BECOM 2 Exam #1 Flashcards
atrial natriuretic factor
found in the myocardium
- Secreted when excessively stretched
- Increases sodium and water loss by the kidneys
Zonula adherens are responsible for what in the myocardium and associated protein
- Anchoring sites for actin filaments of terminal sarcomeres
- α-actinin is main actin-binding protein
Macula adherens are responsible for what in the myocardium and associated protein
- Bind cells together to prevent separation during contraction
- Desmin and vimentin are main intermediate filaments inserting into attachment plaque
Gap junctions are responsible for what in the myocardium and associated protein
-Provide ionic continuity for spread of action potentials between cells
Lipofuscin granules
- Remnants of stuff lysosome cant break down
- Occurs in long-lived cells
3 tunics of heart and what they contain
endocardium (contains purkinje fibers)
myocardium (thickest)
epicardium (adipose and coronary vessels)
Cardiac skeleton purpose
- support valves
- attachment for valve and leaflets
- electrical insulator
Chordae tendineae
Connect cusp free edge to papillary muscle
Blood vessels three layers
Tunica Intima (Inside)
Tunica media
Tunica Externa or Adventitia (Outside and connects vessel to surrounding connective tissue)
what is the role of endothelial layer and sub endothelial layer of the tunica intima
- antithrombogenic via PGI2 which also causes vasodilation
- platelet aggregation
Vasa vasorum
is a network of small blood vessels that supply the walls of large blood vessels, such as elastic arteries (e.g. aorta) and large veins (e.g. venae cavae)
Carotid/Aortic bodies purpose
They are chemoreceptors sensitive to:
- Low oxygen content
- High carbon dioxide concentration
- Low arterial blood pH
Carotid sinus location and purpose
is a slight dilation of the proximal internal carotid arteries:
Contain baroreceptors:
Tunica media layer is thin, allowing the carotid sinus to respond to changes in blood pressure
Pericytes cells role in capillaries
Roles:
- contractile function
- May proliferate and give rise to new blood vessels following injury
Capillary types
Continuous
Fenestrated
Sinusoidal
sites at which white blood cells enter damaged or infected tissues
venules
Left umbilical vein is obliterated
ligamentum teres hepatis
Ductus venosus is also obliterated (right umbilical)
ligamentum venosum
Superior Vena Cava is formed by
Right common cardinal vein and proximal part of right anterior cardinal vein
Left renal vein formed by
Anastomosis between subcardinal veins
Renal segment of IVC formed by
Right subcardinal vein
Post renal segment of IVC
Right supracardinal veins
Proximal part of bulbus cordis forms
right ventricle
Conus arteriosus incorporated into
right ventricle
Conus cordis forms
outflow tracts of both ventricles
Truncus arteriosus forms
roots of aorta and pulmonary trunk
aortic/pulm artery formed by (embryo)
neural crest cells
contruncal septum
separates pulmonary/aortic channels
-formed by L/R conotruncal ridges
Semilunar Valves formed from
endocardium Tubercles on truncus swellings - neural crest cells
Osteum secundum defect
-Leaves a large opening between atria
-Due to excessive resorption of septum primum or
inadequate development of septum secundum
Tricuspid Atresia
Characterized by either absence or fusion of tricuspid valves, resulting in obliteration of right atrioventricular orifice
Most common congenital heart malformation
Membranous Ventricular Septal Defect
Tetralogy of Fallot
Produces 4 alterations:
- Pulmonary infundibular stenosis
- Large interventricular septal defect
- Overriding aorta that arises directly above septal defect
- Hypertrophy of right ventricular wall
Persistent Truncus Arteriosus
- Failure of fusion of conotruncal ridges
- Always accompanied by a defective interventricular septum
- Undivided truncus receives blood from both sides of heart
Transposition of Great vessels
Occurs when conotruncal septum fails to follow spiral course, and instead runs straight down
Because of this aorta originates from right ventricle and pulmonary artery originates form left ventricle
Usually accompanied by an open ductus arteriosus
