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5 signs of Acute inflammation

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Last updated

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Date created

Mar 1, 2020

Cards (166)

Section 1

(50 cards)

5 signs of Acute inflammation

Front

Redness Swelling Pain Fever Loss of fuction

Back

Ischemia

Front

Shortage of blood flow, often resulting from obstruction to circulation.

Back

Neutrophils appearance

Front

Segmented nucleus -2-3 lobes. Purple pink granules.

Back

Pyknosis

Front

Nuclear change indicating cell death, condensation of nucleus and clumping of chromatin. Nucleus becomes a dark shrunken mass.

Back

Dendritic Cell function

Front

- Antigen presenting cells - phagocyte and macrophagocytose - Prime T cells.

Back

Hypoxia

Front

Shortage of oxygen, but not complete lack

Back

Lymphocyte function

Front

Mediate immune responses B cells: produce antibody T cells: CD4 T helper cells secretes cytokines (Th1, Th2, 17 and treg) CD8 Cytotoxic cells induce apoptosis in target cell.

Back

Gangrenous necrosis

Front

Form of coagulative necrosis in a limb, appears dark. Ischaemic coagulative necrosis.

Back

Obese with full metabolic dysfunction

Front

INCREASED inflammation, DECREASED metabolic control, DECREASED vascular function.

Back

Metaplasia

Front

reversible change is adult cell type. A change from one cell type to another as a response to chronic injury. e.g. Smoking leads to squamous metaplasia of the bronchi. (ciliated columnar is replaced by squamous).

Back

Embolism

Front

Mobile thrombus, breaks off from thrombus and travels to new location where can cause clot.

Back

Atrophy

Front

DECREASED SIZE OF CELLS, tissues or organs.

Back

Basophils appearance

Front

Large cells with dark large purple granules.

Back

Atrophy can be due to:

Front

Diminished workload Reduced endocrine stimulation Diminished blood supply Loss of innervation Inadequate nutrition

Back

Basophil purpose

Front

Antigen presenting cell to drive Th2 responses. - secrete histamine, leukotrienes. - numbers are increased in allergic reactions. Can bind IgE

Back

Cardiac tamponade

Front

Compression of the heart due to accumulation of fluid in the pericardial sac. leads to rupture of heart wall. Prevents the heart from beating

Back

Eosinophil purpose

Front

Release granules that contain: -major basic protein - eosinophil cationic protein - Peroxidase

Back

Thrombosis

Front

Formulation of a clotted mass of blood (thrombus) in cardio vascular system.

Back

Eosinophil appearance

Front

Large cells with multilobed nucleus and large orange granules.

Back

Autophagy

Front

Intracellular degradation, self digestion. Lysosomal degradation of cell's' own components.

Back

Eosinophilia

Front

Increased eosinophil production due to IL-5 from mast cells, T cells and macrophages.

Back

NK cells, how are they targeted and what do they do?

Front

Activated by low MHC-1 or activating receptors on target cells. They induce apoptosis on target cells via the extracellular pathway by producing a large amount of cytokines.

Back

Liquefacive necrosis

Front

Inflammatory cells and enzymes liquefy the tissue, hypoxic death of cells in CNS. IF triggered by infection, liquid will contain high amount of neutrophils in the pus, which is eventually removed by phagocytosis leaving a CNS cavity.

Back

Lymphopenia

Front

Decrease in lymphocytes due to some drug therapy (cancerous), AIDs and severe stress.

Back

Lymphocytes T/B cells

Front

Mononuclear, variable in size and shape.

Back

Proliferation

Front

Growing expansion of cells in number and size

Back

Monocyte/macrophage role

Front

Phagocytes, produce pro inflammatory cytokines and present antigen to T cells.

Back

Neutrophilia and causes

Front

Elevated neutrophils Due to: - Infection - Inflammation - Drug induced steroid drugs - leukaemia of myeloid cells, - elevated levels of one type of cell. - promotion of neutrophil production by IL-8.

Back

Monocytosis

Front

increased monocytes - due to prolonged or chronic bacterial infection. Pneumonia or Tb bone marrow cancer

Back

Senescence

Front

Biological aging

Back

Two major reactions of Acute inflammation

Front

Vascular: Vasodilation, increased vascular permeability Cellular: Emigration of leucocytes

Back

Monocyte appearance

Front

Large cells with multilobed nucleus. Differentiate into macrophages when in the tissue. Long lived in tissue.

