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442 Cards in this Set

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Do all arteries carry only oxygenated blood?

Nope

What is autonomic neuropathy associated with?

Silent (painless) myocardial ischemia

T\F a widened pulse pressure is found in shock and congestive heart failure

False

Does skeletal muscle or cardiac muscle have a higher oxygen demand?

Cardiac muscle is higher

What does cessation of blood flow to the myocardium produce?

Immediate ischemia

Does unstable atherosclerotic plaques compared to stable plaques have

Blah

Risk factors for atherosclerotic heart disease

Obesity


Male


Inflammation


Sedentary lifestyle


High LDL


Low HDL

Does cocaine promote thrombosis by activating platelets?

Yes

Is cocaine a vasodilator?

No it's a vasoconstrictor

Does cocaine decrease heart rate?

No it increases it

Neutral pH

7.0

In humans normal arterial blood pH

7.4 (7.35-7.45)


Slightly alkalotic, slight base excess, slight HCO3- excess

Acid =

H+ which = protons

Charge

Increase H+ does what to pH

Decreases pH so it's more acidic/ less base

Decrease H+ does what to pH

Higher pH so less acid and more base

pH equations

pH=-log[H+]


Or


pH= [HCO3] / [paCO2]

Metabolic and respiratory parts that make up pH

Metabolic = HCO3 levels


Resp = paCO2 levels

How does the body deal w acid?

By using HCO3 buffers protons, takes away acid but leaves conjugate base - that has negative charge (aka an anion)

Kidney and HCO3

It is made by kidney but takes few days to make significant level, kidney also saves/re absorbs HCO3 to elevate levels

H2O and CO2- what happens to them in the body

Water/co2 are exhaled by lungs, some h2o is used by body, h2co3 (carbonic acid) an intermediate metabolite is present in very small concentrations, H+ is buffered (removed by proteins)

H2o + co2 <-> ______ <-> ______

H2co3


H+ + hco3

Normal arterial paco2

35-45

Arterial bicarbonate normal levels

Hco3: 24-31


Kidney related

Normal levels of pH, Paco2 and hco3 in arterial blood

PH: 7.35-7.45


Paco2: 35-45


Bicarbonate: 24-31

Respiratory alkalosis blood levels

PH= greater than 7.45


PCo2 = less than 35

Etiology of resp alkalosis

Hyperventilation, anxiety, stress


Drugs. Aspirin/caffeine intoxication


High fever

Metabolic acidosis blood levels

PH less than 7.35


Hco3 less than 22

Metabolic acidosis etiology

Diarrhea, renal tubular acidosis, lactic acidosis, ketoacidosis, shock, cardiac arrest, toxins ethanol, methanol, ethylene glycol

Respiratory acidosis blood leveks

Ph less than 7.35


Paco2 greater than 45

Respiratory acidosis etiology

Narcotic overdose, severe CNS injury


Airway obstruction


Severe asthma pneumonia copd

Metabolic alkalosis

Ph higher than 7.35


Hco3 greater than 31

Metabolic alkalosis etiology

Vomiting


Gastric drainage


Loop diuretics


Too much antacid

If bicarbonate level goes down you can become...

Acidodic

Major buffer for H+ in the body

Hemoglobin / proteins in general

Arterial vs Venous blood

arterial: higher O2 levels, standard for blood gases


Venous: lower O2, higher co2, more acidodic

2 types of immunity

Innate (natural/native)


Adaptive (acquired, specific)

List innate immunity traits

Physical/molecular/cellular defenseman place before infection


Low levels, always ready


Always present


Antigen nonspecific


Respond immediate


No immunologic memory


Attacks nonself


Doesn't distinguish between different microbes

What does innate immunity recognize

General classes of molecules shared by related groups of microbes that are essential to their survival


Does not recognize specific antigens

Examples of innate immunity

Epithelial barrier (skin, cilia, mucus, stomach acid, saliva, tears)


Macrophages, neutrophils, eosinophils, nk cells, dendritic cells


Plasma proteins


Lysosomes

Immune system that doesn't distinguish between different mucrobes

Innate

Physical/molecular/cellular defenseman place before infection


Low levels, always ready


Always present


Antigen nonspecific


Respond immediate


No immunologic memory


Attacks nonself


Doesn't distinguish between different microbes

Innate immunity

Epithelial barrier (skin, cilia, mucus, stomach acid, saliva, tears)


Macrophages, neutrophils, eosinophils, nk cells, dendritic cells


Plasma proteins


Lysosomes

Innate immunity

Natural killer cells are part of__ immunuty

Innate

Less rapid but more effective immunity

Adaptive

Initially naive but then develops memory, 1st must recognize foreign agen then process then produce amplified response

Adaptive immunity

Antigen specific immunity

Adaptive

Immunity that attacks specific microbes at specific antigens

Adaptive

2 types adaptive immunity

Humoral (antibody proteins in blood)


Cell mediated (phagocytic cells)

Humoral immunity

B cell


Antibody proteins in blood

Cell mediated immunity

T cells


Phagocytic cells

Immunity that recognizes general class of lipopysaccharide molecules in gram- bacterial walls

Innate

Immunity recognizes antibody specific to endotoxins o antigen of e.coli in cell wall

Adaptive

T cells come fron

Thymus

B cells come from

Liver, then thymus, then bone marrow, then blood

Immunity you need to be exposed a second time for response

Adaptive

More specific immunity

Adaptive

First identified as antigens that evoke rejection of transplanted organs

Mhc ( majorhistocompatabity complex)

Aka HLA (human leukocyte antigen) in humans

Mhc

Mhc

Major histocompatibility complex


Important in organ transplant


The better the match of similar antigens between recipient and donor, the less rejection of organ by recipient

