CR2 OVERVIEW Flashcards
Cardioinhibitory centre
Parasympathetic innervation to the heart - synapsing with the vagus nerve
Release of ACh
Cardioacceleratory centre
Sympathetic innervation of the heart - synapsing with sympathetic trunk and general visceral afferents in lateral horn of grey matter
Autonomic region of the grey matter within the spinal cord
Lateral horn - T1 to T4
Vagus nerve nuclei
Nucleus ambiguus
Dorsal motor nucleus
Solitary nucleus
Mechanism of action of ischaemia of the heart - angina
Nociceptors on the ends of the general visceral afferents are activated via the build up of lactate
Nerve roots of general visceral afferents
T1-T4
Where is angina referred to?
T1-T4 - inferior medial aspect of the arm and under the jaw
Also referred to the epigastrium - T5-T9
Surfaces of the heart
Anterior (top)
Right pulmonary
Left pulmonary
Diaphragmatic (bottom)
Blood supply to the interventricular septum
Posterior descending artery and the LAD
Define afterload
The end load against which the heart contracts to eject blood
Consequence of left ventricular hypertrophy
Reduced size of the ventricle chamber - reduced cardiac output and reduced compliance of the wall of the left ventricle
In which valvular disease will the atrium large?
Mitral valve stenosis
What is the consequence of left atrial enlargement?
Atrial fibrillation - stroke
Loss of atrial kick
Decreased filling of the left ventricle - reduced cardiac output
Can result in emboli entering the circulation
Pulmonary oedema vs plural effusion
PO - collection of excess fluid at the base of the lungs
PE - collection of excess fluid in the plural cavity
Isoforms of NOS
1 - bNOS - calcium dependent
2 - iNOS - not calcium dependent - inflammatory cytokines
3 - eNOS - vascular endothelium - calcium dependent
How does exercise activate the sympathetic nervous system?
Exercise causes activation of the sympathetic nervous system via activation of the alpha-1 receptors
Receptors causing vasoconstriction
Alpha-1 receptors
Receptors causing vasodilation
Beta-2 receptors
Chemicals causing vasodilation of exercising muscles
NO
Adenosine
Reduced cerebral blood flow - when does this result in reversible and in permanent brain damage?
Reduced by half - reversible brain damage
Reduced by 3/4 - irreversible brain damage
Formula to calculate BP
BP = CO x SVR
Hypotension
BP less than 90/60
Hypertension
BP greater than 140/90
Prehypertension
BP in the range of 135-139/85-89
Define cardiac output
The volume of blood pumped out of the heart per minute
Concentric hypertrophy
The wall of the left ventricle increases in size - hypertrophy of the muscle wall and the size of the chamber decreases - must increase HR to maintain CO
Eccentric hypertrophy
The size of the whole of the left ventricle increases - leads to heart failure
Hyponatremia? Exact value
Low sodium levels in the blood - below 135mm/L
RAAS pathway
Angiotensinogen to angiotensin 1 via renin
Angiotensin 1 to angiotensin 2 via ACE
Angiotensin 2 - release of aldosterone, increased production of ADH and activation of sympathetic NS
Location of baroreceptors
Mechanoreceptors in the carotid sinus and in the aortic arch
Mechanism of thiazide diuretic
Inhibits reabsorption of sodium chloride from the distal convoluted tubule
‘Myeloid tissue’
Bone marrow
Production site of EPO
Fibroblasts in the proximal convoluted tubule of the kidney
Function of haemoxygenase enzyme
Conversion of haem to biliverdin
Enzymes involved in haem to bilirubin conversion
Biliverdin reductase
What are the three stages of atheroma formation?
Endothelial damage - activation
Uptake of modified LDLs and adhesion and infiltration of macrophages
Smooth muscle proliferation and formation of a fibrous cap
What is meant by glycation?
Bonding of sugars to a lipid/protein
What are monocytes transformed into?
Macrophages
What is the role of macrophages in ateriosclerosis development?
