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MEDSCI 203 > Metabolic, Cardiovascular Disease > Flashcards

Metabolic, Cardiovascular Disease Flashcards

1
Q

Atherosclerosis

A

Disease affecting the innermost layer of large and medium side arteries

Plaques or atheroma which are deposits of fibrous tissues and lipids

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2
Q

Tunica intima

A

Endothelial cells separated by tight junction, scattered myointimal cells
A basement membrane underlying ECs. Have tight junctions and a thin cytoplasm for gas exchange

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3
Q

Functions of tunica intima

A

Regulation of blood flow
Barrier function
Blood clotting
Inflammation and immune function
Angiogenesis
Regulate BP

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4
Q

Tunica Media

A

Smooth muscle cell layers
Regulate flow by contraction and stabilise EC by secreting ECM and activating TGF-B

Elastic lamina layers - assist continuous flow

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5
Q

Tunica externa

A

Connective tissue containing:
Fibroblasts
Leukocytes
Nerves
Lymphatics
Blood vessels

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6
Q

Arterioles

A

small branches within tissues

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7
Q

Muscular arteries

A

e.g coronary arteries
media largely of smooth muscle cells
few elastic fibres
separate internal/external elastic laminae

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8
Q

Large elastic arteries

A

Aorta and common carotid
Prominent elastic laminae in their media
Internal/external elastic laminae continuous
Exposed to high pulsatile pressures
Elastic recoil assists the continuous flow

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9
Q

Aetiology of atherosclerosis

A

Still not completely understood

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10
Q

Four major positive risk factors of atherosclerosis

A

Hyperlipidaemia
Cigarette smoking
Hypertension
Diabetes mellitus

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11
Q

Negative risk factors of atherosclerosis

A

High levels of circulating HDL
Moderate alcohol consumption
Cardiovascular fitness

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12
Q

Pathogenesis of atherosclerosis

A

Initiation may involve endothelial cell injury
Progression involves most cellular components of the vessel wall
Atherosclerosis is an example of chronic inflammation

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13
Q

Endothelial cell injury

A

Caused by haemodynamic force
Chemical insults
Cytokines

May lead to:
ALtered permeability
Adhesion of leukocytes
Activation of thrombosis
Endothelial progenitors are recruited

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14
Q

Leukocyte migration into plaque

A

Circulating monocytes adhere to endothelial cells and enter the atherosclerotic lesion.

Differentiate into macrophages and ingest large amounts of oxidised lipoproteins and are called foam cells

Die by necrosis or apoptosis and cytoplasmic contents escape into the extracellular space.

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15
Q

Smooth muscle cell activation and migration

A

Macrophages, platelets and endothelial cells produce growth factors that activate vascular smooth muscle cells.

Smooth muscles migrate and proliferate into the tunica intima through failures of IEL

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16
Q

Lipoprotein entry and oxidation

A

Oxidised lipoproteins attract monocytes and release cytokines and growth factors. Cause dysfunction and apoptosis in smooth muscle cells, macrophages and endothelial cells

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17
Q

Aneurysm can be caused by…

A

Mural thrombosis
Embolization
Wall weakening

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18
Q

Occlusion by thrombus can be caused by…

A

Plaque rupture
Plaque erosion
Plaque hemorrhage
Mural thrombosis
Embolization

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19
Q

Critical stenosis can be caused by

A

Progressive plaque growth and ischemia

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20
Q

Consequences of atherosclerosis

A

Atheroma are often silent

Plaques become unstable/vulnerable
- thin fibrous cap at luminal aspect of plaque
- high lipid content of core
- inflammation

causes symptoms due to
- Rupture
-haemorrhage
-thrombosis
-dissection

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21
Q

Common clinical consequences of atherosclerosis

A

Myocardial infarction
Peripheral vascular disease
Cerebrovascular disease

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22
Q

Haemostasis

A

Haemostasis is the physiological response of a blood vessel to injury. Serves to prevent blood loss by plugging leaks in injured vessels. In healthy vessels, haemostasis is off to maintain the blood in a fluid state

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23
Q

Endothelial cells inhibit haemostasis by

A

Physically insulating tissues from blood

Producing enzymatic and chemical inhibitors of platelet activation
Nitric Oxide (NO)
Prostacyclins