Where are different lymphocytes generated and where do they mature

Generated from stem cells in bone marrow or fetal liver


B cells mature in bone marrow


T cells mature in thymus then go to lymph nodes to wait to be activated by antigen presenting cells

T lymphocyte functuon

Functions in cell mediated immunity


- virus


-rejection of tissue grafts


-delayed hypersensitivity reactions (ex. Tb skin test)


-intracellular microbes (ex. Legionella pneumonophila)


-graft vs host


- contact sensitivity

CD4+

Type of t lymphocyte


Master regulator for the immune system


Important in aids

Types of t lymphocytes

Memory cells


Cd4+


Cd8 (become cytotoxic T cells)


Regulatory T cells (suppress immune response)

Cytokines

Small cell signaling proteins


Act through cell surface receptors


After releasing cells itself, immediate adjacent cells, distant cells


Specific kinds released by different types of cells

Cytokines difference from hormones

-Higher initial concentration


- much greater increase 1000 fold trauma and infection


-made by different types of cells


- erythropoietin is a cytokine hormone

Erythropoietin

Cytokine hormone made by fibroblasts in kidney and CNS neurons and astroglia for memory


Tells precursor to Rbcs to start making rbcs

Are cytokines hirmones

No

Def of hormones

Secreted by discrete glands (ie B cells in pancreas) and affect distant cells and tissues

Effect of low concentration of cytokines

Local effects

Effects of high concentrations of cytokines

Systemic effects

1918 flu pandemic

Relatively more deaths in young people


Healthy immune system liability (produce stronger immune response, greater cytokine response, caused cytokine storm)

Cytokines

Cytokine storm

Cause of 1918 flu pandemic deaths


Fever, erythema, swelling, cachexia, fatigue, lack of cytokine regulation, loss of feedback loop


Implicated in sirs (systemic inflammatory respond syndrome)


So many cytokines killed virus but good cells too

What does cytokine storm cause

Inflammation, organ failure, infection

Plasma cells

Typically not in peripheral blood- found in lymph nodes


Part of B cell humoral adaptive immunity


Short lived, needs continuous colony stimulator factor


Produces antibody against antigen

Typically not in peripheral blood- found in lymph nodes


Part of B cell humoral adaptive immunity


Short lived, needs continuous colony stimulator factor


Produces antibody against antigen

Plasma cells

Immuniglobulins secreted by plasma cells

Igg


Igm


Iga


Ige

IGG

Immunoglobulin secreted by plasma cells


75% of all antibodies in normal individual


Crosses placenta, protects fetus

Igm

Immunoglobulin secreted by plasma cells


1st antibody to respond to antigen


Does not cross placenta

IGA

Immunoglobulin secreted by plasma cells


Mucosal production


Tears, gut, milk, saliva

IGE

Immunoglobulin secreted by plasma cells


Lowest concentration of any immunoglobulin


Parasites, allergy, hypersensitivity (anaphylaxis)

Immunoglobulin of highest concentration

IGG

First antibody to respond to antigen

IGM

Immunoglobulin in mucosal

(Tears, saliva, milk, gut) IGA

Lowest concentrated immunoglobulin

IGE

Immunoglobulin associated with parasites and allergy

IGE

Immunoglobulin that c tosses placenta

IGG

Immunoglobulin levels at birth

Newborn has high IGM and no IGG, if elevated IGG it is from mom so the baby had an infection in utero

At birth origin of IGG is...

Maternal

If elevated IGG at birth...

Baby got infection from mom in utero

Primary immune response

Macrophages phagocytize antigen, present to t helper cell that processes it, TH then activate B cells that produce antibodies


Takes 2-3 weeks

How long does primary immune response process take

2-3 weeks

What kind of response to vaccines produce

Primary immune response

Secondary immune response

B memory cells respond to antigen immediately


Plasma antibody levels rise w/in days

Boost shot produces what type of immune response

Secondary

IGG in response to antigen exposure (describe graph)

Primary antibody response levels go up then start to decline but in response to 2nd exposure go way up even higher

IGM in response to multiple exposures to antigen (graph)

Levels go up in each response but quickly got back to zero after each response so each response is the same level as before

What is Passive immunity

ATB pass directly into body from external source instead of body making them

Artificial examples of passive immunity

Diphtheria antitoxin


Antivenom


IV immunoglobulin


Rabies vaccine

Examples natural passive immunity

IGG through the placenta


IGA through breast milk

Natural active immunity

Exposed to antigen, develop disease and acquire immunity

Artificial active immunity

Vaccine exposed to antigen but no symptoms or very mild

Vaccination

Substance that produces immunity

Immunization

Process by which person becomes protected from disease


By vaccines or being exposed to the disease

Vaccination vs immunization

Vaccination: substance that produces immunity


Imm: process by which person becomes protected from the disease

Active immunity produces _____ so if re exposed, b and T cell response if _____

Immunologic memory


Rapidly mobilized

Types of vaccines

Inactivated or dead


Part of microbe


Attenuated live or viable

Inactivated or dead vaccines typically..

Need a booster

Live or viable vaccines

Less need for boosters


Can be excreted and inoculate others


Cannot be used in immunoconpromised (ex. Polio persists in intestines)


Do better job at stimulating cell mediated immunity

Do most vaccines do a good job of stimulating cell mediated immunity

No they do a poor job


But live attenuated do it better

Do vaccines stimulate innate immunity

None do currently

Immunoconpromised people and vaccines

May not develop immunologic response to vaccine antigen


Can develop vaccine associated disease from live attenuated virus

Can host develop disease from vaccine?

