Cardiorespiratory 2 Flashcards
name the small ligament which attaches the aorta to the pulmonary artery
ligamentum arteriosum (aka Botallo’s ligament)
what does ectoderm (germ layer) give rise toy
ECTODERM= skin, CNS, PNS, eyes + internal ear
what does mesoderm (germ layer) give rise to
MESODERM= bones, connective tissue, skeletal muscle, urogenital system, cardiovascular system
what does endoderm (germ layer) give rise to
ENDODERM= lungs, gut + associated derived tissues e.g. pancreas, liver etc.
what type of mesoderm does the foetal heart develop from?
the foetal heart develops from CARDIOGENIC mesoderm (lateral plate)
at 35 days gestation what will the following give rise to:
1) truncus arteriosus
2) primitive atria
3) bulbus cordis
4) primitive ventricle
1) truncus arteriosus= proximal aorta + pulmonary artery
2) primitive atria= left + right atria
3) bulbus cordis= ventricular outflow tracts + right ventricle
4) primitive ventricle= left ventricle
what is dextrocardia (+when is it seen in clinic)
dextrocardia= heart is positioned to the right side of the chest instead of the normal left position
caused by mistake in ‘looping’ process during early foetal development
dextrocardia can be seen in situs invertus patients or can be ISOLATED dextrocardia
what is foramen ovale
foramen ovale is an opening/ shunt which allows blood to flow from the right atrium to the left atrium (during fetal development)
what is an atrial septal defect (ASD)
ASD= have a hole between the left and right atria
what is the function of foetal ductus venosus
ductus venosus= shunts blood from umbilical vein to IVC (bypassing liver)
what is the function of foetal ductus arteriosus
ductus arteriosus= shunts blood from pulmonary trunk to ascending aorta (bypassing lungs)
what is the treatment for a patent ductus arteriosus
administration of a prostaglandin inhibitor e.g. ibuprofen
what type of contrast is the gold standard for coronary angiogram
iodine contrast
which arteries supply the bundle branches of the heart?
the interventricular (descending) arteries supply the bundle branches
which coronary artery supplies the SA node?
right coronary artery (RCA) supplies SA node
RCA also USUALLY supplies the AV node (but circumflex can also supply AV)
define preload and explain in what pathologies does preload increase?
preload= volume of blood in the ventricles at the end of diastole
preload increases in patients with:
-hypervolemia (aka fluid overload)
-valve regurgitation
-heart failure
define afterload and explain when afterload increases
afterload= resistance ventricle must overcome to circulate blood
Afterload increases in patients with:
-hypertension
-vasoconstriction
-valve stenosis
-outflow stenosis
what is the difference between atherosclerosis and arteriosclerosis
atherosclerosis= a type of specific arteriosclerosis involving build up of fatty deposits (plaques) inside arteries
arteriosclerosis= general term for thickening and hardening of arterial wall (usually caused by atherosclerosis but not always)
what is the mechanism of atheroma formation?
n.b. atheroma= a fatty substance that builds up in your arteries over time
mechanism of atheroma formation:
1)endothelial damage
2) uptake of modified LDL particles, adhesion + infiltration of macrophages
3) smooth muscle proliferation + formation of a fibrous cap
= run risk of rupture + thrombosis/stenosis
name the main vasodilating and vasocontricting substances of the endothelium
endothelium releases various vasoactive factors to maintain vasomotor tone.
These can be vasodilatory factors such as nitric oxide (NO), prostaglandin 12 (PG12) and endothelium derived hyperpolarizing factor (EDHF) or vasoconstrictive factors such as thromboxane (TXA2) and endothelin-1 (ET-1).
why do patients with diabetes mellitus have accelerated rates of atherosclerosis?
GLYCATION: Glycation of LDL occurs chiefly due to the nonenzymatic reaction of glucose and its metabolites with the free amino groups of lysine in which LDL is rich.
this glycation is facilitated by the high glucose levels in diabetics. Glycated LDL is more likely to become oxidised and therefore become Ox-LDL and build up plaque
what is the difference between stable and unstable fibrotic caps?
stable fibrotic caps= slow growing, thick fibrin, unlikely to rupture, reduced blood flow, stable angina following exertion
unstable fibrotic caps= fast growing as rapid lipid deposition, thin + fragile fibrin cap, likely to rupture (with or withou haemorrhage, release of platelet tissue factor/ clotting cascade, collagen is exposed causing platelet aggregation =thrombus formation/ reduces lumen diameter
n.b. in unstable plaque thrombus formation it may occlude lumen completely = STEMI
or partially/ subocclusive= NSTEMI
Describe the mechanism of aspirin
- low dose inhibits COX-1, high dose inhibits COX-2
*COX-1 converts arachidonic acid into PGH2–> PGH2 is a precursor for other prostaglandins
*PGH2 converted to thromboxane A2 which is a potent stimulator of platelet aggregation!
so aspirin inhibits COX-1 which inhibits PGH2 which inhibits platelet aggregation == why its essential in PREVENTING CLOT IN MI
What type of drug is Clopidogrel/ Ticagrelor; describe their mechanism of action
Clopidogrel/ Ticagrelor are P2Y12 antagonists.
