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Clinical Diagnosis > Lecture 3 - Blood and Introduction to Blood Pressure > Flashcards

Lecture 3 - Blood and Introduction to Blood Pressure Flashcards

1
Q

What are some functions of blood?

A

Transporting oxygen and nutrients to lungs and tissues
Forming blood clots (to prevent excessive blood loss)
Brings waste products to the kidneys and liver to filter and clean the blood
Regulates body temperature

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2
Q

What are the cellular components of blood?

A

Erythrocytes (aka RED BLOOD CELLS)
Thrombocytes (aka PLATELETS)
Leukocytes (aka WHITE BLOOD CELLS)
Neutrophils
Eosinophils
Basophils
Monocytes
Lymphocytes

And PLASMA

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3
Q

What is the liquid component of blood?

A

Plasma

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4
Q

What percentage of plasma is water?

A

90%

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5
Q

What percentage of blood is ions, proteins, nutrients, wastes & dissolved gasses?

A

10%

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6
Q

What are the ions, proteins etc found in plasma important for?

A

The ions, proteins etc found in plasma are important for maintaining blood pH & osomotic balance alongside albumin.

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7
Q

What are some of the more specialised functions found in plasma?

A

hormones acting as long distance signals.
Antibodies recognize & neutralize pathogens
Clotting Factors Promote Blood Clot Formation at the site of wounds

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8
Q

Within the 10% of ions/ protein etc found in plasma, we group them as either ?

A

Organic or inorganic components

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9
Q

What are the organic components of blood plasma? (7% of total)

A

Albumin
Immunoglobulins (more later)
Transport proteins e.g.:
Transferrin, caeruloplasmin
Complement proteins (e.g., C1-C10)
Clotting proteins (e.g., prothrombin, fibrinogen)
Hormones e.g. insulin
Pre-cursor hormones (e.g., angiotensinogen)
Secreted substances e.g. Prostatic specific antigen, CA 125
Enzymes – Gamma GT – can be markers for disease
Glucose, uric acid

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10
Q

Why would we look at levels of organic components in blood plasma?

A

because they can be indicators of disease.

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11
Q

What are transport proteins?

A

These are proteins that transport substances across biological membranes or enable a compound to become plasma soluble.

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12
Q

What is Albumin?

A

Is a protein made by your liver.
It helps keep fluid from leaking out of your blood vessels into other tissues.

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13
Q

What is the clinical application with Albumin?

A

Low levels of albumin can be a sign of liver or kidney disease (or another medical condition).
High levels may indicate dehydration
(Blood Test will appear as: ALB or Serum Albumin)

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14
Q

What condition can result from low albumin?

A

HYPOALBUMINEMIA

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15
Q

What is GAMMA - GT(GTT) Test for?

A

High levels of GTT indicates your liver is not functioning as it should.

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16
Q

What conditions do high levels of GTT indicate?

A

Obstructive liver disease
bile duct blockage
Viral Hepatitis.

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17
Q

What waste products of plasma are there?

A

UREA and CREATININE

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18
Q

What is Urea?

A

Urea is a waste product of the breakdown of amino acids and is excreted by the kidneys.

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19
Q

What is the UREA cycle?

A

This a process in which waste (ammonia) is removed from our body .

When we eat proteins, the body breaks them down into amino acids.
Ammonia is produced from the leftover amino acids and must be removed from the body.
The liver produces enzymes which convert ammonia into urea. Urea can be easily removed in the urine.
If this process is disturbed, ammonia levels will rise.

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20
Q

What is creatinine?

A

Is a waste product of creatine phosphate from normal muscle metabolism.
Creatine Phosphate is an important molecule for energy production in muscles.

The higher someone’s muscle mass, the higher their creatinine levels (generally speaking, males will have higher creatinine levels than females).

Creatinine is filtered through the glomeruli, not reabsorbed in the tubules and then excreted in urine.

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21
Q

What are the clinical indications of Urea and Creatinine?

A

Increased urea and creatinine levels in blood can indicate either kidney injury or disease.

Causes:
Kidney Damage
Kidney Infection
Dehydration

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22
Q

Where are blood cells made?

A

Bone marrow

Bone marrow is the spongy tissue inside bones
It produces
Erythrocytes (aka RED BLOOD CELLS)
Thrombocytes (aka PLATELETS)
Leukocytes (aka WHITE BLOOD CELLS)

The spine & hip have the richest source of bone marrow cells

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23
Q

What are Erythrocytes?

A

These mature in red bone marrow
An immature erythrocyte is called a reticulocyte
They do not contain endoplasmic reticula and so do not synthesize proteins
They are bi-concave disks which can fold to pass through blood vessels
They contain hemoglobin molecules which can bind to oxygen

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24
Q

What is the clinical relevance of changes in erythrocytes?

A

Changes in the levels of RBC can have significant effects on the body’s ability to effectively deliver oxygen.

