Cardiovascular Block Flashcards

Question

Why is the total blood volume found in the systemic capillaries so small and its function?

Answer 1

Very small blood vessels so the amount of blood found here is small. The large CSA means that the velocity in these areas are much slower - allows for nutrient exchanges.

Answer 2

Which of the following would increase the proportion of blood in systemic arteries? 1. Decreased cardiac output 2. A reduction in total peripheral resistance (This will allow more blood enter the veins) 3. Vasoconstriction (pressure increases in veins which means greater flow into atrial pressure, more filling of ventricles which means greater stroke volume -\> end up with more blood in the systemic artery.)

Answer 3

Which of the following would increase the proportion of blood in systemic veins? 1. Decreased cardiac output (Yes, less goes to arteries) 2. A reduction in total peripheral resistance (Yes more blood enters the vein) 3. Venoconstriction leads to squeezing of blood into the arteries.

Answer 4

Veins are much more compliant than arteries. This makes arterial pressure much more sensitive to volume changes.

Answer 5

This involves the vasoconstriction of the veins which will transfer the blood to the arterial system to allow for more blood to be used for blood flow.

Answer 6

If the heart stops moving the blood will equalise on both sides. The eventual pressure depends on blood volume and vessel compliance. - 7 mmHg

Answer 7

An increase in cardiac output will: 1. Increase venous pressure 2. Decrease venous pressure (correct) 3. Venous pressures stays the same

Answer 8

Shows what happens to venous return when cardiac output varies.

Answer 9

More blood means that there will be a larger mean circulatory filling pressure. This also means that there will be larger pressures at all points.

Answer 10

This means more blood will be in the veins. TPR does not cause the blood pressure to go up itself. As your CO increases there will be a larger volume pumped into the veins (increasing it more than usual).

Answer 11

1-5mmHg in the great veins right outside the heart. It is slightly higher than the right atria to allow flow. This can be assessed by JVP (Jugular Venous Pressure)

Answer 12

This curve shows the effect of venous pressure on cardiac output.

Answer 13

A decrease in venous pressure: 1. Increase cardiac output 2. decrease cardiac output (correct)

Answer 14

This can be done by combining both cardiac and vascular function curves. But this would increase venous pressure and thus increase cardiac output.

Answer 15

This will increase the cardiac output and decrease venous pressure.

Answer 16

It will increase cardiac output and increase venous pressure.

Answer 17

This is the pressure needed to fill the heart. Failing heart causes it to rise. It falls when venous return is pool

Answer 18

Can alter smooth muscle contraction by releasing substances. NO (dilator), endothelin (irreversible constrictor) and prostaglandins (does both) Also mediates circulating angiotensin, thrombin and bradykinin (vasodilator)

Answer 19

Results in vasodilation and occurs due to hypoxia, physical stimuli, circulating factors or paracrine factors.

Answer 20

NO, histamine and cytokine

Answer 21

Thrombin, ADP (vasoconstriction) and Thromboxane A2. These enhance coagulation and platelet aggregation.

Answer 22

Competitive antagonism and non-competitive (functional, pathway inhibitors or modulators)

Answer 23

It is simply binding to the receptor without eliciting a response. It is mostly dependent on affinity.

Answer 24

It competitively binds to B-adrenoceptors

Answer 25

It inhibits the actions of L-type calcium channel and it is slightly cardio selective (pathway inhibition).

Answer 26

It inhibits any positive inotropic stimulus by acting as a functional antagonist.

Answer 27

This is drug binding to an alternative binding site other than the orthostatic binding site. This will then modulate the receptor's response to stimulus.

Answer 28

1. Modulate orthosteric ligand affinity. 2. Modulation of orthsteric ligand efficacy. 3. Modulation of receptor activation

Answer 29

It makes it very hard to make selective drugs. But allosteric sites are very variable that allow for selectivity.

Answer 30

There is selectivity between sub-type receptors. It is safe in overdoses because it simply modulates receptors - meaning normal physiological control is in place.

Answer 31

This is when the response maximum is unchanged but only the dosage needed. Competitive reversible antagonism: generally surmountable in vivo but sometimes not. Non-competitive antagonism is generally insurmountable (at high levels)

Answer 32

Absorption, distribution, metabolism and excretion.

Answer 33

Patient convenience, cost, bioavailability and local/systemtic?

Answer 34

It has less side effects. Use a poorly absorbed drug or a low enough concentration to just elicit a local response.

Answer 35

Oral, skin, lungs, rectal, nose, injections (subcutneous, intramuscular and intravenous). Only intravenous is directly entering tthe blood.

Answer 36

This model assumes that the drug distributes very quickly to reach distribution equilibrium. Then most drugs are eliminated at a rate proportional to their concentration.

Answer 37

Molecular size, binding to plasma proteins and lipid solubility. Also the blood flow to carry it around.

Answer 38

Only lipid soluble drugs can access the BBB. Any polar compounds cannot cross it (such as proteins).

Answer 39

These are sites around the body where drugs accumulate. They can prolong drug action, end it earlier or lead to slow distribution. Usually the reservoirs are fat (poor blood supply), plasma proteins and cells.

Answer 40

This tells us how concentrated a drug is in the plasma? Vd = X/C

Answer 41

There is glomerular filtration, tubular secretion and tubular reabsorption.

Answer 42

This is depending on the lipid solubility and the different pH levels. Such as acidic drugs in acidic pH will be able to cross cell membranes.

Answer 43

We can give NaHCO3 which makes the urine basic. This increases ionised aspirin making it unable to reabsorb -\> increased excretion.

Answer 44

This is the amount of drug cleared by the kidney. CLrenal = GFR + TS - TR

Answer 45

Biotransformation of drugs usually in the liver. Aims to increase water solubility to facilitate drug excretion. Inactivation, active metabolic, new activity, be toxic, undergo phase I metabolism (creates functional group on the drug - cytochrome P450), conjugates a water soluble molecule to a functional group.

Answer 46

Red cells - oxygen delivery, White cells - fight infections, platelets - stop bleeding, plasma - clots or bleeds

Answer 47

Pancytopenia - lack of all cells Anaemia - Lack of blood cells Leukopenia - Lack of WBCs Neutropenia - Lack of neutrophils Lymphopenia - lack of lymphocytes Thrombocytopenia - lack of Thrombin

Answer 48

Polycthaemia - RBC Leukocytosis - Leukocytes Thrombocytosis - Platelets

Answer 49

Measure Hb instead of RBC count - defined as lower levels for the particular age and _gender_

Answer 50

Delivery = CO x Hb x %saturation x 1.34 1.34 = mL of oxygen carried by one gram of normal cell.

Answer 51

Allows us to determine when to use blood, inotropes or oxygen

Answer 52

It reduces oxygen to tissues. It can be compensated by CV changes. Therefore Hb numbers is not the only factor.

Answer 53

Pale, tachycardia, ischaemia, hypoxic (confused and disorientated), failure to thrive, lethargic

Answer 54

Short term generally shows a quicker jump. Whereas it is not as significant in the long term causes because of adaptation of increased SV (usually it can only be changed over a long time).

Answer 55

Either unable to produce RBC, active loss/destruction of RBC or inappropriate production.

Answer 56

Hb - reported in grams/L RCC (red cell count) - how much RBCs per litre (5 x 10^12 per L) Hct (Hermatocrit) - Proportion of RBC volume compared to plasma volume MCV (mean corpuscular volume) - Allows for differential diagnosis to categorise the type of anaemia. MCH (mean corpuscular haemogloblin) - Amount of Hb in the cell MCHC - Concentration RDW - is the standard deviation around the mean of MCH and MCV Plts - Count of platelets WCC (white cell counts) - Differential for lymphocytes, eosinophils and basophils Blood film - microscope of blood. Looks at morphology of cells

Answer 57

Size (normocytic, microcytic, macrocytic) Shape (many variations - each with different meaning) Colour (normchromic, hypochromic, polychromasia)

Answer 58

Regeneration and Aregenerative. Regenerative: This implies that it was an acute event that caused a rapid decrease in Hb. Aregenerative: Means there is a gradual loss of cells which allows the body to adapt slowly

Answer 59

Increased production: see reticulocytes and polychromasia (formation of Hb) Increased destruction: Jaundice (serum bilirubin), Haptoglobins, LDH

Answer 60

This means there could be rapid reduction in Hb \> rapid reduction in oxygen delviery. So we may have limited time to compensate - Haemolysis is extremely dangerous.

Answer 61

RBC - 3-5 x 10^12 cells/L 120 days WBC - 2-6 x 10^9 cells/L replaces 3-5 days Platelets - 150-400 x 10^9 / L replaced every 10 days

Answer 62

First few weeks: Yolk sac 6weeks - 7months: Liver and spleen (could be recruited later again) 7months - life: bone marrow

Answer 63

Self renewal, ability to differentiate, few found in bone marrow, cannot identify

Answer 64

It provides a specific microenvironment for bone marrow to grow. Changes in CAM will change the progression of the cells through the stroma and when it is ready to enter the circulation. Bone marrow is in continuity with the circulation.

Answer 65

Cells and ECM. Just know that it is involved in cell processing

Answer 66

The growth factors are usually glycoprotein hormones with local and circulating actions. There is a lot of redundancy of the growth factors. - Effects varies on where it is found: Premature cells GM-CSF proliferates but in neutrophil stage it will be activation instead. - Can use factors for therapeutic treatment in specific cases

Answer 67

Iron, Vitamin B12, Folate Iron: essential for haemoglobin function and maintain RBC population (usually troubling in large blood loss) Vitamin B12: Needed for blood cell production. Deficiency usually from poor diet (in animal products) or poor absorption. Folate: Important in RBC production. Deficiency usually from diet or drugs that affect uptake

Answer 68

Haemostasis is the stopping of blood flow in the case of injury. Involves platelets, coagulation factors and inhibitors, fibrinolytic processes and _blood vessels/endothelium_ This means that the haemostasis you see will be different in different parts of your body.

Answer 69

This is the initial platelet plug to stop the bleeding. Vasocontraction, platelet adhesion and aggregation.

Answer 70

This involves formation of fibrin and activation of coagulation factors. This is then shaved off until it is smooth (fibrinolysis process - not part of secondary haemostasis).

Answer 71

Vessel wall, blood flow and blood composition

Answer 72

This is the endothelial cell surface which is ery dynamic - which can be antithrombotic or prothrombotic depending on what is expressed on the wall. - Unable to test for its integrity so usually diagnosed by exclusion.

Answer 73

Intrinsic and extrinsic pathways lead to common pathway. Usually it is Extrinsic signals. VII \> activated X \> activates II \> catalyses fibrinogen to form fibrin. Intrinsic signals: XII \> XI \> IX (not as important) _THROMBIN_ is key in this process

Answer 74

1. Initiation: Vessel exposed which has TF (tissue factor) that activates XII. These then activate IX and X. X binds to Va on the cell surface. 2. Amplification: X/V activates thrombin (II). 3. Propagation: This is when the thrombin burst occurs to form fibrin from fibrinogen

Answer 75

Binding to thrombomodulin will inactivate thrombin by irreversible inhibition.

Answer 76

It is a test of artificial construct to predict clinical behaviour. Must be validated against clinical outcomes. Used to test the integrity of the blood.

Answer 77

Bleeding (no effective test), platelets (number, function and appearance) and the coagulation system.

Answer 78

Sample integrity, standard curve, control samples, duplicate testing and multiple consistent tests.

Answer 79

Involves taking blood and adding calcium. Then activate XII (intrinsic pathway) and time how long it takes for fibrinogen to activate. Just gives information about pathway integrity. - Can also test for presence of warfarin or lupus anti-coagulant

Answer 80

It is similar to APTT but instead it tests for the VII pathway (extrinsic). Values given in INR = (PT/PTavg)^(ISI) Simply a standardised value.

Answer 81

Usually tests for functioning enzymes/proteins. Functional, chromogenic (colour change when binds to particular cell) or immunological.

Answer 82

They affect the data retrieved and are to be adjusted to the appropriate age groups.

Answer 83

Simply to confirm whether my protein is functional or not

Answer 84

This is an allosteric tetrameric protein that is used to carry oxygen. The haem moieties in Hb and Mb binds to oxygen.

Answer 85

Fe (II) has 6 co-ordinating bonds. 4 in the same ring, 1 up and 1 down. Oxygen is found in one of these and the other one binds to proximal histidine.

Answer 86

This is the globular protein found in muscle tissues to deliver oxygen.

Answer 87

Needs to have high affinity to bind many oxygen. Be able to transfer oxygen to myoglobin when it reaches the tissues (sigmoidal curve).

Answer 88

It is a monomer with a compact globular structure with haem. There is transient breathing of alpha helices to allow oxygen to bind. It has high oxygen affinity to take oxygen from Hb.

Answer 89

It has two alpha and beta chains that forms a tetramer. Haem group present and there is cooperativity in binding and release of O2 (changes with O2 concentrations).

Answer 90

When oxygen binds it pull the Fe into plane \> conformational change affects adjacent subunits. - Explains the sigmoidal O2 binding

Answer 91

It is a ligand that does not bind to the normal ligand site that modulates function. It stabilises deoxy-Hb so locks out oxygen from rebinding. - Synthesised via glycolytic pathway in RBC. - _Decreases_ Hb affinity for O2 \> shifts curve right (at high altitudes this is good so that more oxygen is given up in the tissue)

Answer 92

CO₂ produced in tissue is carried by Hb (15%). deO₂ Hb binds CO₂ with more affinity than O₂Hb. Dumps CO₂ in the lungs which gets converted to acid leading into the _Bohr Effect_

Answer 93

Bohr effect is lower shift in pH levels (acidic). This stabilises the 'T' state. Shifts the affinity curve to the right (decrease affinity) but also means it can deliver more oxygen at the tissue level.

Answer 94

It it made up of two alpha and two gamma chains and has a greater affinity than the mother's HbA - allows foetus to access the oxygen.

Answer 95

T - Tense: usually has low affinity for oxygen R - Relaxed: usually has high affinity for oxygen

Answer 96

Synthesis, storage, release, receptor, reuptake/metabolism and degradation.

Answer 97

Exception is that Ach goes to sweat glands and adrenal glands

Answer 98

Choline transported by choline carrier into the cell. Choline + Acetyl CoA with choline-acetyltransferase produces ACh. ACh is then carried into the vesicle via ACh carrier.

Answer 99

Tyrosine is taken up into the cell. Tyrosine hydroxylase then acts on it to produce L-DOPA. L-DOPA is then acted on by DOPA decarboxylase to produce Dopamine. Dopamine is take up into the vesicles by carriers to be acted on by Dopamine B-hydroxylase to produce NA.

Answer 100

It follows the same pathway as NA but has one extra step in the vesicle. PNMT (phenylethanolamine-N-methyl-transferase) acts on NA to produce Adr.

Answer 101

This is the release of more than one transmitter substance. Usually ATP or NPY

Answer 102

It has acetylcholine-esterases found in the synapses of the vesicles which breakdown ACh.

Answer 103

The NA is taken up from the synapse through neuronal high affinity uptake-1 channels.

Answer 104

ACh - somatic, parasympathetic, pre-ganglionic transmission and exception at sweat and adrenal glands. NA - found on the sympathetic system

Answer 105

Nicotinic Receptors (NicR - ligand gated ion-channel) Muscarinic Receptors (M1,M2,M3 - GPCR)

Answer 106

alpha and beta adrenoceptors (GPCRs)

Answer 107

Muscarinic receptors

Answer 108

It is a nicotinic antagonist.

Answer 109

Phenylephrine - alpha agonist Isoprenaline - Beta agonist

Answer 110

It is a pentamer - ligand gated ion channel

Answer 111

It binds to NicR with high affinity and antagonises it. Shows selectivity of receptors.

Answer 112

It prevents the formation of SNARE proteins which is needed for vesicle docking onto the membrane. This prevents the exocytosis process. - Enzyme does the cleaving of SNAP-25, synaptobrevin so only needs small doses. - Used cosmetically and for Blepharospasm.

Answer 113

This inhibits acetylcholine-esterase enzyme which prevents ACh breakdown in the synapse.

Answer 114

It is used to Myasthenia Gravis (autoimmune disease against own NicR). It is an antcholinesterase which will increase ACh in synapse to diagnose for Myasthenia. - Can be treated with neostigmine

Answer 115

Can be used to help with smoking cessation - nicotine patches

Answer 116

These can be used as pre-surgery muscle relaxants. - Non-depolarising: _tubucurarine_ Or ganglion blockers: _hexamethonium_

Answer 117

Generally rule is SLUD Salivation, lacrimation, urination and defecation Furthermore: sweating, bradycardia, bronchoconstriction _Pilocarpine_: used in glaucoma to increase drainage

Answer 118

It inhibits the neuronal high-affinity uptake 1 channel. NA can no longer be taken up from the synapse.

Answer 119

It inhibits monoamine oxidase found in the neurons that metabolise NA. Which will increase the amount of NA in the synapse. COMPT is found on the post-glanglionic cell to metabolise NA.

