KEY wk 7 lec 1

Question 1

atelectasis

Answer 1

collapse or incomplete expansion of part of or all lungs

reduce gas exchange in alveoli

Question 2

3 types of atelectasis

Answer 2

1. resorption atelectasis (obstruct airway, i.e. tumor, aspire foreign body, mucous plug from asthma or bronchitis, reduced tidal volume)
2. compression atelectasis (compress from outside i.e. pleural space from tumors, fluid accumulation, pneumothorax )
3. contraction atelectasis (fibrosis of lungs, reduced compliance and expansion, restrictive pulmonary disease)

Question 3

atelectasis is not a ____ but increases risk for _____

Answer 3

disease

pulmonary infection/ pneumonia, ventilation-perfusion mismatch

Question 5

pleural effusion

Answer 5

excess fluid in pleural cavity

normal: 10-25mL

Question 6

type of epithelial tissue for pleura

Answer 6

mesothelium (for fluid transport)

Question 7

nerves in each layer of pleura

Answer 7

visceral (inner): none-ish

parietal: intercostal nerves and phrenic nerves –> pain

Question 8

replace pleural fluid how often

Answer 8

12x/day via lymphs

Question 9

how do layers of pleura never touch

Answer 9

negative charges repel

Question 10

pneumothorax (air in pleural space) from

Answer 10

trauma, obstructive lung disease

Question 11

hemothorax

Answer 11

blood in pleural space from trauma or vascular rupture

Question 12

hemorrhagic pleurites

Answer 12

blood and inflammatory fluid (leukocytes, protein, exudate)

Question 13

empyema

Answer 13

purulent inflammation in pleural space

adhesion from visceral to parietal pleura

Question 14

2 types of pleural effusions

Answer 14

transudative
exudative

Question 15

transudative vs exudative pleural effusion

Answer 15

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)

Question 16

parapneumonic effusion

Answer 16

pleural effusion from pneumonia complication; infection spread to pleura

can become empyema (pus in pleural cavity)

Question 17

3 stages of infectious pleural effusions

Answer 17

1. exudative phase (sterile fluid rich in protein goes into pleural space)
2. fibrinopurulent stage (bacterial invade and neutrophils; pus)
3. organization stage (fibroblasts grow into exudates between pleural layers; membrane inelastic and prevent inflammation)

Question 18

3 types of pleural effusions

Answer 18

1. uncomplicated (exudate w neutrophils, no microbes- get antibiotics)
2. complicated (bacteria invade but rapidly cleared- drainage needed)
3. empyema (pus- need drainage, from bacterial pneumonia 70%)

Question 19

sx of pleural effusion

Answer 19

dyspnea
chest pain

Question 20

influenza syndrome vs influenza microbe

Answer 20

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)

Question 21

influenza A and B

Answer 21

orthomyxovirus; negative ssRNA

RNA polymerase to get into host ribosome

Question 22

proteins in influena

Answer 22

neuraminidase

viral hemagglutin

RNA-dependent RNA polymerase

Question 23

hemagglutinin spike, neuraminidase spike, and PB protein (RNA dependent RNA polymerase) in influenza virus

functions

Answer 23

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

Question 24

life cycle of influenza A and B

Answer 24

bind via hemagglutinin

bud via neuraminidase

Question 25

pathogenesis of influenza

Answer 25

1. viral entry and replication: get into respiratory tract and use glycoproteins (hemaglutin and neuraminidase) to get in host cells (replicate in URT) 2. viral replication and spread (viral RNA use template and hijack host to make new proteins) 3. immune response (initial;; macrophage mediated also..., dendritic, T and B cell) 4. inflammation and tissue damage (cytokine storm can cause pneumonia and acute respiratory distress syndrome ARDS) 5. resolution or complications

Question 26

most severe influenza type

Answer 26

A (epidemic and pandemic), then B (some epidemic) influenza C is most mild

Question 27

mutations in influenza types

Answer 27

antigenic drift and shift in influenza A antigenic drift in influenza B and C

Question 28

unique proteins in the influenza's

Answer 28

influenza A- M2 influenza B- NB influenza C- HEF

Question 29

antigenic shift vs antigenic drift

Answer 29

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)

Question 30

when influenza has antigenic shift

Answer 30

influenza A (most virulent)

Question 31

why does antigenic drift occur

Answer 31

RNA-dependent RNA polymerase has a high error rate (no proof-reading)

Question 32

mutations in what cause antigenic drift

Answer 32

surface glycoproteins hemagglutinin (HA) and neuraminidase (NA).

Question 33

most common H and N of influenza

Answer 33

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

Question 34

features of influenza

Answer 34

cough, sore throat, rhinorrhea, nasal congestion fatigue, myalgia, headache, shaking chills ~2 days , <1 week

Question 35

complications of influenza

Answer 35

bacterial superinfection --> severe pneumonia (i.e. from s. pneumonia, h. influenza, s. aureus) systemic: myositis, myocarditis, Guillain barre syndrome, encephalitis, reye syndrome

Question 36

cause of COVID 19 and structure of RNA

Answer 36

SARS-CoV-2, a betacoronavirus enveloped + ssRNA bound to a nucleocapsid

Question 37

4 structural proteins in covid 19

Answer 37

S (spike), E (envelope), M (membrane), and N (nucleocapsid) proteins several other surface proteins, including hemagglutinin- acetylesterase glycoprotein, membrane glycoprotein, and small envelope glycoprotein

Question 38

covid 19 replicated in the

Answer 38

cytoplasm

Question 39

transmission of covid 19 and influenze

Answer 39

influenza= droplet/cough covid= droplet, contact with colonized surface (i.e. hands, objects) to eyes/ respiratory tract

Question 40

R0 rate of covid 19 and infleunza

Answer 40

R0 rate is between 5 and 6 (influenza is between 1 and 2) so very contagious

Question 41

where does covid19 replicate

Answer 41

upper airways (very transmissible)

Question 42

COVID19 binds the _____ enzyme viral entry via cleavage of spike protein by _____ which leads to formation of

Answer 42

ACE2 TMPRSS2 (transmembrane protease serine 2) endosome (for invasion)

Question 43

cytokine storm can cause which cytokines

Answer 43

acute respiratory distress syndrome (ARDS) IFNy and TNFa, IL1, IL6

Question 44

how does covid19 infect the lungs

Answer 44

The serine protease TMPRSS2 promotes viral uptake by cleaving ACE2 and activating the SARS- CoV-2 S-protein

Question 45

covid 19- late inflammation in the lungs what is released from what and what does this lead to what is it controlled by

Answer 45

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.

Question 46

what proinflammtory cytokines contribute to vascular leakage and edema in lungs fromCOVID

Answer 46

(TNF, IL-1, IL-6) and NO

Question 47

how is renin-angiotensin-aldosterone system involved in COVID 19?

Answer 47

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)

Question 48

sx of covid

Answer 48

fever, chills, cough, SOB, fatigue, aches, loss of smell or taste, diarrhea, N/V severe: dyspnea, cyanosis, chest pain, confusion

Question 49

when COVID pneumonia progresses from acute lung injury to acute respiratory distress syndrome can cause

Answer 49

hypoxemia

Question 50

complications of COVID19

Answer 50

death, heart attack, myocariditis cerebrovascular disease acute renal failure