Very rarely and typically milder


Immunosuppressed can from live vaccines

Very rare things vaccines can cause

The illness itself


Act as super antigen and overstimulate immune system


Cause allergic reaction to egg protein because it is produced in embryonic chicken eggs

Vaccine autism myth

Thine risk (ethyl Hg) does not cause autism, it is almost never used anymore but autism is increasing

Adjuvant

Added to vaccine to stimulate immune response to target antigen

Hapten

Small molecule that can elicit immune response when attached to lrg protein carrier cannot elicit response by itself

Hapten is associated with...

Type IV cell mediated immunity

Immunosnescense

Deterioration of immune system w/ age


Decreased response to infection


Decreased immunologic memory especially to vaccination

What decreases in immunosenescence

Hematopoietic stem cells

Why do hematopoietic stem cells decrease in immunosenescence

With increasing age, oxidative damage to DNA and telomere shortening cause this

Disorders caused by the immune response are called

Hypersensitivity reactions

What are Hypersensitivity reactions

Excessive or inappropriate activation of immune response


Damage to body by immune response rather than by antigen

Types of hypersensitivity reactions

Type I - IV

Type I hypersensitivity reaction mediated by

IGE mediated


Type I hypersensitivity reaction aka

Immediate hypersensitivity


Antigens are called allergens


Pollen, dust, animal dander, food, chemical, drug


Can be localized or systemic, mild to life threatening

Anaphylaxis

Type I hypersensitivity


Acute, potentially fatal


Multi organ involvement


Release mediators from mast cells, basophils, eosinophils

Where are mediators released from in anaphylaxis

Release mediators from mast cells, basophils, eosinophils

What does anaphylaxis require

Previous sensitization and reexposure

Steps of anaphylaxis

1: previous exposure


2: reexposure


3: IGE release


4: mediator release (mast cells, basophils, eosinophils)


5: symptoms

Non IGE hypersensitivity reaction

Anaphylactoid


Mast cell and basophils activation rather than IGE


Can occur rarely in humans


Need prior sensitization unless complement activation on first exposure

Ex. Anapgylactoid hypersensitivity reaction

Radiocontrast dyes

What cells are covered with IGE and what happens when an antigen specific to IGE binds to it

Basophils, mast cells, eosinophils


Inflammatory agents are released like histamine

Routes of anaphylaxis

Oral


Parenteral


Topical


Inhalational

What does histamine do

Increases capillary permeability to allow WBCs and proteins to disperse to infected areas


Stimulates parietal cells to produce stomach acid

Morphine and histamine

Certain drugs like morphine displace histamine in granules release

List what histamine causes

Bronchoconstriction


Vasodilation


Separation of endothelial cells which inc capillary permeability


Arrythmogenic and myocardial depressant

Leukotrienes

More potent but slower than histamines in anaphylaxis

What is atopy

Exaggerated tendency to mount IGE response to a wide variety of environmental allergens


Inc circulating ige

% affected by atopy in western world

40

What is atopy frequently associated with

Eosinophilia

Examples of atopy

Hay fever, eczema, asthma

Local (atopic) reactions in type 1 hypersent reaction

Strong genetic component but contact w allergen must occurred before reaction develops


Hay fever rhinitis


Food allergies


Atopic dermatitis


Hives

Type II hypersensitivity reaction

Antibody mediated, cytotoxic


IGE and IGM bind to antigens on own cell surface

2 types of antigens

Intrinsic- part of own cell wall


Extrinsic- foreign antigen absorbed on to cells

Antibody mediated hypersensitivity reaction aka

Type II cell mediated

Steps of type II hypersensitivity reaction

1- drugs bind to Rbc membrane recognized as different


2-IGM or IGG bind to antigen


3- activate complement pathway


4- acute inflammation


5-cell membrane attacked


6- cell lysis

Example of type II cell mediated hypersensitivity

Penicillin induced hemolysis (not anaphylaxis)

Type III immune complex mediated hypersensitivity reaction

Formation of insoluble antigen-antibody complexes form in circulation


Localized or systemic

Steps of type III hypersensitivity reaction

1- deposited on endothelial blood vessels or tissues


2- activate complement


3- attract neutrophils


4- release inflammatory response


5- necrosis

Ex of type III immune complex mediated hypersensitivity reaction

Glomerulinephritis

Serum sickness

Immune complexes deposited in heart, joints, kidney, and skin

Causative agents of serum sickness

Antiserum


Horse antitoxin to diphtheria


Anti venom snake bites


Human blood products


Penicillin


NSAID


Monoclonal bodies

Type IV hypersensitivity reaction. Aka

Cell mediated

Type IV cell mediated hypersensitivity reaction T cells attack what

Antigen, not antibody-antigen

What does type IV hypersensitivity reaction primarily respond to

Mycobacterium species


Virus


Fungi


Protozoa

Type IV delayed type hypersensitivity

tB skin test ex. Mantoux


Allergic reactions ex. Poison ivy


Hypersensitivity pneumonitis

Def self tolerance

Ability of immune system to differentiate self vs nonself

What happens in autoimmune disease

Self tolerance breaks down and immune system destroys body tissue


Can be types I, II, III, or IV

Why can't autoimmune disease be type I

No disease mimics type I

Factors associated with autoimmune disease

Genetic: familial clustering


Environment: molecular mimicry

Environmental factor of autoimmune disease molecular mimicry

Microbe shares epitope with host, and cell walls hve human antigens in streptococci

Examples of Environmental factor of autoimmune disease molecular mimicry

Heart: rheumatic fever


Kidney: glomerulonephritis

Heart


Kidney

Superantigens

Coca using hyperactivation and release of large amounts of cytokines

Types of grafts

Xeno:different species


Allo: same species


ISO: identical twins

Host vs graft

Immunocompetent host recognizes foreign antigens on grafted tissues or cells and mounts an immune response which results in rejection