Back

Karyolysis

Front

Nucleus fades

Back

Hyperplasia

Front

Enlargement of an organ, due to INCREASED NUMBER OF CELLS . Can only occur in LABILE or STABLE tissue (those that undergo mitotic division)

Back

Hypertrophy

Front

Enlargement of an organ or part due to the INCREASE IN CELL SIZE, usually in muscle or organs such as the kidney.

Back

Lean with normal metabolic function

Front

Normal inflammation, metabolic control and vascular function

Back

3 stages of nuclear breakdown

Front

Karyolysis - nucleus fades pyknosis - nucleus becomes shrunken mass karyorrhexis - pyknotic nucleus breaks up.

Back

Coagulative necrosis

Front

Protein denaturation typically caused by ischemia or infarction. In coagulative necrosis the architecture of dead tissue is preserved for at least a couple of days.

Back

Obese with mild metabolic dysfunction

Front

INCREASED inflammation, DECREASED metabolic control and SAME vascular function.

Back

Caseous necrosis

Front

'cheese like' necrosis e.g. seen in TB.

Back

Neutropenia and causes

Front

Low neutrophils - Marrow suppression drugs - Infections (viral or bacterial) - Genetic

Back

Necrosis

Front

Cell changes due to cell death. Lysis of the cell - burst membrane and spilled cell contents.

Back

Opsonisation

Front

Coating of a particle with a substance that helps it to attach to a phagocytic leukocyte . Important opsonin is C3b of complement and antibody.

Back

Apoptosis

Front

Programmed individual cell death, not involved with inflammation. characteristics include - pyknosis and formation of apoptotic vessels containing nucleus and shit.

Back

Steatosis

Front

Accumulation of Triglycerides - most likely in liver cells. Accumulation of small lipid droplets in cytoplasm.

Back

Infarction

Front

Area of necrosis brought on by obstruction of the circulation.

Back

Lymphocytosis

Front

Increase in lymphocytes Common in acute viral infections or in neonate response to infection.

Back

Dysplasia

Front

Disordered growth, occurs after persistent injury or irritation.

Back

Oedema

Front

Swelling due to build of fluid in the tissue.

Back

Karyorrhexis

Front

Pyknotic nucleus breaks up

Back

Section 2

(50 cards)

Keloid

Front

Too much proud tissue (granulation tissue) or collagen - replaced with scar tissue

Back

Diapedesis

Front

process of vasodilation and increased vascular permeability of the affected areas blood vessels via chemical mediators, Monocytes, neutrophils and endothelial cells become STICKY from secretion of adhesion molecules (SELECTINS AND INTEGRINS) and adhere to the the endothelial cells - MARGINATION. Once adhered, the can move between the endothelial cell gaps - this process alone is called diapedesis. Neutrophils will die via apoptosis after 24-48 hours in the tissue - releasing destructive enzymes into tissue.

Back

What is sequestrum?

Front

Dead bone in osteomyelitis

Back

Clonal Proliferation

Front

Cells that have uncontrolled growth and fail to die. When clone is big enough it can replace normal marrow and infiltrate into other tissues, replacing and destroying normal cells.

Back

Exudate

Front

Due to the pooling of neutrophils, macrophages and protein rich plasma in injured areas (oedema). Globulin is present in selective protein rich exudate.

Back

Two processes of tissue repair

Front

- regeneration of cells of the same type These cells must be labile or stable and must have structural framework. - Replacement by connective tissue: fibrosis or scarring. When cells are permanent (brain and heart) or structural framework has been severely damaged.

Back

What are the 4 mechanisms of action that complement has?

Front

- To split C3 to generate C3a and C3b these then generate... - Opsonise microorganisms - Degranulate mast cells to release inflam and chemotactic mediators e.g. histamine - Assemble the membrane attack complex which causes perforation of target membrane.

Back

Chemotaxis

Front

the act of diapedesis and movement towards the affected area once through the vessel wall.

Back

Erythrocyte Sedimentation rate

Front

Fibrinogen is converted to fibrin which we can measure in the blood. Fibrinogen causes RBCs to stick together.

Back

Fibrinolytic pathway is activated by what?

Front

Plasmin - which has a main function of lysing fibrin clots. Can also cleave c3 to c3a and activate Factor XII.