Producing antithrombin on their surface which binds and inactivates the coagulation enzyme thrombin

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24
Q

Haemostasis is accomplished between

A

Endothelial cells
Platelets
Clotting cascade

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25
Q

Endothelial cells promoting haemostasis by…

A

Produce endothelin which causes vasoconstriction

Loss of endothelial barrier, activating platelets and coagulation cascade

Produce von Willebrand factor, promoting platelet adhesion to ECM exposed by vessel injury

Produce tissue factor = thromboplastin which activates coagulation cascade

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26
Q

Platelets

A

Produced by cytoplasmic fragmentation of megakaryocytes in bone marrow

Lifespan of 7 days

Chocolate chip structure - alpha and dense granules that contain chemical mediators of haemostasis

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27
Q

Platelets promote haemostasis by

A

They become activated by ECM proteins

Secrete chemical signals including Thromboxane A2, vasoactive amines and ADP

Signals promote combination of vasoconstriction and platelet aggregation

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28
Q

Reduced platelets

A

Purpura (bleeding from skin capillaries)
Major spontaneous haemorrhage

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29
Q

Coagulation cascade promoting haemostasis

A

Coagulation system is a cascade of proteolytic reactions

Zymogens are activated

Cascade is initiated by several stimuli including tissue factor

Activation of thrombin catalyses fibrinogen -> fibrin monomers

Fibrin polymerise into fibrin strands

Fibrin strands form a meshwork with fused platelets to form a stable plug

Counter-regulatory mechanisms limit haemostatic plug to the site of injury

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30
Q

Thrombosis

A

Thrombus - Mass formed from blood constituents with the circulation during life

Thrombi are made of fibrin, platelets and entrapped RBC and WBC

May form in arteries or veins

Obstruct lumen, or break off as an embolus

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31
Q

Blood clot

A

Formed in static blood
Clot is soft, jelly-like, unstructured and composed of a random mixture of blood cells suspended in serum proteins

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32
Q

Virchow’s Triad components

A

Endothelial injury
Abnormal blood flow
Hypercoagulability

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33
Q

Types of endothelial injury

A

Atherosclerosis
Hypoxia
Infection/inflammation
Physical damage - crushing veins and haemodynamic stress
Chemical damage

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34
Q

Formation of thrombi

A

Artificial surfaces can activate the intrinsic coagulation cascade, bind pro-inflammatory complement cascade proteins and bind other proteins that may activate platelets

Vascular implant patients must take anticoagulant drugs

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35
Q

Abnormal blood flow

A

Turbulence caused by narrowing, aneurysms, infarcted myocardium and abnormal cardiac rhythm

In veins, stasis (pooling of venous blood) causes this
- Failure of RHS of heart
- Immobilisation
- Compressed veins
- Varicose veins
- blood viscosity

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36
Q

Changes to blood cause

A

Platelets coming into contact with endothelium
Impaired removal of pro-coagulant factors
Impaired delivery of anti-coagulant factors
Directly cause injury or activation of endothelium
Atherosclerotic plaques which are pro-coagulant

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37
Q

Genetic causes of hypercoagulability

A

Deficiency of antithrombin III
Deficiency protein C

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38
Q

Acquired causes of hypercoagulability

A

Tissue damage
- acute phase response from liver
- pro inflam/pro coag/ complement
- cytokines causes platelet release

Post-operative
Malignancy
Cigarette smoke
Elevated blood lipids
Oral contraceptives

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39
Q

Mechanisms to limit coagulation

A

Antithrombins
Proteins C & S - vitamin K dependent
Tissue factor pathway inhibitor

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40
Q

Arterial thrombosis

A

Formation of thrombosis in arteries

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41
Q

Mural thrombosis

A

Form along wall of heart or blood vessel and are usually after infarctions

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42
Q

Venous thrombosis

A

Thrombosis formation in veins which can lead to embolization to lungs

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43
Q

Pulmonary Thromboembolus

A

Blood clot deep in deep veins of the leg

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44
Q

Emboli

A

Intravascular mass carried by blood flow from its point of origin to distant site