Graft vs host

Immunocompromised host grafted with foreign immunocompetent lymphoid cells with immunoreactive T cells in the graft recognize the host tissue as foreign and mount immune reaponse

Hygiene hypothesis

Lack or early childhood exposure to antigens such as infections, symbiotic flora, parasites, increased susceptibility to allergic disease later in life


Lack of exposure leads to defective immune tolerance


When exposed later in life exaggerated response

Groups with higher allergic disorders because of hygiene hypothesis

Small families


Not go to daycare


Live in clean, like city vs farm


Used antibiotic in 1st year


Inc in affluence

Primary immunodeficiency disorders

Congenital: most recessive (autosomal or xlinked)

Secondary immunodeficiency disorders

Loss immunoglobulins through GI tract


T cell deficiency after viral disease


Drugs and toxins


Aging

Importance of early detection of immunodeficiency disorders

Prevention of exposure


Available treatment


Avoid live virus vaccines when indicated

IGA deficiency

Most common (1/700 Caucasians)


GI/eye/nasopharyngeal infections because that's where IGA is secreted


Treatment with IVIg can cause anaphylaxis

Most common immunodeficiency

IGA deficiency

Combined T and B cell defects

Lymphoid progenitor cells defective so bothT and B cell lineages are affected


Infants suffer recurrent infections, especially opportunistic


Spectrum from mild to fatal

SCID

Severe combined immunodeficiency disorder


-absent t and B cell immunity and absence of circulating T and B cells


-infants course resembles aids

Treatment of scid

Bone marrow transplant

Infants with SCID symptoms

Like aids


- failure to thrive


- diarrhea


- opportunistic infections

HIV

Human immunodeficiency syndrome is a single strand of RNA retrovirus that incorporates into host cell dna


12 genes

What does hiv attack

Cd4 t lymphocytes which coordinates with response to infection


Until cd4 count very low patient is asymptomatic

In hiv, what does infection risk correlate with

Cd4 count

Are antibodies to hiv protective

No but it is helpful in diagnosis

Hiv causes

Immunosuppression


Infection


Malignancy


Waisting


CNS degeneration

___ is the virus ____ is the disease

Virus- hiv


Disease- aids

How hiv is transmitted

Blood (transfusion, needles)


Semen


Vaginal secretions


Breast milk

First stage of hiv

Acute infection


2-4 weeks after expose influenza like synptoms


Very high viral load but may be seronegative (test negative)

Second stage of hiv

Clinical latency


3-20 years (avg 8 years)


Generalized lymphadenopathy, weight loss, fever

3rd stage of hiv

AIDS ( acquired immunodeficiency syndrome)


Typically initial symptom is respiratory

HIV in infants

Failure to thrive


CNS abnormalities, higher incidence of encephalopathy than older patients


Developmental delay


Maternal antibodies can persist for up to 18 months

How is hiv transmitted to infants

Vertical


-in utero


-birth canal


Breast feeding

Signs of congenital hiv

Most appear clinically normal


Neurodevelipmental disorders


Early encephalopathy with microencephaly


Failure to thrive and growth retardation

Why some congenital hiv will show synptoms

Comirbidities such as ETOH or drug exposure or other congenital infections especially CMV are present

How to reduce mother to child hiv transmission

Cdc through key interventions reduced it from 35% to 5%


- testing


- antiretroviral medication to mother and exposed infant


- safe feeding practices

Hiv drug resistance

Hiv mutations common because virus replicates rapidly and doesn't contain proteins to correct mistake in replication


Reduce risk by using 2 antiretrovirals

Ebola barrier protection

Fluid impermeable gown, gloves, mask


Goggles or face shields


If copious secretions double glove and leg and shoe covering


If aerosol generating N95 mask and negative pressure room

Cardiac output=


Equation

Heart rate x stroke volume

3 major determinants of stroke volume

Preload


Contractility


afterload

Statins

Lower cholesterol in liver

70% of cholesterol is made where

In the liver

Co=

Hr (heart rate per min) x sv (stroke volume ml)

Flow =

Pressure / resistance

Radius of blood vessel=

Blood pressure - 1/r^4


Factor in resistance

Total blood volume is about...

5.5L

Def stroke volume

Blood pumped/ beat by each ventricle

Cardiac output def

Volume of blood pumped/ min by each ventricle

Thrombus

Blood clot, stationary

Emboli

Blood clot, migrates

Blood in pulmonary artery is..

Unoxygenated

Normal co for adult women and men

Men- 5.5


Women- 4.9

Normal HR

75

Normal stroke volume

70ml

What happens if co goes down a little, a lot, or to zero

A little: congestive heart failure


A lot: shock


Zero: cardiac arrest

Fick equation

Calculates blood flow to an organ

Preload is blood..

Pumped into the heart to be pumped out

Preload when standing

Blood pools in lrg veins in legs

Preload when laying down

Blood evenly distributed in veins


Inc central venous pressure-> inc diastolic volume -> inc sv-> inc pulse pressure

In the frank starling mechanism as ventricular end diastolic volume increases...

Stroke volume increases until a certain point it evens out and then too high will plummet

When patient was placed laying down with head lower than feet

Adverse outcome when used in shock


Called trendelenburg position

Increased preload effect on stroke volume

It will inc sv to an extent but will eventually overstretched the heart muscles and dec sv such as in fluid overload in congestive heart failure

When does the heart get blood

During diastole

Perfusion of the myocardium is during..