Back

What is the NK cell killing mechanism?

Front

1. receptors on NK cells bind to surface molecules on target cell. 2. NK cells release PERFORIN which cause transmembrane channels in target membrane -> GRANZYMES enter cell and DNA fragmentation leads to death. OR 3. NK surface molecule Fas ligand binds to target cell surface molecule Fas which leads to apoptosis.

Back

Process of Neutrophil movement

Front

Initiated by TNF-a and IL-1 secretion from activated macrophages at site of infection. 1. Rolling of leukocytes along endothelial wall (Adhesion molecules - selectins are responsible for rolling) 2. Integrin (integrin ligand ICAM 1)adhesion molecules - cause leukocytes to adhere by high affinity to blood vessel wall. 3. Chemokines (mainly IL-8) produced at site of infection enter the vessel and bind to endothelial cells surface. 4. Migration of leukocytes occurs across endothelial cells into tissue - diapedesis - caused by histamine, serotonin and C3a and C3b.

Back

Acute inflammation is initiated and lasts..

Front

Initiated within minutes and lasts around 2-3 days

Back

Does the scar tissue achieve normal strength once healing process has occurred?

Front

NO, the scar only achieves 70-80% strength of normal tissue by 3 months. Never regain 100%

Back

Dendritic cell types of endocytosis

Front

- Phagocytosis - unspecific - Pinocytosis - more specific - smaller amounts - Receptor mediated endocytosis

Back

What mediators stimulate migration and proliferation of fibroblasts and where are they secreted from?

Front

Growth factors - TGF-B, PDGF, EGF, FGF from activated endothelium and macrophages - IL-1 and TNF-a

Back

Involucrum?

Front

New bone in the repair of osteomyelitis

Back

Healing by primary intention vs. secondary intention?

Front

Primary intention - clean incision with line of closure that fills with clotted blood, the dehydration of that tissue and blood result in a scab formation. Secondary intention - large tissue defect ( large gap in epithelium) which results in more inflammation, more granulation tissue - wound contraction due to myofibroblasts and secondary infection is very common with ulcer formation.

Back

Pus contents

Front

Dead tissue Living and dead leukocytes antibodies

Back

The three acute phase proteins

Front

Fibrinogen CRP- 1 Haptoglobin ALL RELEASED BY LIVER DURING INFLAMMATION

Back

Granulation tissue is composed of what and when does it appear in the healing process?

Front

-Pink, soft -Contains new thin walled blood vessels.(Endothelial channels over time differentiate into new blood vessels) -Fibroblasts -Connective tissue matrix (ECM) Appears 3-5 days after injury

Back

Membrane attack complex is composed of what?

Front

C5b links to c7,c8 and c6 with a ring of C9 on the outside. this complex punches a hole into the cell wall of bacteria causing lysis of the cell.

Back

3 ways acute inflammation is regulated

Front

- only occurs when there is tissue injury - Terminated when injurious agent is eliminated as mediators are short lived. - Activation of acute inflam. also triggers anti inflam reactions.

Back

What is acute osteomyelitis?

Front

Infection within the bone marrow cavity

Back

Natural killer cells respond how to MHC class 1?

Front

NK cell activity is inhibited when they recognise their own MHC 1 on target cells.

Back

Adhesion molecules

Front

Selectin and integrin regulated by cytokines released in response to infection or tissue necrosis.

Back

Which pathway ends up with more complement and why?

Front

Classical pathway, because you get a higher yield of the enzyme that chops up C3 and C5 so end up with more complement than the alternative pathway.

Back

Angiogenesis

Front

Formation of new blood vessels - mobilised by EPC being released from bone marrow.

Back

Can stable cells regenerate?

Front

Can go back into cell cycle once it has been stimulated. e.g. liver and kidney. IF they are hurt WITH original connective tissue they can repair. IF NOT they have to be replaced via fibrosis or scarring.

Back

Can permanent/quiescent cells regenerate?

Front

NO, they do not have ability to re enter cell cycle and be replicated. e.g. myocardial fibres in heart and brain cells. No fibroblasts present in CNS.

Back

Bradykinin as a vasoactive mediator facilitates..

Front

Dilation, permeability and pain.

Back

What does the innate immune response involve?