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45
Q

Types of emboli

A

Thrombus
Fat
Air
Atheromatous Debris
Bone marrow
Amniotic fluid

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46
Q

Effects of emboli

A

Stenosis - narrowing of vessels leading to occlusion

Emboli from leg veins will lodge in pulmonary artery (pulmonary embolus). Causes pulmonary infarction, reduced CO, right heart failure, in worst case death

Emboli from left side of heart or aorta will enter the systemic arterial system and may pass to the brain, spleen, kidney, gut, legs, etc

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47
Q

Ischaemia

A

Inadequate local blood supply to a tissue

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48
Q

Hypoxia

A

deficiency of oxygen which causes cell injury by reducing aerobic respiration

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49
Q

Anoxia

A

complete lack of oxygen

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50
Q

Infarction

A

necrosis of a tissue due to ischaemia

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51
Q

Causes of iscahemia

A

external occlusion - tumours
internal occlusion - atherosclerosis
Spasm
Capillary blockage
Shock
Increased demand
Venous obstruction

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52
Q

Susceptibility of different cells with increasing sensitivity to ischaemia

A

Fibroblasts and macrophages
Skeletal muscle
Myocardium
Renal proximal tubular epithelium
Neurons

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53
Q

Ischaemia

A

If doesn’t kill - reduces ATP and activation of signalling cascades

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54
Q

Ischaemia causes decreased ATP by

A

Decreased oxidative phosphorylation with down the line leads to ER swelling, cellular swelling, loss of microvilli, blebs, clumping of nuclear chromatin and lipid deposition

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55
Q

Apoptosis vs necrosis

A

apoptosis requires energy so not in ischemic cells

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56
Q

Neutrophils and ischaemia

A

Off the scale
Resistance to cell death is enhanced by hypoxia

57
Q

O2 regulated gene expression

A

Anoxia causes increased HIF transcription system activity. This increases NFkB activity and pro-survival target RNAs

58
Q

Effects of ischaemia at tissue level (increasing in damage)

A

Function defects due to sub-optimal tissue perfusion
- myocardial dysrhythmia
- renal insufficiency
Adaptation, atrophy and shutdown
Apoptosis
Infarction

59
Q

Factors influencing outcome of vessel occlusion

A

Size
Speed
Duration
Reperfusion
Metabolic demands
Adequacy

60
Q

Red infarcts

A

Haemorrhagic
Occur in tissues with a dual blood supply such as the lung and tissues where blood flow is reestablished after arterial occlusion

61
Q

White infarcts

A

Anaemic
Occur in solid tissues supplied by a single artery, often wedge shaped

62
Q

Usual pattern after infarction

A

Coagulative necrosis in solid organs

63
Q

Ischaemic heart disease syndromes

A

Angina Pectoris
Chronic ischaemic heart disease with heart disease
Myocardial infarction
- Transmural infarction
- Subendocardial infarction
Cerebral ischaemic injury

64
Q

Timing of infarction

A

<24 hours - neutrophils develop from viable margins
1-3 days macrophages and lymphocytes appear
Fibroblasts and endothelial cells are then recruited (organisation) to form granulation tissue
6-8 weeks the infarct is organised and replaced by a fibrous scar

Some tissues (e.g liver) may attempt regeneration

65
Q

Treatment of myocardial infarction

A

Thrombolytic agents (streptokinase or tissue-type plasminogen activator)

Mechanical re-expansion of the occluded vessel or coronary artery bypass grafting

Problem of further damage by reperfusion injury

66
Q

Complications of myocardial infarction

A

Mural thrombus
Dysrhythmias
Heart failure
Reperfusion injury

67
Q

Effects of reperfusion

A

Short period of ischaemia followed by reperfusion may result in complete reversal of ischaemic cell injury

Longs periods of ischaemia followed by reperfusion may cause additional damage to cells

68
Q

Reactive oxygen species

A

ROS are produced in cells after blood flow is reintroduced after long periods of ischaemia

Accumulation of ROS causes cell injury called oxidative stress

69
Q

Reperfusion damage due to free radicals (ROS)

A

Attack double bonds in UFAs -> lipid peroxidation

Oxidase aa side changes -> enzyme damage

React with thymine -> DNA damage

70
Q

Hypovolemic shock

A

A sudden decrease in circulating blood volume e.g vessel rupture and extensive haemorrhage