Answer 120

These are administered which is taken up through the same reuptake channel as NA. They are also taken up through the vesicle channels so that it now displaces NA. This case is now a passive leakage of NA into the synapse.

Answer 121

Amphetamine, Ephedrine and Tyramine. Tyramine can cause unwanted CV effects. Since it is normally broken down by MAO in the gut usually. When used with MAOi it can lead to high BP

Answer 122

In the same order: non-selective B, B1 and B2

Answer 123

Propranolol - non selective B Atenolol - B1

Answer 124

Phenotolamine: non selective alpha agonists Phenylephrine: a1 agonists Prazosin: a1 antagonists

Answer 125

They are rapidly metabolised or diluted beyond their biologically active range close to their site of release

Answer 126

Mast cells (tissues and particular mucosal surfaces/skin) and basophils (blood) It is also secreted by enterochromaffin-like cells (GIT) that regulate stomach acid

Answer 127

Induced by antigen via IgE, complement fragments (C3a/C5a), cytokines, physical trauma and bacterial components.

Answer 128

They act on histamine receptors (H1,2,3,4) which are all GPCRs

Answer 129

Reddening - Vasodilation Wheal - increase in vascular permeability (local oedema) Flare - spreading through sensory fibres

Answer 130

Competitive reversible H1 receptor antagonists Sedative: promethazine (was able to enter CNS) - affected lifestyle Non-sedative: terfenadine - caused sudden ventricular arrhythmia Newer non-sedative: loratidine, cetirizine (reduced cardiac risk)

Answer 131

Cimetidine blocked H2 receptors and was used for peptic ulcers by limiting stomach acid production.

Answer 132

This is a local peptide mediator in pain and inflammation. It is produced AFTER plasma exudation during inflammation. Prekallikrein \> kallikrein (by factor XII when it becomes active outside the blood). Acts on HIGH molecular weight kininogen to bradykinin

Answer 133

Kininase II (also known as ACE) cleaves the bradykinin.

Answer 134

Dilates arterioles and venules, increases permeability, stimulates pain sensory nerve endings. Also contracts uterus, airways and gut Acts on B1 and B2

Answer 135

Used in hereditary angioedema. It is a selective B2 antagonist. The HA is caused by C1esterase inhibitor deficiency - this means the Kallikrein pathway is overactivated which can cause deep tissue swelling.

Answer 136

In-vivo it vasodilated whereas in-vitro it vasoconstricted. Turns out that the endothelium was releasing a relaxing factor.

Answer 137

It was found to be NO Other endothelium derived vasoactive factors are: PGI₂, NO and endothelin (constricts)

Answer 138

Leads to increased calcium, that activates NOS (nitric oxide synthase) which converts arginine to NO and citrulline.

Answer 139

NO activates guanylate cyclase, which produces cGMP. The cGMP is what causes relaxation of the SMC.

Answer 140

nNOS (nerves), iNOS (inducible macrophages and smooth muscle) and eNOS (endothelial cells)

Answer 141

There is a basal level of NO that regulates vascular tone. Inhibits platelet adhesion and aggregation And flow-dependent vasodilation

Answer 142

Most of these drugs are actually NO donors which elicit the response. Glyceryl trinitrate (GTN) and nitroglycerin.

Answer 143

It is an eicosatetranoic acid (20:4) omega 6 fatty acid that make biologically active molecules

Answer 144

Can be found in our diet indirectly (linoleic acid - which must be transformed) or directly.

Answer 145

It is stored in the plasma membrane by esterification of C2 glycerol onto the AA.

Answer 146

This is done by PLA₂ which can be activated by ERK or increase intracellular calcium

Answer 147

The AA is metabolised by COX (1 - constitutively active, 2- inducible by inflammatory stimuli) - found in _all cells_ Or it can be metabolised by 5-lipoxygenase to produce leukotrienes. Only found in _inflammatory cell (mast cells and eosinophils)_.

Answer 148

These are products of COX which are highly unstable and are only intermediates to the product.

Answer 149

Produces stable prostaglandins by _isomerases_ that act on the reactant. Produces PGD₂, PGE₂ and PGF_2a. _-_ PGF and PGD are bronchoconstrictors. PG is broken down by endothelial cells in the pulmonary capillaries.

Answer 150

Anti-inflammatory, anti-pyretic and analgesic

Answer 151

- Increases blood flow \> tissue reddening and oedema (affects vasculature not cells) - Sensitises pain fibres but does not cause it. - Causes fever by having PGE₂ produced in the hypothalamus which acts to increase temp set point. - Promotes blood flow, angiogenesis, mucus secretion and reduce acid secretion in the stomach

Answer 152

These are short lived (T1/2 = 3 min) - Produced by _endothelial_ cells that cause vasodilator and reduces platelet aggregation. Protect against coronary artery disease

Answer 153

It is produced in the _platelets_. - Increases platelet activation and vasoconstricts Opposes prostacyclin and promotes coronary disease.

Answer 154

1. Acetylation of COX and vascular protection. Inhibits COX irreversibly so that it cannot re-synthesis COX in platelets for 8 days. Endothelium can re-sysnthesise in hours. Leads to PGI2/TxA2 ratio increased. 2. Aspirin triggers lipoxins (15-epi leukotrienes) which are analogous to those found in the body. Inflammatory resolvers.

Answer 155

They will produce PGI₃ and TxA₃. Because of the structure the thromboxane is dysfunctional. Causing an increase in PGI/TxA ratio.

Answer 156

Acts on AA and produces leukotriene A₄. Seems to only be involved in inflammation.

Answer 157

LTB₄ and LTE₄ These are highly active compounds that cause vasodilation and bronchoconstriction - trouble in allergy, inflammation and asthma

Answer 158

Bronchoconstrictor, vasoactive, leaky vessels. It can be antagonised by leukotriene receptor antagonist cysteinyl-leukotrienes blocking by _montelukast_ No action on SMC but promotes inflammation by attrack leukocytes

Answer 159

Descriptive (how common is a particular disease) and analytical (cause and effect)

Answer 160

There are observation and intervention studies. Some fall under descriptive and analytical. Case reports, cross-sectional studies, ecological - descriptive Case-control, cohort, clinical trials (intervention) - analytical

Answer 161

Cohort and clinical trials. Case reports, ecological, cross-sectional and case-control are non-longitudinal

Answer 162

These have no follow up on the subjects - information collected in one encounter

Answer 163

Information collected over multiple encounters and follows up on study subjects

Answer 164

Number of existing cases of an outcome in a defined population at one defined point in time. Usually given a proportion or percentage. % of current smokers % of 65y.o with CHD

Answer 165

These are the number of new cases of an outcome _arising_ from a defined population during a time interval - Expressed as a rate (denominator includes time component) - Drawn from longitudinal studies - Number of non-smokers start smoking in 2012

Answer 166

Probability of disease occuring in disease free population during a specific time period. - Risk = n/P n - new cases in defined period, P - population at risk

Answer 167

Probability of disease happening in a disease free population during total person-time of follow up E.g. rate = 3/1000 person-years for cases of lung cancer

Answer 168

Cause and effect, correlation

Answer 169

This is an isolated measure of risk/rate. - There is no indication of association with exposure (no indication of cause)

Answer 170

Provides indication of association by using the comparison of 2 absolute risk/rate measurements

Answer 171

RR= R(exposed)/R(unexposed) Indicates relative magnitude of change in risk/rate of outcome associated with exposure

Answer 172

AR = R(exposed) - R(unexposed) Indicates the _absolute magnitude_ of change in risk/rate of outcome associated with exposure

Answer 173

AR% = [(Re- Ru)/ Re] x 100 Proportion of incident disease _among exposed_ people that is **due to exposure**

Answer 174

PAR = Rt\* - Ru Rt - incidence measure in the total population

Answer 175

Known as the preventable fraction

Answer 176

Small increase in risk/rate of common disease leading to greater additional disease than large increase in risk/rate of rare disease

Answer 177

Carotid sinus, aortic arch and includes juxtaglomerular apparatus (pre-arteriole kidney)

Answer 178

It is found in the brain stem - medulla. It has both pressor and depressor centres which operates via sympathethic and parasympathethic nerves

Answer 179

- Increases heart rate - Decreases AV conduction time - Increases cardiac contractility (by increasing intracellular calcium during depolarisation) - Increases TPR - Increases Venous tone

Answer 180

- Reduces HR - Increases AV conduction time - Reduces TPR (dilates a few blood vessels but it will not reduce the TPR)

Answer 181

This is the baroreflex that stabilises the pressure and smooth out variations such as posture, eating, defecation and noise

Answer 182

These are used as detection when the blood pressure drops below 60mmHg (baroreceptors stop firing). Found on carotid and aortic bodies outside the arteries. - Stimulated by low flow, low O₂, high CO₂ and low pH

Answer 183

CHD, stroke, cardiac hypertrophy, heart failure, kidney failure NOT liver failure

Answer 184

It is unimodal distribution with skewing of the curve to the upper values

Answer 185

Men typically have higher blood pressure than woman. This is representative of the average there are cases when women BP are higher than men.

Answer 186

Blood pressure increases with age

Answer 187

Pulse pressure increases due to the decrease in compliance of the arteries in elder people. Typically diastolic no longer increases and may even decrease.

Answer 188

The bigger the body size the higher the BP

Answer 189

Lower night BP (20mmHg), less variability at night, less sympathethic activity at night

Answer 190

Sweat \> loss of blood volume and reduce cardiac output. Vasodilation during summer due to heat. Body weight changes between summer and winter (winter usually gains weight)

Answer 191

It is simply the upper end of the distribution defined arbitrarily. It has been falling over time - about 140mmHg at the moment.

Answer 192

In a population where more deaths occur in the larger number of people at moderate risk than in the smaller number of people at highest risk

Answer 193

Breast has glandular tissue that secrete milk. Also made up of fibrous, adipose tissue, blood vessels, nerves and lymphatics. It is located on the lateral border of the sternum out to the mid axillary line. Also notice the axillary process superior laterally - which means there is more glandular tissue in the upper quadrant of the breast (thats why more carninomas occur here)

Answer 194

Vertically the breast extends from the 2nd to 6th rib. The deep aspect of the breast is concaved due to having 2/3 of it being over the pectoralis major. The remaining 1/3 lies over the serratus anterior. Another significant landmark is the _retromammary_ space which separates the glands from the muscles and ribs. This allows the breast some degree of movement and is also the location for breast implants.

Answer 195

It shares the blood vessel system with the thoracic and upper limbs. So laterally the artery that supplies the breast are the axillary artery. The medial aspect is suppled by the internal thoracic artery. Similar system is found for the veins. Laterally it is drained by the lateral mammary vein or the lateral thoracic vein. Medially drained by internal thoracic vein which all drain to the internal jugular vein.

Answer 196

Laterally drained to axillary lymph nodes and medially to the intercostal lymph nodes. Carcinoma of the breast can use the lymphatic vessels to metastasise into the thoracic wall.

Answer 197

Ribs articulate anteriorly with costal cartilages. The upper 1-7 articulate with the sternal complex. Costal cartilage 8,9,10 articulate with the costal cartilage from above. This forms the costal margin. 11-12 do not articulate at all (called floating ribs).

Answer 198

Ribs articulate with the facets found on the vertebra with the head first. Then the smooth facet on the tubercle is what articulates with the transverse process.

Answer 199

Consists of the head which has a superior and inferior articular facet for attachment to the vertebral body. Then forms the tubercle which has two facets - smooth medial (for articulation) and rough lateral (for ligaments). This leads into the body and finally the anterior sternal end where it slots in with the costal cartilage. Costal groove is found inferior to the body of the rip where the blood vessels and nerves are located.

Answer 200

11-12 are atypical ribs because they have no neck or tubercle. 1-2 ribs, particularly the first rib it is almost horizontal and short. Bares distinct grooves for the subclavian vessels. It only articulates with T1 so it only has a single facet on the head.

Answer 201

Costal facets on the body (superior and inferior), facets on the transverse process and long vertically spinous process helps identify thoracic vertebral body.

Answer 202

Head of the ribs articulate with the vertebral body. Articulates onto the IV disc and on two consecutive vertebras. Exception to T1. There are strong radiate ligament of head which reinforces the joints.

Answer 203

Between the transverse process of the vertebra and the tubercle of the rib. Between the medial facet of the rib with the facet on the transverse process. This joint also has an incredibly strong three part costotransverse ligament of neck and tubercle. These joints are very strong and typically rib fractures occur first before these joints are broken.

Answer 204

The superior aperture is narrow compared to the inferior aperture. The supre-pleural membrane further narrows the superior aperture but does not close it off entirely. The inferior aperture is completely closed off by the diaphragm

Answer 205

Usually with blunt traumas it will cause fractures of the ribs. Typically these form different rib segments. It impacts on respiration and does not influence of the join itself. Causes independent movement of the different sections.

Answer 206

It is a muscle that has a circumferential origin of the inferior aperture. It attaches to the xyphoid process, costal margin, to the tips of the 11-12 ribs then we head towards the vertebral volume. Posteriorly there is a lateral and medial arcuate ligaments which are overlying the muscles. The medial arcuate ligament is thickening in the psoas fascia. The most posterior attachment is onto the lumbar vertebra.

Answer 207

This is the tendinous structures that is found extended inferiorly from the diaphragm to the vertebral column. The right one is higher than the left one due to the liver.

Answer 208

Clubbed shaped central tendon. Three many hiatus in the diaphragm: IVC passes through the central tendon at the level of T8 (to the right of the mid line). Oesophagus passes the level at T10 (to the left). Aorta passes more behind the diaphragm rather than through it (between the pleura).

Answer 209

Where one lung is paralysed the functional diaphragm will go down with inspiration. Because it simply moves substances (organs) will go up instead up the other dome. - Each dome is supplied independently by the phrenic nerve.

Answer 210

EICM: the fibres are directly downwards and forwards like our hands in our pockets. - Anterior part of each space is replaced by external ICM membrane. - This is used to elevate and expand the rib cage (expand it) IICM: It is a back pocket muscle with fibres directly downwards and backwards. The muscle fibres fill the space anterior and laterally and replaced by membrane posteriorly. - It will pull the ribs down and in which is a muscle that splits and holds down the ribs during expiration. Innermost is the same as direct of muscles as IICM but it is usually only found laterally and deepest layer. There are some muscles found anterior and posteriorly. Sub-costalis is the name for the muscle fibres in the posterior aspect of the rib. - Discontinuous lining of the rib

Answer 211

Each space has its only vein, artery and nerve (same order from superficial to deep). They run at the top of the space and runs just in the groove of the costal groove. The bundle lies between the internal and innermost ICM. Usually we see smaller branches (co-lateral branches) of each of these nerves and blood vessels running in the bottom of the space (only small amounts).

Answer 212

Ventral ramus of the thoracic spinal nerve forms the intercostal muscle nerves. Anterior intercostal artery comes from the internal thoracic artery. Posterior intercostal artery usually comes from the aorta. Feeds anteriorly and posteriorly which joins to anatomise later together laterally. Anterior comes from the internal thoracic artery and the posterior comes from descending thoracic aorta. - The veins mirror the arteries so there are anterior and posterior intercostal vein which will drain into the internal thoracic vein. Posterior intercostal veins are different its equivalent and drains into the azygous veins.

Answer 213

A-P directions, vertical and lateral directions

Answer 214

Any increase in volume of the thorax will drop the pressure inside the thorax. This will create a gradient for air to flow into the thorax.

Answer 215

Lifting it up will push the sternum superior and anteriorly which will change the AP dimension. Expansion of AP will increase volume and decrease pressure

Answer 216

When elevated the ribs will move laterally and increase lateral dimension of the thorax

Answer 217

These are muscles that attach to the ribs which can affect respiration by acting as accessory muscles

Answer 218

It surrounds the heart and attaches to the central tendon of the diaphragm to prevent it from falling down

Answer 219

This is the cavity in the thoracic cage

Answer 220

Division is at T4/5

Answer 221

Anterior, middle and posterior

Answer 222

It is found in the middle region in front of T5-8. Behind the body of the sternum.

Answer 223

It is the tough layer found outside of the heart and outside of the serous membrane too. It consist of the parietal layer.

Answer 224

It is a serous pericardial envelop that is punched in by the heart. This forms a continous membrane with two layers. Contains the visceral layer.