Front

- NK cells - activation of the alternative complement pathway - Phagocytosis - Acute phase proteins NO T OR B cells are involved in innate immunity.

Back

Margination

Front

The adhesion of monocytes and neutrophils to the endothelial wall of a blood vessel as a result of adhesion molecules.

Back

The three phases of scar formation and the time phrames

Front

1. Inflammation ~24 hours 2. Granulation tissue formation, with angiogenesis, fibroblast migration and proliferation and new ECM. ~3-7 days 3. Scar remodelling ~weeks - months - never regain full functionality. Get white hard scar + 3months.

Back

Myeloid stem cells become:

Front

Basophil Neutrophil Eosinophil Monocyte Can also become ethyroid cell - RBC. Are the main cell type associated with acute inflammation.

Back

What are the four stages of tissue repair?

Front

1. Angiogenesis - formation of new blood vessels 2. fibroblast migration and proliferation 3. Deposition of ECM 4.maturation and organisation (remodelling) of scar tissue

Back

Oxinisation

Front

The splitting of C3 and C5 into a and b subtypes for activation of complement system.

Back

What does Factor XII do and how does it get to tissue?

Front

Factor XII triggers both the kinin and coagulation cascades (clotting and fibrinolysis), it triggers this response by diffusing through the blood vessel epithelia as part of the plasma transudate when vessel has increased permeability. Once in the tissue, it is activated on contact with collagen or basement membrane of vessel wall.

Back

Chemical mediators involved with PAIN

Front

Bradykinin and prostaglandins

Back

Chemical mediators involved with HEAT

Front

TNF and IL-1

Back

Chemical mediators involved with Vasodilation

Front

- Histamine - Nitric Oxide - Prostaglandins

Back

C3a and C5a Facilitate what 6 things?

Front

Recruit neutrophils into the site Acute inflammation Vasodilation Chemotaxis Transudation - process of fluid crossing membrane Phagocytosis

Back

In innate immunity, once macrophages have been activated what do they secrete and what does that result in?

Front

TNF-a and Il-1 - Leads to E-selectin secretion (increased adhesion secretion) and ICAM-1 - act on blood vessel wall epithelia. Il-8 - recruits neutrophils

Back

Chemical mediators involved with Leukocyte recruitment, activation and chemotaxis

Front

- Cytokines ( TNF and IL-1) - Chemokines (IL-8) - C3a and C5a

Back

Can labile cells regenerate?

Front

Yes they are always in the cell cycle e.g. gut epithelium and skin. Usually always dying and dividing.

Back

timelines of healing.

Front

Back

Three types of leakage of blood vessels

Front

Normal - plasma proteins stay in vessel Transudate - fluid leakage due to increased hydrostatic pressure and decreased colloid osmotic pressure. Exudate - Fluid and protein leakage

Back

Thrombin as a key mediator of the clotting system does what?

Front

Converts fibrinogen to a fibrin clot and has proinflammatory effects (increased permeability and endothelial cell activation).

Back

Natural killer cells can acquire antibody via what?

Front

CD16 Fc receptors which allow specific antigen recognition.

Back

Chemical mediators involved with increased vascular permeability

Front

- Histamine - serotonin - C3a and C5a

Back

Section 3

(50 cards)

What is atherosclerosis?

Front

Lipid materials acting as a pathogen that is not eliminated causing a chronic inflammation response.

Back

What is Dyslipidemia?

Front

Elevated plasma cholestereol and TG, lower concentrations of HDL-C - contributes to atherosclerotic risk.

Back

Three phases of bone repair and the time frames

Front

Inflammatory phase 1-5 days (first week) Reparative phase - 7 days -few weeks Remodelling phase - long term

Back

What is hypercholesterolemia outcomes?

Front

Increase in cholesterol via LDL - big increase in serum cholesterol - serum TG levels are normal - High atherogenecity

Back

Hypertriacylglyceridemia

Front

Increase in VLDL Normal to slightly elevated sreum cholesterol increased TG serum levels has relative atherogenicity.

Back

Systemic miliary Tb

Front

The organisms spread through the blood system Almost every organ in the body can be seeded Lesions resemble those in the lung

Back

B Cells and T cells produce what?

Front

B cells produce antibody (IgM, IgG, IgA and IgE) T cells divide into CD4 T helper cells which secrete cytokine TH1. TH2, TH17 and Treg. CD8 cytotoxic cells induce apoptosis in target cell.

