORY: (decreased co2 levels) -hyperventilation -anxiety -pain -hypoxaemia

Answer 113

increased renal reabsorption of bicarbonate

Answer 114

Polydipsia= excessive thirst.

Answer 115

The major reason why patients with COPD on too much o2 the main reason co2 retention increased is vq (ventilation-perfusion) mismatch and haemoglobin w o2 cant carry as much co2 Oxygen-therapy-induced hypercapnia in patients with chronic obstructive pulmonary disease (COPD) who retain CO₂ is primarily attributed to ventilation-perfusion (V/Q) mismatch; supplemental oxygen decreases hypoxic pulmonary vasoconstriction, leading to increased perfusion of poorly ventilated alveoli and thus exacerbating CO₂ retention. Secondarily, the Haldane effect contributes to hypercapnia; this effect describes how increased oxygenation of haemoglobin reduces its capacity to carry carbon dioxide, resulting in elevated plasma CO₂ levels (West, 2018). But this plays less of a role than the primary mechanism: V/Q mismatch. N.B. HYPOXIC DRIVE IS A MYTH! been disproven medically

Answer 116

SIADH (Syndrome of Inappropriate Antidiuretic Hormone Secretion) is a condition where the body produces excess antidiuretic hormone (ADH), leading to water retention and hyponatraemia (low sodium levels). Key Features: * Excessive ADH causes water retention. * Hyponatraemia (low blood sodium) due to dilution. * Concentrated urine despite low sodium. * No oedema (normal fluid volume). Causes: * CNS disorders: Brain injury, stroke, infections. * Lung diseases: Pneumonia, small-cell lung cancer. * Medications: SSRIs, anticonvulsants. * Tumors: Ectopic ADH production, especially in lung cancer. Symptoms: * Mild: Nausea, confusion, headaches. * Severe: Seizures, altered consciousness, coma. Diagnosis: * Low plasma osmolality, high urine osmolality. * Hyponatraemia with euvolaemia. * Normal adrenal, thyroid, and kidney function. Management: * Fluid restriction. * Hypertonic saline for severe cases. * Vaptans (ADH antagonists), demeclocycline. * Treat underlying cause (e.g., infections or tumors). Careful sodium correction is crucial to avoid osmotic demyelination syndrome.

Answer 117

leukocytosis= WBC overproduction leukopenia= WBC underproduction neutropenia= reduction in number of neutrophils agranylocytosis= distinct reduction in neutrophils leading to serious susceptibility to infections lymphocytopenia= lymphocyte redistribution rather than number decrease (induction of specific proteins that regulate lymphocytic cell migration)

Answer 118

antibody= immunoglobulins in plasma which react with specific antigen= produced against antigens not present on patient's own red cells immune/acquired= only form following contact w blood group antigen naturally occurring= form following exposure to environmental antigens similar to blood group antigens

Answer 119

Chronic myeloid leukemia is caused by a rearrangement (translocation) of genetic material between chromosome 9 and chromosome 22 aka Philadelphia chromosome

Answer 120

myocardial ischaemia= reduced/lack of blood supply to myocardium myocardial infarction= necrosis of myocardium (due to lack of blood supply)

Answer 121

C3,C4,C5 (keep the diaphragm alive)

Answer 122

For a vein to be useful for central line placement it needs to have a large lumen and be relatively superficial for ease of access. Therefore the Femoral, Internal jugular and Subclavian veins are used for central lines.

Answer 123

-ectomy= removal -otomy= incision

Answer 124

major criteria: Paroxysmal nocturnal dyspnea: (difficulty breathing at night) Neck vein distention: (visible swelling of neck veins) Rales: (crackling or bubbling sounds in the lungs) Radiographic cardiomegaly: (enlarged heart on X-ray) Acute pulmonary edema: (fluid buildup in the lungs) Third heart sound (S3 gallop rhythm) Weight loss >4.5 kg in 5 days in response to treatment Hepatojugular reflux: (rise in jugular venous pressure when pressure is applied to the liver) Increased central venous pressure (>16cm H20) Orthopnea (shortness of breath that occurs while lying flat and is relieved by sitting or standing)

Answer 125

Amiodarone is a class III antiarrhythmic indicated for the treatment of recurrent hemodynamically unstable ventricular tachycardia and recurrent ventricular fibrillation. MoA= blocks potassium channels, thereby prolonging the repolarization phase (phase 3) of the cardiac action potential. This action increases the refractory period and helps prevent abnormal heart rhythms SEs; Blue-Gray Skin Discoloration (75%), pulmonary fibrosis, thyroid dysfunction, rarely hepatotoxicity, neurological effects (tremor, ataxia, peripheral neuropathies, gait disturbance)

Answer 126

Chest expansion: Reduced Tactile vocal fremitus/vocal resonance: Reduced Percussion note: Hyper-resonant Breath sounds: Absent

Answer 127

Eosinophils are essential in fighting parasitic infections, therefore those affected typically present with eosinophilia Eosinophils are granulocytes, which have a characteristic bilobed nucleus ('sunglasses' appearance) and eosinophilic (pink) cytoplasm. Cytokines involved in their maturation and survival are IL-5 and IL-13.

Answer 128

Pericarditis on an ECG trace typically has concave ST elevation/saddle ST (as shown in this trace) and PR depression.