Answer 225

This is the potential space created by the serous membrane that allows the heart to have frictionless movement

Answer 226

The heart is twisted so that we mainly see the right atrium and ventricles but still see some left ventricle. Right border of heart RA \> RV\> LV. Apex of the heart at bottom and the base is where the major vessels are. The different compartments are divided by a sulcus: coronary sulcus, anterior interventricular sulcus. Auricle are like ear lobes out of the atrium that wraps around the vessels (indicates anterior orientation) Blood drains into RA by SVC and IVC then pumped out through pulmonary artery. Ligamentum arteriosum found between aorta and pulmonary artery

Answer 227

Similar to anterior there is mostly LA, LV and little bit of RA. Right border is still formed by the RA. Most other complexes are similar to the anterior view such as the coronary sulcus and posterior interventricular sulcus

Answer 228

Thin posterior wall, fossa ovalis, coronary sinus, IVC and SVC supplies, tricuspid valve, musculi pectinati (rough end found anterior to this section), crista terminalis (smooth area) and sinus venarum (smooth posterior wall)

Answer 229

Tricuspid valve, chordae tendinae, papillary muscle, thicker wall, trabeculae carnae (rough surface found around the ventricles), conus arteriosus/infundibulum smooth area right before the pulmonary valve. Three papillary muscles that are simply extensions of the trabeculae carnae (still ventricles)

Answer 230

LV has a much thicker wall. the valve present is the mitral valve (bicuspid) - so only two papillary muscles are found. RA simply has four openings for the four pulmonary veins.

Answer 231

Muscle fibres of the heart is anchored to the fibrous skeleton. It has four rings that surround the orifices of the valves. Atrial and ventricular muscle mass are two separate muscle masses that are separated by the fibrous skeleton. This means that they are electrically isolated too. - Also the fibrous skeleton provides an attachment for the base of each valve cusp

Answer 232

Anterior, posterior and septal cusps The chordae tendinae and papillary muscle have nothing to do with valves closing

Answer 233

It is a rough surface with chordae tendinae. Closure of valves are due to changes in ventricular pressures. The papillary muscles simply keep the valves closed longer to prevent back flow

Answer 234

Each set attaches to the adjacent cusps of two cusps. So when it contracts it will create a water tight seal.

Answer 235

Aortic and pulmonary valves

Answer 236

These are semi-lunar valves with its base attached to the internal surface of the wall vessel it is in. L and R are inverted in the picture

Answer 237

There are no chordae tendinae attached to the valves. It is semi-lunar valves (three). The origin of the coronary arteries are found in these valves.

Answer 238

SA node, AV node, bundle of His, R bundle branches (Purkinje fibres) SA node found in the RA right at the top at the cristae terminalis. AV node is also found in the RA. Bundle of His is the bridge between atrium to ventricles.

Answer 239

The cardiac plexus is found at the base of the heart which then splits off into SNS and PS nervous system.

Answer 240

Right and left coronary arteries come out from the aorta near the valves. Left coronary artery \> circumflex branch and anterior interventricular branch. Right coronary artery \> marginal branch and extends around posteriorly.

Answer 241

Right coronary arteries supplies to SA node, AV node, RA and RV. Left coronary arteries branch off to two vessels one that runs down the front of the heart and the circumflex branch around to the posterior which forms an anastomosis.

Answer 242

This means that acute level blocks in these arteries will not give them sufficient time for the anastomoses to adjust adequately. Leading to myocardial infarction

Answer 243

Coronary sinus drains blood into the right atrium. Some anterior cardiac veins will also drain directly into the RA. However the great, middle and oblique will drain into the coronary sinus then into the RA.

Answer 244

Acts by targeting the SA and AV node, by using the transmitted ACh to act on muscarinic receptors which eventually slows the heart rate (bradycardia)

Answer 245

Giving atropine caused the heart rate to increase from 60 HR (base) This also shows that there is a baseline PS stimulation to maintain appropriate HR

Answer 246

This targets SA nodes, conducting tissue and myocardial cells by using NA or Adr. The receptors are B-adrenoceptors. Results in increase HR as well as force (positive inotropic effect)

Answer 247

Use of propranolol showed a decrease in Heart rate. Implies that there is a baeline sympathethic activation present.

Answer 248

The Parasympathethic nervous system affects the heart rate the most

Answer 249

The baseline heart rate was found to be at about 100beats/min

Answer 250

The parasympathethic nervous system acts on K+ channels while the SNS acts on Ca²⁺ channels.

Answer 251

P - atria contraction QRS - ventricle contraction T - ventricle contraction

Answer 252

Phase 0: Depolarisation which involves Calcium (+) ion influx Phase 3: Repolarisation phase with influx of K+ Phase 4: Spontaneous depolarisation, influx of Na+ and Ca²⁺ influx - Involves Ifunny, I Calcium T and I Calcium L Stable membrane potential - 60mV +/- 20mV

Answer 253

ACh acts on M2 muscarinic receptors \> decreases cAMP \> opens K+ channels Efflux of K+ ions \> slows Na+ and Ca²⁺ fluxes \> slowed prepotential phase \> _longer to reach threshold potential in SA and slows rate of conduction (AV node)_

Answer 254

NA, Adr acts on B-adrenoceptors \> increases cAMP \> opens Ca²⁺ channels _Increases slope of Phase 4 depolarisation (SA and AV node) \> increased firing rate and more rapid conduction (AV node)_ It can trigger dysrhythmias

Answer 255

Phase 0: Depolarisation by Na+ in Phase 1: Rapid depolarisation by K+ efflux Phase 2: Extended plateu by Ca²⁺ in and K+ out Phase 3: Repolarisation by K+ out Phase 4: Stable membrane potential Resting membrane is about -90mV

Answer 256

This is any variation from the normal rhythm of the heart beat - seen as palpitations, fluttering or forceful contraction after a missed beat.

Answer 257

Shortness of breath, fainting, fatigue, chest pains

Answer 258

Need ECG to determine rhythm (flutter/fibrillation) and rate (tachycardia/bradycardia)

Answer 259

- Altered pulse formation: in pacemaker cells or genereation of AP other than SA node Altered impulse conduction: Conduction blockage or by re-entry Triggered activity: Early or late after-depolarisation from excess sympathethic activation

Answer 260

Na+ blockers, B-adrenoceptor antagonism, K+ blockers and Ca²⁺ blockers

Answer 261

Reduces Phase 0 slope and peak of ventricular action potential

Answer 262

Decrease rate and conduction of SA node

Answer 263

Delay of phase 3 of ventricular activation potential, so it prolongs APD

Answer 264

Most effective at SA and AV node which reduces rate and conduction

Answer 265

Affects _ventricular action potential_: all of these shotern maximum AP and rate of depolarisation 1a: _Quinidine_: moderate Na+ block (also affects Ifunny no atrium) 1b: _Lignocaine:_ mild Na+ block 1c: _Flecainide_: marked Na+

Answer 266

Above 4ug/mL starts to show side effects. The effective dosage is 2-3ug/mL so there is a small therapeutic window. Na+ channels found in skeletal muscle and CNS so side effects are found with higher doses Given IV in acute situations to restore rhythm. It's also a local anaesthetic is given topically instead of IV.

Answer 267

Prevents sympathethic activation on cardiac muscles. So it decreases sinus rate, conduction velocity and aberrant pacemaker activity. Stabilises membranes in Purkinje fibres Adverse effects include: Bradycardia, reduced exercise capacity, hypotension, AV conduction block and cause hypoglycemia and bronchoconstriction (Blocks B2 activation)

Answer 268

Used for ventricular arrthymias caused by re-entry of conduction and muscle damage - Prolongs cardiac action potential (slowing Phase 3 repolarisation of ventricles) Leads to reduced re-entry but can cause _increased trigger events_ (slower pulse and act during non-refractory periods) - Example: Amiodarone - blocks Na+, Ca+ and B adrenoceptors. Side effects: Reversible photosensitisation, skin discolouration and hypothyroidism and pulmonary fibrosis with long term use. UNIQUE.

Answer 269

Verapamil acts preferentially on SA and AV nodal tissue (Ca²⁺ for initiation of AP - used for _atrial tachycardias_) It slows conduction velocity and increases refractoriness May cause facial flushing, peripheral oedema, dizziness, bradycardia, headache and nausea

Answer 270

Stroke, AMI, ischemic heart disease, cardiac heart failure, aortic aneurism, renal failure, death

Answer 271

Smoking, diet, weight and stress

Answer 272

Reduce the known risk factors: risk, diet (alcohol, salt, saturated fats), weight and stress

Answer 273

This will lower our cut off for hypertension

Answer 274

NA --\> a1 adrenceptors, B1 adrenoceptors and the kidneys (Renin) a1 - blood vessel constriction B1 - heart (rate and contractility) Kidneys - Renin -\> ANG II ANG II \> acts on kidney to release renin, positive feedback to SNS, release of aldosterone, affect the heart contractility, vasoconstrict blood vessels

Answer 275

ABCD - Angiotensin system, B-adrenoceptor, Ca²⁺ blockers and Diuretics

Answer 276

B1 receptors on kidney \> Renin \> Ang I \> (ACE) ANG II \> acts on AT1 receptors Cell growth (heart and blood vessels), vasoconstriction, aldosterone (salt and water retention) and enhances sympathetic system (positive feedback)

Answer 277

It prevents the production of ANG I to ANG II. Reduces vascular tone, aldosterone production and cardiac hypertrophy. Bradykinin is not broken down Adverse effects: First dose hypertension, dry cough, loss of taste, _hyperkalaemia_ (use with thiazide diuretics), acute renal failure. _Contraindications:_ Pregnancy, bilateral renal stenosis and angioneurotic oedema E.g. Captopril, Enalapril. Perindopril

Answer 278

Blocks AT1 receptors causes reduced vasoconstriction, aldosterone, cardiac hypertrophy, sympathetic activity. Adverse effects: similar to ACEi but without dry cough - has kyperkalaemia (+ thiazide diuretics), headache, dizziness. Same contraindications are ACEi - pregnancy and renal stenosis E.g. losartan, candesartan

Answer 279

B-adrenoceptor antagonists which reduces cardiac output and reduce renin release (also affects blood volume, TPR) Lipid solubility of these drugs can affect the CNS - lucid dreams E.g. Propranolol (non-selective B), Atenolol (B1 selective)

Answer 280

Cold extremities - due to reflex a1 activation and blocking B2 receptors Fatigue - reduced CO (B1 blocking) it is _contraindicated_ in diabetes. As well as from B2 blockage (constriction of skeletal muscle vessels) Dreams, insomnia - lipid solubility Bronchoconstriction - B2 blockage in airway smooth muscle _contraindicated in asthma_

Answer 281

Asthma, diabetes, AV block and take care with heart failure and metabolic syndrome. Generally want to select for human heart/kidney therefore B1 selectivity is preferred

Answer 282

Inhibits L-type calcium channels found in the vasculature and in the myocardium \> reduces cardiac/vasculature contractility There are cardiac and vascular selective drugs. Non-selective: verapamil, Diltiazem (less pronounce on cardiac cells) Vascular selective: _Dihydropyridines_ - Felodipine and Nifedipine

Answer 283

Both types of blockers show: oedema, flushing and headache (due to dilation of blood vessels) Verapamil, Diltiazem - also causes bradycardia Dihydropyridines - Reflex tachycardia since blood vessels cannot reflex contract

Answer 284

Decreases Na+/Cl- reabsorption in renal tubules this means there will be increase water excretion from kidney. Also means a _loss of K+_ from collecting duct. This lowers blood volume and decreases blood pressure.

Answer 285

K+ loss, gout, hyperglycemia, allergic reaction. K+ loss is why you use it in combination with ACEi E.g. Hydrochlorothiazide

Answer 286

Information collected at one point in time, subject contributes data only once (_no follow up subject_) Data is collected through questionaires, examinations investigations Attain _prevalance_ numbers Can explore associations among variables but it provides weak evidence for causality

Answer 287

Compares _previous_ exposure status between people with and without the outcome. Controls are matched with cases to eliminate confounders. - Researcher comes in once outcome has happened Used to study _rare disease_ Key output = Odd ratios (approximation of relative risk conferred by exposure) These are non-longitudinal so cannot estimate incidence measures

Answer 288

It is simply the same as relative risk.

Answer 289

This is longitudinal study that has follow-up on the subjects. Can collect _incidence_ data. Compares outcomes between subgroups (not exposed vs exposed to risk factor). Derives _relative risk_ These studies can include multiple exposures and outcomes - Difficult to study rare diseases Research hypotheses can be addressed *post hoc* in established cohorts

Answer 290

Prospective and retrospective cohort studies. The difference is when the researcher comes into the picture but they still follow up on the patients. Key: explicit knowledge about the temporal relationship (time course) between exposure and outcome

Answer 291

Recruited 5000 people and follow up to them looking at the risk factors of stroke and cardiovascular disease.

Answer 292

It confirmed risk factors and looked at the relationship/interplay of more than one risk factor

Answer 293

All stroke patients have active follow up for three months after the episode. There are plans to do 'passive' follow up by database linkage across hospitals

Answer 294

Bias is an error or systematic difference between groups that cause under/over estimation of true results. The two main types of bias is selection bias (from people) and information (measurement - how we collect data) bias

Answer 295

Usually the selection of participants (from those who volunteer) are systematically different from the other groups. Does not give a generalising cross-section of the population. - May be systematic differences in the case and control groups purely because they are from different sources (hospital vs community) - Systematic differences between those who drop out and those who don't

Answer 296

- Recruit a representative sample and have case/controls from the same source - Maximise response - Minimise lost to follow-up

Answer 297

Systematic differences from method of information collection (especially subjectivity). Recall bias: between subjects with and without MI Women seeking help first: gives a suggestion that women are more biased to disease despite simply more volunteering

Answer 298

Using standardised tools and objective assessment of the participants.

Answer 299

This is a third factor involved that independently affects outcome but also has a relationship with the exposure

Answer 300

Usually it is age and sex. 1. Age: Association between use of blue hair rinse and bowel cancer 2. Sex: Association between baldness (exposure) and CVD (outcome) Men tend to be bald and also higher risk of CVD.

Answer 301

Matching by confounder and restriction. In the analysis stage use restrictions, stratification (analysis by sub-group) and multivariate analysis

Answer 302

Epicardium (outer), myocardium (muscle and capillaries) and endocardium (inner)

Answer 303

Contains a simple squamous cell, _sub-epicardial connective tissue_, blood vessels, fat and nerve tissues

Answer 304

Endothelial layer, sub-endocardial connective tissue and _conducting tissue_

Answer 305

Striated muscle forms myocardium that can contract spontaneously, cells are small, central nucleus, joined by intercalating discs, gap junctions - to electrically couple cells locally.

Answer 306

This is achieved via conduction pathway found in the endocardium - Purkinje fibres. DO NOT initiate heart beats.

Answer 307

These are modified cardiac muscle cells - larger. It has loss its contractile function, full of glycogen and forms bundles in the _sub-endocardium connective tissue_

Answer 308

Tunica intima, media and adventitia (innermost to outer)

Answer 309

Tunica Intima

Answer 310

Tunica Adventitia

Answer 311

It has a simple squamous epithelium (endothelium), lies on a basal lamina which is then supported by a thin layer of connective tissue, Endothelial cells bulge and are elongated in the direction of blood flow.

Answer 312

Actively inhibits the clotting process, but in the underly sub-endothelial connective tissue there are Von Willebrand factors that cause clotting. Endothelium also releases vasoactive substances such as NO and endothelin

Answer 313

Middle layer that contains smooth muscle which is arranged concentrically so it constricts lumen. This increases blood pressure. Also has elastin in its structure.

Answer 314

The smooth muscles themselves produce the connective tissue

Answer 315

Connective tissue found - collagen type I, elastin, ground substance and fibroblasts. Acts to anchor to surrounding tissue. If the vessel is large enough it has its own blood supply _Vasa vasorum_

Answer 316

These are found closer to the heart due to the BP fluctuations. The elastin in the media stores energy and then compresses the blood for continuous flow.

Answer 317

They distribute blood to tissue with elastin in the media. Elastin found in two places - internal and external elastic laminae. Internal (found subendothelial) and external found between media and adventitia. Contractions regulate blood pressure

Answer 318

These are very small arteries and contribute the most to blood pressure - resistance is the power of 4 inversely.

Answer 319

These are intermediate vessel with incomplete smooth muscle coat. Single smooth muscle cells act as sphincters controlling capillary flows.

Answer 320

These have diameter less than that of RBC, thin walled to help exchange, most cells in the body are very close to a capillary. - No identifiable media (SMC) Made of single endothelial rolled into a tube, sealed with tight junction, basal lamina, sometimes it has pericytes (media), surrounded by only a few collagen fibres (adventitia)

Answer 321

These are thinner capillaries than normal which are found in pancreas, intestines and endocrine glands.

Answer 322

Blood is collected in the veins - about 70% of blood and acts as a blood reserve.

Answer 323

Have the same layers as arteries. But which a thinner media and a thicker adventitia. Veins have valves to force blood one way. Blood is pushed through the vein by muscular contraction

Answer 324

Blood from capillaries then moves into the venules. The media is initially SMC but then replaced by smooth muscle. - This is the site of diapedesis of leukocytes.

Answer 325

Adventitie is gradually enlarged at the expense of the media. This is to allow it to resist the hydrostatic pressure especially when the volume increases.