ADP is found in platelets + stimulates platelet aggregation (+ve feedback mechanism for platelet aggregation)
P2Y12 receptors are found on platelets; by inhibiting P2Y12 then we inhibit platelet aggregation and this prevents thrombus formation
Name and explain the mechanism of action of beta blockers
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)
Name and explain the mechanism of action of ACE inhibitors
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
Name and explain the mechanism of action of calcium channel blockers
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
Name and explain the mechanism of action of Statins
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
Define Systemic Vascular resistance (SVR) aka TPR
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.
What is the role of nitric oxide in the CVD?
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!
what is intermittent claudication
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
what is the difference between stable and unstable angina
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.
what are platelets produced by and under the influence of which hormone
platelets are produced by megakaryocytes in bone marrow under influence of thrombopoietin (hormone)
what is haemophelia?
Explain difference between haemophelia A and B
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)
what is von willebrands disease? Explain the 3 types.
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
define the following
* thrombosis
* embolism
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
Patients with chronic inflammatory disease such as rheumatoid arthritis, IBD are more at risk of blood vessel wall pathology.
Explain with reference to the role of heparan sulfate and thrombomodulin why patients with chronic inflammatory conditions are more at risk of clot formation.
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
what is the most common heritable risk factor for DVT/PE?
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)
What is a D-dimer test, how is it carried out and what does it indicate?
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
what is the guideline for DVT (deep venous thrombosis) diagnosis
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)
what is an INR blood test?
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.
define circulatory shock
circulatory shock= acute circulatory failure with inadequate or inappropriately distributed tissue perfusion resulting in cellular hypoxia + end-organ damage
define hypoperfusion
Hypoperfusion is a life-threatening condition characterised by poor circulation of blood from heart and lungs to the body’s organs.
How does the body regulate peripheral vasculature?
- vasodilation
*vasoconstriction
describe these mechanisms
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
Describe the 4 stages of circulatory shock
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
Explain the 4 classifications of circulatory shock
- 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
Obstructive shock can be caused by a tension pneumothorax. A life-threatening condition caused by continuous entrance + entrapment of air in pleural space= this compresses lungs, heart + blood vessels. Blood flow through the collapsed lung is severely obstructed this impair left ventricular filling by obstructing venous return to the heart (preload)
What are the signs and symptoms the patient wld experience in this scenario?
- tachycardia + tachypnoea
*hypoxia
*chest pain
*reduced breath sounds on affected side
- deviated trachea, AWAY FROM AFFECTED SIDE
Obstructive shock can be caused by a cardiac tamponade. A cardiac tamponade is the accumulation of pericardial fluid, blood, pus or air within pericardial space. Leads to increase in intra-pericardial pressure, restricting cardiac filling + decreasing cardiac output.
What are the signs and symptoms the patient wld experience in this scenario?
- tachycardia
-hypotension
-distant heart sounds
- elevated jugular venous pressure
What are the 3 stages of hypertension? Also mention the values for low BP, normal BP, Prehypertension:
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
Describe the mechanism of angiotensin receptor blockers (ARBs)
ARBs bind to and inhibit the angiotensin II type 1 (AT1) receptor and are indicated to treat hypertension, congestive heart failure, and diabetic nephropathy.
what are natriuretic peptides (NPs) and what is the difference between ANP and BNP. What are their functions?
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)
what is rheumatic heart disease
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)
How does infective endocarditis present and what is its cause
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
Define aortic stenosis + its causes.
What are the signs, symptoms + treatments?
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)
Define aortic regurgitation + its causes.
What are the signs, symptoms + treatments?
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
Define mitral stenosis + its causes.
What are the signs, symptoms + treatments?
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
Define mitral regurgitation + its causes.
What are the signs, symptoms + treatments?
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)
what nerve innervates
sternoclaidomastoid?
cranial nerve XI (spinal accessory)
what nerves innervate pectoralis major and pectoralis minor?
pectoral nerves C5-T1
what nerve innervates serratus anterior?
long thoracic nerve (C5-C7)
what nerves innervate rectus abdominis?
intercostal + subcostal nerves (T7-T12)
what nerves innervate the external intercostal muscles?
intercostal nerves (T2-T11)
what is thoracocentesis, how and why is it performed?