Valvular Stenosis
Semilunar valves are fused for a variable distance, reducing the opening of the vessel
Ectopia cordis
Heart lies on surface of chest due to failure of closure of ventral body wall
Phases of infectious disease progression Prodrome Invasive Acme Decline Convalescence `
Incubation – interval btwn infection and signs/symptoms Prodrome – mild symptoms Invasive – classical signs/symptoms Acme – signs/symptoms peak Decline – dwindling signs/symptoms Convalescence – healing
Three components of LPS
outer oligosaccharide chains (O-antigen)
Core polysaccharide
Inner Lipid A (a.k.a. ENDOTOXIN)
Sepsis-Related Organ Failure Assessment
Brain: Altered mental status
Lungs: Tachypnea (>22 bpm)
Cardiovascular: Low SBP (<100 mmHg)
2 or more = septic
Bacterial propeller made of
flagellin
Eukaryote whip made of
tubulin
Key Spore-formers
Actinomyces anaerobe
Bacillus aerobe
Clostridium anaerobe
usually gram pos rods
likes it HOT (42°C)
Campylobacter
likes it COLD (< 5°C)
Listeria monocytogenes
Yersinia entercolitica
Aeromonas hydrophila
Peptidoglycan
Lipopolysaccharides (LPS/endotoxin)
Flagellin
receptor recognition
TLR-2
TLR-4/CD14
TLR-5
Strict anaerobes
Freaks Can't Breath Air Fusobacterium Clostridium Bacteroides Actinomyces
What does IgA Protease do and presenting pathogens
-cleaves antibody produced by mucus membrane (IgA) allowing these bacteria to adhere to mucus membrane
-My SHiN protects my spleen
Str. Pneumoniae
H. influenza
Neisseria
What is M protien and what pathogen carries it?
-doesnt allow the bacteria to be phagocytosed via Breaks down C3 convertase, prevents opsonization by c3b
Str. Pyogenes (Group A strep)
What is protein A and pathogen?
-Binds Fc portion of IgG, inhibiting phagocytosis
Staphylococcus aureus
how does Protein A work
binds Fc portion of IgG flipping it and not allowing phagocytosis to occur
Endotoxins cause cytokine release … via …
TNFalpha and IL-1 via TLR4 and CD14
LOS releases from
Neisseria meningitides
capsule facts
antiphagocytosis
can cross blood brain barrier (meningitis)
many produce IgA protease
M gate
activation Na+ gate
H gate
inactivation Na+ gate
Gram Pos only
- endotoxins (LPS) - lipid A
- porin channels
- reistant to lysozyme and penicillin
Gram neg only
- teichonic acid
- no porins/endotoxins
- vulnerable to penicillin
bacteria vs human ribosome construciton
70s (50s + 30s)
80s (60s + 40s)
Peptidoglycan structure and what breaks it down
Amino acids cross linked with sugars (NAG and NAM)
- transpeptidase binds AA to each other (penicillin binds to transpeptidase)
- lysozymes cleave sugars (NAG and NAM)
enterotoxins
pyrogenic toxins
neurotoxins
gut toxins
produce fever
paralysis
Main capsule bacteria and all mneumonic
Make spleen protects my SHiN -Strep pneumonia -H. influenza -Neisseria meningitidis YES, Sadly Some Bad Killers Have Pretty Nice Capsules
Yersinia Pestis (F1 capsule) E. coli (meningeal strains only) Streptococcus agalactiae (Group B strep) Salmonella typhi Streptococcus pneumoniae Bacillus anthracis (protein – Poly-D-glutamate) Klebsiella Haemophilus influenzae Pseudomonas aeruginosa Neisseria Cryptococcus neoformans (fungal pathogen)
Exotoxins group A and B component
‘A’ component is active/toxic
‘B’ component binds to cell receptor
Protein Synthesis Inhibitors (pathogens and action)
Corynebacterium diphtheria (Diphtheria toxin) (gray plaque on throat) Pseudomonas aeruginosa (Exotoxin A) -Mechanism: ADP-ribosylating A-B toxin inactivates elongation factor 2 (EF-2) Both toxins (Diphtheria and Exotoxin A) add ADP- Ribose to EF-2 Addition of ADP-Ribose makes protein dysfunctional
Shigella causes and how
-Causes bloody infectious diarrhea
-Secretes shiga toxin
Binds to 60S ribosome in cells
Removes a specific adenine residue from rRNA in the 60S ribosomal subunit
Blocks protein synthesis
***Toxin causes tissue destruction, but invasion of GI mucosal cells is main cause of disease
Enterohemorrhagic E. coli (EHEC) causes
-Causes bloody infectious diarrhea
-Secretes shiga-like toxin (Same mechanism as shiga toxin)
**EHEC does not invade GI mucosa
Unlike shigella, the shiga-like toxin does the damage!