Answer 129

Bacteria: Streptococcus pneumoniae Haemophilus influenzae Mycoplasma pneumoniae Chlamydophila pneumoniae Viruses: Type A influenza Respiratory syncytial virus Adenovirus Rhinovirus

Answer 130

G6PD deficiency causes intracellular oxidative damage to RBC on consumption of fava beans

Answer 131

Chest X-ray findings in individuals with a diagnosis of heart failure include ('ABCDE') Alveolar oedema ('Bat wing sign') B lines (Kerley B lines) Cardiomegaly Dilation of upper lobe vessels Effusions (pleural)

Answer 132

- Common carotid artery - Internal jugular vein - Vagus nerve (CN X) - Sympathetic plexus

Answer 133

Low Hb, normal MCV, high LDH and Unconjugated bilirubin, and low haptoglobin indicate a haemolytic anaemia low Hb but normal MCV, characterise normocytic anaemia, and the high LDH, unconjugated bilirubin, and low haptoglobin indicate the underlying process is haemolytic

Answer 134

Nasal passages, oral cavity, pharynx (part), larynx. Clinical border between upper and lower resp tract Clincal = aditus laryngis (entrance of the cavity of the larynx) ENT clinical border = rima glottidis (opening between 2 vocal cords)

Answer 135

Pseudostratified ciliated columnar epithelium with goblet cells (mucus production). Clinical: Lamina propria contains mucous glands; Kiesselbach’s plexus (Little’s area) is a common site for nosebleeds.

Answer 136

Sphenopalatine artery (branch of maxillary). Veins drain → pterygoid plexus → maxillary vein → internal jugular. Clinical: Nosebleeds in elderly/hemostasis disorders can be dangerous

Answer 137

Cricothyroid membrane (between thyroid and cricoid cartilages). Clinical: Emergency airway if obstruction at/above vocal cords (e.g., foreign body at C5-C6).

Answer 138

Mucosal thickening + bony wall sclerosis (osteitis). Clinical: Maxillary sinus most commonly affected.

Answer 139

Insert needle superior to the rib (nerve runs inferior to rib). Clinical: "Safe triangle" for chest drain: 5th ICS mid-axillary line (bordered by latissimus dorsi, pectoralis major, nipple level).

Answer 140

Phrenic nerve (C3, C4, C5). Clinical: Diaphragm hiatuses: IVC (T8), oesophagus (T10), aorta (T12)

Answer 141

Visceral: covers lungs; Parietal: lines thoracic wall/diaphragm (innervated by intercostal/phrenic nerves). Clinical: Pneumothorax → collapsed lung; blunted costophrenic angle = pleural effusion.

Answer 142

Great vessels, trachea, esophagus, vagus/phrenic nerves, thoracic duct. Clinical: Recurrent laryngeal nerve loops around aortic arch (left) → damage → hoarseness.

Answer 143

Pupil dilation, bronchodilation, tachycardia, vasoconstriction

Answer 144

Diagnosis: Confirm with spirometry, FeNO, and symptom history. Initial treatment: Low-dose ICS. Stepwise add-on: - Add LABA if not controlled. - Then increase ICS dose or add LTRA. - Consider theophylline or oral steroids in severe cases. Monitoring: Regular reviews using ACT; adjust treatment. Self-management: Asthma action plan + inhaler technique + trigger avoidance.

Answer 145

Assessment: Check symptoms, RR, O2 sats, and PEF. Initial treatment: - High-dose salbutamol (via spacer/nebulizer). - Add ipratropium if severe. - Oral/IV steroids (e.g., prednisolone). O2 to maintain sats 94–98%. Escalation: - Monitor PEF/vitals. - IV magnesium sulfate if life-threatening. - Hospital admit if no improvement. Aftercare: Follow-up within 48 hrs + review chronic plan.

Answer 146

Intrinsic Pathway: Activated by endothelial damage; involves factors XII, XI, IX, VIII. Extrinsic Pathway: Triggered by tissue factor (factor III) release; involves factor VII. Common Pathway: Both pathways converge at factor X activation, leading to thrombin formation and fibrin clot development

Answer 147

If a PE/DVT is suspected, the clinical probability of this diagnosis is calculated using the Well's score (not calculated for pregnant women and those who are haemodynamically unstable). If the probability is high (score is >4), then a CT pulmonary angiogram (CTPA) is carried out. If the probability is low (score is

Answer 148

A massive PE is characterised by haemodynamic instability, whereas with a non-massive PE, individuals are stable. On examination, apart from tachycardia and tachypnoea, there are usually no other abnormalities noted, and this is typical in PE.

Answer 149

Use Wells score for DVT or PE to guide further testing

Answer 150

Likely DVT (Wells >4): Urgent ultrasound → if negative, do D-dimer Unlikely DVT (Wells 4): Immediate CT Pulmonary Angiography (CTPA) Unlikely PE (Wells

Answer 151

Non-massive PE/DVT management: - Direct oral anticoagulants/DOACs (e.g., apixaban or rivaroxaban) - If DOACs unsuitable: Low molecular weight heparin (LMWH) i.e. Enoxaparin → warfarin Massive PE management: (patient is hemodynamically unstable) Thrombolysis (alteplase)

Answer 152

Provoked: 3 months Unprovoked: ≥3 months, reassess risk Cancer-associated: LMWH for 6 months (then reassess)