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Hugh's Foundation and Cardiovascular > Cardio Week 7 > Flashcards

Cardio Week 7 Flashcards

1
Q

Why is the subendocardium the most susceptible to MI?

A

That area is subject to the greatest pressure during systole hence has the most restricted blood flow.

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1
Q

How can you increase O2 supply to the heart?

A

Dilate coronary arteries - atherosclerotic arteries may be dilated maximally already

Decrease HR - increases the time of diastolic coronary a. blood flow

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1
Q

What occurs in Type I error (alpha)?

A

The study shows an effect when in reality there is none.

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1
Q

The major burden of pathology in Australia is from which genetic disease?

A

CF

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1
Q

Are genetic and congenital diseases the same?

A

No, congenital diseases are just those apparent at birth; not all congenital diseases are genetic (eg thalidomide poisoning)

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1
Q

What is contained in mast cell’s preformed granules?

A

Histamine, heparin, tryptase, chymase and TNF-alpha

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2
Q

Which coronary generally supplies the SA and AV nodes?

A

The right coronary artery

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3
Q

At what level is vomitus likely to drain into?

A

Apical segment of the lower lobe of the right lung - because it has the shortest distance from the trachea.

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4
Q

What is ApoB-100

A

Protein that is the mechanism for recognition of lipoprotein in the liver. Expressed on LDL

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4
Q

What factor in a study determines its power?

A

Sample size

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4
Q

What is the name of the sleeve of pleura that hangs down below the hilum and what does it allow for?

A

The pulmonary ligament. It allows room for veins to expand into if they overfil with blood

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4
Q

Define allergy?

A

Immune mediated response to environmental antigen that are otherwise harmless

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4
Q

What is special about the Fc(epsilon)R?

A
  1. On mast cells and binds IgE
  2. Only FcR that can bind antibody that isn’t already bound to ag
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5
Q

What are the 3 fates of cholesterol that is synthesised in the liver?

A
  1. Ester formation - made into VLDL for export
  2. For production of bile acids that are used to emulsify fatty meals
  3. Membranes
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5
Q

Is it possible to see bronchial arteries and veins?

A

Generally no but it is possible to see lymph nodes sometimes due the carbon pigment.

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6
Q

What are the possible side effects of statins?

A

Depletion of Q10 causing skeletal and cardiac muscle complications

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6
Q

How can you tell the right lung?

A

It has three lobes and therefore 2 fissures. The imprints of the great veins may be seen.

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6
Q

How can you tell the left lung?

A

2 Lobes, 1 Fissure. Clearly defined indentation of the aorta and heart. Cardiac notch present.

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6
Q

What is the general shape of a segment of the lung?

A

Pyramid with the apex pointing towards the hilum and the base on the surface of the lung

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6
Q

What are names of the three lobes of the right lung?

A

Upper, middle and inferior

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6
Q

What is the name of the gene that is mutated in CF? On which chromosome does it lie?

A

CFTR: Cytic fibrosis transmembrane conductance regulator

Chromosome 7.

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7
Q

What is the normal function of HDL?

A

HDL is a cholesterol scavenger that take cholesterol back to the liver for production of bile salts. It also acts on macrophages to stop them becoming foam cells.

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7
Q

In terms of antigens, what is special about delayed type hypersensitivity?

A

Antigens are persistent in delayed type - this causes an accumulation of T cells and macrophages attempting to clear it.

eg. TB

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8
Q

What are 4 mechanisms of antibiotic antagonism?

A
  1. Bacteriostatic antibiotics that stop bacteriocidals working eg tetracycline (static) stops penicillin (requires bac to be growing to kill)
  2. Induction of enzymes eg amoxycillin is a good inducer of betalactams while pippercillin isn’t therefore they are not good together
  3. Competitive binding for the same target
  4. Inhibition of target
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8
Q

Where is the pulmonary artery in relation to the bronchus in the right lung?

A

Anterior

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9
Q

What is mendel’s second law?

A

Different genes are inherited differently, unless they are on the same chromosome.

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9
Q

What is Marfans syndrome characterised by?

A

Bone overgrowth and joint laxity, increases susceptibility to aortic dissection.

Mutation in fibrillin 1 gene

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9
Q

What is Der p 1?

A

Allergen from house mites - the mite faeces

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10
Q

What occurs in type 2 error (beta)

A

Study shows no treatment effect when in reality there is one.

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10
Q

Why is the left lung smaller than the right?

A

Its development is impeded by the heart

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11
Q

What are the names of the fissures of the right lung? What which lobes does they separate?