Clinical Relevance
A form of Anemia can be due to insufficient numbers of RBC
(there are multiple causes of anemia)

HYPOXIA
Occurs when there is not enough oxygen to meet the demands of the body.
A pulse oximeter is an easy, non-invasive way we can measure the amount of oxygen carried by the erythrocytes.
We call this arterial blood oxygen saturation (or Sa02 for short)
A Pulse oximeter measures the saturation of peripheral oxygen - Sp02.
A sp02 of 95% of greater is considered normal.
Anything below that is considered low
If it falls below 85%, it is considered potentially life threatening.

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25
Q

Erythrocytes are produced at what rate?

A

more than 2million cells per second.

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26
Q

For Erythrocytes to be produced, what trace elements need to be present?

A

adequate nutrition are needed
IRON
COPPER
ZINC
B Vitamins

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27
Q

Tell me about Iron

A

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.

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28
Q

Tell me about copper

A

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.

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29
Q

Tell me about B vitamins

A

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!

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30
Q

What are Clinically Relevant Conditions Relating to Erythrocytes?

A

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

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31
Q

What are Leukocytes?

A

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.

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32
Q

What are the 2 main groups of Leukocytes?

A

Granular and non granular

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33
Q

What are granular leukocytes?

A

Basophils, Eosinophils, Neutrophils

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34
Q

What are non granular leukocytes?

A

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

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35
Q

What is Haemostatis?

A

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.

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36
Q

During haemostasis what three steps occur in a rapid sequence?

A
  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.
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37
Q

What is Primary Haemostasis ?

A

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.

38
Q

What is secondary Haemostasis?

A

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.

39
Q

What are the events of clot formation?

A

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.

40
Q

What is the coagulation cascade?

A

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).

41
Q

What 3 pathways does coagulation consist of?

A

Extrinsic
Intrinsic
Common Pathways

42
Q

In coagulation, What is the extrinsic pathway?

A

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

43
Q

In coagulation, What is the intrinsic pathway?

A

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

44
Q

In coagulation, What is the common pathway?

A

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

45
Q

What are the stages of primary haemostasis?

A

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

46
Q

What is the stage of secondary haemostasis?

A

Formation of stable fibrin clot

47
Q

What is the name of what happens when there is too much aggregation of platelets?

A

Thrombus

48
Q

What are the Three Main Factors Predispose To Thrombus Formation?

A

1.Endothelial Dysfunction
Direct injury e.g. trauma or inflammation
Damage to the endothelium occurs in association with atheroma.

  1. 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.
  2. 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.
49
Q

What is warfarin?

A

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

50
Q

What is Heparin?

A

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

51
Q

What damage does high blood pressure do to Endothelium?

A

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.

52
Q

What is systolic?

A

How much pressure your blood is exerting against your artery walls

53
Q

What is diastolic?

A

The pressure in the arteries when the heart rest between beats

54
Q

Your Blood Pressure is recorded as two numbers. Explain?

A

DIASTOLIC (the pressure in the arteries when the heart rest between beats)
120
—–
80

55
Q

What is the blood pressure equation?

A

BP = CARDIAC OUTPUT X PERIPHERAL VASCULAR RESISTANCE

56
Q

What does CO =?

A

how much blood leaves the heart per minute

57
Q

What is heart rate?

A

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

58
Q

What is stroke volume?

A

how many litres (approx. 5l) pumped out

59
Q

increase HR or SV =?

A

Increase CO

60
Q

Vascular resistance =?

A

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

61
Q

What are some general facts of blood pressure?

A

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.

62
Q

What is considered normal blood pressure?

A

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

63
Q

What is considered high blood pressure?

A

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

64
Q

What is low blood pressure considered to be?

A

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

65
Q

What is stage 1 hypertension

A

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

66
Q

What is stage 2 hypertension?

A

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

67
Q

What is severe hypertension?

A

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

68
Q

What are the causes of primary hypertension (Aka. Benign Essential Hypertension) ?

A

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)

69
Q

What are the causes of secondary hypertension?

A

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.

70
Q

Tell me about primary hypertension?

A

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!

71
Q

What is benign essential hypertension?

A

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

72
Q

What is the morbid anatomy of Benign essential hypertension?

A

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.

73
Q

What are the pathological effects of benign essential hypertension?

A

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

74
Q

How does malignant phase hypertension present?

A

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

75
Q

What is some information about malignant phase hypertension?

A

<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.).

76
Q

What are complications of malignant phase hypertension?

A

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

77
Q

What is atheroma?

A

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

78
Q

What is Arteriolosclerosis?

A

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

79
Q

What is Atherosclerosis?

A

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

80
Q

How is an antheroma made?

A

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).

81
Q

What are environmental factors of atheroma?

A

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).

82
Q

What are risk factors for atheroma?

A

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.

83
Q

What are clinical complications of atheroma?

A

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).

84
Q

What is a Thrombus?

A

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

85
Q

What is thrombosis?

A

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

86
Q

What is an embolus?

A

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

87
Q

What is thrombolysis?

A

is the breaking up of a blood clot

88
Q

True or false? A thrombus can travel around the body, and depending where it blocks a vessel, will have different symptoms.

A

True

89
Q

What are the associated morbidities of a thrombus?

A

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

90
Q

What are the common places for thrombus formation?

A

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

91
Q
A

Clinical Diagnosis (22 decks)

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