Increased Fluid Secretion pathogens
Bacillus anthracis
Enterotoxigenic E. coli (ETEC)
Vibrio cholera
Bacillus anthracis toxins and action
Edema toxin = protective antigen + edema factor
- Acts like adenylyl cyclase
- inc AC -> inc cAMP -> inc Cl- secretion, inc H2O secretion
Enterotoxigenic E. coli (ETEC) toxins and action
- Heat Labile Toxin (LT): Activates adenylyl cyclase/increases cAMP
- Heat Stable Toxin (ST): Activates guanylyl cyclase/increases cGMP
Vibrio cholera toxin and action
cholera toxin: permanently activates Gs to increase cAMP
neurotoxin bacteria and action
Clostridium tetani: Tetanospasmin, Inhibits inhibitory neurons (GABA and glycine) -> RIGID (muscles always on)
- Clostridium botulinum: Botulinum toxin, Prevents Acetyl choline release (no contraction) -> FLACCID paralysis
- infants slow, adults fast
Superantigens action and classic case (toxic shock)
Non-specifically activate MASSIVE numbers of T-cells
-staphylococcus aureus + packed wound (women and tampons or surgical packed wounds)
toxic shock syndrome pathogens
Sta. aureus (packed wounds) (Staff that is Hot and Red with a Rash has the Runs!)
Str. Pyogenes
Ventricular myocyte action potential (01234)
0: Depol. (Na+ influx)
1: ——-
2: Ca2+ influx, K+ efflux at lower rate
3: K+ efflux
4: Na+/K+ pump, K+ leakage
Why do cardio myocytes have such a long AP?
a long AP in myocytes causes a long refractory period that allows the heart to relax, preventing tetany
Nodal cell action potential (403)
4: slow Na+ influx, K+ blocked
0: Ca2+ influx
3: K+ efflux
Norepinephrine and Acetylcholine effect on nodal cells
NE: B1 receptors, inc rate of Na+ entry -> faster phase 4
Ach: M2 receptor, inc K+ permeability and inhibit If channels
Funny (If) channels
slow Na+ channels on nodal cells that are triggered by hyperpolarization (Na+ perm inc, K+ perm dec)
Fungal cell wall are composed of?
chitin, ergosterol, and B glucan
yeast and mold growth temps
yeast: 37°C
molds: 25°C
- Candida albicans is the opposite
Only yeast to have a capsule
Cryptococcus neoformans
Primary fungal pathogens
Blastomyces dermatitidis Coccidioides immitis Histoplasma capsulatum Paracoccioides brasiliensis -All infect via inhalation of large numbers of spores
Fungi-Like Bacteria
Actinomyces israelii (Forms microscopic “sulfur” granules) Nocardia asteroides (often mistaken for TB,Causes pulmonary abscesses and cavitations)
athlete’s foot
Tinea pedis
Potassium hydroxide (KOH) used for
Used to visualize fungal elements
-Fungal elements visible in skin scrapings (hyphae)
Rose Gardner’s Disease pathogen and reaction
- Sporothrix schenkii
- Ascending lymphangitis
Candida albicans can cause and test
Oral thrush Vulvovaginitis (yeast infection) Diaper rash - test: “Germ tube test” Positive - opportunist pathogen so occurs in immunosuppressed individuals
Virus like bacteria that like to hide in a host cell
Rickettsia and Chlamydia
Tropism
viruses are tissue selective
Capsid
protein coat surrounding virus core (DNA/RNA)
dsDNA viruses and ssDNA virus
HHAPPPy hepadenovirus herpesviruses adenovirus papillomaviruses poxvirus
parvovirus
Reverse transcriptase viruses
HIV and Hep B
Two types of virus spikes
Hemagglutinin(HA)..attachment
Neuraminidase(NA)..release/budding (exiting)
drift vs shift