A

Oblique - the inferior from the middle and upper

Horizontal - the middle and the upper

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13
Q

At what level does the trachea bifurcate?

A

T4/5

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13
Q

Where does the apex of each lung sit?

A

Tightly in the concavity of the 1st rib.

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14
Q

What are some non atherosclerotic related causes of coronary a. occlusion in MI?

A

Ventricular thrombus

Inflammation/vasculitis

Aortic dissection

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16
Q

Which areas of the heart does the left anterior descending coronary artery supply?

A

The LV, RV and 2/3 of the intraventricular septum

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17
Q

What are the 3 types of dyslipidaemias

A

Hypercholesterolaemia

Hypertriglyceridaemia

Mixed Hyperlipidaemia

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18
Q

What are some problems with bile acid sequestrants/resins?

A
  • bloating, constapation
  • decreased absorption of other drugs
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19
Q

What is the mechanism of nicotinic acid / niacin to lower LDL?

A

Mechanism unknown

Decreases VLDL secretion from the liver

Decrease plasma LDL and triglyceride

Increases HDL

Usually used in combination

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20
Q

How is a greater O2 demand in the heart met?

A

Can only be done by increasing blood flow (by dilation of coronary vessels) as the maximum O2 is already removed from blood.

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21
Q

What are the charactistic immunogical features of an atopic individual?

A
  • Elevated IgE
  • High numbers of eosinophils
  • large numbers of IL-4 secreting Th2 cells.
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23
Q

What are the vessel level consequences of atherosclerosis?

A
  1. Vessel narrowing
  2. Inability to vasodilate or produce vasodilators that could act downstream on smaller vessels
  3. Possible plaque rupture and thrombosis
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25
Q

What must be in a full chest xray for it to be proper?

A
  1. 7 ribs from top of chest to the bottom, all along the mid clavicular line.
  2. Full picture of the lungs right to the diaphragm
  3. Trachea and spinous processes aline
  4. Labelled
  5. Scapulae out of the way
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26
Q

Kinks in collagen indicate which disease?

A

Osteogenesis imperfecta

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27
Q

What lipid mediators do mast cells produce in response to activation and long does it take?

A

Leukotrienes and prostaglandins, 10-30mins

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28
Q

An elevation in which pancrease secreted substance indicates CF?

A

Immunoreactive trypsin (IRT)

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30
Q

… was the first disease to be routinely tested for at birth and treated as required.

A

Phenylketonuria (PKU)

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31
Q

What is meant by number needed to treat?

A

The number of people needed to be treated inorder to prevent the outcome in one person.

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32
Q

At what level does the trachea start?

A

C6

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32
Q

What is the name of the muscle that connects of the U-rings of the trachea?

A

Trachealis muscle

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34
Q

What is meant by external validity?

A

The extent to which the results of trial are relevant to a given clinical situation. A trial must be internally valid to be externally valid but not vice versa.

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35
Q

What are Jawetz’s law (referring to antibiotic antagonism vs synergism)

A

Bacteriostatic + bacteriostatic = no difference

Bacteriostatic + bacteriocidal = antagonism

Bacteriocidal + bacteriocidal = synergism

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36
Q

What is internal validity?

A

The extent to which the results are valid for the sample patients being studied. Depends on:

  • study design
  • data collection
  • data analysis
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37
Q

What is the mechanism of reduction in LDL for bile acid sequestrants/resins

A

Bind to bind acids causing increase in bile secretion > increases the demand for LDL from the blood to make new bile acids in the liver > LDL uptaken via upregulation of cholesterol receptors in hepatocytes

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38
Q

What is the reaction protein in celiac disease

A

Gliadin from gluten

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39
Q

What are the five requirements of a proper X-ray?

A
  1. Standing
  2. Scapulae out of the way
  3. Full inspiration
  4. Posterior to Anterior
  5. Close to the film
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41
Q

What are some X-linked disease?

A

Colour blindedness, male pattern baldness, Haemophilia A, Duchenne muscular dystrophy,

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42
Q

What are the mediators of type III hypersensitivity/Immune complex hypersensitivity

A

IgM and IgG immune complex disposition

44
Q

What percentage of plasma membrane consists of cholestrol?

A

8% - optimised for rigidity at 37C

46
Q

Down’s syndrome is caused by a trisomy of which chromosome?

A

21

47
Q

How are the lungs divided on chest xrays?

A

Upper, middle and lower. The upper half of the upper segment is called the apex while the lower segment of the lower zone is called the base

49
Q

What changes in the managable risk factor can you make in response to hyperlipidaemia?