Back

High levels of ESR, HDL, Ferritin, Homocysteine and blood glucose, monocytes are indicators of what?

Front

Chronic inflammation

Back

What are fatty acids made out of?

Front

Carboxylic acid with an aliphatic chain.

Back

What is the synoviums function

Front

Lines the non-articulating aspects of the joint, secretes synovial fluid which acts as lubricant.

Back

What are foam cells?

Front

Macrophages that have engulfed oxidised LDL. These form fatty streaks in the arterial intima and start off atherosclerosis.

Back

The synovial Knee joint is protected against bone ends grating together by which secretions?

Front

Type II collagen, aggrecan (major proteoglycan - provides hydrated gel structure) and proteoglycans.

Back

Involucrum

Front

The new bone that is laid down beneath the periosteum which entraps the sequestrum causing chronic osteomyelitis.

Back

Define Antigen

Front

Any substance that can bind to an antibody and generate an immune response.

Back

What is osteoarthritis?

Front

A change in the homeostasis of chondrocytes, cartilage is degenerated as synthesis of proteoglycans and collagen are decreased and their degradation increases. This disease leads to fibrillation of cartilage. 1. Fibrillation 2. Eburnation 3. Sclerosis 4. Subchondral cysts 5. Osteophytes.

Back

Miliary pulmonary disease

Front

Organisms drain through lymphatics into the lymphatic ducts, and to right side of heart Miliary lesions may expand and coalesce to yield almost total consolidation of large regions or even whole lobes of the lung

Back

Wound rupture (dehiscence), ulceration (inadequate blood supply - common in diabetics, and infection are all examples of what?

Front

Factors leading to inadequate scar formation.

Back

What are the key components of a normal joint?

Front

1. Cartilage 2. Synovium 3. Supporting ligaments and joint capsule

Back

Which two lipids contribute most to disease?

Front

Triacylglycerols and cholesterol.

Back

What are epitopes?

Front

It is the part of the antigen recognised by the antigen combining site of an antibody or T cell receptor. Conformation is important as it determines the degradation and recognition of the antibody.

Back

What is osteomyelitis?

Front

chronic Inflammation of the bone marrow. starts off as acute due to infection. Usually caused by Staph. Aureus.

Back

What is a callus composed of?

Front

Granulation tissue containing bone or cartilage.

Back

IDL composition

Front

25% TG and 35% cholesterol

Back

What is the primary complex?

Front

when Tb has infected the apex area of the lung and a lymph node - isolated ghon complex +lymph node.

Back

APO E is located on what lipoproteins?

Front

Chylomicrons, remnants, VLDL, HDL, IDL. Acts as LDL receptor ligand

Back

three outcomes of chronic inflammation

Front

-Abscess - via liquefactive necrosis -Persistent inflammation - chronic, due to failure to completely eliminate injury to the tissues. -Healing

Back

What is rheumatoid arthritis?

Front

The pathogen is part of the synovial tissue/cells - destruction of tissue and joints occur from continued pathogen.

Back

Joint immobility via fibrous tissue or bone fusion prevents movement in rheumatoid arthritis is called what?

Front

Ankylosis

Back

Bile acid, sex and adrenal hormones and vitamin D all need what lipid component?

Front

Cholesterol.

Back

sequestrum

Front

Dead bone resulting from either pressure within the marrow cavity or due to loss of the blood supply because of the lifting of the periosteum,

Back

LDL

Front

5% TG and 60% cholesterol

Back

APO B-100 is present on what lipoproteins and has what function?

Front

VLDL, IDL, LDL Acts as LDL receptor ligand.

Back

What are the components of a granuloma?

Front

inside - the silica (foreign body like TB) then layer of macrophages which can form giant cells with multiple nucleus's, then have collagen, granulation tissue, lymphocytes and neutrophils are the outside.

Back

What is rheumatoid arthritis?

Front

The formation of a pannus in the joint which erodes the cartilage and bone, causing joint deformation and pain. treated with steroids, immunosuppressants and physiotherapy.

Back

Chylomicron composition

Front

85% TG and 10% cholesterol

Back

Duration of chronic inflammation?

Front

Weeks

Back

What is psoriasis

Front

Immune response triggers skin to reproduce heavily which builds up outer layers (epidermis and keratin) - the epidermis thickens and blood flow increases causing red skin with grey scales.

