Lecture 3 - Blood and Introduction to Blood Pressure Flashcards

Question

Erythrocytes are produced at what rate?

Answer 1

more than 2million cells per second.

Answer 2

adequate nutrition are needed IRON COPPER ZINC B Vitamins

Answer 3

Approx 20% of dietary fiber we consume is absorbed. Heme – Iron (from animal products) is absorbed more efficiently than non- heme – Iron (from plants). Upon absorption, iron becomes part of the total iron pool. Iron is stored in the bone marrow, liver and spleen as protein compounds ferritin and hemosiderin When EPO (a hormone that your kidney’s make to trigger your bone marrow to make RBCs) is released, iron is also released from storage, bound to transferring and carried to the red marrow where it attaches to erythrocyte precursors.

Answer 4

Is vital for hemoglobin production Enables oxidation of iron from Fe2+ to Fe3+ In copper deficiency, iron synthesis decreases and iron can accumulate in the tissues leading to organ damage.

Answer 5

The B Vitamins, Folate and B12 function as co-enzymes that facilitate DNA synthesis and so are crucial for synthesis of new cells – including RBCs. Clinically important!

Answer 6

SICKLE CELL ANEMIA IRON DEFICIENCY ANEMIA VITAMIN – DEFICIENT ANEMIA (B12 & Folate) Megaloblastic Anemia Pernicious Anemia THALASSEMIA

Answer 7

These lack hemoglobin They have a nucleus and are capable of motility. They defend the body against infection (remember last 2 weeks of inflammation lectures!) Produced by the bone marrow, and are regulated by the spleen, liver and kidneys.

Answer 8

Granular and non granular

Answer 9

Basophils, Eosinophils, Neutrophils

Answer 10

Lymphocytes & monocytes. Eg. Natural Killer Cells, T- Cells and B Cells Monocytes E.g. Macrophages, dendritic cells

Answer 11

Is your body’s normal reaction to an injury that causes bleeding. This reaction will stop you bleeding, and is therefore essential in keeping you alive. However, if the processes that control hemostasis malfunction, the individual can have potentially serious or life threatening problems with bleeding or clotting.

Answer 12

1. Vascular spasm is the first response as the blood vessels constrict to allow less blood to be lost. 2. Platelet plug formation, platelets stick together to form a temporary seal to cover the break in the vessel wall. 3. Activation of fibrin deposition.

Answer 13

Is a clot forming process Defined by the formation of a primary platelet plug Activated Platelets are mainly involved Primary Homeostasis is when your body forms a temporary plug to seal an injury. It does this by activating platelets (active platelets allow them to recruit further platelets to help form the plug). Active platelets also cause vasoconstriction of damaged blood vessels.

Answer 14

Also clot forming process but it associated with the propagation of the clotting process via the intrinsic and extrinsic coagulation cascades. In this process, you have the formation of insoluble cross- linked fibrin Activated coagulation factors are mainly involved. Now the platelet plug has been formed to stop the bleed, it needs help to keep it in place  this is Secondary Homeostasis. Secondary Homeostasis involves molecules called the “coagulation cascade” which amplify the clotting effects. The Coagulation Cascade forms FIBRIN which makes the clot a stable clot.

Answer 15

Endothelial damage results in exposure of collagen and Von Willebrand Factor – which mediate adhesion of platelets. Platelets express surface glycoprotein receptors which bind to these ligands. Glycoprotein Ia (GPIa) binds directly to collagen Glycoprotein Ib (GPIb- IX) binds to Willebrang Factor  This is turn binds to collagen. Adherent platelets undergo a shape change and aggregate. ADP is released from granules which further stimulates aggregation of platelets  forming a platelet plug Prostaglandin Thromboxane A2 is synthesized by platelet and causes: further platelet aggregation vasoconstriction Receptors are expressed on the platelet surface which interact with coagulation factors (Collectively called the Platelet Factor 3) The Coagulation Cascade generates the insoluble protein FIBRIN Final stage Platelets express glycoproteins on their surface which act as a receptors for fibrinogen and Von Willebrand Factor which helps form a firm hemostatic plug.

Answer 16

The ultimate aim of the coagulation cascade is to form a solid plug of cross linked proteins (FIBRIN) which seal a defect in a blood vessel. To achieve this, a number of different proteins interact together in a cascade (they are numbered from I- XIII).