A

Stop smoking

Stop drinking alcohol

Improve diet (reduce sat fats)

Increase exercise

Reduce weight

50
Q

What cytokines do mast cell produces in response to activation and how long does it take?

A

IL-3, IL-4, IL-5, IL-13, TNF-alpha. Hours

51
Q

What is the chance of phenylketonuria in a new born

A

1/14,000

52
Q

Why does puncturing the parietal pleura cause severe pain?

A

The parietal pleura is innervated by somatic nerves hence the produces a painful response while autonomic innervation produces dull, non-localised pain

54
Q

What cardiac factors contribute to cardiac workload?

A

HR and contractility

Preload

Afterload

55
Q

What occurs at a tissue level during the early phase of type I hypersensitivity?

A

Wheel and flare: There is vasodilation and leaking of plasma - localised swelling. Squishy to touch

56
Q

What are the phases of type I hypersensitivity?

A

Sensitisation: first exposed to allergen, usually not noticed

Response: immune reaction to second exposure to allergen, can be local or systemic and has immediate (30s) and late phase (6-10 hours)

57
Q

Usually a combination of drugs are used against TB infection, when do you only use one?

A

When treating someone who has been exposed to an infected and contagious TB patient

58
Q

What are statins?

A

Competitive ihibitors of HMG-CoA reductase which is the enzyme that catalysises the rate limiting step of cholesterol production.

59
Q

What is porphyria?

A

Blood disease, plasma is red over UV light. King George the V had it.

60
Q

Ehlers Danlos Syndrome is characteristed by what?

A

Flexibility

61
Q

Cholesterol inhibits which enzyme in the pathway of cholesterol production?

A

HMG-CoA reductase

62
Q

What is the mechanism of phenylketonuria?

A

A lack of phenylalanine hydroxylase - Phe can’t be converted to tyrosine - instead Phe is converted to phenylpyruvate - this builds up and damages the brain and inhibits tyrosinase the melanine making enzyme > you get blond children from black haired parents.

63
Q

What is the name of the pleura that lines the thoraxic wall?

A

Parietal pleura

65
Q

How does the right main bronchus different from the left?

A

It is shorter, wider, and more vertical.

66
Q

What are some life-threatening consequences of MI?

A

Fatal arrhythmias: 1-2 hours post MI

Acute Cardiac Failure

Pulmonary oedema and drowning

Ventricle wall rupture - Tamponard

Thrombus in LV - travel brain = stroke

Aneurysm of ventricle wall - thrombus formation

67
Q

At what stage of the heart cycle is coronary artery blood flow the greatest? Why?

A

Diastole, because during the ventricular contraction (systole) pressure is put on the vessels which restricts blood flow.

68
Q

What occurs during sensitisation?

A

DCs activate CD4 T cells to differentiate them into Th2 cells. IL-4 is required for Th2 differentiation - This comes from basophils either after they receive IL-33 from the DCs or they can present the allergen to the T cell directly (on MHCII) and produce the IL-4 directly

Th2 cells direct B cells to isotype to IgE producing plasma cells via secreting IL-4 and IL-13

69
Q

What enzyme is defective in albinoism?

A

Tyrosinase

70
Q

How long does it take for release of preformed granules?

A

30-45 seconds

71
Q

What is abnormal in abinism?

A

There is defective tyrosinase > tyrosin isn’t converted into melanin > melaninocytes have no pigment to give to surrounding cells > blood hair and white skin

71
Q

What occurs at a tissue level during the late phase of type I hypersensitivity?

A

8-12 hours later, there is leukocyte infiltration due to cytokines synthesised. These include eosinophils, Th2 cells, neutrophils. There is also smooth muscle contraction and sustained oedeam. The skin is hard/firm to touch due to the cell present.

72
Q

What is the mechanism of action of ezetimibe?

A

Specifically inhibits cholesterol absorption in the intestines by binding to sterol transports

73
Q

Order the following tissues in order of most e-dense to least:

soft tissue, metal, calcium, fat, air, contract agents (iodine, barium)

A

Metal > Contrast agents > calcium (bone) > soft tissue > fat > air

75
Q

What is the angle louis?

A

Junction of the manubrium and sternun

76
Q

What happens with eosinophils in allergy?

A
  1. They are over produced in the bone marrow and activated by IL-5 from Th2 cells
  2. They are recruited to the site allergen and activated by epithelials, via CC chemokines (eotaxins)
  3. They are have a lower threshold for activation and degranulation
78
Q

What are the type of antibiotic combinations?