Answer 326

Extracellular fluid drainage, it has very thin walled and valves

Answer 327

Absense of red cells, some white cells present, with valves and the large vessels look like veins

Answer 328

Contain blood in normal pressure, not leaky and not clotting. As well as interact with blood components when appropriate - inflammation and coagulation

Answer 329

Yes it can but this will cause thickening/fibrose

Answer 330

Elastic arteries - has many layers Muscular arteries - has two layers internal and external elastic lamina - This layer is thicker in the arteries than veins to allow for pulsatile blood flow and maintain blood pressure

Answer 331

Primarily made of connective tissue filled with fibroblast, collegan and blood vessels

Answer 332

Disease of wear and tear (arterioslerosis and arteriolosclerosis), atherosclerosis, aneurysm, dissection, thrombosis, embolism all leading to Ischaemia and infarction

Answer 333

The intima is damaged and leads to thickening of arteries.

Answer 334

This is commonly seen in ageing and hypertension. It leads to arteries losing elasticity and narrowing lumen.

Answer 335

It impairs the artery's ability to control blood pressure and can impair blood supply to subsequent tissues

Answer 336

SMC produce too much matrix and protein from the blood then leaks through damaged endothelium (immunoglobulin and albumin). This is known as_ hyaline arteriolosclerosis_ this is just a glossy look and smooth walls.

Answer 337

This is the damage and thickening of the intima in the arterioles - that has a glossy look. Leading to poor blood supply to tissues and possibility of microaneurysms and haemorrhage (gunk that can be extended and bleed)

Answer 338

Cerebral haemorrhage, benign nephrosclerosis (ischaemia from narrowed arterioles) and retinopathy

Answer 339

This is the blocking of arteries that involves a build up of inflammatory, fibrotic, necrotic and fatty materials. ## Footnote **Must have fibrous cap and necrotic lipid core**

Answer 340

It can slowly narrow arteries or rupture catastrophically

Answer 341

1. Fatty streaks 2. Damage, inflammation, cholesterol and fibrosis 3. Stable atherosclerotic plaque 4. Unstable atherosclerotic plaque

Answer 342

These are foam cells (macrophages that ingested lipids) found in the intima.

Answer 343

It is a fibrous cap with a necrotic lipid core and chronic inflammatory cells

Answer 344

Foam cells, inflammatory cells (mononuclear), cholesterol clefts (clean needle shaped spikes), calcification, _thickened intima_, narrowed lumen, fibrous cap, necrotic core, _thinned media_ (inability to get blood through thickened intima) and neovascularisation

Answer 345

1. Dystrophic calcification - areas of cell degeneration 2. Metastatic calcification: serum calcium levels are too high that they are above the precipitation threshold and form in blood vessels and kidneys.

Answer 346

Vulnerable Plaques are prone to acute plaque event, which is rupturing. Often occurs in plaques with thin fibrous cap (with ulceration), larger necrotic core and has more inflammatory cells. But vulnerable plaques take up less stenosis so are generally asymptomatic

Answer 347

When something goes wrong in the plaque. - Plaque rupture, haemorrhage into plaque or erosion of endothelium. Leads to thrombosis, thromboembolism, atheroembolism

Answer 348

Chronic ischaemia when \>70% stenosis - leading to stable angina or peripheral vascular disease (claudication - ischaemic leg disease) Aneurysm - weakening of media and can risk rupture/haemorrhage

Answer 349

Non-modifiable: Age, gender, family history, certain genes, already having atherosclerosis Modifiable: smoking, diabetes, high BP, cholesterol and sedentary lifestyle

Answer 350

Endothelial dysfunction/activation is the start of atherosclerosis. The endothelium becomes leaky and adhesive to WBC, produce cytokines and growth factors and is now pro-coagulant. Takes up LDLs into intima (once activated and gets oxidised) and becomes pro-inflammatory. Also allows monocytes into intima (macrophages enters phagocytose oxidised LDL and produce inflammatory cytokines.

Answer 351

HDL take up lipid from the peripheral. LDL accumulates in the intima and oxidises. Toxic to endothelium and other cells. Taken up by macrophages and SMC (form foam cells). Which stimulates inflammatory cytokines and produces free radicals in intima

Answer 352

The process of atherosclerosis is started by cholesterol but sustained by cytokines. Inflammation perpuates endothelium dysfunction via cytokines. - RoS, cytokines, MMPs

Answer 353

It migrates to intima and changes phenotype by - proliferating and producing ECM. Produces collagen and the _fibrous_ cap

Answer 354

This is abnormal dilatation of blood vessels due to weakening of the media.

Answer 355

There is a risk of rupture and haemorrhages. There are true and false aneurysms. True - All three layers are dilated (saccular vs fusiform) False - blood enters the adventitate layer

Answer 356

Aneurysm associated with atherosclerosis due to weakened ECM. Generally contains thrombus (which can emoblise). Risk of rupture when it increases above 5cm diameter.

Answer 357

This is found in the cerebral circulation, weakening due to congenital defect. Major cause of subarachnoid haemorrhages.

Answer 358

This is when we get blood in the media (rupture of intima and blood enters media). Highly associated with hypertension. Classified into type A and B dependent on how close it is to the aorta

Answer 359

Embryo - hyperplasia then stops after a few months Childhood then undergoes cell hypertrophy which parallels to body growth. LV is thicker than RV.

Answer 360

Depends on body size/surface area, genetics, blood pressure, athletic conditioning and ANG II

Answer 361

Increase in LV mass relative to body size

Answer 362

Thickness/Diameter LV wall thickness/LV chamber size

Answer 363

LV dimensions measured by echocardiography or MRI. Can use this to calculate volume which then can be used to find the mass (myocardial specific gravity)

Answer 364

Changes in size and function occurs after injury.

Answer 365

Myocardial infarction, volume overload (valve dysfunction), pressure overload (aortic larger pressure or aortic stenosis) and cardiac damage (myocarditis)

Answer 366

Concentric (Increase LV mass and wall thickness) and eccentric (increase LV mass and no change to wall thickness) And remodeling - normal LV mass and increase wall thickness

Answer 367

Concentric from pressure overload and sarcomeres in parallel. Eccentric from volume overload and sarcomeres in series

Answer 368

Thick, dilated, thick and dilated, intermediate

Answer 369

Increase myocardial cell size (more mitochondria, myofibrils, SR), increase fibroendothelial cell numbers and increased interstitial matrix.

Answer 370

Thicker walls will reduce and normalise wall stress. This is to maintain LVEDP and CO.

Answer 371

To compensate for the volume load. In order to maintain stroke volume, increase LVEDV and increase ejection fraction.

Answer 372

At one point there is marked ventricular dilatation, with marked reduced systolic function and CO. Increase LDEDV, increase LVESV and decrease ejection fraction. Leads to increased LVEDP and eventually cardiac failure

Answer 373

Pressure overload, volume overload, myocardial infarction, following cardiac injury, obesity, diabetes, renal failure and infiltration (proteins are laid down in the heart) Hypertrophic cardiomyopathy and Fabry's disease (enzyme function loss - renal failure) for genetics

Answer 374

Forceful apex beat, ECG (tall voltage and T wave inversion), CXR, Echo, MRI and Cardiac CT

Answer 375

Will see asymmetric septal hypertrophy (septum is thickened)

Answer 376

Angiotensin, Aldosterone, catecholamines, local factors and some cellular & molecular mechanisms

Answer 377

Increased risk of ischemic heart disease, cardiac failure, atrial fibrillation and stroke. Functionally: diastolic dysfunction (ventricles are stiff and do not fill easily)

Answer 378

Concentric hypertrophy \> eccentric \> concentric remodelling

Answer 379

Thick muscle is stiff, increased LVEDP to achieve same LVEDV. Leads to increased LA and pulmonary vein pressure. - Likely pulmonary congestion - Making us sensitive to both fluid loading (heart failure) or dehydration (low BP) - Makes atrial kick more important - atrial fibrillation

Answer 380

Underlying problem (valves?), hypertension and weight loss

Answer 381

Believe its caused by Renin-Ang-Aldos system, adrenergic, endothelin, cytokines and local factors. So prevent this by: Angiotensin and B-adrenergic blocking

Answer 382

Congenital, pulmonary hypertension (lung disease - pulmonary arterial hypertension, pulmonary embolus and chronic L heart failure), right heart valves (pulmonary stenosis/regurgitation and tricuspid regurgitation)

Answer 383

Autosomal dominant, mutation in sarcomere proteins, most commonly in B-cardiac myosin heavy chain, cardiac myosin binding protein and cardiac troponin I and T

Answer 384

Varying marked hypertrophy at the septum -Increased LV thickness, hypertrophy, myocyte disarray, LV outflow tract obstruction, diastolic dysfunction. _Ventricular arrhythmias_ - especially big risk with hypertrophy

Answer 385

Mild to asymptomatic LVH But with severe LVH: outflow obstruction, ventricular arrhythmias, shortness of breath, heart failure, syncope and sudden cardiac death

Answer 386

Multiple causes but perhaps genetics. Particularly mutation in cytoskeleton.

Answer 387

Bradycardia normal with increased exercise training. Moderate exercise reduces the risk of heart attack and stroke.

Answer 388

Found in competitive athletes, eccentric hypertrophy (RV) with normal cardiac function - usually regresses with deconditioning. May become enlarged in RV, will not regress after deconditioning and is a possible cause of ventricular arrhythmia

Answer 389

Rate, contractility, afterload resistance and preload (venous return)

Answer 390

Larger sarcomere length, increase cross bridges, increase sensitivity of Ca²⁺ of troponin and finally increase force of contraction

Answer 391

Increase preload (EDV), increase cardiac contraction and increase SV and CO Larger force generated with bigger stretch of the heart

Answer 392

Dehydration - Low CO and BP (drop in BP, drop in VR and decreased SR) Fluid overload - Oedema (Increase in VR will cause increase in CO at the expense of fluid leaking out of the tissue)

Answer 393

1. Catheter inserted via vein and through the tricuspid valve. 2. Measure the RA pressure because RA pressure = ventricular pressure = _Jugular Venous Pressure_

Answer 394

1. Catheter inserted via an artery across the aortic valve 2. Measure the LA pressure since Artial pressure = ventricular pressure = _pulmonary artery wedge pressure_

Answer 395

Catheter entered into the pulmonary artery, balloon is blown up which blocks it. Momentarily the tip only measures the pressure ahead of the balloon which will measure the _pulmonary venous pressure_.

Answer 396

Measured after the arteriole from the pulmonary artery to the pulmonary vein. Making the pulmonary venous pressure the significant contributor to the pressure. Usually lower than the pulmonary artery pressure.

Answer 397

Artery \> arteriole (this usually restricts the pressure) so it is mainly venous pressure in the capillary. Gradient (hydrostatic pressure) decreases as it goes towards the veins. Osmotic pressure (oncotic pressure from proteins pushes fluid into the capillary).

Answer 398

Causes fluid to leak out and cause oedema. Excess fluid cannot be taken out by the lymphatics quickly enough. Increase in arterial pressure is simply blocked off by the arteriole.

Answer 399

Increased venous pressue (heart failure), decreased osmotic pressure (loss of proteins - renal/liver failure), blocked lymphatics (cancer invade lymph nodes) and increased capillary permeability (infection)

Answer 400

1. Measure of ventricle filling (pre-load) 2. Measure of venous pressure driving fluid out of capillaries. Left - Preload LV function and measure of lung capillaries Right - Preload RV function and measure of peripheral capillaries (JVP)

Answer 401

At a particular point when the EDP excedes - it will cause fluid to begin to leak out. (Usually associated with increase in CO too)

Answer 402

This is when the cardiac output is less than what the body requires. -Usually due to systolic failure (loss of contractility) rather than increase in body needs (very rare)

Answer 403

The curve is lower in CO at every point of LVEDP.

Answer 404

Maintain CO by increase fluid retention (pushing LVEDP higher). But this leads to oedema in legs and lungs (pulmonary congestion). Reduced oxygenation also leads to shortness of breath

Answer 405

Compenstion for decrease in contractility is right before the LVEDP needed for pulmonary congestion to begin

Answer 406

When CO is low and the lungs become congested because of the increase in LVEDP (causing pulmonary congestion)

Answer 407

Oedema due to increase in venous pressure NOT arterial pressure. Arterial pressure may put a strain on the ventricles which may _eventually_ lead to ventricular failure.

Answer 408

Mechanisms are usually loss of myocardial muscles (ischemic heart disease and cardiomyopathy), pressure overload and volume overload

Answer 409

Ischemic heart disease valvular heart disease, hypertensive, congenital, cardiomyopathy, _cor pulmonale (right hear)_ - right heat failure due to severe lung disease and pericardial disease (thickened and filled with fluid)

Answer 410

Right heart failure - oedema Left heart failure - Shortness of breath, fatigue, tachycardia (to maintain CO) and lung 'creps' (crackles in lungs)

Answer 411

Na+ and water retention (to increase EDV), K+ loss, vasoconstriction, Renin-Ang-aldosterone system and sympathetic nervous system

Answer 412

Decrease in cardiac output intially \> decrease renal blood flow \> activate RAS \> fluid retention, Na+ retention, K+ loss (most likely arrhythmia) and vasoconstricton (increase afterload)

Answer 413

SNS stimulated \> release NA \> increase contractility \> long term deleterious effect \> vasoconstriction, _arrhythmias_ (ventricular) anad direct toxic effect

Answer 414

Increase LVEDP, Increase CO, Increase LAP, Increase Pulmonary venous pressure, fluid leaks out of the pulmonary capillaries, pulmonary congestion, _shortness of breath_

Answer 415

Na+ and water retention \> Increase RVEDP \> Increase RAP \> Increase JVP \> peripheral oedema and _liver_ congestion

Answer 416

Global heart disease (cardiomyopathy), specific right heart diseases (RV cardiomyopathy, Right valves, shunts, pericardial disease, pulmonary hypertension, lung disease or pulmonary embolism) OR due to Left heart failure: Pulmonary venous hypertension, pulmonary congestion, chronic hypoxia, pulmonary vasoconstriction (via _endothelin)_, pulmonary arterial hypertension leading to right heart failure

Answer 417

It has normal systolic function, reduced LV compliance (due to scarring from infarct or stiff from hypertrophy), increased LVEDP to fill the LV and therefore increase pulmonary venous pressure.

Answer 418

Main goals are to _remove fluid (decrease preload) and vasodilate (decrease afterload)_ Diuretics, Aldosterone antagonists, ACE inhibitors, Ang receptor antagonists

Answer 419

By reducing preload we reduce the pulmonary venous pressure therefore no longer have pulmonary congestion. But we may reduce CO too low and reduce BP. Decrease in afterload (vasodilation) will increase the Starling curve - allowing better CO per a particular LVEDP

Answer 420

Digoxin (mild positive inotropic effects), B-blockers to protect heart from toxic effects of NA Positive inotropic drugs only helpful in the short run

Answer 421

Coronary artery bypass, valve replacement, hypertension, biventricular pacemaker, implantable defibrillator and cardiac transplantation.

Answer 422

ACE inhibitors, B blockers, Aldosterone antagonists, biventricular pacing and implantable defibrillator.

Answer 423

It contains the thymus which cannot be seen in post-mortum. Fat and lymph nodes are also found here.

Answer 424

Yes it can (oesophagus)

Answer 425

This is the area right above the heart. From the anterior perspective into the posterior. Thymus \> great veins \> aortic arch, vagus + phrenic nerves \> trachae, oesophagus, thoracic duct and Left recurrent laryngeal nerve Thymus is only present during adolescent

Answer 426

It is located to the right side more because the veins need to drain into the RA which is found towards the right.

Answer 427

This is the vein where the subclavian vein and internal jugular vein drain into. The left BC vein is longer and more horizontal than the right (it must travel to the right side to form the SVC).

Answer 428

At the first right costal cartilage

Answer 429

It is pretty much vertical from the SVC so it provides the closest measurement to the RA pressure.

Answer 430

At the third right costal cartilage.

Answer 431

These are veins that collect blood from the entire thorax region.

Answer 432

It runs against the back of the posterior aspect then it arches forward to plug into the posterior aspect of the SVC. This happens at the second costal cartilage.

Answer 433

The phrenic nerve and the vagal nerve

Answer 434

The aorta extends upwards, posteriorly and to the left. This will extend until the level of T4/5 where it will will begin to descend. This occurs above the left lung root.

Answer 435

This is where the two coronary arteries are found.

Answer 436

This is the remnant of the duct that bypassed the blood form the pulmonary trunk into the aorta.

Answer 437

The BC trunk comes off first which then splits into the right common carotid and subclavian artery. The branch is found to the right of the trachae. The next branch to come off is the left common carotid artery. Both the right and left common carotid artery forms a 'v' shaped grasp over the trachae. Finally the third branch is the left sub-clavian artery.

Answer 438

No it is not necessarily in the usual fashion. A key anomaly. The right common carotid artery and subclavian artery do not branch off from a BC trunk. The right sub-clavian artery branches off last in the arch so it must come back around to the right side. It travels _behind_ the oesophagus and can make it difficult to breath.

Answer 439

Phrenic nerve C3,4,5 keeps the diaphragm alive. Comes from the nerve and runs down along the scalenus anterior then passes _between_ the subclavian vein and artery. It will always pass anterior to the lung roots on both sides. Phrenic nerve are always the most lateral structure in the mediastinum (taking the central as the border). The phrenic nerves then pierces the diaphragm since it supples it too.