71
Q

Cardiogenic shock

A

A dramatic decrease cardiac output e.g heart attack, arrhythmia

72
Q

Circulating vasoconstrictor mediators and neural factors

A

Angiotensin II
Catecholamines
Thromboxane
Leukotrienes
Endothelin

a-adrenergic

73
Q

Circulating vasodilator mediators and neural factors

A

Prostaglandins
Kinins

B-adrenergic

74
Q

Systemic arterial hypertension

A

Systemic arteries

75
Q

Pulmonary hypertension

A

Pulmonary vascular circuit

76
Q

Portal hypertension

A

Hepatic portal veins and its tributaries

77
Q

Smoking and damage to endothelial cells

A

Chemical insult from free radicals and oxidants. Create a pro-oxidative environment.

Superoxide anion reacts with NO to form peroxynitrite & leads to protein nitration. Damaged & dysfunction endothelial cells. Leads to increased deposition of oxidized lipids

78
Q

Dysfunction endothelial cells

A

Increase expression of adhesion molecules provoking the development of a procoagulant and inflammatory environment

79
Q

Diabetes mellitus and damage to endothelial cells

A

Hyperglycemia results in glycation of amino-acids. Advanced glycation end products

Damages function and structure of proteins. Damages endothelial and smooth muscle cells. Generates oxygen-free radicals and is pro-inflammatory

Perturbed lipid metabolism, elevating circulating free fatty acids increasing chances of atheroma formation

80
Q

Hypertension BP

A

Over or equal to 140/90mmHg

81
Q

Micro-angiopathy in hypertension

A

Sclerotic damage in small blood vessels of the glomerulus of kidney and the retina of the eye can result in kidney damage and blindness

82
Q

Hypertension increases risk of

A

Myocardial infarction
Blindness and kidney disease
Cerebrovascular hemorrhage
Aortic dissection/aneurysm
Left ventricular hypertrophy
Cardiac failure

83
Q

Left ventricular hypertrophy

A

Heart has to increase cardiac output. Pathological cardiac hypertrophy is a compensatory response to the increase peripheral vascular resistance in hypertension to minimise the stress on the myocardial left ventricle.

84
Q

Pathological hypertrophy

A

Stimuli is the pressure overload in myocardium. Accompanied by the increase in the number of myocardial capillaries

Fibrosis occurs within hypertrophic myocardium.
Increased migration of fibroblasts into the myocardium these become activated into myofibroblasts.
Interstitial fibrosis
Deposition of excessive and inappropriate ECM

85
Q

Heart failure

A

Fibrosis causes cardiac dysfunction
Weak contractile function
Impaired electrical conduction

86
Q

Dilated heart failure

A

The fibres of the muscular wall become weakened & stretched - not typically directly hypertension related

Coronary artery disease
Ischaemia
Reparative fibrosis
Hypertrophy
Weakened ventricle wall & dilation
Heart failure

87
Q

Infarction of heart

A

Detected as cardiac troponin release
Cardiomyocytes cannot be replaced by cell division
Functional tissue is replaced by collagen

88
Q

Oedema

A

Abnormal and excessive accumulation of transudate fluid in the interstitial space of tissues

89
Q

Transudate vs exudate

A

Clear and acellular vs cloudy, inflammatory cells and protein rich

90
Q

Left sided heart failure

A

Decreased emptying of LV
Increased volume in LV and PV
Increased volume in pulmonary capillaries
Movement of fluid from capillaries into the alveoli
Rapid filling of the alveolar spaces = pulmonary oedema
Breathlessness

91
Q

Right sided failure

A

Increased pressure in the pulmonary system will eventually lead to right-sided heart failure
Causes back pressure on systemic venous circulation
Observed as venous congestion of visceral organs
Lower legs oedema

92
Q

Obesity

A

Increased accumulation of adipose tissue which arises when energy intake exceeds energy expenditure

93
Q

Subcutaneous fat

A

Less dangerous health wise
Pear shaped
More fat around buttocks and legs
Greater hip circumference
More common in women

94
Q

Intra-abdominal fat (visceral fat)

A

More dangerous health wise
Apple shape
Shows up as fat in gut
Greater waist circumference
More common in men