A
  1. No difference (1+2 = 3)
  2. Synergism (1+2 = 4)
  3. Antagonism (1+2=2)
79
Q

What are some side effects of statins? When are they contraindicated

A
  • mild GI tract symptoms, headache
  • myopathy

Contraindicated

  • when on antibiotics
  • when pregnant
80
Q

An ST elevation on an ECG indicates what type of damage to the myocardium?

A

Transmural infarction

81
Q

In a normal person, what is the ratio of heart to diaphragm on a chest xray?

A

> 1/2

82
Q

What is the name of the pleura that line the lung?

A

Visceral pleura

83
Q

What do eosinophils produce?

A

Toxin granules contain free radicals and basic proteins that are designed to damage parasites but cause tissue damage in allergy.

They also produce chemical mediators for epithelial cell activation, inflammatory cell recruitment and activation

84
Q

T/F Statins have a linear relationship between dose and effect

A

False, the therapeutic effect of statin quickly tapers with increasing dose

85
Q

What substances stimulate dilation of coronary arteries?

A
  1. Local metabolites - adenosine, lactate, H+
  2. Vasodilators - prostocyclin, NO
  3. Innervation
87
Q

What does the trachaelis muscle do?

A

Control bronchonstriction and dilation

88
Q

What are 3 mechanisms of antibiotic synergy?

A
  1. Block sequential steps of a pathway - eg co-trimoxazole = trimethoprim and sulphamethoxazole. Both interfere with folic acid synthesis
  2. Inhibit enzymatic degradation - eg co-amoxyclav
  3. Facilitate entry into cell - eg beta-lactams + aminoglycosides
89
Q

Why does dyspnoea occur during acute myocardial ischaemia?

A

Ischaemia > depletion of ATP > both contraction and relaxation is energy depend > impaired relaxation causes increase LV diastolic pressure > pressure backup > pulmonary congestion

90
Q

Why might having “normal” total blood cholesterol not mean a healthy blood cholesterol?

A

The ratio between HDLs and LDL might not be proper.

91
Q

What factors effect myocardial O2 demand?

A

Ventricular wall stress - thickening of the wall reduces demand to a point

HR

Contractility

92
Q

What are some treatments for allergy?

A

Adrenaline for anaphylaxis

Inhaled beta-adrenoceptor agonist (eg salbutamol) for asthma

Anti-histamines for hives, allergic rhinitis

Corticosteroids

93
Q

What is the most common mechanism in sudden cardiac death?

A

Cardiac arrhythmic arrest

eg Ventricular fibrillation

95
Q

What are some non-vascular occlusion causes of MI ischaemia?

A

LV hypertrophy that impairs flow

Rapid tachycardia

Shock

Hypoxaemia

96
Q

What structure imprint in the right lung?

A

SVC, azygous vein, RA

97
Q

Which areas of the heart does the circumflex coronary artery supply?

A

Part of the left ventricle

98
Q

What is Mendel’s first law?

A

Parents have two copies of a gene for a character

99
Q

What are the mediators of type II hypersensitivity/Antibody mediate hypersensitivity?

A

IgM and IgG against cell-bound or extracellular matrix Ag

101
Q

What is the product of the CFTR?

A

Chloride channel protein - Cl- ions travel through them

102
Q

What 5 factors influence choice of antibiotic to treat an infection?

A
  1. Clinical presentation - certain clinical presentations are only caused by certain bugs
  2. Microbiology analysis
  3. In vitro susceptible - R, I and S
  4. Properties of antibodies - eg whether it can get into the urinary tract
  5. Host factors - eg bacteriocidal in immunocompromised
104
Q

When do you use antibiotic combinations?

A
  1. To treat ill patients
  2. To prevent the emergence of resistance
  3. To reduce toxicity
  4. To produce an synergic effect
  5. To treat mixed infections
106
Q

What are lipoproteins?

A

Structure filled with tri-glyceride and cholesterol with a monolipid membrane and ApoB-100 protein for its recognition in the liver.

107
Q

Which areas of the heart does the posterior descending coronary artery supply?

A

Inferior part of the L and R ventricle

109
Q

Where is the pulmonary artery in relation to the bronchus in the left lung?

A

Superior

110
Q

Newer MI are sometimes surrounded by what?

A

Haemorrhage

112
Q

colour blindness, Duchenne muscular dystrophy, haemochromatosis, haemophilia, neurofibromatosis, polycystic kidney disease, Prader-Willi syndrome, sickle-cell disease and Tay-Sachs disease are all what?

A

Pathologies related to specific gene

113
Q

What does Allergen crosslinking of FceR cause?