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
what nerve innervates the diaphragm?
phrenic nerve (C3,C4,C5)
C3,4,5 KEEPS DIAPHRAGM ALIVE
explain the symptoms + management of DCM (Dilated cardiomyopathy)
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)
explain the symptoms + managements of HCM (hypertrophic cardiomyopathy)
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
explain the symptoms + managements of RCM (restrictive cardiomyopathy)
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
explain what is meant by ventilation vs perfusion when we talk about lung gas exchange
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.
explain the difference between type 1 and type 2 respiratory failure
type 1 resp failure:
hypoxemia only
PaO2= below 8kPa
PaCO2= normal
type 2 resp failure: hypoxemia + hypercapnia
PaO2= below 8kPa
PaCo2= above 6kPa
what is asthma pathology? what is PEFR vs FEV1?
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)
whats the difference between how an asthmatic shld take a aerosol inhaler vs a dry powder inhaler (DPI)?
aerosol inhaler= inhale slow + steady
dry powder inhaler (DPI)= inhale quick + deep
explain the role of muscarinic vs beta-2 receptors in lungs and what drugs do we use in asthma patients
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)
what is MART (in asthma management)
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
is salbutamol a LABA or a SABA
salbutamol is a SABA (short acting beta-2 agonist)
If a patient has confirmed spirometry below 0.7 and confirming history they have confirmed COPD. What is the 1st line treatment then 2nd line
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
what is bronchiectasis? symptoms, risk factors and management
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!
explain the mechanism of action of ICS (inhaled corticosteroids) which are used in managing asthma + COPD
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
Explain anatomically what makes up the upper vs lower respiratory tract
upper respiratory tract: nasal cavity, pharynx + larynx
lower respiratory tract: trachea, primary bronchi, lungs
what is the pathophysiology of human rhinovirus (HRV)
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
explain mechanism behind why asthmatics are more susceptible to HRV infection
n.b. estimated that human rhinovirus (HRV) infections account for 50-80% asthma exacerbations
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
Explain the mechanism of otc nasal decongestants
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)
what is peak flow?
peak flow= max speed of expiration
what is tidal volume?
tidal volume= volume of air move in + out of ur lungs at rest
what is forced vital capacity?
forced vital capacity= max volume of air forcibly exhaled after taking deep/full breath
what is inspiratory reserve volume
inspiratory reserve volume= volume of air u can draw into ur lungs
what is expiratory reserve volume
expiratory reserve volume= volume of air u can expel from ur lungs
what is residual volume
residual volume= volume of air that remains in lungs even after max exhalation
which cells in the arteries produce elastic fibres
the smooth muscle cells (SMC) produce elastic fibres
what is mesothelium?
mesothelium= the epithelium that lines the pleaurae, peritoneum and pericardium
what is difference between bronchitis and bronchiolitis
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
what are the symptoms of acute bronchitis
- sore throat
-cough
-fatigue
-runny/stuffy nose
-fever
-body aches
-vomiting
-diarrhea
symptomatic up to 2wk
minority: severe illness + require hospital admission (ventilator support)
what do docs mean when they say ‘consolidation’ in lungs on CXR
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
what is pneumonia?
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
The CURB65 score assesses mortality risk. Tell me the criteria of CURB65
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)
what is idiopathic pulmonary fibrosis; symptoms + management
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!
what is sarcoidosis? symptoms + management
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
how do we treat hypoxaemia
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
Virchow’s triad describes the three broad categories of factors that are thought to contribute to thrombosis. name them
The 3 factors of Virchow’s triad:
venous stasis,
vascular injury,
hypercoagulability
what is microcytic anaemia and its 5 causes
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
av.person need 10-15mg of iron a day; where does iron absorption occur in body?
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)
describe iron absorption + transport in gut
- 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!
describe cellular iron uptake in cells (other than enterocytes)
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
explain the regulation of iron absorption via hepcidin
- 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)
Ferritin blood test often ordered for patients w suspected anaemia. What is the clinical relevance of ferritin?
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
define the following:
-haematopoiesis
-erythropoiesis
haematopoiesis= formation of blood cellular components
erthropoiesis= subtype of haematopoiesis referring to generation of RBCs
what hormone controls erythropoiesis and where is this hormone synthesised
erythropoiesis is controlled by peptide hormone ERYTHROPOIETIN (EPO)- produced by kidney interstitial cells around proximal tubules: PERITUBULAR INTERSTITIAL FIBROBLASTS
If a patient has inflammation and suspected anaemia, what blood test will you do as opposed to ferritin blood test?
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
how do proton pump inhibitors (PPIs) cause anaemia
PPIs and H2 blocker-induced iron deficiency reduces iron absorption by altering the acidic environment of the gastrointestinal trac
why do oral iron supplements not correct anaemia of inflammation (anaemia chronic disease)?