95
Q

BMI

A

Height in m / (body weight in kg) ^2
Doesn’t asses which depot the fat is in

96
Q

Circumferences and diameters at waist and hips

A

Give some idea of degree of obesity and relative amount of fat in visceral vs subcutaneous

97
Q

Skinfold thickness

A

Idea of amount of subcutaneous fat

98
Q

BMI for healthy people, overweight and obese

A

BMI of 18.5 -24.9 = healthy weight
25 - 29.9 = overweight
BMI > 30 = obesity

99
Q

Hydrostatic weighting

A

Compares body weight inside and outside a tank of water since fat is lighter than lean tissues. Doesn’t tell you where the fat is located

100
Q

Impedence

A

Can measure relative amounts of fat but lacks accuracy by electric currents

101
Q

Ultrasound

A

Measure total amount of body fat. Gives only total level of fat

102
Q

DEXA or CAT

A

Gives high degrees of accuracy is assessing total %. Downside is the cost.

103
Q

NMR can identify the presence of biological molecules such as fat

A

Can identify the presence of biological molecules such as fat in tissues. Can accurately define how much fat is in the body and where it is, downside is cost

104
Q

Women and men fat

A

Women have higher percentage of fat and also more lower body fat

105
Q

Adipocytes in obesity

A

Consist up to 95% stored lipid as triglycerides

Insulin is an anabolic hormone and one of its major actions is stimulating lipid accumulation

Adrenergic receptors regulate lipid release from adipocytes

Can be over 100um

Specialized in storing triglycerides safely and triglyceride deposition in other cells is highly deleterious

Deleterious effects on glucose metabolism resistance that leads to Type-2 diabetes. Damaging spillover of lipid into other tissues such as liver .

106
Q

Triglycerides being broken down process

A

Perilipin controls access of enzymes to lipid droplets
First fatty acid is removed by adipose tissue triglyceride lipase (ATGL)

The second fatty is removed by hormone sensitive lipase (HSL)

The third fatty acid is removed by monoglyceride lipase (MGL)

107
Q

Adrenergic receptors activate…

A

Protein kinase A which phosphorylates perilipin and increases access of lipases to lipid droplets. PKA phosphorylates and increases the activity of HSL.

Insulin stimulates lipid accumulation by shutting down HSL

108
Q

Causes of increase accumulation of fat

A

Environment factors - less exercise, warm, easily digestible foods, stimulating more insulin release
MC4R gene
Psychological factors
Fetal programming resulting changes to fetus
Illnesses affecting endocrine system such as hypothyroidism which can affect basal metabolic rate and reduces energy expenditure
Side effect of prescribed drugs

109
Q

Signals regulating appetite

A

Integrated in hypothalamus and brainstem.

Hormonal signals to hypothalamus
Neuronal and hormonal signals to brain stem

110
Q

Sensory mechanisms regulate appetite and metabolism

A

Signals from mouth and nose via nerve cells to modulate food intake and metabolism and prepare digestive system by secreting saliva and stomach acid.

111
Q

Gut influence on food intake (Ghrelin)

A

Ghrelin and vagus nerve link stomach to brain to regulate appetite. Ghrelin is high in fasted state and promotes hunger. Falls rapidly after meal

112
Q

Gut influence on food intake (CKK)

A

Cholecystokinin (CKK) induces sense of fullness in response to mechanical stretch of stomach and gut

113
Q

Gut influence on food intake (L and K cells)

A

Secrete hormones that have powerful effects on appetite and energy expenditure. These include GLP1, GIP and GDF15.

114
Q

Hormone influence on food intake

A

Insulin and leptin from fat acts in the hypothalamus to regulate appetite

115
Q

Leptin

A

Receptors are mainly found in two sets of neurons in the arcuate nucleus of the hypothalamus

Leptin acts to shut down the production of the appetite promoting hormone AGRP

Alpha-MSH binds to melanocortin 4 receptors (MC4R) in nearby neurons

Together they suppress appeptite

116
Q

Consequences of obesity

A

CBF reading allat

117
Q

Treating obesity

A

Diet, exercise and behaviour modification
Recombinant leptin in ppl with genetic leptin deficiency
GLP1 agonists reduce appetite and SGLT2 inhibitors increases glucose loss into urine
Gut bypass surgery

118
Q

How does diabetes arise

A

Beta cells are destroyed so insulin cant be made (Type 1)

Insulin cant act on its target tissues. Beta cells make more insulin to compensate and loss of insulin action becomes evident

119
Q

Hypoglycemia

A

brain starts to malfunction

120
Q

Hyperglycemia

A

Glucose spills into the urine so energy is lost.

