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Disease Processes > Haemodynamics > Flashcards

Haemodynamics Flashcards

1
Q

Duties of the right and left ventricle

A

Right Ventricle  Pulmonary Circuit (low pressure)

Left Ventricle  Systemic Circuit (high pressure)

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2
Q

Where does gas exchange occur

A

Capillary beds

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3
Q

Blood presence percentage

A 
Systemic veins - 60%
Systemic arteries - 15%
Pulmonary blood vessels - 12% 
Heart - 8% 
Capillaries - 5%
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4
Q

Aorta and vein structural difference

A

Artery - thick wall, has an internal elastic lamina and smooth muscle layer
Vein - thinner wall, loose muscle, able to dilate and absorb blood

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5
Q

What is vasoconstriction and vasodilation

A

Vasocontriction – narrowing blood vessel (increase in BP)

Vasodialtion – dilation of blood vessel (drop in BP)

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6
Q

Renal Physiology

A

Important for bone mass, and synthesis of bicarbonate reabsorption

Kidneys activate vitamin D

Formation of urine – removal of wastes

Regulates plasma ions (Na+, Cl-, PO43-, K+, Ca2+)
Regulates pH (H+, HCO3-)

Endocrine Function (Vitamin D, Renin-angiotensin-aldosterone system, EPO)

Regulation of blood volume

Regulation of blood pressure

Metabolism – deamination of αα, detoxification of drugs/toxins

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7
Q

Describe RAS

A

Nephron (filters blood)  kindeys activate RAS  increase in vasodilation and the release of angiotensin II  smooth muscles in blood vessel constrict  cause increase in HR and sympathetic tone  angiotensin II can also lead to the release of aldosterone

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8
Q

Kidney and erythropoietin relationship

A

Hypoxia –> leads to more EPO production —> increase RBC production

Hypoxia —> leads to anaemia if EPO doesnt occur—> lethargy and increased heart rate

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9
Q

Haemopoiesis

A

the production of all of the cellular components of blood and blood plasma. Immune cells are formed through this process

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10
Q

What is anaemia

A

decreased number or quality of RBCs
Excessive loss or RBCs

Reduced synthesis (decreased EPO, dietary deficiency of iron, vitamin B12 or folic acid)

Increased destruction

Can be passive or sudden onset

Can be caused by ulcers or cancer

Can affect the CNS  can make the heart work harder

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11
Q

Lymphoma and leukaemia

A

always malignant cancers involved with blood or lymph

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12
Q

Lymphoid organs categories and names

A
  1. Primary lymphoid organs
    Bone marrow
    Thymus
  2. Secondary lymphoid organs
    Spleen
    Lymph node
    Lymphoid tissues of the Alimentary tract
    Gut-associated lymphoid tissue (GALT)  Peyer’s patches
    Respiratory tract
    Mucosa-associated lymphoid tissues (MALT)  tonsils
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13
Q

Duty of lymph nodes

A

Lymph nodes filter blood and look for targets for the immune system –>microorganissms enter the interstitial tissue –>potentially enter the lymph –>naïve lymphocytes which haven’t been presented with antigen target antigen presenting cells present the targets to the lymphocytes

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14
Q

Duty of spleen

A

Filters old and new RBCs
Filters circulating blood
Immunological response against blood borne antigens

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15
Q

Functional unit of the liver

A

Hepatocytes (liver cells) make straight lines  in between are sinusoids (leaky capillaries)

Portal Tract (portal triad)  located around the functional units  has bile duct, portal vein and hepatic artery

Has two blood supplies (venous and arterial)

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16
Q

Functions of the liver

A
  • Storage of vitamins (A, B12).
  • Metabolism of bilirubin
  • digestion of fats through production of bile salts
  • metabolism carbohydrates, fats, proteins, vitamins
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17
Q

Hydrostatic pressure

A

forces fluid from vessel into the tissue

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18
Q

Exudate formation

A

in a acute inflammation because of hyperamia (active increase in blood flow to the area)  increase in hydrostatic pressure

Epithelial cells increase permeability thus allowing for the protein to leak out of the vessel

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19
Q

Congestion

A

within venous system due to passive build up or due to failing heart in which the muscle doesn’t contract as forcefully and oedema

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20
Q

Categories of oedema

A
  • Increased Hydrostatic Pressure: Reduced venous return
  • Reduced Plasma Osmotic Pressure: Reduced protein (hypoproteinemia)
  • Lymphatic Obstruction: Inflammatory, cancer, post-op/irradiation
  • Sodium Retention
    Renal & endocrine disorders
  • Inflammation
    Acute, chronic & angiogenesis
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21
Q

What is haemorrhage

A

Escape of blood from ruptured vessels

22
Q

Consequence of haemorrhage determined by?