drift: small mutations over time (why vaccines need to be tweaked)
shift: abrupt/major assortment (pandemics)
avian influeza
H5N1, H7N9
How to detect viruses
IgM antibody: acute
IgG antibody: longer
and symptoms
Virus replication cycle
Attachment Penetration Biosynthesis Maturation/Assembly New viruses are assembled Release
Latency
period of dormancy
Lytic
cell rupturing
Hepatitis B virus cancer
liver cancer
HIV / HHV-8 cancer
Kaposi sarcoma
P wave
PR interval
QRS
P wave: .06 - .11
PR interval: .12 - .20
QRS: >.12
small box in sec
.04 sec
P
QRS
T
P: atrium depol
QRS: ventricle depol (Q: septal depol)
T: ventricle repol
Depolarization direction and deflection
- ———-> + depol, up
- ———-> - depol, down
V wave
filling of the atrium w a closed AV valve to opening of AV valve
ST segment depression
subendocardial injury (ischemia)
ST segment elevation
epicardial injury (ischemia)
Identify the bacterial pathogen that causes the body to produce anti-streptolysin O (ASO) antibodies
Streptococcus pyogenes
acid fast and is commonly confused with TB
Nocardia asteroides
S4 sound
Atrial kick: Fill a ventricle with low compliance (stiff) sound produced
Dihydropyridine channels
Ca2+ channel through T tubule
ryanodine channels
Ca2+ channels on the sarcomere
phospholamban
wedges next to Ca2+ pump to SR (inhibitor). Phosphorylate phospholamban will cause it to leave Ca2+ pumped into the SR at a faster rate (dec AP length)
-SERCA2
Ca2+/Na+ exchanger
Ca2+ out, Na+ in
Methylxanthine
inhibits phosphodiesterase, inc in cAMP, inc in intracellular Ca2+
stretching of the myocardial muscle casues
high affinity of troponin to Ca2+
get myosin and action closer together
cardiac glycosides (digitoxin)
- inhibits Na+/K+ ATPas
- Less extracellular Na+
- Ca2+ out, Na+ in (exchange) –> more intracellular Ca2+
Virus Replicates in Cytoplasm
poxvirus (pox-like lesion)
Herpes Virus family
- herpes simplex viruses 1 and 2 (HSV-1 and HSV-2)
- Varicella-Zoster virus (VZV, which may also be called by its ICTV name, HHV-3)
- Epstein–Barr virus (EBV or HHV-4)
- Human Cytomegalovirus (HCMV or HHV-5)
- Human Herpesvirus 6A and 6B (HHV-6A and HHV-6B)
Greatest influenza threat to humans
H5N1 and H7N9 (avian influeza)
Hemagglutinin (H)
facilitates attachment and penetration of virus into host cell
Neuraminidase (N)
assists the virion into entry and budding (escaping) host cell
Human Papilloma Virus cancer
cervical, penis, mouth, anus, throat, vaginacancer
Hepatitis B Virus cancer
Liver Cancer
Hepatitis C Virus cancer
Liver Cancer
Human T-cell leukemia virus cancer
T-Cell Leukemia
HIV/HHV-8 cancer
Kaposi sarcoma
main place that regulates blood pressure
arterioles because high sympathetic innervation
compliance equation and meaning
compliance = delta V / delta P
more volume = more compliance
ohm’s law equation and meaning
F = deltaP / R
more pressure = faster flow
more resistance = slower flow
POISEULLE’S LAW most important factor of flow
radius of vein/artery
-inc/dec by 16 times
POISEULLE’S LAW
Pi (Pi - Po) R^4 / (8 x viscosity x length)
Sheer force
- All flowing fluids exert “rubbing” force against the inner wall of a cylinder
- High flow rate reduces the lateral pressure BUT increases the sheer stress on the arterial wall
Reynolds Number
(velocity) (diameter) (density) / viscosity
