KEY wk 7 lec 1 Flashcards
atelectasis
collapse or incomplete expansion of part of or all lungs
reduce gas exchange in alveoli
3 types of atelectasis
- resorption atelectasis (obstruct airway, i.e. tumor, aspire foreign body, mucous plug from asthma or bronchitis, reduced tidal volume)
- compression atelectasis (compress from outside i.e. pleural space from tumors, fluid accumulation, pneumothorax )
- contraction atelectasis (fibrosis of lungs, reduced compliance and expansion, restrictive pulmonary disease)
atelectasis is not a ____ but increases risk for _____
disease
pulmonary infection/ pneumonia, ventilation-perfusion mismatch
pleural effusion
excess fluid in pleural cavity
normal: 10-25mL
type of epithelial tissue for pleura
mesothelium (for fluid transport)
nerves in each layer of pleura
visceral (inner): none-ish
parietal: intercostal nerves and phrenic nerves –> pain
replace pleural fluid how often
12x/day via lymphs
how do layers of pleura never touch
negative charges repel
pneumothorax (air in pleural space) from
trauma, obstructive lung disease
hemothorax
blood in pleural space from trauma or vascular rupture
hemorrhagic pleurites
blood and inflammatory fluid (leukocytes, protein, exudate)
empyema
purulent inflammation in pleural space
adhesion from visceral to parietal pleura
2 types of pleural effusions
transudative
exudative
transudative vs exudative pleural effusion
transudative: pressure imbalance (starling forces) and minimal protein and cells in the fluid accumulation (i.e. CHF, nephrotic syndrome, cirrhosis, pericarditis, atelectasis)
exudative: inflammation, infection, protein rich (i.e. malignancy, lupus, RA, infection, pulmonary emboli, drugs, pneumonia)
parapneumonic effusion
pleural effusion from pneumonia complication; infection spread to pleura
can become empyema (pus in pleural cavity)
3 stages of infectious pleural effusions
- exudative phase (sterile fluid rich in protein goes into pleural space)
- fibrinopurulent stage (bacterial invade and neutrophils; pus)
- organization stage (fibroblasts grow into exudates between pleural layers; membrane inelastic and prevent inflammation)
3 types of pleural effusions
- uncomplicated (exudate w neutrophils, no microbes- get antibiotics)
- complicated (bacteria invade but rapidly cleared- drainage needed)
- empyema (pus- need drainage, from bacterial pneumonia 70%)
sx of pleural effusion
dyspnea
chest pain
influenza syndrome vs influenza microbe
syndrome: fever, malaise, myalgia and respiratory sx (i.e. dyspnea, cough, URTI rhinitis and sinusitis)
microbe: influenza virus (anywhere in in respiratory tract i.e. rhinitis vs pneumonia)
influenza A and B
orthomyxovirus; negative ssRNA
RNA polymerase to get into host ribosome
proteins in influena
neuraminidase
viral hemagglutin
RNA-dependent RNA polymerase
hemagglutinin spike, neuraminidase spike, and PB protein (RNA dependent RNA polymerase) in influenza virus
functions
hemagglutinin: virus bind and invade host via silica acid
neuraminidase: virus disengage from cell and spread
PB protein: transport to nucleus where viral mRNAs are produced
life cycle of influenza A and B
bind via hemagglutinin
bud via neuraminidase
pathogenesis of influenza
- viral entry and replication: get into respiratory tract and use glycoproteins (hemaglutin and neuraminidase) to get in host cells (replicate in URT)
- viral replication and spread (viral RNA use template and hijack host to make new proteins)
- immune response (initial;; macrophage mediated also…, dendritic, T and B cell)
- inflammation and tissue damage (cytokine storm can cause pneumonia and acute respiratory distress syndrome ARDS)
- resolution or complications
most severe influenza type
A (epidemic and pandemic), then B (some epidemic)
influenza C is most mild
mutations in influenza types
antigenic drift and shift in influenza A
antigenic drift in influenza B and C
unique proteins in the influenza’s
influenza A- M2
influenza B- NB
influenza C- HEF
antigenic shift vs antigenic drift
shift: large change in RNA sqeuqnece (making previous antibodies/adaptive immunity less effective; change in spike proteins so antibodies cant bind)
drift: small point mutations in RNA genome (less effect on antibodies, RNA polymerase has high error rate bc no proof reading)
when influenza has antigenic shift
influenza A (most virulent)
why does antigenic drift occur
RNA-dependent RNA polymerase has a high error rate (no proof-reading)
mutations in what cause antigenic drift
surface glycoproteins hemagglutinin (HA) and neuraminidase (NA).
