Cardio Flashcards
What is haematocrit
the percentage of blood volume occupied by red blood cells
what causes a high haematocrit - i.e. Polycythaemia?
Excessive production of RBCs and dehydration (which reduces plasma volume)
what causes low haematocrit?
anaemeia
sites of haemolysis
spleen, bone marrow, lymphnodes
which leukocytes are the most abundant
neutrophils
neutrophils - function and appearance
phagocytosis - they are the first line of defence during acute inflammationthey have multi lobed nuclei with relatively translucent cytoplasm
function of basophils + appearance
responsible for anaphylaxis - produces histamine| multi lobed and has so many purple/bluey granules you can barely see the nucleus
eosinophils - function and appearance
Combats parasitic infection and neutralises histamine.| Double lobed nucleus with bright pink eosinophilic granules.
what do monocytes differentiate into? and where? give some specific exampleswhat is their function? what do they look like?
they are monocytes in blood and differentiate into macrophages in tissue.Examples: microglial cells (CNS), Kupffer cells (Liver), tissue macrophages, alveolar macrophagesFunction is phagocytosis of foreign materialLarge, fine white granule-looking-things, kidney shaped nucleus, kinda wobbly round the edges
Name the 3 types of lymphocytes and give some extra info e.g site of production and function.
T cells: progenitors originate in bone marrow but they migrate to and mature in thymus - have many functions but naive t cells identify specific antigens; helper t cells help activate other immune cells, produce cytokines and help B cells with antibody production; cytotoxic cells kill cells by releasing cytotoxic granules; there are also memory t cellsB cells: originate and mature in bone marrow - plasma cells produce antibodies and memory cells remain in case of reinfectionBoth have large round nucleus and are agranularNatural killer cells - kill virus infected cellsHas large round nucleus but is granulated
platelets: structure, function, production
structure: anucleate and discoid - becomes spiculated (spikey) with pseudopodia (temporary protrusions) when activatedfunction: produce platelet plug along with clotting factors for haemostasisproduced as fragments of cytoplasmic material derived from megakaryocytes and modulated by thrombopoeitin
haemostasis? primary? secondary?
Haemostasis is the process to prevent and stop bleeding.Primary involves platelet plugs and the 3 As after vessel injury: Adhesion, Activation, AggregationSecondary: coagulation cascade and fibrin clot formation
What happens when vessel injury occurs?
Endothelial wall becomes exposedSmooth muscle contracts to limit blood lossMechanisms of contraction:- Endothelin release- Nervous stimulation
what happens in the adhesion phase of primary haemostasis?
Subendothelial collagen becomes exposed| Platelets bind to collagen via vWF (von Willebrandβs factor) using their receptor GP1B
what happens in the activation phase of primary haemostasis?
Once bound to the subendothelium, platelets change shapePlatelets release alpha and electron dense granules, to escalate haemostasis processAlpha:vWF, Thromboxane A2, fibrinogen and fibrin-stabilizing factorElectron-dense:ADP, Ca2+, Serotonin
Aggregation
Lots of platelets binding to each other using GP2b/3a receptors and fibrinogen - forms platelet plug
The important parts of the coagulation cascade
Prothrombin (II) -> Thrombin (IIa) (catalysed by Xa and/or Va)Thrombin converts Fibrinogen (I) -> Fibrin (Ia)Fibrin is stablised by Fibrin-stabilising factor (XIIIa)this causes a cross-linked fibrin clot to be formedfactor IV (Ca2+) is also important
Which factors in the coagulation cascade are Vitamin-K dependant?
X (precursor to what activates thrombin), IX, VII, II (Prothrombin)Remember 1972
fibrinolytic pathway
plasminogen -> plasmin which then mediates fibrin -> fibrin degradation products (important in PE and DVT - D-Dimer??)can be inhibited by thrombin activatable fibrinolysis inhibitor
types of blood transfusion.
homologous (emergency transfusion from other person - have to test safety, recipient serum mixed with donor blood to check for reaction)autologous (self-transfusion)
blood types? how are they classified? presence of antigens and antibodies?