less than 2000 = laminar flow
Law of LaPlace
Stress (S) = pressure (P) x radius (r)/ width (r)
-inc radius or pressure = inc stress
Mean arterial pressure (MAP)
MAP = diastolic pressure + 1/3 pulse pressure
pulse pressure = systole - diastole
stiff aorta arterial pulse wave form
inc systole pressure
dec dicrotic notch
aortic incompetence arterial pulse wave form
very low diastole because it will equal out with left vent pressure during diastole which is close to zero
aortic stenosis arterial pulse wave form
low systole pressure bc dec blood in aorta
slow pressure rise to systole
atherosclerosis arterial pulse wave form
multiple wave as pressure decreases because of reflective waves
a1
b1
b2
a1: vasoconstriction
b1: inc HR
b2: vasodilation
Vasoconstrictor center
Rostral ventrolateral medulla (RVLM)
-and also CARDIO STIMULATORY CENTER
Vasodilator center
Caudal ventrolateral medulla (CVLM)
Cardioinhibitory center
Dorsal motor nucleus of vagus (DMNV) and Nucleus Ambiguous (NA)
Arterial Baroreceptor Reflex location
carotid sinus and aortic arch (baroreceptors)
-short term
histamine
vasodilation
oncotic pressure
albumin inside the vessel keep H2O in vessel through osmotic pressure counteracting hydrostatic pressure
arterioles vs veins (filtration vs reabsorption)
arterioles: favor net filtration
veins: favor net reabsorption
result of blood loss
vasoconstriction which will end up favoring reabsorption because fluid will be borrowed from tissue to make up for lack of blood
Function of Lymph Capillaries
- Remove excess fluid and proteins from interstitial space.
- Take up differential between filtration and reabsorption for return back to central circulation
edema is caused by
- Reduction in plasma proteins
- Increased capillary hydrostatic pressure
- Increased protein permeability in post capillary venules
Kwashiorkor Protein Deficiency
low protein diet has reduced albumin in blood resulting in inc fluid in the tissue
chemoreflex
-PERIPHERAL chemoreceptors on carotid and aortic body measure blood oxygen, CO2, and pH
CENTRAL in brain
-low O2, high CO2 and low pH dec parasympathetic stimulation and inc sympathetic stimulation
-Result: inc heart rate (stroke volume), vasoconstriction, and
Cardiopulmonary Reflexes
Goal is to minimize changes in blood pressure in response to changes in blood volume
-Located at artrio-venous junctions and pulmonary vessels of heart
-Activation: Diuresis (inc urine) (inhibition of RSNA)
ANP release (natriuresis: sodium loss)
Vasodilation – sympathetic inhibition
CAUSES LOSS OF CIRCULATING VOLUME
-Inhibition: Antidiuresis (RSNA increase)
ANP inhibition
Vasoconstriction – sympathetic activation
Hypothalamic Mechanisms
when high low BP the hypothalamus stimulate the post. pituitary gland to release Vasopressin/Antidiuretic Hormone (ADH)
angiotensinogen
inc blood pressure (released from liver)
pressure equation
delta P = Q (flow) x resistance
adenosine
vasodilation
Short PR (delta wave) meaning
indicates that the heart may have an alternate faster
conduction route around the AV node, indicative of “pre-excitation”
long PR interval meaning
AV block (reduced speed of conduction through AV node from atrial depolarization to ventricle depolarization)
ST segment shift means
elevated?
depressed?