A

Site
Amount lost
Speed of loss

23
Q

Hematoma

A

Accumulation of blood

24
Q

Signs of shock

A

Low peripheral blood flow

Excessive sympathetic stimulation

Thirst, altered skin temp, decreased BP, increased HR, decreased venous pressure, decreased urine output,

Decreased cellular perfusion, increased lactic acid, cell death

Once entering shock  cannot come back

25
Q

Anaphylaxis

A

Body overreacts to a specific substance

Inflammatory response

26
Q

Thrombus

A

Blood clot attached to the wall of the vessel or ventricle of the heart

27
Q

Embolus

A

Undissolved mass travelling in the blood

could be a thrombus or fat from a bone fracture

28
Q

Aneurysm

A

an abnormal, localised, dilatation of an artery or ventricle

29
Q

Causes of necrosis

A

Blockage in arterial system – Ischaemia - Necrosis

Blockage in venous system – congestion of poorly oxygenated blood- Haemorrhage -Necrosis

30
Q

Normal haemostatic process

A

The maintenance of fluid blood & the formation of a haemostatic clot in response to injury
Vital for everyday to repair damage to endothelial lining

31
Q

3 components of haemostatic process

A

Vascular wall, endothelium

Platelets

Coagulation cascade

32
Q

Steps following injury

A

Lose endothelial cells which normally make anticoagulants

Underlying CT is procoagulative

Coagulation cascade begins and the activation of platelets

Forms blood clots

33
Q

Abnormal Blood Flow

A

often described as turbulent blood in the arterial system (RBCS bashing against the vessel wall – can lead to endothelium damage) /  Venous Circuit – Static Blood (blood isn’t moving)

34
Q

Hypercoagulation

A

Increased blood coagulation

35
Q

Risk factors of venous thrombus

A
  • Stasis: blood not moving

- Hypercoagulation: higher chance of forming a clot

36
Q

Superficial venous thrombus

A
  • rarely embolise

Overlying skin has a high number of nerve endings

Oedema downstram  blood below clot can passively form a clot

Ulceration of overlying skin

37
Q

Deep venous thrombus

A

Often silent or asymptomatic

May cause swelling of the limb

Deep vein thrombi often embolise
For transiently  iliac or femoral veins  forms large mass or clot  can dislodge and embolise

Those at greatest risk are bed bound

Embolis will enevitably always go towards the lungs

38
Q

Atheroma

A

Sclerotic plaque in an artery

39
Q

Atherosclerosis

A

the chronic inflammatory process of changes (accumulation of lipids, Ca2+, inflammatory cells, etc) within the intima lining of an artery

40
Q

Risk factors for atherosclerosis

A

Increasing age
Male gender
Genetics
Smoking

Diabetes

Systemic Hypertension

Hyperlipidaemia (high LDL, low HDL)
/dyslipidaemia

Visceral adiposity

Infection (e.g.
Herpes virus, cytomegalovirus)

Immune/autoimmune processes

41
Q

Evolution of arterial wall changes in the response to injury hypothesis

A
  1. Platelet activation & adhesion at the site of endothelial injury.
  2. Leukocytes & monocytes attracted to injury & migrate into vessel wall where the latter mature into macrophages
  3. Smooth muscle cells migrate into the intima from the medial layer and proliferate
  4. Inflammatory mediators released from platelets, macrophages, lymphocytes, smooth muscle cells etc propagate the process
  5. Smooth muscle cells secrete components of the ECM
  6. Lipid accumulates within the lesion
  7. Smooth muscle cells & macrophages engulf lipid (macrophage foam cells)
  8. Cells undergo necrosis and stimulate further inflammation
  9. A fibrous cap forms over the lesion
42
Q

Risk factors of atherosclerosis

A

Reduced vascular elasticity
Increased vascular resistance
Swelling/bleeding in plaque
Leading to systemic hypertension

43
Q

Atherosclerosis–>Vascular Pathology

A

Arterial Circuit  Thrombus builds up passively  bits can break off (become embolus)  aneurysm can form in the area of atherosclerosis

44
Q

Atherosclerosis–>Death

A
  1. Bleeding & swelling within the lesion–>Vessel Occlusion –>Infarct
  2. Thrombus formation –>Occlusion –>Infarct
  3. Thrombo-embolus –>Occlusion –>Infarct
  4. Aneurysm –> Rupture –> Hypovolemic shock, death
  5. Aneurysm –> Thrombus & embolus –> Infarct
45
Q

Blood circuit of the brain

A

carotid and cerebral arteries

- branching arteries have a high risk of atherosclerosis

46
Q

Aorta and atherosclerosis

A

Abdominal aorta very prone to forming atherosclerosis

Embolus is an issue because it can cause an infarct or damage in the lower limb  not necessarily gonna lead to death

Atherosclerosis will lead to death if aneurysm forms and ruptures  aorta is heamorraging internally  die of shock

47
Q

Differences between venous and arterial thrombi

A
  1. Venous - Initiated by stasis & increased coagulation
    Red (more RBCs)
  2. Arterial - Initiated by endothelial injury & atherosclerosis
    White or striped (more platelets)
48
Q

How does venous and arterial system treat thrombi

A

Venous  target the coagulation cascade

Arterial  target the risk factors for atherosclerosis

49
Q

Hypertension and types

A

Elevated BP

Systemic Hypertension  risk factor for the development of hypertension

Pulomary Hypertension  can be caused by COPD –> high blood pressure in pulmonary circuit

50
Q

Transudate

A

fluid with low protein, due to increased hydrostatic pressure and decreased osmotic pressure

Disease Processes (13 decks)

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