Glucose is a chemically reactive species so at high blood glucose, proteins in circulation and blood vessels become glycated and are damaged.

121
Q

How does insulin control blood glucose

A

Food is absorbed from gut, levels of blood glucose rise above 5mM

Triggers insulin release

Triggers uptake of glucose into liver, muscle and fat. Lowers BGL

If BGL fall below 5mM, glucagon is released

122
Q

How does insulin leave the pancreas

A

Portal vein and reaches the 3 main targets which have the highest cell surface levels of the insulin receptor at their cell surface

123
Q

Glucagon + adrenaline

A

Stimulate releases of glucose from glycogen

124
Q

Other way of producing glucose

A

Certain amino acids can be converted to glucose via gluconeogenesis

125
Q

Increasing rate of glucose transport into cells

A

Liver has GLUT4. Insulin causes GLUT4 molecules to move from intracellular sites to plasma membrane It can transport more glucose and during exercise it can be translocated to PM using a different signalling pathway

126
Q

Impacts of diabetes

A

Hyperglycemia, damages proteins in the body leading to diabetic complications
Tiredness
Polyuria and polydipsia
Muscle wasting
Ketoacidosis

127
Q

What happens when there is no insulin?

A

Wasting of tissues
Acidification of blood

128
Q

Dangers of high levels of blood glucose

A

Damage to retina (retinopathy)
Infections and gangrene due to damage to small blood vessels
Neuropathy
Nephropathy
Atherosclerosis

129
Q

High sugar causing damage

A

Results in high sorbitol
Causes osmolar imbalance and water accumulates in cells and cell swells and dies. Particularly affects tissues where aldose reductase is expressed such as nerves, retina and kidneys

Causes glycation

130
Q

HbA1c

A

When blood glucose are high, glucose is added to proteins by non-enzymatic mechanism. Haemoglobin becomes glycated.

Monitoring HbA1c allows an estimate of longer term exposure to glucose.

HbA1c levels correlate with risk of diabetic complications

131
Q

Different types of diabetes

A

Type 1
Type 2
Monogenic (Maturity onset diabetes of the young)
Maternally inherited diabetes and deafness (MIDD)
Gestational diabetes
Malnutrition induced diabetes

132
Q

Type 1 diabetes

A

Absence of insulin due to loss of function beta cells
Usually seen in younger subjects
0.3%
HLA genes that control autoimmune response
Auto antibodies against B-cells can be detected in blood
Viral infections, cancer and immune checkpoint inhibitor therapy for cancer can cause type-1 diabetes

133
Q

Type-2 Diabetes

A

5-10%
Obesity is major risk factor
Progressive diseases and mainly affects older people
Beta cells lose ability to secrete insulin or die
Do not have islet cell antibodies

134
Q

What causes Type-2 diabetes

A

Insulin resistance - becomes less effective
BGL cant be controlled
Obesity is major driver
- release of IL-6 interferes with insulin receptor signalling
- Increases levels of lipids in circulation also interfering with insulin receptor signalling
Variants in TCF7L2 gene links increases risk of b-cell failure

135
Q

Gestational diabetes

A

Abnormal regulation of glucose metabolism during pregnancy
Low insulin secretory capacity in women results in increases in circulating glucose levels that reach the definition of diabetes

Symptoms disappear after birth but 60% of these women develop diabetes in later life suggest pre-disposition

136
Q

Type 2 diabetes drugs - Metformin

A

Reduces BGL by increasing use of glucose in cells of gut

137
Q

Type 2 diabetes drugs - Sulfonylurea

A

Force b-cells to release more insulin to compensate for insulin resistance

138
Q

Type 2 diabetes drugs - modulate GLP-1 signalling

A

improve insulin sensitivity

139
Q

Type 2 diabetes drugs - SGLT2 inhibitors

A

Block re-uptake of glucose in kidney, so it lost in urine

MEDSCI 203 (7 decks)

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