Monocytes bind to receptors that are sticking out into the lumen from the endothelium and then enter the blood vessel - transformed into macrophages - these release of proinflamamtory cytokines e.g. PDGF
Pick up excess levels of LDL via scavenger receptor - formation of foam cells
What is a foam cell?
LDL laden macrophage/fat laden macrophage
How is a foam cell formed?
Macrophage normally picks up LDL due to apolipoprotein B100 receptor - modified LDL not recognised by this receptor and is picked up by scavenger receptor - excess levels picked up –> foam cell
Summarise formation of atheromatous plaque
Activated endothelium
Uptake of modified LDL and infiltration of macrophages - formation of foam cells
Release of growth factors - migration of smooth muscle cells which lay down collagen
Formation of fibrous cap
Rupturing of fibrous cap - exposure of underlying collagen and platelets can stick here to form thrombus
What are the different levels of an artery?
Tunia adventia
Tunica media
Tunica intima
What is contained within the polypill?
Aspirin
ACE inhibitor/Beta blocker
Diuretic
Statin
Through what artery is a stent usually inserted for atherosclerosis?
Radial artery (rather than femoral artery)
Arteriosclerosis vs. atherosclersosis
Ateriosclerosis - stiffening/hardening of arterial wall
Atherosclerosis - narrowing of an artery due to plaque build up
How does LDL modification occur?
Oxidation from ROS
Glycation
Common sites of atheroma formation
Aortic bifurcation
Carotid bifurcation
Common iliac artery - lateral wall
Coronary arteries
Ferric reductase
Ferrous 2+ to ferric 3+
Chemical presentation of ferrous iron
Fe2+
Chemical presentation of ferric iron
Fe3+
What are the normal levels of haemoglobin in males and females? (NEED TO KNOW)
Males - 13.5
Females - 11.5
Define hypochromic
Paler than normal in colour (less colour)
MCV of microcytic anaemia
<76
MCV of macrocytic anaemia
> 96
What is a pencil cell?
Cell that has shrunk down into a tube
Indicative of microcytic anaemia
What are plasma ferritin levels indicative of?
Indicative of the level of iron that is stored in the body (diagnostic marker)
Factors to increase iron absorption
Increased haem consumption Pregnancy Iron deficiency Ferrous (Fe2+) salts Acid pH
Factors to impair iron absorption
Alkali pH Consumption of non-heam iron (veg) Ferric salts Iron overload Inflammatory disorders Drugs use e.g. PPIs
Cause of macrocytic anaemia
B12/Folate deficiency
Where is B12 and where is folate absorbed in the body
B12 - absorbed in the ileum
Folate - absorbed in the duodenum and the jejunum
Cells that produce intrinsic factor
Parietal cells in the gastric mucosa
Cause of spherocytic anaemia
Haemoloysis - lack of proteins to hold the cell in bioconcave shape
Splenomegaly occurs in what type of anaemia and why
Spherocytosis because there is increased premature haemolysis occurring
Glucose-6-phosphate dehydrogenase
G6PD - enzyme that prevents/reverses the oxidation of RBCs
Significance of G6PD deficiency
Deficiency results in premature oxidation of RBCs - premature haemolysis
Inheritance of G6PD deficiency
X-linked
Clinical tests to test for the presence of antibodies to red blood cells (haemolytic anaemia)
Direct coombs test
Direct antiglobulin test
RR interval represents?
Heart rate
PR interval represents?
Action potential from the atria to the Bundle of His
P wave represents?