Back

Pus oozing into soft tissue in chronic osteomyelitis is called what?

Front

Abscess

Back

VLDL composition

Front

55% TG and 20% cholesterol

Back

Eburnation

Front

The grinding of bone that results in the surface becoming shiny and smooth - like ivory bone.

Back

Hyperlipidaemias

Front

increase in cholesterol and TG only

Back

What are the four major lipids in the body?

Front

1. Cholesterol 2. Phospholipid 3. Fatty acids 4. Triacylglycerol

Back

Abscesses may open onto the skin surface forming what?

Front

A sinus.

Back

HDL

Front

5% TG and 20% cholesterol.

Back

What are triacylglycerols made out of?

Front

Glycerol and 3 fatty acids.

Back

What are phospholipids made out of?

Front

Glycerol, 2 fatty acids and a phosphate group.

Back

Fibrillated cartilage

Front

Cartilage breakdown - edges become frayed and jagged - fibrillation occurs as cartilage is lost over time.

Back

Pannus is made of what?

Front

granulation tissue, proliferation of synovial lining cells and fibrous connective tissue. Macrophages, neutrophils and dendritic cells will also be present.

Back

Wound contraction is most common in what victims and why?

Front

Burn victims, because there is too much wound contraction over a joint so can lose joint function - common in burn victims as healing is accelerated and most skin has been destroyed.

Back

Outline the key stages in atherosclerosis

Front

1. Damage in blood vessel epithelia 2. LDL enters the intima and becomes oxidised. 3. Monocytes enter the wounds and convert to macrophages where the uptake the oxidised LDL. 4. The macrophages become foam cells that either die to release cytokines and cholesterol increasing plasma levels. 5. Cytokines act on smooth muscle cells so that they replicate and proliferate and form the fibrous cap on top of the lipid core from the LDL cholesterol. 6. the plaque/cap can rupture or become weakened and become a thrombus or detach and become an embolism.

Back

Section 4

(16 cards)

What is angina pectoris?

Front

Chest pain due to the increased demand of oxygen by the heart. This DOES NOT cause myocyte necrosis as it is caused by MI but not sufficient enough to cause necrosis.

Back

What are the ECG changes in MI?

Front

- Elevation of ST - Inversed T wave - Increased amplitude of Q wave.

Back

What are the cells involved with atheroma?

Front

- Endothelial cells - platelets - Smooth muscle cells - Macrophages - lymphocytes - Neutrophils

Back

Permanent myocardial injury from MI occurs after how long?

Front

2-4 hours so rapid diagnosis is very important in treatment.

Back

ApoA1 containing lipoproteins are what?

Front

Atheroprotective.

Back

Diabetes has what effect on cholesterol levels?

Front

Decreases VLDL clearance and increases VLDL production. Due to no VLDL uptake from plasma, insulin causes FFA to be released into blood stream and packaged as VLDL by liver.

Back

Increased IDL outcomes

Front

Increase IDL and chylomicron remnants. Increased serum TG and cholesterol concentrations. High atherogenicity.

Back

Types of angina

Front

- Stable angina (most common) - Unstable angina ( may occur at rest or sleep).

Back

Defective Apo E function outcome

Front

IDL no reuptake into the liver of endogenous pathway. NO uptake of remnants via remnant receptor into the liver in exogenous pathway. This will decrease VLDL production.

Back

LPL deficiency outcomes

Front

- Elevated chylomicrons - Cholesterol serum concentration is normal to slightly high. - Sever increase to TG serum levels. - no atherogenicity.

Back

What biomarkers are released from injured myocytes during ischaemia?

Front

- Cardiac Troponins T and I - Creatine Kinase

Back

Acute rheumatic heart disease usually follows a strep throat infection?

Front

Yes.

Back

Aneurysm?

Front

Localised abnormal dilation of a blood vessel.

Back

LDL receptor deficiency outcomes

Front

LDL and IDL cannot get into the liver ( no clearance) and go through endogenous pathway. will increase IDL, and LDL plasma levels. Decreases HDL production from LDL through extrahepatic tissue.

Back

Tangier disease is what?

Front

Extremely low HDL-C levels.

Back

What are the layers of an artery?

Front

Endothelial cells Intima (internal elastic lamina) Media Adventitia

Back