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