Diastole

Arteriosclerosis

Gardening and loss of elasticity of medium and larg arteries

What kind of disease is atherosclerosis

Chronic and slowly progressive


A symptomatic for decades


Symptoms depend on which artery and organs are involved


Very abrupt onset of symptoms when narrowing or obstruction of blood flow to organs occurs

Steps of atherosclerosis formation

1- endothelial cell injury


2- migration inflammatory cells


3- lipid accumulation & smooth muscle proliferation


4- plaque formation


5- occlusion and or rupture with thrombosis

First step of atherosclerosis formation

Endothelial cell injury


- smoking/pollution/ldl/mechanical stress(hypertension)->>> endothelial injury->> adhesion monocytes and platelets

Second step of atherosclerosis formation

Migration inflammatory cells


-endothelial cells express chemotaxic adhesion molecules


Monocytes and other inflammatory cells accumulate


Monocytes migrate to intima, become macrophages and engulf lipoproteins (especially ldl)

Third step of atherosclerosis formation

Lipid accumulation and smooth muscle proliferation


- activated macrophages release ROS that oxidize ldl-> macrophages ingest oxidized ldl and form foam cells-> macrophages induce migration and proliferation of smooth muscle cells and increase extracellular matrix

Fourth step of atherosclerosis formation

Superficial fibrous plaque made of smooth muscle cells and extracellular matrix (especially collagen) secreted by smooth muscle cells ->> necrotic core of fatty debris and lipid filled foam cells -> monocytes continue to infiltrate

Fifth step of atherosclerosis formation

Occlusion, rupture, and thrombosis


- rupture, ulceration, or erosion of fibrous cap initiates activation of extrinsic clotting system that forms thrombosis and obstruction


Can totally stop blood and kill tissue


May reorganize and cause stenosis

Determinants of plaque instability

Inflammation


Size of lipid rich core


Lack stabilizing smooth muscle cells


Stability and thickness of fibrous cap

What triggers plaque rupture?

Sympathetic stimulation often triggered by anger

How much occlusion or coronary artery can you have w/out symptoms

70%

Trigger for acute cardiovascular events

Outbursts of anger (sympathetic activity) causing changes in blood flow

Major risk factors for atherosclerosis

Hypertension


Diabetes


Smoking


Family history


Low levels of HDL


High levels of ldl

HDL vs ldl good and bad

Good- HDL


Bad- ldl

Importance of hdl

Takes days back to liver to be recycled


So if low levels foam cells accumulate causing plaque to accumulate and stick out more

Treatment of atherosclerosis

Lifestyle modifications (diet, exercise)


Stop smoking


Lower bp


Drugs (statins, low dose aspirin)


Invasive procedures (stents, bypass)

What gives blood flow a pulse

Contraction/ relaxation of left ventricle

Nicotine effect on blood flow

Causes vasoconstriction, so has a dose response curve with strain on the heart and blood vessel damage


Also causes inflammation and dysplasia

Vasoconstriction effect on peripheral vascular resistance, blood flow, and co

Periph resist- higher


Blood flow- lower


Co- less

What is blood flow proportional to

Radius^4

Systolic pressure

Peak pressure in arteries


Higher value in blood pressure notation


Occurs near end of cardiac cycle when ventricles contracting

Contributing factors to systolic pressure

Closure of aortic valve


Force and rate blood is ejected


Elasticity of aorta and large arteries


Ventricle contracting

Peak pressure in arteries is called

Systolic pressure

In blood pressure notation top number is ___ and bottom number is ____

Top is systolic bottom is diastolic

Diastolic pressure

Minimal pressure in arteries


Occurs when ventricles are relaxed and filling w blood

Contributing factors to diastolic pressure

Closure of aortic valve


Energy (rebound) stored in elastic fibers


Resistance to flow through arterioloes and capillaries

Pulse pressure what is

Difference between systolic and diastolic pressure


Proportional to sv (but not =)


About 40mmhg (120-80)

Autonomic nervous system regulation of heart

Parasympathetic via vagus nerve lowers HR


Sympathetic inc. HR (chrinitropic) and inc contractil it's (inotropic)

Autonomic nervous system regulation of blood vessels

Sympathetic vasoconstriction leads to inc peripheral resistance

Inc after load does what to the heart

Puts a strain on the heart

2 systems that regulate bp

Nervous- autonomic nervous systems (symp and parasympathetic)


Humoral (renin-angiotensin-aldosterone, and ADH)

Angiotensinogen

Made by liver and is just circulating in the blood until kidney secreted renin

How does the kidney secrete renin

The juxtaglomerular apparatus senses decreased renal perfusion so it secreted renin

Renin

Secreted by kidney


Converts angiotensinogen to angiotensin I

What triggers renin-angiotensin-aldosterone

Dec BP, extracellular fluid volume, and extracellular Na

ACE

From endothelial cells (esp in lungs) converts angiotensin I to angiotensin II


Reduce vasoconstriction and dilate arteries so it's used to treat hypertension

Angiotensin II

Active form


Strong vasoconstrictor

Aldosterone

Released by adrenal cortex


Deans orbs Na in the kidney

Systolic and diastolic #s in hypertension

Syst- greater than 140


Diast- greater than 90

Systolic greater than 140

Hypertension


LV hypertrophy


Inc myocardial O2

Normal diastolic and systolic pressure

Systolic less than 120


Diastolic less than 80

Per hypertension diastolic and systolic pressure

Systolic- 120-139


Diastolic- 80-89

Hypertension diastolic and systolic pressure

Systolic- greater than 140


Diastolic- greater than 90

Studies have shown a reduction of just __mmHg can reduce stroke

5 mmHg

Types of hypertension

Primary= essential, most common, due to weight gain and sedentary lifestyle


Secondary= due to other diseases, only 10%

Primary hypertension

Chronic elevation without other diseases present, no identifiable cause


90%


Inc metabolic demands, co inc


Ren-ang-ald elevated

Secondary hypertension types

Renovascular


Hyperaldosteronism


Oral contraceptive pills


Amphetamines/cocaine/alcohol


Decongestants


Hyperthyroidism


Sleep apnea

Most common secondary hypertension

Renovascular

Renovascular hypertension

Renal artery stenosis from fibromusculad dysplasia or atherosclerosis dec. blood flow which stimulates renin secretion