Answer 440

The right phrenic nerve runs lateral to the _venous_ structures (SVC, atrium and IVC). It will pierce the diaphragm with the IVC. The left phrenic nerve is lateral to the _arterial_ structure (aortic arch and Left ventricle). It will pierce the diaphragm at the apex of the heart with its own hole.

Answer 441

Done by the phrenic nerve motor nerves. Sensory nerves are also sent to the mediastinal + diaphragmatic pleura and pericardium

Answer 442

T8 - caval opening T10 - Oesophageal hiatus T12 - Aortic hiatus (From top to bottom in the picture)

Answer 443

It is directly adjacent to the IVC (caval orifice)

Answer 444

Begins in cranial cavity \> neck \> thorax \> abdomen It descends through the neck postero-lateral of the common carotid artery (aims to be anterior aspect of oesophagus). Comes down with the bundle (IVJ, common carotid artery and vagus nerves). _Moves_ behind of the lung root. Then moves anterior to oesophagus.

Answer 445

It will pierce it at the level of T10 with the oesophageal hiatus.

Answer 446

As the right vagus nerve moves anteriorly to form the oesophageal bundle and it gives contribution to cardiac and pulmonary complexes.

Answer 447

Vagus nerve heads posterior as the phrenic nerve heads anteriorly. Lateral to aortic arch, moves behind the lung root, then runs anterior to the oesophagus.

Answer 448

This is when the left vagus nerve misses a spot. It must go back up as it does it hooks under the ligamentum arterios. Then it tucks into the left trachae oesophageal groove.

Answer 449

The recurrent nerve remembers earlier than the left. It is found at the level of the right sub-clavian artery.

Answer 450

The trachae is found in this area and bificates at the T4/5 level. Descends down the superior mediastinum and along the posterior mediastinum. The oesophagus is the next structure behind the trachae.

Answer 451

As it runs down oesophagus is mid line and the aorta is the left. As it reaches the diaphragm the oesophagus moves slightly to the left and the aorta is now more mid line.

Answer 452

At the superior start and the inferior end has normal narrowing. In the middle there are also narrowing by the aortic arch impinging on the oesophagus.

Answer 453

Runs along the back of the oesophagus. Down to the aortic hiatus at T12 between the pleura. Drains all the upper limb and abdomen lymph nodes to it. Travels up the thorax slightly to the left. It will arch to the left and drain into the IJV and the subclavian vein. As it descends it also drains the lymph from the left side of the head, neck, limb and abdomen. The right upper limb and the right side of the thorax enters to the SVC at the level of subclavian and IJV. It splits it into 1/3.

Answer 454

This is the upward pathway. Travels between the descending aorta and azygous vein. Then moves posteriorly left then drains into the IJV and subclavian vein at T5.

Answer 455

There is the descending aorta, oesophagus plexus, thoracic duct, azygous system of veins.

Answer 456

Intercostal, bronchial, pericardial and oesophageal

Answer 457

Most variable system in the body. Everyone has a right sided vertical azygous that lies on the posterior wall and arches into the posterior aspect of the SVC.

Answer 458

Antibiotics are naturally occuring

Answer 459

Chemotherapeutic are synthetic whereas semi-synthethic are modifications made to naturally occuring agents.

Answer 460

This is so we can alter the pharmacodynamic and pharmacokinetics of the naturally occuring agent to suit our therapeutic needs. - Or to extend patents

Answer 461

There are bacteriostatic and bactericidal (which actively kills bacteria and needs 3log reduction - 99.99%)

Answer 462

Bacteriostatic agents are fine as long as they have a functioning immune system. Use bactericidal drug in the case the immune system is compromised. Most cases the two different drugs make no difference.

Answer 463

Antibiotics. Usually has rapid elimination from the blood so needs multiple doses. Modified drug allowed it to stay longer in blood.

Answer 464

Penam (penicillin) first one to be discovered.

Answer 465

Naturally occuring antibiotic. Really good because it has no toxicity unless you are allergic. However it does need to be injected.

Answer 466

Used for GPC, GPR and GNC (but not for pseudomonas, it is for E.coli) Weak orally, and very low toxicity

Answer 467

Used against GPC, GPR, GNC But its good orally and has low toxicity

Answer 468

It is used for GPC (but especially for GPC - Penicillin resistant Staphylococcus). Two disadvantages was that it needed to be injected and it had some toxic effects on the liver and renal.

Answer 469

Methicillin resistant Staph Aureus

Answer 470

Works a broader spectrum than penicillin G and V. Active against: GPC, GPR, GNC and _GNR_ Works well orally and has no toxicity. Extension to this molecule is amoxicillin.

Answer 471

Works specifically for GNR (pseudomonas) but often needs large doses. Very weak orally and low toxicity.

Answer 472

_Cell wall_ (B-lactams and glycopeptides), cytoplasmic membrane - not as good because it is similar to ours, _ribosomes_ - smaller than ours so they can be a good target, _nucleic acid,_ and folic acid (we need to ingest it but bacteria produce it themselves for use).

Answer 473

Quinolones acts on DNA folding and rifamycin acts on transcription

Answer 474

The layer is made up of alternating N-acetyl-glucosamine and N-acetyl muramic acid (derived from the glucosamine). Off the Muramic acid it has a peptide chain coming off it which then binds to a pentapeptide bridge to connect the layers (to the next peptide chain)

Answer 475

The peptide chain has alternating D and L-amino acids - giving it the rigid effect. L-Lys binds to above pentapeptide bridge. D-ala binds to the bottom pentapeptide bridge.

Answer 476

Precursor made in the cytoplasm. Becomes immobilised on inner aspects of plasma membrane. Then synthesis of building block. Once this is down its exported to the exterior membrane and links to the growing peptidoglycan chain.

Answer 477

The glycine on the pentapeptide chain replaces the second D-ala in the chain.

Answer 478

Vancomysin are glycopeptides used to treat MRSA. They act by binding directly to the D-ala, D-ala terminal directly, this prevent cell wall production.

Answer 479

This is because the vancomycin is large sized and negatively charged complex. Cannot transport through the cell membrane of the Gram -ve bacteria.

Answer 480

The cells instead of having two D-ala it is substituted by another sugar - _D-lac._ These are Gram +ve cocci.

Answer 481

Vancomysin intermediate resistant Staph Aureus. They confer resistance by producing a thicker peptidoglycan wall.

Answer 482

The cross linking process is catalysed by transpeptidases or penicillin binding proteins. Drugs are able to bind to this enzyme that catalyse these reactions.

Answer 483

The structures are very similar. So when penicillin G is given the transpeptidase will bind and cleave the pencillin G instead of the D-ala. Once the enzyme is used it also becomes inactivated. Penicillin is bactericidal - lack of cell wall causes the bacteria to respond by breaking down the wall.

Answer 484

The cell wall is destroyed and because the cytoplasm is hypertonic fluid will flow into it.

Answer 485

These are able to hydrolyse B-lactam bonds found in the penicillin which confers penicillin resistance.

Answer 486

1. B-Lactamase 2. Altered penicillin binding protein (new transpeptidase that does not bind to penicillins anymore)

Answer 487

Some bacteria have different penicillin binding proteins, hard to access the PBP and the susceptibility of antibiotic to B-lactamase.

Answer 488

This is a B-lactamase inhibitor so it prevents bacteria from hydrolysing B-lactam rings on particular antibiotics.

Answer 489

This is so that the amoxillin can be effective against bacteria that produce B-lactamase as resistance.

Answer 490

Recognition - _aminoglycosides_, tetracyclines Peptidyl transfer, translocation, isoleucyl-tRNA synthesis, formation of initiation complex.

Answer 491

_Tobramycin_ acts on the recognition stage of protein synthesis. There is also gentamicin and amikacin

Answer 492

It interferes the recognition process by binding to the tRNA side and distorts it - essentially preventing protein synthesis.

Answer 493

1. Modified outer membrane leading to reduced entry 2. Efflux 3. _Enzymatic modification_ to the aminoglycoside leading to reduced entry (making it polar) 4. _Ribosomal mutation_ leading to the reduced binding.

Answer 494

Drug inactivation (by hydrolysis or covalent modification), altering the target of drug action (modify target to less sensitive form or overproduce it (VISA)), reduce acess of drug to target (decrease influx and increase efflux) and failure to activate inactive precursor of drug (good against pro-drugs).

Answer 495

Platelets - stick to injured surface via vWF and contract and cemented with fibrin to form plug Thrombin - Coagulation cascade to eventually activate fibrinogen to form fibrin. Also activates platelets Fibrin - Stick to things

Answer 496

The normal endothelium produces thrombomodulin (inactivates thrombin) and does not bind platelets. Fibrinolysis - activation of tissue plasminogen activator (tPA) binds to fibrin and activates Plasmin - breaks down fibrin

Answer 497

This is a clotted mass of blood in an _unruptured_ CV system (within blood vessels) during life. It is also abnormal.

Answer 498

Platelets, fibrin, red and white cells.

Answer 499

This is lines of red and white layers which contain either red cells or platelets + fibrin layer. This is indicative of thr thrombus being formed within a living being.

Answer 500

Arterial thormbi - white due to higher proportions of platelets and fibrin. Occurs due to endothelial damage/dysfunction. Best prevented by aspirin. Venous thrombi - red due to higher proportions of blood cells (and fibrin), associated with _blood stasis and hypercoagulability_. Best prevented with _warfarin._

Answer 501

Usually an imbalance within the Virchow's triad. Blood flow, blood contents and endothelium

Answer 502

Loss of endothelium exposes collagen and vWF. But activation/dysfunction of endothelial cells will reduce anti-coagulant activity and increase pro-coagulant activity. - Causing thrombosis in the absence of injury

Answer 503

Can be caused by inflammatory cytokines, toxins, hypertension, cholesterol and smoking.

Answer 504

Causes turbulence and stasis so that there is loss of laminar flow. Cells that were not meant to touch the endothelium now do - activating the endothelium. Allows platelets to aggregate now.

Answer 505

Genetic (primary) is Factor V Leiden and Non-genetic (secondary) can be caused by cancer, smoking, obesity and age.

Answer 506

1. Dissolution - fibrinolysis: tPA, protein C and S 2. Organisation and recanalisation: Formation of granulation tissue with capillaries piercing it 3. Propagation: grow longer 4. Emoblisation: breaks off and clogs else where

Answer 507

This is an intravascular mass carried in the blood stream (away from the site of origin) which then blocks the vessel it lodges into.

Answer 508

Pulmonary embolus - from DVT lodged into pulmonary artery Arterial thromboembolism - Usually from atheroma or heart and will block a vessel downstream causing ischaemia and infarction. Other examples include: amniotic fluid embolism, septic embolism, atheroembolism, fat embolism and gas embolism

Answer 509

Significant thromboemboli arise from deep veins and usually travels to the right side of the heart and lodges into the pulmonary artery.

Answer 510

Involves turbulence and platelets adhering to dysfunctional blood vessel surface. Can lead to blockage where it forms. Can be embolised further down and cause ischaemia in that organ. Emboli from the heart can affect any organs downstream (rare for it to return back to the heart)

Answer 511

This is the inadequate oxygenated blood supply to tissues. Due to: Local vascular narrowing, increased demand for oxygen or systemic reduction in tissue perfusion.

Answer 512

This is tissue due as a result of the lack of oxygen.

Answer 513

Hypoxia is just the lack of oxygen whereas hypoxaemia is the lack of oxygen in the blood

Answer 514

Some tissues are more sensitive than others (neurons 3-5 minutes). Some organs have other blood supplies (lungs have bronchial and pulmonary). Chronic ischaemia may stimulate collateral supply.

Answer 515

Coronary thrombosis, thromboembolus from LA to the brain causing transient ischaemic attack, walking up steep hills with atherosclerotic arteries (angina and claudication), torsion or volvusion blocking a vein and shock (reduced blood supply to everything).

Answer 516

Atherosclerotic disease cause atrophy or lower limbs, renal artery stenosis causing renal atrophy and hyaline arteriolosclerosis causing benign nephrosclerosis.

Answer 517

This is infarction where there is blood entering the infarct area. Usually due to dual blood supply, collateral blood supply, venous infarction or reperfusion.

Answer 518

Infarction where there is no haemorrhage. Usually blockage of an end artery and found in most organs such as the kidney, heart and spleen.

Answer 519

This is a time dependent drug. Will increase ventricular contractility. But later it may cause late after depolarisation (dysrhythmias).

Answer 520

Inhibits Na+/K+ ATPase, increased Na+ inside cell will decrease calcium extrusion. Leaves more calcium in SR and therefore more calcium per contraction.

Answer 521

Low therapeutic index. Affects all excitable tissues. Half life of 40 hours because it has high affinity to muscle (Vd - 400L).

Answer 522

Gut (nausea, diarrhoea and anorexia), CNS (drowiness, confusion) and cardiac (ventricular dysrhythmia but treats _atrial dysrhythmias_)

Answer 523

Low K+ (less competition for digoxin), high Calcium (less gradient for calcium efflux so accumulates) and _renal impairment_.

Answer 524

Activation of the B1 adrenoceptor will cause an increase in cAMP and then increase calcium influx. Another drug that can do this is phosphodiesterases inhibitors which inhibit the degradation of cAMP. Then increasing calcium.

Answer 525

Intravenously for short term support of heart failure.

Answer 526

Increases cardiac work and O2 demand. They both have risks of arrhythmias (calcium build up).

Answer 527

Chronic overactivation of B1 receptors will lead to desensitisation. By reduced receptor expression and impaired B1 adrenoceptor coupling.

Answer 528

Inotropes are good for symptom relief, but it increases work. Disease does progress by chest pain, fainting then death. Cardiac muscles eventually remodel to cope.

Answer 529

Increase sympathetic outflow, vasoconstriction, renin stimulation, increase Ang II, aldosterone which _Increases_ both afterload and preload on the heart.

Answer 530

Venodilators - nitrates (used in angina and undergoes 1st pass metabolism and has tolerance) Diuretics - Frusemide is used to treat oedema and act on the Loop of Henle Aldosterone receptor antagonists Aquaretics: vasopressin receptor antagonists

Answer 531

Inhibit aldosterone on the cortex and distal tubules. - K+ sparing diuretic so it causes accumulation of K+. Improves survival with combination therapy in severe heart failure

Answer 532

Hyperkalaemia and renal function

Answer 533

Arterial vasodilators (cause reflex tachycardia), ACE inhibitors (affects both pre and afterload), AT1 antagonists (same as ACE inhibitors) and B-adrenoceptor _antagonists_.

Answer 534

Effective at all levels of heart failure. Improves both symptoms and disease progression (delays). Given as titrate dosage (so the body won't have huge reflex compensation). Can maintain at tolerated dose with other therapies.

Answer 535

Blockade of B1 still increases stroke volume. Need to titrate to maintenance dosage. It reduces tachycardia, cardiac work, inhibits renin release and protects against receptor down regulation.

Answer 536

Platelets attach to exposed collagen and activate. Release of ADP and 5-HT from platelets. The 5-HT is a potent vasoconstrictor.

Answer 537

ADP from platelets causes others to activate and change shape. Mediates (thromboxane) are synthesised. Platelets aggregate and adhere via fibrinogen briding between GPIIb/IIIa receptors Then soft plug is formed

Answer 538

Thrombin, ADP, thromboxane and collagen

Answer 539

Fibrin formed from fibrinogen. Fibrinogen is cleaved by thrombin. It must be produced by activation of prothrombin.

Answer 540

Extrinsic (in vivo): damaged tissues release _thromboplastin_ Intrinsic (in vivo in relation to blood): exposed collagen and other materials

Answer 541

The extrinsic pathway is much faster than the intrinsic becaues it has less steps.

Answer 542

Enzyme inhibitors such as antithrombin III -\> cascade inhibition Fibrinolysis by plasmin. Plasminogen activation requires. Thrombin + thrombomodulin, Protein C which inactivates the inhibitors -\> produces plasmin to cleave.

Answer 543

Coagulation, platelets and fibrinolysis

Answer 544

It enhances the activity of _antithrombin III_ which naturally inactivates Xa and Thrombin. Heparin binds to it to expose the active site.

Answer 545

LMW heparin acts in a similar mechanism. It has the same effect on Xa but less on thrombin. Heparin is large and not orally available. LMW heparin is not orally available and has a longer elimination half life (used for patients at home)

Answer 546

Inhibits along the intrinsic pathway of the cascade as well as the common pathway Thrombin and Xa.

Answer 547

Activated Partial Thromboplastin Time (APTT) Time for clot formation after you add calcium and contact activator. It is a measure of the intrinsic pathway.

Answer 548

Haemorrhage, thrombocytopenia (platelet deficiency) and osteoporosis (mechanism unsure) So we should use heparin during ICU then it shifts to oral medications (warfarin)

Answer 549

It is essential for the formation of factor II, VII, IX and X

Answer 550

Coumarin derivatives form _warfarin_. It inhibits the reduction of Vitamin K. This step then inhibits gamma carboxylation of glutamate factors II, VII, IX and X. It inhibits Vitamin K reductase.