classified by presence of specific antigens and antibodiesA - A antigens and Anti-B antibodiesB - B antigens and Anti-A antibodiesAB - A and B antigens but NO antibodies (universal recipient)O - NO antigens but has anti-A and anti-B antibodies (universal donor)focus on antibodies for recipients, and antigens for donor suitability
Rhesus factor (D protein presence)
Rh+: - contains D-antigen (most immunogenic), no antibodies- can receive from both Rh+ and Rhβ only donates to Rh+Rh-:- contains no antigens, and anti-D antibodies- can donate to both Rh- and Rh+- only receives from Rh-the antibodies are not naturally occuring unlike anti-a and -b. anti-d will only be made if RH- blood comes into contact with Rh+ blood
formation of primitive heart tube
during week 3/4 the visceral mesoderm forms 2 heart tubes which then fuse. There is some craniocaudal folding which makes it look kinda like a funky shrimp. It has 5 divisions.
divisions of heart tube
truncus arteriosus: ascending aorta and pulmonary trunkbulbus cordis: smooth outflow portion of ventriclesprimitive ventricle: majority of the ventriclesprimitive atrium: both auricular appendages, all of left atrium, anterior portion of right atriumsinus venosus: smooth part of right atria where VC connects, the Vena Cava, coronory sinus
septation
(formation of atrial septum - occurs after looping of heart tube to make something kinda c shaped and more like a heart)1. septum primum starts developing from top - the open part is foramen primum2. septum primum has a bit at top and a bit in middle - top hole is foramen secundum, below is foramen primum3. septum primum is only at top and bottom with septum secundum forming at the top on right side of primitive heart - foramen primum completely closed4. septum secundem is at top and bottom now but the top part is partially going over the foramen secundum (in between the two bits of septum primum) - the part between the 2 parts of septum secundum that blood can actually flow through is the foramen ovale5. foramen ovale closes
aortic arches - time period, names , what they form
weeks 4-6symmetrical, sprouts from aortic sac - 6 of them (but 6th one is actually pulmonary arteries from the pulmonary trunk)I - maxillaryII - stapedialIII - common carotids and proximal part of internal carotids (distal part made from extensions of dorsal aortae)IV - aortic arch and right subclavian (both sides join with 7th intersegmental)V - regresses completelyVI - pulmonary arteries and ductus arteriosus on left 7th segmental arteries (not an aortic arch) form the left subclavian and part of right subclavian
extra embryology facts
Heart appears in 3rd week (starts beating ~day 23)Constriction of ductus arteriosus > ligamentum arteriosum 10-15 hours after birthObstetrical climbing = constriction of umbilical vein > ligamentum teresIncrease L atrial pressure & decreased R atrial pressure due to first breath causes foramen ovale to close > fossa ovalisDuctus venosus constricts > ligamentum venosum shortly after birth
membrane potential definition
the difference in electrical potential between the interior and exterior of a celle.g. if inside is +1 and outside is 0 the membrane potential is +1if inside is 0 and outside is +1 the membrane potential is -1
membrane potential of cardiac myocyte at rest
-90mV| more positive outside cells
is a cardiac action potential longer or shorter than in skeletal muscle
cardiac action potential is around x100 linger than in skeletal muscles. Voltage gated Ca2+ channels open more slowly and stay open longer than Na+ channels (sometimes called L-type Ca2+ channels i.e. long lasting or dihydropyridine - target of amlodipine treatment - antihypertensive)skeletal muscle action potential is a spike, cardiac myocyte action potential is more like a wiggly water slide that peaks lower and slightly after the skeletal action potential
action potential/cardiac cycle phases
phase 4: resting phase - -90mV. SAN generates an action potential which causes depolarisation. If it reaches the threshold, phase 0 starts.phase 0: depolarisation - threshold (-60mV) reached and Na+ channels open.phase 1: partial repolarisation - at +30mV Na+ channels close and there is transient K+ channels open allowing K+ out of the cellsphase 2: plateau - L-type Ca2+ channels open to allow an influx of Ca2+ into the cell to balance the efflux of K+phase 3: repolarisation - Ca2+ channels close allowing repolarisationthere is a bit of overshoot and over polarisation which is when the refractory periods happenphase 4: resting
In what phase of the cardiac cycle does contraction occur?