ACUTE injury
- damaged tissue (MI) or ischemic tissue
- when tissue completely dies there will be no ST segment shift
faster part of laminar flow
center
korotkoff sound
the sound turbulent flow makes when passing through narrow area
flow velocity through aorta -> capillaries
High flow velocity in aorta and decreases in arterioles and bottoms out in capillaries
inhalation S2 sound
aortic closes before pulmonic resulting in two sounds
-inhalation inc venous return, requiring the right ventricle more time for systole, resulting in a delay of the pulmonic valve closing
Pulse pressure
pressure difference between systolic pressure and diastolic pressure
arteriole constriction vs dilation
constriction: raises arterial diastolic BP and decreases capillary pressure
dilation: lowers arterial diastolic BP elevates capillary pressure
what happened when hemorrhage occurs and why
dec in BP because a dec in mean systemic filling (venous return)
-acutely blood vessels constrict
inc/dec pressure at baroreceptor
- inc: afferent discharge inc causing dec in efferent sympathetic nerve activity and HR
- dec: afferent discharge dec causing inc in efferent sympathetic nerves activity and HR
NE vs EPI
NE: perdominently alpha 1 (constriction)
EPI: both alpha 1 and beta 2 depending on concentration
Vasodilation goes hand in hand with
opening of capillary sphincters (need more nutrients)
Inc/dec HR effect on stroke volume and why?
Inc HR = dec SV
Dec HR = inc SV
-in order to maintain a constant CO on a beat to beat basis
inotropic force
contractility (without inc EDV)
venous return factors
blood volume
sympathetic tone
muscle pump
how to identify muscular arteries
internal elastic lamina
Mean systemic filling pressure (Psf) =
right atrial pressure when venous return equals zero
Semi lunar valves are anchored to
annuli fibrosae
Where are purkinje fibers found
in the subendocardium layer of the endocardium
sinus venosus
right atrium, vena cava, coronary sinus
primordial atrium
right and left auricle and left atrium
primordial ventricle
left ventricle
bulbus cordis (proximal 1/3)
muscular right vent
bulbus cordis (conus cordis)
smooth outflow portion of right and left ventricle
bulbus cordis (trunks arteriousus)
proximal aorta and pulmonary trunk
aortic sac
aorta and pulmonary artery
Vitelline veins form
superior mesenteric (right), splenic, and converge to make hepatic portal vein
superior mesenteric vein comes from
right Vitelline Vein
Left umbilical vein is obliterated
ligamentum teres hepatis
Ductus venosus is also obliterated (right umbilical vein)
ligamentum venosum
Double Inferior Vena Cava
persistent left sub cardinal vein
S1 Ejection Click S2 OS S3 S4
S1: closure of the mitral and tricuspid valve
Ejection Click: opening of aortic valve (aortic stenosis)
S2: closure of aortic and pulmonic valve (aortic then pulmonic)
OS: opening of mitral/tricuspid valves (abnormal stenosis)
S3: sudden tension of chordae tendinea
S4: atrial kick (stiff ventricle)
Accentuated S1
Diminished S1
- exercise, sympathetic stimulation, mitral stenosis (mild)
- AV block, high diastolic filling pressure (stiff ventricle), and severe AV stenosis
holosystole
all of systole (regurgitation)
splitting occurring in expiration
-reversed splitting (LBBB)
endothelin
vasoconstriction
Natriuretic peptide
inc in renal blood flow, sodium loss
-fluid loss
pressure inc/pressure dec, afferent discharge
inc/dec
Angiotensin II
stimulates ACE
- vasoconstrictor
- inc thirst
- reabsorption of Na+ -> fluid retention
Long term control of blood pressure
- cardiovascular compensation mechanism
- Renin-angiosten alderstone system
- Renal mechansim
- Hypothalamic mechanism
- Atrial natriuretic peptide hormone
Short term control of blood pressure
- baroreceptor reflex
when and where is coronary blood flow least
endocardium left ventricle during isovolumic contraction
why is aortic regurg high for MI
in systole more than normal
inc contraction puts more compression on CA
how does enterotoxin work?
inhibits NaCl resorption
activates NaCl excretion
kills intestinal epithelial cells
bacteria with capsule not made from polysaccharide
Bacillus anthracis
most common viral nucleic acid
ssRNA
During peak 0 phase of a cardiomyocyte what does the electrical and chemical gradient favor for Na+
chemical: in
electrical: out
PR interval represents and long PR interval
AV conduction (AV block)
Wide QRS
R/LBBB or Pre ventricular contraction (PVC) do to ischemia raising cell excitability
Heart beat intervals
300 150 100 75 60 50 42
paced by junctional tissue near the AV node
The absence of “P” waves along with a normal QRS complex morphology
Cor triloculare biventriculare
Complete absence of atrial septum