Atrial depolarisation
Normal range for heart rate
60-100pbm
Normal length for p wave
<80
Normal length for PR interval
120-200
Normal length for QRS interval
<120
Atrial fibrillation vs. atrial flutter
AFib: Many sites in the right atrium are firing action potentials to compete with the SAN
AFlut: One overexcited site of excitation in the left atrium competing with the SAN
Ventricle tachycardia vs. ventricle fibrillation
Tachy: Abnormal but regular QRS complex
Fib: Abnormal and irregular QRS complex - no sign of organisation at all and the ventricles only quiver
Junctional rhythm
Some form of damage to the SAN/the path through here and so the main pacemaker shifts to the AVN
Supraventricular tachycardia
Atrial tachycardia
Significance of right bundle branch block
Damage to the right hand side of the heart
Significance of left bundle branch block
Heart disease
Wolff-Parkinson White syndrome
Formation of a new (pathological) connection between the atria and the ventricles - known as the Bundle of Kent
Atrioventricular nodal reentrant tachycardia
There are two activations of the AVN - a fast cycle and a slower cycle SO inbetween each AVN depolarisation - there is another, pathological one
Why does a low grade fever occur when you have an MI?
MI - ischaemia - there is a leakage of proteins and this can stimulate an inflammatory response
Cardiogenic shock
Inadequate circulation of blood and insufficient perfusion of tissues to meet the O2 demand
Cardiac arrest
A sudden stop in effective blood flow due to a failure of the heart to contract effectively
Thromboembolytic drugs (name two main)
Streptokinase
Tissue plasminogen activator (tPA)
What is the main problem with thromboembolytic drugs?
Major risk of haemorrhage and bleed
Why can streptokinase only be used once?
Develop antibodies against it - risk of anaphylaxis and allergy
Define dyspnoea
Difficult or laboured breathing where the subject is short of breath
Undue awareness of breathing/difficulty breathing
What are J receptors?
Pulmonary c-fibre receptors (slow)
Sensory nerve endings in alveolar walls innervated to vagus nerve
Feedback - shortened expiration and increased respiratory frequency
Value for hypoxia
pO2 <8kPa
Value for hypercapnia
pCO2 >6.8
Type 1 vs type 2 respiratory failure
Type 1 - hypoxia and hypocapnia
Type 2 - hypoxia and hypercapnia
Different types of heart block
a
How can you recognise macrocytic anaemia from blood film?
a
Cause of macrocytic anaemia
a
Common causes of sinus bradycardia
a
Cause of type 1 respiratory failure
Ventilation/perfusion mismatch
Cause of type 2 respiratory failure
Inadequate alveolar ventilation
What is released from the blood vessel when it is damaged? Local effect of this?
Endothelin - vasoconstriction
Sepsis vs. septic shock
Sepsis - systemic response to the presence of pathogens in the blood
Septic shock - sepsis + hypotension
Stroke volume vs cardiac output
a
Obstructive vs. restrictive disease
a
Vitalograph and function
a
Define tidal volume
a
Define expiratory reserve volume
a
Define inspiratory reserve volume
a
Define vital capacity
a
Define functional residual volume
a
Define residual capacity
a
Define total lung capacity
a
Define peak flow rate
a
Vitalograph and function
a
Obstructive vs. restrictive disease
a
Peak flow rate morning vs. evening
a
Define asthma
a
Investigation to determine presence of obstructive vs. restrictive disease
a
Asthma - on which cells are the IgE receptors found?
a
Which mediator results in the immediate bronchoconstriction in asthma?
a
Pathophysiology of bronchoconstriction in asthmatics (immediate and delayed)
a
Main immunoglobulin (Ig) involved in asthma/allergies/atopic condtions
a
Four substances that can trigger asthma
a
Alpha-1-anti-tripsin and cause
a
Main cause of emphysema
a
Significance of virchow’s node
Metastasis from the gut
Where is the lymphatic drainage to and which is most major?
Right - right lympatic duct
Left - thoracic duct - this is the major drainage
Right - only from the right arm, right side of head and the right thorax
Where are the superficial lymph nodes located?
Cervical - drain above the clavicle
Axillary - drain between clavicle and the umbilicus
Inguinal - drainage below the umbilicus
State the lymph nodes of the head adn neck
Think from osce
Two groups of inguinal lymph nodes
Horizontal - superficial to the inguinal ligament - drain from perineum and the external genitalia
Vertical - along great saphenous vein - drain from the leg