Answer 551

It must work on clotting factors found in vivo. It has a delayed onset because it does not act on already active factors.

Answer 552

Haemorrhage - requires titrate dose and this is determined by INR Reversal: Can be achieved by Vitamin K (competing with warfarin).

Answer 553

It has unpredictable pharmacokinetics. It is rapidly absorbed and is strongly bound to plasma proteins (99%) so small changes makes significant changes.

Answer 554

Vitamin K deficiency, hepatic disease (impaired synthesis of clotting factors), hypermetabolic states (increased metabolism of clotting factors) and by drug interactions (drugs that affect cytochrome P450 will also affect warfarin and aspirin to impair platelet aggregation).

Answer 555

Pregnancy (it is contraindicated in pregnancy because its teragenic). Also by other drug interactions.

Answer 556

We test this by using PT (prothrombin time) - this is the time for clot formation after adding calcium and tissue factors. Tests the extrinsic pathway. Measured by using the international normalised ratio (INR).

Answer 557

LMW and orally available. It has more predictable dose-response which reduces laboratory monitoring. Indirect Xa inhibitor. Direct Xa and thrombin inhibitors.

Answer 558

ADP receptor antagonists, thromboxane synthesis inhibitors (aspirin) and glycoprotein IIb/IIIa receptor antagonists.

Answer 559

It undergoes first pass metabolism in the liver. But aspirin only needs to act in platelets found in the hepatic vein.

Answer 560

It is a monoclonal antibody used against the receptors and must be given intravenously.

Answer 561

It prevents ADP binding to its receptors on platelets and therefore prevent activation. It is typically given orally as a prodrug.

Answer 562

Streptokinase and Alteplase

Answer 563

They activate plasminogens.

Answer 564

Streptokinase - antigenic can only be used once intravenously Alteplase - Human recombinant tissue plasminogen activator (hrtPA), it's not antigenic, IV infusion, short half life and _more active on fibrin bound plasminogen_.

Answer 565

They open and close by changes in pressures.

Answer 566

Closing of the heart valves

Answer 567

1/3 systole and 2/3 diastole

Answer 568

70mL with 140mL EDV

Answer 569

SV/EDV - 50%

Answer 570

It is to hold the valves in place so that it won't fly into the atrium when the ventricle is in systole.

Answer 571

This is narrowing of valves that restricts flow. There is now a _pressure gradient_ across the valves. It will lead to higher pressure in the previous chamber. Pressure overload

Answer 572

This is valve regurgitation where the valves do not fully close and the blood flows back into the previous chamber. Heart will need a larger EDV to pump the same SV again. Increases ejection fraction. Volume overload

Answer 573

This is just turbulence of blood usually around stenosed or incompetent valves - causes _murmurs_ Visible in echo cardiogram High flow can cause innocent murmurs (children, fever, anaemia and pregnancy)

Answer 574

Sometimes due to previous rheumatic fever. Now its mostly due to degenerative conditions (may be congenital).

Answer 575

Mild and moderate lesions are generally asymptomatic and the heart can easily compensate for this level of lesion. To the point where some severe lesions can be asymptomatic for a few years.

Answer 576

Eventually ventricular enlargement is too big and this is an irreversible failure. Leads to shortness of breath (which is a late feature which indicates poor prognosis). The irreversible LV changes usually occurs at the time of regurgitation. But in aortic stenosis it indicates the time to intervene - LVH changes can regress.

Answer 577

History, examination, ECG and most importantly echocardiography. Echo can show LV changes before they are irreversible in aortic and mitral regurgitation.

Answer 578

Mitral valvotomy (using finger to pierce scar tissue in a closed operation), valve replacements (bioprostheses), valve repair (mitral valve), balloon valvotomy and stent valves (delivered percutaneously - through femoral artery)

Answer 579

Narrowing of aortic valve by fibrosis or calcification. The pressure gradient could increase to \> 50mmHg. Increase in ventricular pressure with no changes to aortic.

Answer 580

Creates pressure overload, concentric hypertrophy, larger EDP to fill LV due to stiffer walls. Atrial contraction important to fill LV now. Usually reversible after surgery.

Answer 581

Usually calcify in older patients - sometimes congenital and rheumatic. Most common valve lesion

Answer 582

Due to aortic stenosis - and the pressure gradient rises during systolic ejection. The murmur is crescendo decrescendo meaning that it becomes louder, louder then slower. This is the murmur that comes after S1 then followed by S2.

Answer 583

The aortic leaftlets are damaged by endocarditis or rheumatic fever. The aortic roots dilate so leaflets do not close.

Answer 584

Volume leaks back into LV, to maintain SV needs to pump more per beat. Volume overload, Increase EDV, Increase ejection fraction leading to normal ESV. - There is no gradient across the valve. But aorta pressure will increase with the increase SV too. - We see a very wide pulse pressure in aortic regurgitation.

Answer 585

Increase SV, Increase pulse pressure, reduced aortic diastolic pressure and _early diastolic murmur_. No symptoms if its mild and moderate aortic regurgitation. Lub Dub pwosssh (comes after second sound).

Answer 586

Myxomatous degeneration (mitral valve prolapse - long chordae tendinae or mitral leaflets), ruptured chordae tendinae, infective endocarditis, ruptured papillary muscle, rheumatic fever, collagen vascular disease, cardiomyopathy (changes in ventricular shape)

Answer 587

Small volume is ejected into the LA. To maintain CO, LV pumps a greater SV per beat. Causes volume overload. Increased EDV, increased ejection fraction, normal ESV --\> leads to increased LA volume and pressure. Eventual decompensation

Answer 588

Risk of atrial fibrillation, thrombus in LA (possibly embolus), increases pulmonary venous pressure (congestion, oedema, hypoxia). The hypoxia leads to pulmonary artery pressure (constriction in response to hypoxia).

Answer 589

Systolic murmurs due to the pressure gradient LV to LA. It is a pansystolic mumur (same level of mumur after the S1)

Answer 590

Due to rheumatic fever especially in women - leading to fibrotic and narrowed mitral valve. There is a pressure gradient over the valve and reduces LV filling. LV systolic function is unaffected whereas the LA contraction become more important.

Answer 591

It is similar to mitral valve regurgitation. Increase in LA pressure and volume - risk of atrial fibrillation. Thrombus in LA that could embolise. Pulmonary venous pressure increases and also increase in pulmonary artery pressure.

Answer 592

Lub Dub kajflksdjf (long sound in the diastolic period)

Answer 593

Cells adapt by hypertrophy, hyperplasia, metaplasia or neoplasia. Determined by the type of cell in question labile, stable and permanent. As well as the present growth factors and environment

Answer 594

Increase in the size of cells without change in number. Increase intracellular structure production, nucleus can change size and shape. Typical route for permanent cells.

Answer 595

An increase in number of cells. Stem cells stimulated to grow. Typically done by labile cells or stable cells.

Answer 596

A _reversible_ change in which one adult cell type is _replaced_ by another cell type. At junctions of different epithelial types. Can be protective or do nothing.

Answer 597

Proliferative endometrium (cyclic hormone)

Answer 598

Parathyroid hyperplasia

Answer 599

Grave's disease in thyroid where the antibody stimulates the thyroid growth.

Answer 600

Swelling of the tissues exposes the endocervical muscus to the acidic vaginal environment.

Answer 601

Barrett oesophagus due to the bile acid reflux that induces metaplasia of the oesophageal stratified squamous epithelium to an intestinal type - mucus secreting goblet cell.

Answer 602

This is dysregulated/uncontrolled cell division that occurs in the absence of stimulus due to genetic mutations. Can be benign or malignant.

Answer 603

It is controlled division under a stimulus. Alters gene expression instead of genome. Usually benign but can increase risk for neoplasia. - Reversible if stimulus taken away

Answer 604

This is a decrease in cell or organ size - usually due to inactivation, loss of innervation, stimulation, aging, loss of blood supply.

Answer 605

Occurs during growth periods (infants and childhood). Growth of ventricle walls are _proportional_ to the chamber. Increased capillary density and no loss of systolic/diastolic function. It is reversible.

Answer 606

Usually occurs in valvular disease and hypertension. Growth of ventricle wall with reduced/enlarged cavity (not in proportion). Switching on of fetal embryonic genes. Reduced function Deposition of matrix (fibrosis) meaning that it cannot regress

Answer 607

Concentric and eccentric

Answer 608

Increases work without stretch, for pressure overload (valve stenosis, hypertension). The mean myocyte diameter is larger.

Answer 609

Increased work with stretch in volume overload (regurgitation, shunt/wall defect, cardiac failure). Increase in myocyte length rather than diameter

Answer 610

Normal LV \<= 15mm Normal RV \<= 5mm

Answer 611

Women \> 400g Men \> 500g For hypertrophic heart

Answer 612

Enlarged rectangular nuclei, bi-nucleated and increase connective tissue (fibrosis).

Answer 613

Myocardial hypertrophy \> impaired perfusion \> ischaemia \> arrhythmia & cardiac failure. Cardiac failure \> increase EDV \> eccentric hypertrophy \> LV stiffness \> cardiac failure Catecholamines worsen these situations

Answer 614

Regional infarction will increase workload on the surrounding muscles

Answer 615

Calcification and bicuspid anomaly

Answer 616

Prolapse, papillary muscle rupture or fibrosis

Answer 617

Aortic and mitral valve disease

Answer 618

Aortic stenosis

Answer 619

These are floppy valves that have problems closing causing regurgitation or mitral valve prolapses

Answer 620

Thickening of the chordae tendinae by chronic rheumatic valve disease. Occur due to Streptococcus antigen molecular mimicry. Affects all valves. Common cause of mitral stenosis

Answer 621

It is a softer ball than calcium and the rest of the valve is normal (calcification usually thickens everything). It also begins to eat the valves.

Answer 622

Fever, worsening or new murmur and sometimes embolism.

Answer 623

Longitudinal studies to access if an intervention will change the incidence. Expect intervention to decrease incidence and usually has a control group.

Answer 624

These are made very frequently

Answer 625

It is the gold standard for causality - since we can change the exposure and in a tightly controlled environment. Provides most evidence for evidence based practice

Answer 626

Relative Measure: Relative risk, Hazard ratios Absolute Measure: Absolute risk/rate reduction, number needed to treat Survival analysis

Answer 627

Use randomisation so that all the confounders are found in equal parts for the two groups. Treatment groups are identical in all aspects other than the intervention.

Answer 628

This is achieved by blinding the experiment - usually double blinding Removes the systematic differences in the way information is collected.

Answer 629

This is dealt by using 'intention to treat' analysis. There is systematic difference within the groups being compared. Drop outs may skew the result to a healthier group. Assume the subjects remain in the randomised group regardless of cross over.

Answer 630

It always gives an _under-estimate_ of any treatment effect. Since it gives a conservative estimate we are more confident that the result is true.

Answer 631

Continuously updated, instantaneous rate done in longitudinal studies (close follow ups). Can take week-week hazard (rates) while it adjusts for the sample population of interest.

Answer 632

This is a measure of time to reach a particular event. Usually measures how long we can avoid an outcome. _Kaplan-Meier curve_: plots hazar vs time

Answer 633

This is conceptually the same as relative risk. Ratio Hintervention:Hcontrol Applies to the entire time period. Meaning at any point in time within the period of follow up, the probability of outcome in an intervention group is 'Hazard ratio' of the control group

Answer 634

The Hazard ratio is the average weighted risk across all points whereas relative risk shows it at one particular time.

Answer 635

Relative risk and absolute reduction

Answer 636

This is the numer of people treated so that one person is prevented from the outcome. NNT = 1/absolute risk reduction

Answer 637

NNT refers to the efficiency of the intervention. Despite the RR being the same the starting change is not given. It is important that we know that as well.

Answer 638

This is the same as NNT but when the intervention increases the incidence of outcome. NNH = -NNT

Answer 639

Physical, mental and social wellbeing of people

Answer 640

1. Social gradient (shorter life and more disease the lower the social class) 2. Stress 3. Early start (early development and education) 4. Social exclusion (poverty and social exclusion) 5. Work (more control of work better health) 6. Unemployment (Job security \> better health) 7. Social support 8. Addiction (turn to alcohol and drugs) 9. Food (access to food for health) 10. Transport (healthy transport is less cars and more PT and bikes)

Answer 641

Stage 1: No growth Stage 2: Birth \> death Stage 3: Birth \> death (begins to diminish) Stage 4: Birth = death

Answer 642

Pestilence and faminine (infectious disease and malnutrition) \> Receding pandemics (reduce infectious disease and begin to see chronic diseases) \>Degernative and man made disease (smoke, alcohol, fat - chronic conditions dominate infectious) \> Delayed degenerative diseases

Answer 643

Yes it does: worse child well-being, lower levels of trust, more drug use, higher infant mortality rates, lower educational scores, more drop outs, poorer innovation, more crime, higher teenager birth rates

Answer 644

Drug filtration at the glomerulus difficult to excrete proteins. Proximal tubules is where the drug secretion occurs. After the proximal tube reabsorption occurs along the entire tract.

Answer 645

Proximal tubule 60-70% of water reabsorption, loop of henle has about 20-30%, distal tubule has 5-10% and collecting duct has whatever is remaining.

Answer 646

Proximal - Absorption Distal and collecting ducts - secretion

Answer 647

Diuretics, urine pH changing and change of organic molecule secretion (drug secretion stage)

Answer 648

Increase Na+ excretion which leads to water excretion. Usually done by preventing Na+ reasborption. Remember that it acts at a local part in the nephron then affects distal components.

Answer 649

Loop diuretics, thiazide diuretics, K+ sparing diuretics and osmotic diuretics.

Answer 650

Most powerful diuretic since it can excrete 15-20% of Na+ into filtrate. Acts on the Loop of Henle (thick ascending limb) by inhibiting Na+/K+/2Cl- carrier into cells. Increase Na+ in cells make it hypertonic so water will also move out.

Answer 651

Decreased hypertonicity in interstitium and increased Na+ in the distal tubule

Answer 652

Absorbed from gut and onset \< 1hour. They are bound to plasma proteins so must be secreted to enter the kidney tubules to work. Last for 3-6 hours.

Answer 653

K+ loss from distal tubules due to increase Na+ found there. This means increases Na+ reabsorption which is more K+ secretion in the distal tubules. Causes hypokalaemia. H+ excretion (metabolic alkalosis) Reduced extracellular fluid (elderly) - hypovolaemia and hypotension

Answer 654

Salt and water overload in acute pulmoanry oedema, chronic heart failure, ascites (liver cirrhosis) and renal failure. Hypertension

Answer 655

Moderately powerful diuretics with true thiazides and thiazide-like Act on the _distal convoluted tubule_ by inhibiting Na+/Cl- cotransporter

Answer 656

Orally active and is excreted into the urine. Max effect 4-6 hours and lasts for 8-12 hours.

Answer 657

K+ loss from _collecting ducts_ so usually administrated with K+ supplement. Increase in uric acid (inhibits tubular secretion of uric acid - gout) These effects are less with the thiazide-like diuretics.

Answer 658

Hypertension and severe resistant oedema (used in combination with loop diuretic)

Answer 659

This has limited diuretic effect. Usually used with K+ losing diuretics to prevent further K+ loss (especially in heart failure) Act on the collecting tubule and ducts by aldosterone receptor antagonist. - Binds to the receptor on Na+ channels and reduces activation and reduces stimulation of Na+ pump synthesis.

Answer 660

This is the aldosterone receptor antagonist acting in the collecting ducts.

Answer 661

Orally active but slow onset (interferes steroid action to reduce receptor numbers). Short half life but metabolite has long half life.

Answer 662

It causes hyperkalaemia if used alone (less K+ secretion due to Na+/K+ co transporter)

Answer 663

Used in combination with loop or thiazide diuretics. Heart failure and hyperaldosteronism.

Answer 664

These are K+ sparing diuretics that act directly to block _luminal_ sodium channels in collecting tubules and ducts. Inhibits Na+ reabsorption and K+ secretion.

Answer 665

It is much faster. Triamterene is well absorbed (fast onset) whereas amiloride is poorly absorbed (slow onset)

Answer 666

They are pharmacologically inert but make up oncotic pressure in the tubules to prevent water leaving. It can be filtered but not reabsorbed - affects water permeable parts of nephron. -Proximal tubule, descending limb of loop and collecting tubules

Answer 667

Increase in intracranial and intraocular pressure. Used to prevent acute renal failure (when GFR is low and NaCl and water are reabsorbed). Not used for Na+ retention (does not affect Na+)

Answer 668

25% of blood goes here, and substances are concentrated (so drugs are too), kidney can metabolise so create ROS and contribution from extrarenal events.

Answer 669

Direct or via metabolite that create ROS (cell damage), interfere with Ca²⁺ metabolism and protein/enzyme binding (that inhibits the enzyme function or starts immune response)

Answer 670

There is direct toxicity, vasoconstriction, binds to groups on proteins to make them immunogenic, changes to proximal tubule cells.