What causes primary hypertension

No specific disease but it is associated w excessive Edith gain and sedentary lifestyle

What causes secondary hypertension

Specific lesions

Treatment of hypertension

Lifestyle changes (diet/dec Na, exercise, weight loss, stress reduction)


Medications (ace inhibitors, beta blockers, calciumu channel inhibitors, diuretics)

Medications that treat hypertension

ace inhibitors, beta blockers, calcium channel inhibitors, diuretics



ABCD

Blood pressure in elderly

Age related inc in systolic bp


Loss elasticity of arteries (dec baroreceptor response, inc peripheral resistance)

What happens to blood vessels in elderly

Aorta and lrg arteries elastin replaced by collagen, increases wall stiffness, inability for vessels to distend and adjust to systolic bp, can't store energy needed to maintain diastolic bp

Thrombus vs embolism

Thrombus in vein with inflammation can occlude or break and cause embolism

Risk factors for venous thrombosis

Immobilization, bed rest, dehydration, surgery and inflammation injury to vessel wall, vein injury or compression, malignancy, inc blood coagulability aquired or inherited coag inhibitor factors

Pulse pressure relationship with stroke volume

Proportional but not equal, so if pulse pressure is 55 sv isn't 55 but it does inc

Effect of exercise on pulse pressure

Increases it

Normal pulse pressure

30-40

High and wide pulse pressure characteristics

Inc sv


Anemia


Fever


Thyrotoxicosis


Av fistula

Low and narrow pulse pressure

Hypovolemia


Shock


chf

Heart failure def

Not pump well enough to get O2 to peripheral cells

MI def

Myocardial infarction, aka heart attack, myocardial cells die, can be cause of heart failure, a systole, and death

Coronary artery disease def

Impaired blood flow, often to heart due to obstruction of coronary arteries


Often caused by atherosclerosis so used synonymously w/ atherosclerotic heart disease but there are other etiologies

Dyslipidemia

Risk factor for Coronary artery disease


LDL inc and HDL is lowered

Diarrhea effect on sv

Dec blood flow so less preload to sv dec

Vascular volume relationship with sv/bp

If it goes up so does sv/bp

Heart is an ____ organ

Aerobic

Interruption of blood flow to the myocardium causes..

Immediate ischemia

Heart and oxygen

Has 70% O2 extraction(very high) so blood flow interruption can cause rapid ischemia and if not reversed necrosis

How does cardiac monocyte get O2?

During diastole, has to go through diffusion and vessels in longer areas

What do you need for forward flow through the arteries

Systole

Determines coronary artery profusion pressure

Aortic pressure

Myocardial blood flow occurs during ___ and is regulated by ___

diastole


Metabolic demands of myocardium

2 vasocontrictors

Endothelin


Angiotensin II

2 vasodilators

Nitric oxide (NO)


Lactate


CO2

Made by endothelium

Nitric oxide and AcE

Causes of endothelial dysfunction

Inflammation such as infection or atherosclerosis

Def endothelial dysfunction

Coronary vessels w atherosclerosis lose ability to release vasodilators substances especially NO

Normally if demand inc... Is reduced which inc --

Coronary resistance dec


Flow inc

If blood supply doesn't meet demand in body

Ischemia will occur such as in an MI

What does lactate, co2, and prostacyclin have in common?

They are vasodilators that will inc blood flow

What does nitric oxide do?

Vasodilators that will inc blood flow

What do inc hr and systolic pressure decrease

Dec diastole and thus myocardial blood flow

Determined mvo2

Ventricular wall stress


Contractil it's


Heart rate (higher the hr lower the myocardial blood flow)

Afterliad

Pressure the left ventricle needs to overcome during systole

Angina

Paroxysmal chest pain/ pressure sensation


Transient myocardial ischemia


Fixed or stable plaque (69-70% occlusion)

Most common cause of coronary artery disease

Atherosclerosis

Legit happens in an MI

Unstable or rupture w platelet adhesion of plaque

Stable angina

Fixed or stable plaque


Precipitated by walkin, stress, cold, meal


Relieved by nitroglycerin

Unstable angine

Occurs at rest


Severe pain


Not respond to nitroglycerin

Nitroglycerin

Converted to NO by mitochondrial aldehyde dehydrogenase


Causes myocardial blood vessel dilation

Nitroglycerin dose for decreased preload

Lower dose

Nitroglycerin dose for a lower after load

Higher dose

Silent myocardial ischemia symptoms and causes

Painless


Autonomic neuropathy ex diabetes


Elderly


Previous mi

Symptoms of heart disease

Chest pain / pressure/tightness


Shortness of breath


Dizziness/ fainting


Fatigue


Pain in neck/ back/ jaw/ both arms

Do men and women have same symptoms

In women more diffuse, have chest pain less often than men

Cocaine effect on heart

Inc hr


Coronary artery vasoconstriction


Promotes thrombosis by activating platelets


Accelerates atherosclerosis

3 problems acute blockag of a blood vessel causes

Goes from aerobic to anaerobic


Loss of contractile function


Loss normal membrane potential causing arrhythmias

Serum biomarkers

A necrotic monocyte releases into the blood enzymes specific to it


Cells become necrotic from ischemia and release intracellular contents


Higher levels of Troponin (I and t specific for cardiac)