A

Exocytosis of preformed granules

synthesis of lipid mediators, cytokines and chemokines

114
Q

What is the incidence of CF in Australia?

A

1/2,500

115
Q

What is the upper limit of cholesterol in the blood?

A

5.5 mmol/L

116
Q

What is the normal function of LDL?

A

Provide cholesterol to the tissues

117
Q

What is the mechanism of gliadin presentation in celiac disease?

A

Gliadin is deaminated by tissue transglutaminase 2 so that it is now able to bind into HLA-DQ2 polymorph on APCs > gets presented to CD4 T cells > Th1 activated > Effector Th1 cells travel to gut mucosa and act macrophages > damage the mucosa.

119
Q

Why can’t you only consider the comparative size of the zone of inhibition when comparing two antibiotics?

A

Different antibodies diffuse through the media at different speeds

120
Q

What is the clinical setting?

A

P: Population

I: Intervention

C: Comparator

O: Outcome

T: Time

121
Q

How do nitrates treat angina?

A

Undergo biotransformation into NO > vasodilate all vessel

Venodilation = decrease preload = decrease O2 demand

Arterodilation = decrease afterload = decrease O2 demand

Coronary arteries = may dilate depending on artherosclerosis statis

122
Q
A
123
Q

Calcium channel blockers in angina, go!

A

Can be cardiac selective - act on AV, SA nodes, cardiac myocytes L-type channels

  • decrease HR, contractility therefore O2 demand
  • decrease HR - increase coronary blood flow

Or vascular selective

  • atrial dilation - reduced afterload and demand
124
Q

When can troponins be detected after MI?

A

3-6 hours

125
Q

What factors are present at sites of delayed type hypersensitivity?

A

IFN-gamma = act. macrophages

IL-3 - act. production of monocytes

chemokines = recruitment of macrophages

TNFalpha = tissue destruction, adhesion molecules via local blood vessels

Reactive oxygen and nitrogen species

126
Q

How does TB infection sometimes cause delayed type hypersensitivity?

A

TB infects alveolar macrophage > it can’t kill it > IL-12, IL-1 and TNF-alpha are produced > Macrophages and DC migrate to the LN > activate Th1 T cells > IL-12 act Th1 cells > Th1 and CD8 T cells go back to site of infection > try to help kill > can’t > persistant inflammatory response > can impair airways function

127
Q

Hair straightness/curliness shows what type of inheritance?

A

Incomplete dominance

128
Q

Macroscopically, how to old MI appear cf to newer ones?

A

Older one are whiter, while more recent ones are paler.

129
Q

What are the mediators of type I hypersensitivity?

A

Mast cells, IgE, lipid mediators

131
Q

What is the mechanism of fibrates to lower LDL?

A

Regulate gene expression to increase the synthesis of lipoprotein lipase - increase lipolysis of lipoprotein triglyceride, moderate increase in HDL

Slower effect as it acts via gene expression

132
Q

What type of T cells are involved in delayed type hypersensitivity?

A

Th1 classically but sometimes CTL

133
Q

Does atherosclerotic plaque rupture always end in MI?

A

No, unstable angina can occur if there isn’t complete occlusion. Also sudden cardiac death can occur.

134
Q

What is an example of a nitrate used for angina

A

Glyceryl trinitrate (GTN)

Given sublingual for acute attack

transdermal for prophylaxis

IV for emergency

Side effects - hypotension, and reflex tachycardia

Tolerance - therefore take patchse off at night

135
Q

T/F there are superficial lymphatics immediately below in the visceral pleura?

A

True

136
Q

What is familial hypercholesterolaemia?

A

Genetically inherited dysfunctional LDL receptors on cells that causes reduced LDL endocytosis and therefore increased LDL in the blood. Results in early atherosclerosis and the appearance of cholesterol despites called xanthomas

137
Q

What is the acrynym for hypersensitivities?

A

A - Anaphylaxis

C - Cytotoxic

I - Immune complex

D - Delayed

138
Q

What are 5 causes of valvular disease?

A

Genetically aquired - eg bicuspid aortic valve (may not effect normal function)

Myxomatous mitral valve - genetic or aquired (mitral valve prolapse)

Age-related degeneration - most common is calcification of aortic valve

Infection - endocarditis

Immune damage - rheumatic fever

139
Q

Are are the complications with having a bicuspid aortic valve?

A

It increases the likeihood of infection and calcification

140
Q

What is a complication of infective endocarditis?

A

Vegetation on the valve can break off and form a embolise that blocks vessels downstream

141
Q
A

Hugh's Foundation and Cardiovascular (7 decks)

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