Answer 17

Extrinsic Intrinsic Common Pathways

Answer 18

Coagulation is initiated by a substance generated from damaged tissues called Tissue Factor, by interaction with Factor VII

Answer 19

Coagulation is initiated by contact with surface agents such as collagen. Activated Factor X form a complex with activated Factor V and convert prothrombin to thrombin

Answer 20

A series of steps that leads to the generation of cross linked fibrin. A key component of this is the formation of thrombin

Answer 21

1 - Vasoconstriction 2 - platelet adhesion 3 - platelet activation 4 -platelet aggregation/platelet plug formation

Answer 22

Formation of stable fibrin clot

Answer 23

1.Endothelial Dysfunction Direct injury e.g. trauma or inflammation Damage to the endothelium occurs in association with atheroma. 2. Change in the flow pattern of blood A major factor is causing a thrombus. Turbulent blood can cause physical trauma to endothelial cells and without laminar flow, can bring platelets into contact with the endothelium. 3. Change in potential blood coagulability Can predispose thrombus formation. May be due to increased concentration of fibrinogen, which can occur for example with estrogen containing oral contraceptive pill.

Answer 24

Warfarin acts by inhibiting the synthesis of vitamin K-dependent clotting factors, which include Factors II, VII, IX, and X, and the anticoagulant proteins C and S

Answer 25

Heparin and related compounds increase the action of antithrombin on thrombin and factor Xa

Answer 26

High Blood Pressure causes damage to endothelium of blood vessels which can cause them to: Rupture Leak High Blood Pressure can cause a thrombus to form in arteries, which can dislodge and travel elsewhere in the body causing a stroke.

Answer 27

How much pressure your blood is exerting against your artery walls

Answer 28

The pressure in the arteries when the heart rest between beats

Answer 29

SYSTOLIC (How much pressure your blood is exerting against your artery walls) ------------------------------------- DIASTOLIC (the pressure in the arteries when the heart rest between beats) 120 ----- 80

Answer 30

BP = CARDIAC OUTPUT X PERIPHERAL VASCULAR RESISTANCE

Answer 31

how much blood leaves the heart per minute

Answer 32

How many times does the heart beat per min (approx. 70)

Answer 33

how many litres (approx. 5l) pumped out

Answer 34

Increase CO

Answer 35

the diameter of the blood vessels. If you narrow the diameter of a blood vessel – you increase resistance – you increase BP.

Answer 36

Systolic pressure is the greatest indicator of the risk of death. Blood pressure increases with age. Risk of death increases exponentially with systolic pressure. Females more resistant up to age 45 years (protected by oestrogen), then rises in parallel with males.

Answer 37

considered to be between 90/60mmHg and 120/80mmHg

Answer 38

High blood pressure is considered to be 140/90mmHg or higher

Answer 39

Low blood pressure is considered to be 90/60mmHg or lower

Answer 40

Stage 1 hypertension Clinic blood pressure is 140/90 mmHg or higher and subsequent ambulatory blood pressure monitoring (ABPM) daytime average or home blood pressure monitoring (HBPM) average blood pressure is 135/85 mmHg or higher.

Answer 41

Stage 2 hypertension Clinic blood pressure is 160/100 mmHg or higher and subsequent ABPM daytime average or HBPM average blood pressure is 150/95 mmHg or higher.

Answer 42

Severe hypertension Clinic systolic blood pressure is 180 mmHg or higher or clinic diastolic blood pressure is 110 mmHg or higher.

Answer 43

Occurs not due to a medical condition, but usually due to obesity, smoking & family history. Most common cause (more than 90% of people have this form)

Answer 44

Secondary to other conditions (<10% of total patients with hypertension). Kidney disease. Adrenal cortex tumour (increased Aldosterone). Adrenal medullary tumour (increased Adrenaline phaechromocytoma). Thyroid disease. Higher centres dysfunction. Cardiac or vessel disease.

Answer 45

most common type - 90– 95% of cases As we age, our BP increases Unsure what causes this. Known as the silent killer as it is asymptomatic. A high cause of death. 50% of adults in the US have hypertension – 50% of those, don’t know they have it. The 50% that do know they have it, are being treated incorrectly it. 1 in 2 people with mismanaged hypertension will die of ischaemic heart disease THIS IS WHY IT IS REALLY IMPORTANT TO CHECK IT!

Answer 46

Most common Gradual increase in BP over many years. It is the most modifiable risk factor for cardiovascular disease

Answer 47

Left ventricular hypertrophy. Thickened vessel walls associated with fibrosis (medium and large arteries). Increased risk of aneurysm: 1) Cerebral vessels (risk of stroke). 2) Aorta (aortic aneurysm). Severity of atheroma. 60% die from cardiac causes such as MI and cardiac failure. 30% die from stroke as a result of haemorrhage, infarct or embolus.