Answer 671

Used to treat Gram -ve infections and interferes with cell signalling causing eventually changes in calcium and cell injury.

Answer 672

Treatment of tumours can cause nephron death as well (cisplatin)

Answer 673

Proper membrane permeability, component of bile acids, steroid hormones and Vitamin D - Also found in atherosclerotic plaques and gall stones

Answer 674

Acetyl CoA till HMG CoA. HMG-CoA reductase forms mevalonic acid. Forms activated isoprene to squalene and finally cholesterol.

Answer 675

Chylomicrons, VLDL, LDL, HDL

Answer 676

It is a positive correlation

Answer 677

There is an inverse correlation between the two

Answer 678

This is best meausre of correlation to risk of heart disease.

Answer 679

Transport - by assembly with VLDL Bile acids - production in gall bladder, used on demand for emulsifying fats Steroid hormones & Vitamin D - synthesised from cholesterol in adrenal glands and skin. Membranes - Sits in kinks makes the membrane less fluid

Answer 680

Areas of concentrated signalling molecule

Answer 681

Stops the pathway at mevalonic acid so that no activated isoprene - which could lead to many other products.

Answer 682

Not soluble in the blood and can alter properties of the membrane if delivered to wrong site. - Esterify the cholesterol to make it more hydrophobic. - Incorporated cholesterol ester into lipoproteins to carry around the blood

Answer 683

Chylomicron delivers cholesterol-esters and TGs from gut. VLDL carries cholesterol from liver to capillaries. In the capillaries the lipoprotein lipases free up the TGs and form FFA. Chylomicrons and VLDL remnants carry concentrated cholesterol back to the liver. Sometimes VLDL will split and form _LDL_ which will last in the blood longer and deposit cholesterol on other tissues. HDL is involved in reverse cholesterol transport (removal of cholesterol from the tissues back to the liver - for bile salt formation)

Answer 684

Chylomicrons are formed in the intestinal mucosa and carry TGs from the diet to tissues via the lymphatic system. This is the largest lipoprotein found in the body.

Answer 685

Formed in the liver and carries cholesterol from liver to the tissues via the blood. This is just smaller than chylomicrons

Answer 686

Derived from VLDL by the loss of Apo E. This is just smaller than VLDL and increased levels lead to risk of heart disease.

Answer 687

HDL are formed in the liver and intestine which conducts reverse cholesterol transport. This is the smallest lipoprotein.

Answer 688

Occurs in the liver ACAT helps and acts directly on cholesterol ester.

Answer 689

LCAT in plasma helps HDL scavenge cholesterol from membranes. Must take the cholesterol off the phospholipid then add an ester group onto it before binding to HDL.

Answer 690

Disorder of lipoprotein metabolisms.

Answer 691

Increase in total cholesterol which includes both free and esterified forms in the blood.

Answer 692

Increase blood levels of cholesterol with LDLs, this will cause increase in oxidised LDL particules which is atherogenic.

Answer 693

This is increase in triglycerides in the blood.

Answer 694

Oxidised LDL accumulates in artery wall. Endothelial reacts and displays adhesion molecules. White cells invade and secrete inflammatory mediators. Macrophages then appear and take up the modified LDLs. Become foam cells. Fibrous tissue develops and traps foam cells (fibrous cap). If the cap is broken can lead to blood clot.

Answer 695

Recent studies have found that overconsumption of cholesterol is not a problem

Answer 696

This enzyme is the rate-limiting step in the synthesis pathway.

Answer 697

These are competitive inhibitors of HMG-CoA reductase. The structures are similar to mevalonic acid so it binds to the enzyme site.

Answer 698

Statins deplete Q10 which can cause heart problems - myotoxicity.

Answer 699

Imbalance between oxygen supply and demand

Answer 700

Perfusion pressure, coronary vascular resistance (atherosclerosis), external compression (from compressing muscles) and intrinsic regulation (endothelium and local metabolites)

Answer 701

They have a hilum and the blood flows from the hilumto the capsule/peripheral.

Answer 702

Flow is form the outside to the inside.

Answer 703

It will form at the end of the blood supply.

Answer 704

Non-transmurable: Transient occlusion that leads to regional subendocardial infarct. Transmurable: Permanent occlusion of LAD (left anterior descending branch) leads to entire entire infarct.

Answer 705

The endocardium is directly in contact with blood in the ventricles which is enough for diffusion.

Answer 706

LAD - Left anterior descending PD - Posterior descending

Answer 707

Flat posterior, round anterior, PD at septum, LAD branches are lateral off septum, look at the direction of papillary muscles/chordae tendinae, more fat anterior.

Answer 708

LAD - Anterior wall and 2/3 of septum PD - Posterior wall and posterior 1/3 of septum LCX - Lateral wall on the left side

Answer 709

An inbalance between oxygen supplied and oxygen demanded resulting in ischaemia and cell death (Myocardial infarction).

Answer 710

Acute plaque event with rupture or haemorrhage of atherosclerotic plaque forming an occlusive thrombus within a coronary artery. These attacks are locally formed thrombus instead of an embolism

Answer 711

Necrosis, acute inflammation, granulation tissue and fibrosis/scar Which will occur with timely progression

Answer 712

Occurs 0-30 minutes. There are no microscopic or macroscopic differences. But can see intracellular changes (swelling of mitochondrial and myofibril relaxation) - rapid loss of contractility. May see ST depression or T wave inversions (ECG)

Answer 713

30 minutes to 12 hours This is irreverisible disruption of cell membrane (leakage of troponin and creatine kinase) also causes current leakage STEMI or NSTEMI - Cardiac enzyme levels generally become detectable 3-4 hours post infarction. (Before when testing for this early - make sure to keep patient at hospital)

Answer 714

Arrhythmia (damaged myocytes are unstable) and cardiac failure (damaged myocytes)

Answer 715

STEMI - ST elevation myocardial infarction (seen in ECG) STEMI - generally implies transmural infarcts NSTEMI - Non ST elevation myocardial infarction NSTEMI - non-transmural MI

Answer 716

Irreversible injury, necrosis, haemorrhage and oedema.

Answer 717

Begin to see necrosis and acute inflammation (neutrophils) At this stage macroscopically still haemorrhagic

Answer 718

Acute inflammation is still going with massive influx of neutrophils. Appears as pus in macroscopic specimen of heart The cardiac proteins levels are at a peak at the moment (troponin). Will gradually drop so another spike implies another event.

Answer 719

End of acute inflammation and start of early granulation. So macrophages infiltrate and digest dead cells. Appearance of fibroblast and vessels of granulation tissue. Collagen lay down at 5-6 days.

Answer 720

Granulation tissue is the new connective tissue and blood supply that forms during the wound healing process. Granuloma is the walling off found in hard to kill pathogens. Involves macrophages and fibroblasts forming a large centre.

Answer 721

Arrhythmia, cardiac failure, mural thrombus (damaged wall not moving properly), rupture (wall is necrotic and weakened), pericarditis (a lot of inflammatory mediators at this point)

Answer 722

Rupture of ventricular wall (blood leaks into pericardium - haemopericardium \> this leads to blood filling and compressing the heart until it stops - Cardiac Tamponade) Rupture of papillary muscle: New onset murmur, mitral regurgitation and cardiac failure Rupture of IV septum: New onset murmur, Ventricular Septal Defect and cardiac failure _All lead to acute severe cardiac failure_

Answer 723

Early and late granulation tissue formation. At the start was highly vascular with little collagen. Eventually reduces vessels and increases collagen. Now its fixed in position, becoming stronger but still flexible to stretch (causes thinning to happen because of the volume acting against it)

Answer 724

Arrhythmia, cardriac failure, but mostly MURAL THROMBIS and ANEURYSM (collagen wall is strong but its flexible so it may stretch and bulge out)

Answer 725

Fibrosis and scarring

Answer 726

MAINLY cardiac failure (remodelling and hypertrophy), also arrhythmia and aneurysm mural thrombus (aneurysm will not regress but the development of scar tissue makes it unlikely to rupture)

Answer 727

Other vascular pathology other than atherosclerosis. - Coronary dissection - Thrombosis due to vasculitis - Thromboembolism from the heart Reduced flow/oxygenation - Hypotension (shock), rapid tachycardia, hypoxaemia

Answer 728

Both are transient ischaemia displying chest pain. Stable Angina (on exertion and goes by rest) and Unstable Angina (at rest)

Answer 729

Due to atherosclerosis usually more than 70% occlusion. Usually has endothelial dysfunction (cannot respond to vasoactive mediators) and causes reversible injury.

Answer 730

Acute plaque event, coronary thrombosis and eventually resolves (clot broken down). NO irreversible damage caused. Chest pain at rest or with exertion (occurs at any time)

Answer 731

Chronic atherosclerotic narrowing of vessels leading to: small areas of subendothelial ischaemia, patchy myocyte necrosis replaced by fibrosis. Has the same risk factors of cardiac failure and arrhythmia.

Answer 732

Unexpected death due to cardiac causes in short period with no previous fatal diagnosis. Majority is caused by ischaemic heart disease - usually from early arrhythmic event or silent myocardial infarction. Common in young people who will not have developed atherosclerosis or ateriolosclerosis

Answer 733

Abnormal lipid profile. Includes hypercholesterolaemia, hypertriglycerdaemia, mixed hyperlipidaemia. Leads to atherosclerosis and increase risk of MI and stroke

Answer 734

No it does not. In fact it is highly dependent on the proportion of HDL and LDL cholesterols.

Answer 735

Consider CV status, risk factors and treat secondary causes (obesity, diabetes, hyperthyroidism). Then manage modifiable risk factors - smoking, alcohol, weight reduction, increase exercise and modify diet.

Answer 736

Reduce LDL and increase HDL intake

Answer 737

Diet or de novo synthesis in the liver

Answer 738

Stored in liver then exported out by VLDL, converted to bile acids and stored in gall bladder or used for membrane synthesis.

Answer 739

Inhibit HMG-CoA reductase which decreases mevalonic acid \> decreasing cholesterol synthesis. This causes compensatory increase in hepatic LDL receptors, increase LDL clearance. Decrease in plasma LDL and total cholesterol. Also leads to increase in plasma HDL.

Answer 740

Doubling dosage has minimal increase in beneficial effects so must consider the additional adverse effects before administering more statins.

Answer 741

Best benefit after 1-2 years of use so that generally relates to low compliance rates. Used for hypercholesterolaemia and mixed hyperlipidaemia.

Answer 742

Drug-drug interaction that uses cytochrome P450 pathway for metabolism. May affect liver because of increase in serum aminotransferase. Contra-indicated in pregnancy, infections (antibiotics - P450 pathway), pre-surgery and post trauma.

Answer 743

These bind to bile acid so they are prevented from being reabsorbed. This will reduce bile acid and therefore increase demand for cholesterol to synthesise bile acid. - Compensatory increase of hepatic LDL

Answer 744

It specifically inhibits cholesterol absorption in the intestine by binding to the sterol transporter. It does not affect bile acid or fat soluble vitamins. Lowers LDL. Used in statin-intolerant patients and in combinations to lower statin doses.

Answer 745

Mechanism is unclear but it decreases VLDL secretion from liver, reduce plasma LDL and TGs, increases HDL and _lowers atherogenic lipoprotein (a)_ which normally inhibits thrombolysis.

Answer 746

Agonists at nuclear receptor that produces peroxisome proliferator activated receptor alpha (PPARa). Essentially increases lipoprotein lipase (LPL) which hydrolyses TGs to fatty acids. Moderate reduction in plasma TGs, increase HDL and variable effect on LDL.

Answer 747

Hypertriglyceridemia because it reduces TGs and VLDL and increases HDL

Answer 748

They tend to be fully dilated already due to the stable angina and therefore application of vasodilators have no significant effect.

Answer 749

Try to increase supply to heart while decreasing demand of the heart. Drugs to relieve symptoms or prevent attacks.

Answer 750

Stable angina (on exertion - coronary artery disease), Variant angina (coronary vasospasms at rest) and unstable angina (crescendo - angina at rest and exercise - potential for thrombi formation)

Answer 751

Dilate coronary arteries by local mediators - but generally maximally dilated already. Reduce heart rate - allows longer relaxation phase so blood will actually enter the coronary arteries (also longer time to fill).

Answer 752

Decrease cardiac output by reducing HR and SV. Reduce preload (dilate veins and reduce venous return) and reduce afterload (dilate arterioles to decrease resistance).

Answer 753

Releases NO \> stimulates guanylate cyclase \> GTP to cGMP \> dephosphorylates myosin LC so it cannot bind to actin \> vascular relaxation

Answer 754

Relaxation of all vessels but MOSTLY veins. This reduces the preload coming back to the heart therefore reducing the demand on the heart. Can dilate arteries to reduce TPR as well but not as significant.

Answer 755

Short acting - GTN has 1st pass metabolism Longer acting - isosorbide dinitrate (pro drug to active isosorbide-5-mononitrate). Can be taken orally.

Answer 756

Postural hypotension due to venous pooling, headache and flushing from arterial dilation. Reflex tachycardia so it is usually used with B-blockers.

Answer 757

Usually interacts with Viagra (PDE inhibitors) - prolongs increase in cGMP so it will cause significant BP drop. Generally do nt use two cardio-depressive drugs with each other.

Answer 758

Develops by depletion of tissue thiols (needed for NO production from GTN). Increased release and/or sensitivity to vasoconstrictor mediators. Increased endothelial free radicals will reduce NO bioavailability. Can treat with N-acetyl cysteine to restore tissue thiols. But mostly use drug-free periods (usually night time).

Answer 759

Acts by blocking calcium entry into the heart at the SA node, AV nodes and muscles. Leading to decreased HR and increases supply to heart. Decrease in HR, SV, CO will also reduce demand. Verapamil and diltiazem

Answer 760

Block calcium entry into vessels which will cause arterial dilation. This reduces afterload and demand on the heart. Nifedipine and felodipine.

Answer 761

Flushing, headache, oedema Bradycardia, AV block NEVER taken with B-blockers (double cardio-depressive)

Answer 762

Flushing headache oedema. Hypotension and reflex tachycardia.

Answer 763

Used prophylactically

Answer 764

Acts on SA, AV node and muscles. Decreases HR, contractility and SV. Increase in diastole leads to better coronary perfusion and supply. Decrease on demand of heart from decreased CO (HR, SV, contractility).

Answer 765

First line therapy for prophylaxis. Atenolol (B1) and propranolol (non selective B)

Answer 766

Selective inhibition of Na+/K+ channel Ifunny at the SA node. Pure reduction in heart rate. Leads to decrease in oxygen demand and maximise oxygen supply. It is different because it actively reduces the risk of MI.

Answer 767

Brightness if visual field because the same receptors are found in the retina. May cause conduction abnormalities.

Answer 768

Use GTN to relieve coronary spasm. Vascular selective calcium channel blockers (dihydropyridine) as prophylaxis. BUT B-adrenoceptor antagonists are contraindicated. Vasospasm via alpha adrenoceptors may be worse if you also block B2 receptors that facilitate coronary dilation.

Answer 769

Similar treatments to angina but you also prescribe aspirin to prevent thrombosis.

Answer 770

Metronidazole is a pro-drug that needs nitric reductase to activate. Bacteria can reduce the production of this enzyme. Failure to activate the prodrug.

Answer 771

Gram positive and negative _anaerobes_, protozoa and amoeba.

Answer 772

It is the typical hospital acquired infection.

Answer 773

Makes it resistant of all four first line of therapy antibiotics. Must used second line of therapy.

Answer 774

Intrinsic (such as Gram negative bacteria resistance to vancomycin and pseudomonas resistance to penicillin). Also acquired through mutation and horizontal gene transfer.

Answer 775

Transformation, phage-mediated transduction (bacteriophages) and plasmid-mediated conjugation (plasmids).

Answer 776

The donor bacterium lyses then DNA fragments. The DNA fragments are taken up by competent cell (cells that can uptake it). Once the DNA enters the cells the fragment will integrate into the bacteria genome and eventually be translated.

Answer 777

Since the DNA fragments are being integrated to the recipient bacterium. In order to be able to integrate it the fragment must be similar to the bacterium. Must be related bacteria so it can integrate into the genome.

Answer 778

Restriction enzymes cleaves DNA. Also methylation of their bacterial DNA.

Answer 779

Temperate phage (lysogenic cycle) and Virulent phage (lytic cycle)

Answer 780

Bacteriophage binds to the surface which releases the genetic material into the nucleus. The genetic material will incorporate into the genome. The cell may function fine with a new phenotype or die because of the virus.

Answer 781

Temperate phages generally produce resistance when phage protein is produced. It is the main cause of the bacteria toxins production too. Dipthera and Cholera toxin. Shiga toxin is produced when cells are induced to replicate and produces the toxins (do not use antibiotics)

Answer 782

Normal and abnormal bacteriophages infect the bacterium. The abnormal bacteriophages causes gene recombination.