Create kinase

ST elevation

Full thickness injury and necrosis to myocardium can cause this

EKG indicators of MI

ST elevation


Wide Q wave


T wave inversion


May not show up early


Many don't have at segment elevation

STEMI

ST segment elevated myocardial infarction

NSTEMI

Partial thickness necrosis, ST segment is not elevated


Has partial occlusion

What is the st segment

Between qrs and t wave


Ventricular re polarization


Initial period of ventricular diastole

STEMI has ___ occlusion

Full// complete

7 treatments of mi

O2


Asa aspirin therapy


Pain control (narcotics)


Re perfusion (catheter)


Beta blockers


After load reduction (ace inhibitor)


Anticiagulation

Consequences of MI

Cardiac arrest


Chf


Cardiogenic shock


Sudden death (arrhythmia, ventricular fibrillation)


Mechanical (aneurysm, papillary muscle necrosis)

Major cause of death in sudden cardiac arrest

Arrhythmia most often ischemic in nature

What happens after an MI

Necrosis becomes scar


Macrophages remove necrotic tissue


Highly vascularized granulation tissue

Characteristics of scar tissue

Less vascular


Non contractile


Not conduct action potentials, abnormal rhythm

Rheumatic fever

Group a beta hemolytic streptococcus pyrogenes


Typically post pharyngitis but also after skin infection

Rheumatic fever body involvement list

Joints ( poly arthritis)


Skin


Brain (Sydenham's chorea)


Heart

Rheumatic fever effect on heart

Acute phase can have ps carditis inflammation


-pericardium 5-10%


Myocardium rare


Long term heart valves esp mitral and aortic affected

What type of reaction is rheumatic fever

Type II hypersensitivity antibody mediated

Glomerulonephritis

Type III antigen antibody


Destruction of glomerular basement membrane

Causes of bacteremia

Surgery


Endoscopy


Dental surgery


IV drug use


Catheter

Are fetal and maternal circulation directly connected

No

Does fetal and maternal blood mix

Not directly

What does placenta do for fetus

O2 and exchange of nutrients and waste

O2 saturation and paO2 of fetus

O2 saturation- 60-70%


Pao2- 30-35

Fetal hemoglobin has a ---- to o2

Higher affinity

Pao2 normal levels in artery

Pao2 level in artery 85-80, much lower in fetus

When does baby take first breath

After cord clamping, no longer placenta so get oxygenation from lungs

Before first breath babies blood flow bypasses...

The lungs, little blood flow 20%

For amen ovale

In fetal heart, blood bypasses the lungs and goes from the right atrium to the left atrium via this

In fetal heart blood goes from the -- to the --- via the ductus arteriosus

Pulmonary artery to aorta

What to check for MIs

Bio markers of MI =CPK and Troponin, elevated at segment, arrhythmias

Preload, contractility, afterload

Determinants of stroke volume


Preload=how much blood ventricle has to pump out


Contractility = how strong <3 muscle is


Afterload= heart has to pump against

Low output failure def

Inspired circulation and vasoconstriction

Compensation for low output failure in heart specifically

<3 stretched and thin so inc in size to inc preload


Or


Inc muscle mass/ wall size to generate greater force of cintraction

Low output failure compensation list

Fluid retention


Inc hr


Vasoconstriction to inc bp


Shunt blood away from less important tissues

How the body increases systemic volume

To inc preload the body uses ten-angiotensin-ald and ADH


Can result in fluid overload w inability to generate adeq. co

2 reasons why inc ventricular diastolic volume too much is bad

Weakened <3 can't pump as much/ as hard


Too much muscle makes the get stuff less fillable

Frank starling- inc preload will cause...

Inc sv, but too much preload will injure cardiac myocytes and actin-myosin will be iverstretched

Left ventricular dysfunction

-dec cardiac output


-dec in periph blood flow causing inc filtration pressure and pulm edema


- most commonly caused by myocardial infarction

Most common cause of left ventricular dysfunction

Myocardial infarction

Right ventricular dysfunction

Engorgement of systemic venous vasculature


Peripheral edema


Enlarged liver and decrement of liver function

In right ventric. Dysfunction engorgement of ___ vasculature occurs

Engorgement of systemic venous vasculature not pulmonary vasculature

In right ventricular dysfunction __ edema occurs and in LVF ___ edema happens

Right- peripheral


Left- pulmonary

High output failure edema

Excessive deman that <3 can't meet


Cardiac function supra normal but metabolic demand is still to high

Higher output failure symptoms

Thyrotoxicosis


Severe anemia


Arteriovebous shunting


Fluid overload ie massive blood transfusion

Shock def

Profound and widespread reduction of effective perfusion leads to 1st reversible, if prolonged irreversible tissue injury


Inadequate blood flow to meet metabolic demands of tissue

Is shock reversible?

At first but if prolonged can become irreversible

Six types of shock

Hypovolemic


Cardiac


Septic


Neurogenic


Anaphylactic


Obstructive

Neurogenic shock def.

Lack of sympathetic stimulation causing vasodilation

Anaphylactic shock def

IGE triggers mediator release leading to vasodilation and bronchoconstriction

Obstructive shock def

Block central flow

Hypovolemic shock def

Decreased circulating blood volume in relation to total vascular capacity


Dec in preload

Cardiac shock def

Cardiac pump failure


MI or heart disease

Septic shock def

Infectious can be initially vasodilated leading to peripheral vasodilation

Most common cause of death in American icus

Septic shock

Shock major contributor to early mortality in trauma

Hypovolemic

Shock associated with cardiovascular disease mortality

Cardiogenic

Cold clammy hands


Blue skin


Tachycardia (weak fast pulse)


Low bp


All symptoms of

Shock

Anxiety


Restlessness


Altered mental state


Symptoms of

Shock

Shallow labored breathing rate


Inc breathing


Thirst


Dilated pupils


Nausea and vomiting


Symptoms of..