most common H and N of influenza
H1, H2, H3 and N1, N2 (most common)
“H” refers to hemagglutinin type ▪ 18 subtypes of hemagglutinin
- “N” refers to neuraminidase type ▪ 11 subtypes of neuraminidase
features of influenza
cough, sore throat, rhinorrhea, nasal congestion
fatigue, myalgia, headache, shaking chills
~2 days , <1 week
complications of influenza
bacterial superinfection –> severe pneumonia (i.e. from s. pneumonia, h. influenza, s. aureus)
systemic: myositis, myocarditis, Guillain barre syndrome, encephalitis, reye syndrome
cause of COVID 19 and structure of RNA
SARS-CoV-2, a betacoronavirus
enveloped + ssRNA bound to a nucleocapsid
4 structural proteins in covid 19
S (spike), E (envelope), M (membrane), and N (nucleocapsid) proteins
several other surface proteins, including hemagglutinin- acetylesterase glycoprotein, membrane glycoprotein, and small envelope glycoprotein
covid 19 replicated in the
cytoplasm
transmission of covid 19 and influenze
influenza= droplet/cough
covid= droplet, contact with colonized surface (i.e. hands, objects) to eyes/ respiratory tract
R0 rate of covid 19 and infleunza
R0 rate is between 5 and 6 (influenza is between 1 and 2)
so very contagious
where does covid19 replicate
upper airways (very transmissible)
COVID19 binds the _____ enzyme
viral entry via cleavage of spike protein by _____ which leads to formation of
ACE2
TMPRSS2 (transmembrane protease serine 2)
endosome (for invasion)
cytokine storm can cause
which cytokines
acute respiratory distress syndrome (ARDS)
IFNy and TNFa, IL1, IL6
how does covid19 infect the lungs
The serine protease TMPRSS2 promotes viral uptake by cleaving ACE2 and activating the SARS- CoV-2 S-protein
covid 19- late inflammation in the lungs
what is released from what and what does this lead to
what is it controlled by
plasma and tissue kallikreins release kinins that activate kinin receptors on the lung endothelium
* leads to vasculars mooth muscle relaxation and increased vascular permeability.
This process is controlled by the ACE2 receptor.
* Without ACE2 blocking the ligands of kinin receptor B1, the lungs are prone to vascular leakage, angioedema, and downstream activation of coagulation.
what proinflammtory cytokines contribute to vascular leakage and edema in lungs fromCOVID
(TNF, IL-1, IL-6) and NO
how is renin-angiotensin-aldosterone system involved in COVID 19?
binds ACE2 receptor which leads to down regulation of it
increases angiotensin II which leads to inflammation, vasoconstriction etc
(ACE2 converts angiotensin II into angiotensin 1-7 which are less harmful than angiotensin II and cause vasodilation and anti-inflammatory, but this is down regulated in covid)
sx of covid
fever, chills, cough, SOB, fatigue, aches, loss of smell or taste, diarrhea, N/V
severe: dyspnea, cyanosis, chest pain, confusion
when COVID pneumonia progresses from acute lung injury to acute respiratory distress syndrome can cause
hypoxemia
complications of COVID19
death,
heart attack, myocariditis
cerebrovascular disease
acute renal failure