Answer 783

Nothing - it does not need to be similar

Answer 784

Formation of cytoplasmic bridge between two different bacteria. The plasmid will replicate and transfer into the other bacterium. Once it has occurred the cells will separate.

Answer 785

The plasmids contain a build up of resistant genes. Treatment of bacteria using one antibiotic may trigger resistance to another antibiotic because it will express the entire plasmid.

Answer 786

The less you use antibiotic the less likely it will develop resistance. Inappropriate use of antibiotics may expose them to highly resistant bacteria.

Answer 787

Clinical diagnosis, microbiological diagnosis, In Vitro susceptibility (Susceptible, Resistance, Intermediate), host factors (such as pregnant? Immunocompromised?) and also the properties of the antibiotics (will it reach the target?).

Answer 788

To know which particular drug can be used against particular bacteria. This is done through dilution and diffusion methods.

Answer 789

Different concentrations of antibiotics is placed into test tubes. The bacteria is then placed into the test tubes. Clear shows that antibiotic works.

Answer 790

Minimum inhibitor concentration. The lowest concentration needed for antibiotic action.

Answer 791

Disc with cultured bacteria then drop antibiotic containing disc. Circle diameter will determine that it is susceptible and measure of MIC.

Answer 792

Susceptible, intermediate and resistance (increasing MIC leads to resistance)

Answer 793

A strip used to measure the diameter of the diffusion antibacterial susceptibility test to determine the MIC.

Answer 794

Antimicrobial spectrum, clinical efficacy, route of administration, route of excretion, pharmacokinetics/pharmacodynamics, availability and costs.

Answer 795

1. Prescribing antimicrobial when it is not needed. 2. Prescribing the wrong antimicrobial. 3. Use the correct antimicrobial inappropriately (dose, patient, course and route)

Answer 796

Is the antimicrobial needed? Safe and reasonable before treating? Are diagnostic samples needed? Have we collected them yet (make sure before antibiotic given)? What is likely the aetiological agents? What are its antimicrobial susceptibility? Will this treatment benefit the patient?

Answer 797

Use it in very ill patient to cover all bases. Delay emergence of resistance. Treat mixed infections. Reduce toxicity? Possible synergistic effects.

Answer 798

Indifference, antagonism (penicillin and tetracycline - penicillin needs actively dividing bacteria but tetracycline stops bacteria dividing) and synergy (amoxicillin and clavulanoic acid).

Answer 799

Usually by blocking sequential steps of a metabolic pathway. Inhibit enzyme degradation (Such as amoxicillin and clavunoic acid). Enhances antimicrobial uptake by bacterial cell (B-lactam and aminoglycoside). B-lactam punches hole in membrane so aminoglycoside (which normally do not have good access) is able to access inside now.

Answer 800

Inhibition of bactericidal activity by a bacteriostatic agent (Penicillin G and tetracyclines). Induction of enzymatic degradation (ampicillin and piperacillin - ampicillin induces B-lactamse). Competition for binding of the same target. Inhibition of target.

Answer 801

Static + static = addictive or indifferent Static + bactericidal = antagonistic Cidal + cidal = synergistic

Answer 802

If white is found below the drawn lines it is synergistic combination. If it is above it will be antagonistic. MIC can be derived from these tests as well.

Answer 803

Equity in health for all people world wide.

Answer 804

Age, gender, diabetes, smoking, obesity, high cholesterol, physical activity, family history

Answer 805

Lower down in the hierachy the more likely you will die early. The mentioned risk factors for CVD only contribute to no more than 40% of the causes of CVD.

Answer 806

Stress. The ability of one to control their work.

Answer 807

Stress is normal in the acute phase. But when it happens and the adaptation becomes pathological because people are without power. Can cause problems.

Answer 808

Higher up the hierachy the better the health. Higher up the hierachy the lower the stress levels.

Answer 809

Visceral and parietal pleura

Answer 810

Covers the surface of the lungs until the hilum of the lung where it reflects away from the lung and towards the mediastinum.

Answer 811

This is the pleura when the visceral is reflected away - it lines the interal thoracic cavity.

Answer 812

This is the potential space between the parietal and visceral pleura filled with serous membrane. This allows for friction free movement - on expansion of the lungs.

Answer 813

Pneuomothorax

Answer 814

Haemothorax

Answer 815

Based on the surfaces that line around the lung. Cervical, mediastinal, diaphragmatic and costal pleura.

Answer 816

This is the space where the lung is not in contact with the diaphragm - only on inspiration.

Answer 817

Parietal pleura that runs over the T1 rib and reduces the superior aperture space. Also posteriorly at the T12 and adjacent to the vertebral column (costodiaphragmatic recess).

Answer 818

This is the pulmonary ligament found on left and right lungs.

Answer 819

This allows for extra space that the veins might require to hold volume and expand.

Answer 820

Pain from the visceral pleura is dull and delocalised. It shares the same nerve supply as the organs it surrounds - lung and heart. Autonomic nerve supply.

Answer 821

The pain is severe, very sharp and well localised. It is the lining of the thoracic wall so it receives somatic nerve supply.

Answer 822

Begins at C6 on the neck and moves superiorly down through the thoracic inlet (superior aperture) into the superior mediastinum. At T4/5 it divides into right and left main bronchus.

Answer 823

Shorter, wider (diameter) and more vertical than the left main bronchus. Foreign bodie will usually lodge into the right main bronchus due to this difference.

Answer 824

It has U-shaped cartilage rings closed posteriorly by trachealis muscle (flattened).

Answer 825

Main bronchus \> lobar \> segmental bronchi.

Answer 826

One lobar bronchus per lobe of the lung.

Answer 827

Each segmental bronchus supplies a bronchopulmonary segment.

Answer 828

Pyramid shape with the base on the surface of the lungs and the apex is towards the hilum.

Answer 829

Supplied by a segmental bronchus artery and vein - The different segments allow for different zones of function.

Answer 830

Apical segment of the lower lobe is drained this way - so it can be filled by lying supinely.

Answer 831

This is typically where the patients will have vomit or foreign bodies lodged there.

Answer 832

The lower lobe is found posteriorly so you have to auscultate there.

Answer 833

Three lobes found in the right lung. Divided by the horizontal and oblique fissures. Oblique - separates upper and middle from lower Horizontal - separates upper and middle.

Answer 834

Both anterior and middle are found anterior to the lung. The posterior is found posterior to the lung

Answer 835

Between the anterior and posterior segments

Answer 836

The costal ribs and the mediastinum grooves.

Answer 837

Right side

Answer 838

Two lobes are found in the left lung divided by the oblique fissure separating the upper and lower lobe.

Answer 839

It must positioned much higher.

Answer 840

This is the imprint formed by the heart found medially to the lung.

Answer 841

This is the hanging lung found posterior to the cardiac notch.

Answer 842

The right main bronchus will have just divided right before entering the root. The left main bronchus will divide later after its in the root.

Answer 843

Airways are found posteriorly. Arteries are found just anterior to the airways. Veins are found anteriorly to the arteries and also found inferiorly.

Answer 844

Because the right hilum has the bronchus branching already the pulmonary artery will also branch. The left hilum pulmonary artery will not branch just yet.

Answer 845

Two bronchus (right upper and intermedius), pulmonary artery, anterior pulmonary vein and inferior pulmonary vein. There are also black lymph nodes (due to carbon).

Answer 846

SVC, arch of azygous vein and right atrium.

Answer 847

Bronchial artery, vein and nerve supply.

Answer 848

Left main bronchus, left pulmonary artery, anterior and inferior left pulmonary vein and lymph nodes.

Answer 849

The aorta and left ventricle - much bigger than those found on the right lung.

Answer 850

Broncial arteries come from the anterior surface from the descending aorta. The bronchial veins drain into the azygous system.

Answer 851

Surface of the lung has blank lining (spider web like) all over the lung - superficial lymphatic of the lungs. Coloured black due to inhaled carbon. The deeper lymphatic vessels that follow the airway and the blood vessels that collects it and drain to the hilum lymph nodes. The superficial and deep meet at the hilum. Then trachae, bronchial lymph nodes. From the hilum lymph nodes are lymphatic channels that will head to the thoracic duct on the left (3/4 of the body) and the right lymphatic trunk (1/4 only right side of head, neck and upper limb). Eventually enters the subclavian vein then SVC back to the RA.

Answer 852

Comes from sympathetic trunk and vagal nerves. It forms the pulmonary plexus which enters the hilum of the lung.

Answer 853

Firing of X-ray to the body which will then interact with the X-ray and be projected against a film. 3D structure is collapsed into a 2D film so it does not show depth.

Answer 854

Blacker image means more X-ray has passed through. Whiter image means less X-ray has passed through. X-rays hit the film to convert silver-halide into silver (black)

Answer 855

The electron density will determine whether or not X-ray will be able to pass. Therefore atomic number and concentration is important.

Answer 856

This is the difference between energy densities of different tissues leading to easier identification through white/black contrasts.

Answer 857

Patient positioning, adequate quality of X-ray and systematic approach to recognition of anatomical structures. (Can go inside out)

Answer 858

Erect - standing so we can see blood fluid and fluid in lungs. MUST be taken with full inspiration. PA = posterior to anterior (so the heart is closer to the heart - less magnification and blurry). Hugging = to pull scapula away.

Answer 859

Count the number of ribs visible. Anteriorly 7 ribs and posteriorly 11 ribs.

Answer 860

Should be able to see through the heart so there should also be white lines down the mid line.

Answer 861

Line something in the back with something in the found that both belong to the mid line. They they are super imposed it will be straight. Usually spinous process and clavicles.

Answer 862

This is generally where fluid begins to accumulate first.

Answer 863

Use the cardio-thoracic ratio by measuring the maximal transverse length of the heart then the thoracic cavity (inside ribs). If it is \<50% it is normal.

Answer 864

Very hard to see pleura unless it is pathological. Apex (upper half of the upper section), upper, middle, lower, base (lower half of the lower section). Each major section is generally 1/3 of the lungs.

Answer 865

Angle between the manubrium/sternum junction to the T4/5 vertebra. Above it - Superior mediastinum Below it - Inferior border of mediastinum (further divided into anterior, middle and posterior)

Answer 866

Fluid will sink to the base of the lungs looking like a meniscus (negative pressure). Air that enters the pleural space will fill up like a glass of water (atmospheric pressure) - Hydropneumonia Thorax.

Answer 867

CT are computed topography so it provides cross sectional views (depth) so it can be presented as 3D images.

Answer 868

The scanner is rotating as the patient passes through it to get multiple snapshots (X-rays).

Answer 869

Still use cathode ray tube, e-density of tissue determines black or white, radiation detector (no film) and shown up as film/computer monitor.

Answer 870

It is a grey scale used instead of film density. Assigns actual numbers which may allow you to discriminate what structures are present.

Answer 871

Look at it as if you are looking from the foot up.

Answer 872

Do not need to make divisions because we can visualise the insides.

Answer 873

Post processing - can better demonstrate anatomical structures. Slice the image in multiple planes. Develop 3D virtual models. Alter brightness and contrast to emphasise specific structures.

Answer 874

Pros: Good spatial resolution and much better contrast discrimination. Cons: Significant radiation exposure and expensive

Answer 875

Parents have two copies of a gene and pass down one to its offspring.

Answer 876

Genotype is the two alleles for a gene and the phenotype is the physical manifestation of that gene.

Answer 877

When the traits are both equally expressed.

Answer 878

This is where different characteristics are independently inherited.

Answer 879

Developmental errors apparent at birth which may or may not have a genetic basis. Thalidomide use as morning sickness treatment - lead to defects in babies.

Answer 880

Lack of phenylalanine hydroxylase which means elevated phenylpyruvate levels. This will cause brain damage and inhibits tyrosinase which makes melanin.

Answer 881

Low phenylalanine diet is first treatment

Answer 882

Genetic disorder that affects the respiratory system, digestive and reproductive system. Leads to the build up of mucus in the lungs which may lead to chest infections. Generally have persistent coughs. They are also infertile.

Answer 883

Mutation in CFTR (cystic fibrosis transmembrane conductance) which affects the Cl- channel protein. Results in salty sweat.

Answer 884

Guthrie heel prick blood test.

Answer 885

Replacement of the central glycine in collagen. Causes disruption to the helix leading to brittle bones.

Answer 886

Mutation in collagen genes that alter structure, production and interactions. Leads to hyper flexibility - Autosomal dominant.

Answer 887

Lack of tyrosinase so it cannot produce melanin. Usually white with red eyes.

Answer 888

Accumulation of porphyrins is toxic to tissue at high concentrations - especially neurologically acutely. The plasma of people with this disease fluoresces red in UV light.

Answer 889

Single base substitution of glutamic acid to valine. This makes the haemoglobin form an insoluble crystalline structure.

Answer 890

Typically it is genetically inherited - autosomal recessively

Answer 891

This is the haemoglobin found in adults - a2B2 (heterotetramer). Each of the chains contains one haem molecule.

Answer 892

there are two identical alpha chains found on this gene and both are transcribed.

Answer 893

They are genes that are not transcribed.

Answer 894

Embryonic uses: ξ₂ε₂, ξ₂γ₂and α₂ε_2. Fetal Hb: α₂γ₂ Adult (at birth): α₂B₂ and α₂δ₂ Initially has a lot of embryonic ones but declines as fetal Hb rises. During fetus period the fetal Hb is large and the adult HbA begins to increase. Post-natal: There is still moderate levels of fetus Hb but HbA begins to rise to 97%. HbA₂ is present at this stage too but stays at 2%.

Answer 895

HbA - 97% HbA₂ - 2% HbF - 0.5%

Answer 896

α₂B₂ (HbA) and α₂δ₂ (HbA₂)

Answer 897

alpha and B thalassemia - decrease synthesis of the globin chains. Structural variants - altered globin polypeptide such as sickle cell disease Hereditary persistence of fetal haemoglobin (HPFH) - which is clinically benign.

Answer 898

Alpha thalassemia - high in SEA Beta thalassemia - Around meditarrian sea: Southern European and Middle eastern countries as well as North Africa, SEA and Indian subcontinent. Sickle cell disease (SCD) - West and Central Africa, Middle East and Indian subcontinent

Answer 899

Usually decreased synthesis of one or more globins. The end result is an imbalance in relative amounts of alpha and beta chains - end up getting homotetramers instead of heterotetramers. The severity of imbalance confers severity of disease.

Answer 900

Alpha - large gene deletions. Beta - caused by point mutations that regulate gene expression.

Answer 901

Alpha - deficiency in the production of alpha chains. Beta - deficiency in the production of beta chains.

Answer 902

If it is homozygous it is called thalaessemia major. Will not produce B chains but still produces alpha chains. Eventually leads to homotetramer of alpha chains. This haemoglobin will precipitate in RBC. This will lead to damage of RBC - haemolytic anaemia.

Answer 903

Normal erythroblast with reduced B-chain production leads to abnormal erythroblast. It will have some HbA but mostly insoluble alpha aggregate. Most of these die in the bone marrows. - If a few leave they are hypochromatic and accumulate in the spleen and die there causing splenomegaly. The lack of erythropoiesis will stimulate iron uptake from gut leading to liver enlargement and heart damage due to Iron overload. Anaemia will also stimule erythropoietin that causes skeletal deformaties (long bones) and liver enlargement.

Answer 904

Marrow expansion - intramedullary erythropoiesis. Frontal bossing, thinning of long bones and hair-end appearance of the skull due to cranial bone thinning. Hepatosplenomegaly.

Answer 905

Tear-drop shaped cell (due to alpha aggregates), microcytic and hypochromatic. Also target cell (looks like a target)

Answer 906

Normal - 97.5% HbA Heterozygous - \>90% HbA Homozygous - Zero in B0 or reduced in B²⁺ Usually asymptomatic in heterozygous (thalassemia minor)

Answer 907

Blood transfusions for the anaemia (need it often), splenectomy (removal of the enlarged spleen), chelation therapy (for the excess iron accumulation). A cure is bone marrow transplant.

Answer 908

B-thalassemia affects after birth. Alpha-thalassemia affects fetal development and adult.

Answer 909

Affects adult and fetal Hb. Produces homotetramers of gamma and beta chains which are less soluble. The severity of the phenotype is highly dependent on the genotype. Since there is two alpha genes found on each chromosome.

Answer 910

--/-- is where hydrops fetalis occurs and is fatal. a-/a- is still manageable so the carrier genotype is very important.

Answer 911

Caused by point mutations leading to a single base substitution from hydrophilic (glu acid) to valine (hydrophobic). When the Hb is deoxygenated it will become sticky which may lead to vaso-occlusions.

Answer 912

Sickle cell anaemia may have normal MCV and MCH. So the sickle cells must be looked at on Hb electrophoresis/HPLC. Or can look at a blood film.

Answer 913

Inteference RNA to target reduction in alpha-globin mRNA in B-thalassemia. Use epigenetic modifications to maintain HbF levels. Use gene therapy of induced pluripotent stem cells (iPS).

Cardiovascular Block Flashcards

(954 cards)