Answer 48

1 - Increased incidence of cerebral haemorrhage + MI. 2 - Hyaline laid down in vessels: thickening and narrowing of small/medium arterioles. 3 - Advanced arteriosclerosis in larger arteries. 4 - Damage to glomeruli (less marked than malignant hypertension). 5 - Left ventricular hypertrophy (concentric).

Answer 49

Headache. May have left ventricular hypertrophy: picked up on ECG or echocardiography (ultrasound). Chest X-ray is asymptomatic.

Answer 50

<45 years. Very high B.P. 210/120 minimum, more usually >250/130. Papilloedema. Renal failure. Usually de novo or superimposed upon benign hypertension. Pathogenic feature is fibrinoid necrosis (damage to arterial walls) in small/medium sized arteries. 50% of untreated cases die within six months. Commonest cause of death is stroke. Renal failure also common (damaged by high B.P.).

Answer 51

Retinopathy Very high incidence of cerebral oedema. Renal glomerular damage. increased B.P. leads to renal failure resulting in increased B.P. etc.

Answer 52

An Atheroma is a plaque of fatty material that builds up inside your arteries. Specific degenerative disease affecting the large and medium arteries. They grow over time, and lead to: Coronary Artery Disease Peripheral Artery Disease Heart Attack (MI) Stroke

Answer 53

Used to describe the thickening and hardening of the walls of the arterioles.

Answer 54

Progression of atheroma. Initially atheroma affects tunica intima, and then progresses to thickening and hardening of the tunica media

Answer 55

Plaques invade tunica media. Ulceration of plaque. Damaged endothelium leads to leukocyte and platelet adhesion. Permeability is increased. Roughness of endothelium narrows lumen and causes increased turbulence and decreased laminar flow resulting in more lipid deposition. Formation of thrombus. Thrombus stops O2 getting to muscles which then atrophy. Arterial wall smooth muscle hardens and calcifies (atherosclerosis).

Answer 56

Inflammatory response around plaques suggests involvement of T-cell and polymorphic neutrophils. Foam cells are the precursors of atheromatous plaques. The foam cells contain lipid globules and create an antigenic response. They are toxic to the endothelium. There is a possibility that the condition may be worsened by stress (increased sympathetic tone, increased vasoconstriction).

Answer 57

Age and sex (increased incidence of ischaemic heart disease after menopause - hormonal). Blood lipid levels. Hypertension (reduced calibre of vessel leads to increase B.P. (BP = peripheral resistance and cardiac output). Diabetes (esp. type 2 onset type). Toxic effects of high blood glucose levels. Genetic disposition. Environmental/lifestyle factors: Decreased exercise increased intake of saturated fats & decreased intake of fish oil fats. Oral contraceptives decreased fibre in diet. High alcohol intake.

Answer 58

Coronary artery disease Can result in myocardial infarction or angina. Localised MI causes damage to the myocardium or can affect the electrical pathways causing arrhythmias. Stroke / TIA cerebral infarction or haemorrhage resulting in stroke (CVA). Transient cerebral ischaemic attacks (TCIA). Especially in the elderly. “Dizzy periods”/semi-collapse. Transient decreased O2 to the brain Mesenteric ischaemia. Claudication in the abdomen -- decreased function. Abdominal pain after food. Ischaemia of bowel (mimics appendicitis). Peripheral vascular disease (intermittent claudication). Exercise related distal muscle pain, increased lactic acid, leg pain (even at rest in severe cases). Reno-vascular stenosis Commonly cause by atheroma, resulting in renal ischaemia. Aneurysms. Usually asymptomatic: can have an aortic aneurysm for years, current screening programme- males only 65yrs single scan. Usually secondary to atheroma. Iliac artery aneurysm, AAA Popliteal artery aneurysm. Cerebral aneurysm (carotid or vertebral arteries). Intracerebral aneurysm (in the Circle of Willis).

Answer 59

is a blood clot that forms inside a blood vessel or cavity of the heart

Answer 60

is the formation or presence of a blood clot inside a blood vessel or cavity of the heart

Answer 61

is a blood clot that moves through the bloodstream until it lodges in a smaller vessel and obstructs circulation

Answer 62

is the breaking up of a blood clot

Answer 63

Brain > Paralysis (non-fatal thrombotic stroke), Heart > Cardiac disability (repeated coronary events), Eyes > Loss of vision (retinal vascular thrombosis) Legs > Deep Vein Thrombosis

Answer 64

Venous Deep Veins of Legs (Low blood flow) Predisposing Factors  abdominal surgery, childbirth, heart disease, and varicose veins, immobility Arterial Aorta, Coronary Arteries, middle cerebral arteries Predisposing Factors Atherosclerosis Cardiac Within chambers of the heart Predisposing Factors  Heart Valve Disorders, MI, Fibrillation