Shock

Golden hour

In hypovolemic shock correct hypotension first then hypo fusion to w in first hour to greatly reduce death rate

Hypovolemic symptoms at 10% blood loss

Well tolerated tachycardia

Hypovolemic shock symptoms at 20-25% blood loss

Failure compensatory mechanisms, hypotension, dec co, orthostasis

Symptoms of hypovolemic shock at greater than 40% blood loss

Overt shock, hypotension, dec co, lactic acidosis

What is the inadequate circulation in cardiogenic shock due to

Primary failure of ventricles to function

Worst manifestation of uncompensated heart failure

Cardiogenic shock

Systolic bp for shock

Less than 90


Co markedly decreased

Number one cause of cardiogenic shock

MI

What is the preload a measure of

How much volume of fluids the ventricle has to pump

Determines preload

Venous return to heart

Dec stroke volume leads to

Dec co, which makes the body inc angiotensin II and norepinephrine which inc vasc resistance, which dec blood flow

Dec blood flow leads to further...

Myocardial ischemia, the release of cytokines, and necrosis

Fuehrer myocardial ischemia leads to...

Cytokines that cause necrosis

Triggers septic shock

Severe infection by gram + bacteria, gram - endotoxins producing bact, less commonly virus and fungi

Septic shock activates __, __, and __ that release __

Lymphocytes leukocyte and macrophages that release cytokines

What do cytokines do in septic shock

Injure endothelial cells, reduce production or anticoagulants, vasodilate, and depress myocardial function

Are cytokines in septic shock vasoconstrictors or dilators?

Vasodilator of myocardial function

Why is septic shock called warm shock

Vasodilation due to dec vasc resistance and hypovalemia


Other forms of shock inc vasc resistance leading to cold and clammy skin

Most common cause of neurogenic shock

Injury to CNS especially cervical area of upper spinal cord


Higher the injury the worse the symptoms

Aka distributive shock

Neurogenic shock

What happens in neurogenic shock

Dec sympathetic NS output so loss vasoconstriction and inc in hr


Unopposed parasymp NS so bract cardiac and vasodilaation

Bradycardia and vasodilation due to unopposed PNS is from

Neurogenic shock

IGE mediated shock

anaphylaxis

Anaphylactic shock major target systems

Resp- airway obstruction


CV- shock, hypotension, loss vasc resistance


GI- nausea, vomiting, cramps, pain

In anaphylactic shock you can have inc ____ ____ with massive ___ shifts

Inc vasc permeability


Fluid shifts


Because of inc in vasc permeability

Etiology of obstructive shock

Pulmonary embolism


Hemothorax


Cardiac tamponade


Pneumothorax

Pneumothorax

Compresses superior and inferior vena cava


Can compress heart


Compromises O2 and co2 exchange


Happens in obstructive shock

SIRS

Systemic inflammatory response syndrome


Locally released but inflammatory cytokines lead to systemic organ failure

Infection+ SIRS =

Sepsis

Tachycardia


Fever greater than 38 deg c


Tachypnea


Leukocytosis

SiRS

Causes of SIRS

Ischemia


Trauma


Pancreatitis


Burn


Seppsis

T/f placental transfer of IGG is an ex of passive immunity

True

TF hapten such as urishol in poison ivy can elicit immune response all by itself

False

TF inactivated vaccines can cause the disease in immunosuppressed host

False

Vaccines guarantee complete protection from disease

No

What immunoglobulin crosses the placenta

IGG

TF b lymphocytes of innate immunity can produce cytotoxic effects

False

Ebola infection serum treatment is an ex of... Immunity

Passive immunity

Joint pain, lymphadenopathy, rash, hives, what does this person have

Serum sickness

Immunoglobulin elevated with parasitic infestation

IGE

Produces IGE

Plasma cells

Newborn with seizures, rash, microencephaly and cataracts


High IGM level most likely due to

In utero stimulation by TORCH microbes

TF anaphylaxis is usually mediated by IGE

False

TF human blood products can cause serum sickness

True

TF eosinophils are only proinflammatory

False

Is IGA found higher in serum or secretions

Secretions

Histamine increases what that can cause edema

Capillary permeability

What do statins promote in the liver

Cholesterol production

TF HDL carries cholesterol from the liver to periphery

False

Can smoking cause hypertension by a mechanism other than atherosclerosis

Yes

Does inflammation play a minor role in atherosclerosis

No

___ myocardial activity inc myocardial blood fliw

Increased

Rupture of atherosclerotic plaque typical will not cause

Angina

What would you do for hypovolemic shock

Administer IV to expand intravascular volume

Does inc sympathetic tone happen in neurogenic shock

No

Dec hr


Dec vasc resistance


Inc vagal parasymp tone


Blue skin

Neurogenic shock

Cardiac output inc when

Preload inc which inc stroke volume

Right sided failure is associated with

Enforcement of periph vasculature and periph edema

Can septic shock be caused by fungi candida albicans

Yes

Left sided ventricular failure will manifest w edema and resp distress TF

True

TF dec urine output in shock is indicative of good renal perfusion

False

TF in hypovolemic shock angiotensin II will stimulate aldosterone production

True

TF aldosterone production by adrenal gland will cause kidney to tea sorb Na and h2o that will dec intravascular volume

False

In high output failure pulse pressure is ___

Increased