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
Megaloblastic anaemias are a form of macrocytic anaemia. Explain the mechanism behind megaloblastic anaemias + examples
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
macronormoblastic erythropoiesis is a form of macrocytic anaemia. Explain the mechanism behind macronormoblastic erythropoiesis + examples
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
what is stress erythropoeisis (macrocytic anaemia). Explain the mechanism behind stress erythopoeisis + examples.
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
how much folic acid shld a woman who wants to conceive take before and during pregnancy?
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)
vitamin b12 (aka cobalamin) is a water soluble vitamin. What is it an essential cofactor for; why do we need b12.
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
describe the mechanism of vitamin B12 absorption
- 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)
what is pernicious anaemia
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
what is a red cell distribution width (RDW) blood test used for?
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
a blood film for a patient with severe burns will show what cell present
blood film will show red blood cell fragmentation with both microspherocytes and microdiscocytes, with budding of these round fragments from erythrocytes
what is the most common hereditary haemolytic anaemia in europeans?
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
define the following red cell membrane disorders:
-elliptocytosis
-ovalocytosis
-stomatocytosis
-hereditary pyropokilocytosis
- 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. - 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. - 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. - 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.
what is the structure of haemoglobin
- 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
what are the treatments for autoimmune haemolytic anaemia (AIHA)
treatment of AIHA:
-folic acid supplementation
-transfusion
-immunosuppression- steroids, rituximab, MMF
-splenectomy
what detoxyfying compound regenerates epithelium of small airways when damaged?
detoxyfying compound cytochrome p450: regenerates epithelium of small airways when damaged
what are the 2 major groups of lung cancers and put most common risk factor next to each
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%
what are the symptoms for lung cancer (n.b. stage I usually asymptomatic)
-cough
-dyspnoea
-wheezing
-haemoptysis
-lung infection
-chest/shoulder pain
-weight loss
-lethargy
-malaise (vague sense of feeling mentally/physically unwell)
Pancoast tumours commonly occur in the superior sulcus of lung upper lobe. Typically they’re non-small cell lung carcinomas and theyre often missed because theyre in a loco where they can be missed.
- 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
In Horner’s syndrome, why is the eyelid only slightly drooped and not fully closed?
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
Explain lung cancer symptoms; regional metastases vs distant metastases
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)
what is meant by pleuritic chest pain
chest pain thats worse on inspiration/ deep breathing
what is lymphatic filariasis (aka elephantiasis) caused by?
more common in countries closer to equator
lymphatic filariasis is a tropical disease where roundword/nematode infection block lymphatic drainage (vector is mosquito)
what is a chylothorax
Chylothorax= build up of lymph (CHYL) caused by rupture of thoracic duct= build up of chyl in pleural space
what vein does the thoracic duct drain into?
left venous angle of subclavian vein
what is the name for the condition which refers to swelling of the interstitium due to blocked lymphatic drainage
lymphedema
what is the normal pH range for
* arterial blood
* venous blood
normal pH of arterial blood= 7.35-7.45
normal pH of venous blood= 7.31-7.41
define acidaemia and acidosis. Describe processes that can lead to acidaemia
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
define alkalaemia and alkalosis. Describe processes than can lead to alkalaemia.
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
A 55 y.o. woman with COPD has worsening dyspnoea + an ABG is obtained. What is the primary compensatory mechanism for her acid-base disturbance?
increased renal reabsorption of bicarbonate
define polydipsia
Polydipsia= excessive thirst.
what is the major reason patients with copd on too much o2 retain co2?
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
what is SIADH (Syndrome of inappropriate antidiuretic hormone secretion)
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.
Define the following:
- leukocytosis
-leukopenia
-neutropenia
-agranylocytosis
-lymphocytopenia
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)
what is an antibody and explain the difference between immune/acquired antibodies and naturally occurring antibodies
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
translocation of which chromosome causes chronic myeloid leukemia?
Chronic myeloid leukemia is caused by a rearrangement (translocation) of genetic material between chromosome 9 and chromosome 22
aka Philadelphia chromosome
define the following
-myocardial ischaemia
-myocardial infarction
myocardial ischaemia= reduced/lack of blood supply to myocardium
myocardial infarction= necrosis of myocardium (due to lack of blood supply)
What level does the trans-thoracic plane lie?
T4/T5
What are the roots of the phrenic nerve?
C3,C4,C5 (keep the diaphragm alive)
Central lines (also known as a central venous catheter) are catheters that can be place in a large vein to give medication or fluids or to collect blood for medical tests.
Given your anatomical knowledge which veins do you think are used for central lines?
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.