phase 2 - contraction occurs when there is a calcium influx
refractory periods
absolute refractory period - when the cell is completely unexcitable (longer for myocytes than skeletal muscle)relative refractory period - when the cell can be depolarised by a greater than usual stimulus
where is the sinoatrial node located? what does it do? what is it modulated by?
in the right atrium - it is the primary pacemaker (rate of discharge: 60-100/min) - vagus stimulation decreases rate, noradrenaline from sympathetic nerves increases rate
pacemaker potential
There is no resting baseline line in normal depol/repol. No plateauing. Phase 4 equivalent - prepotential: slow influx of Na+ through HCN channels (hyperpolarisation activated cyclic nuclotide gated channels - permeable to K+) - slow depol from -60mV to -40mVPhase 0 equivalent - depolarisation: influx of Ca2+ through voltage-gated t type channels (specifically found in heart condutive cells) - -40mV -> +10mVPhase 3 equivalent - repolarisation: Ca2+ channels close and voltage-gated K+ channels open - +10mV -> -60mV (at which point f type Na+ channels open again - they open at most negative membrane potential)
which cells act as pacemakers in heart - what do they do
pacemakers are responsible for automacity of heart. Nodal cells generate the pacemaking potential (1%?)
sympathetic stimulation of pacemaker potential
- noradrenaline binds to beta-1 receptors - increases Ca2+ channels opening - faster depol- steeper phase 0 - increased heart rate and force of contraction
parasympathetic (vagal) simulation of pacemaker potential
- Ach activates K+ channels - hyperpolarises membrane - takes longer to reach treshold potential- reduces influx of clacium so slower depolarisation (shallower slope of phase 0)- decreases heart rate
excitation-contraction coupling
Wave of depolarization (AP) spreads into myocytes via T tubules.L-type Ca2+ channels open π‘ͺ Ca2+ enters the muscle cellCa2+ binds to Ryanodine Receptor π‘ͺ release of more Ca2+ from Sarcoplasmic Reticulum (Ca2+ induced Ca2+ release.)Ca2+ binds with Troponin which uncovers active site on tropomyosinCross-bridge cycling = Muscle contraction
What causes contraction in excitation-contraction coupling?
The presence of Ca2+ in the cytosol. Force of contraction is directly proportional to cytosolic Ca2+ levels.drugs and chemicals that increase cardiac contractility (like adrenaline, Digoxine, cardiac glycosides) are increasing the levels of cytosolic Ca2+
Electrode and lead (for ECG) definitions
Electrode is the object placed on the body to pick up electrical signalsA lead is a specific plane in which you are observing the heart
shapes of ECG graphs
+ve going to a positive electrode = curve goes up+ve to -ve electrode = curve goes down (as in it is inverted/peaking underneath the baseline instead of above it)-ve to +ve electrode = curve goes downif the charge is going at an angle and so only part of the vectored charge is picked up (e.g. like how a thrown ball has a horizontal and vertical part that combines to form the final vectored trajectory) - then the curve will just be shorter but the same width and shape
list all the ECG leads
6 limb leads:I - goes from right arm (-ve) to left arm (+ve) - bipolar - (the leaving part is always negative and receiving part is positive) II - from right arm (-ve) to left leg (+ve) - bipolarIII - left arm (-ve) to leg (+ve) - bipolaraVR - right shoulder - unipolaraVL - left shoulder - unipolaravF - left ankle - unipolar6 chest leads:Lead V1 β 4th IC space to right of sternal borderLead V2 β 4th IC space to the left of sternal borderLead V3 β midway between V2 and V4Lead V4 β 5th IC space, mid-clavicular lineLead V5 β anterior axillary line at same level as V4Lead V6 β midaxillary line at same level as V4 and V5
Key parts of ECG:
P wave - atrial repolarization. QRS - ventricular depolarisation. T wave - ventricular repolarization. PR segment - delay in AVN ST segment - plateau phase of ventricular repolarization.PR interval - atrioventricular conduction time - this is when atrial systole happensQT interval - Total ventricular contraction during systole.
What is a segment in ECG
A period of isoelectric neutrality
What is an interval in ECG
A region including magnitude
what is the ejection fraction
the proportion of the EDV that is pumped out the LV per beat, SV/EDV, provides an indication of the contractility of the heart
