BMS test 2 Flashcards
sneezing and rhinorrhea (mucus) from what in allergic rhinitis
histamine –> trigeminal nerve –> sneeze
histamine, leukotrienes, prostagladings –> mucus
early and late phase of allergic rhinitis
early: mast cell degranulation via IgE, Th2
late: cytokines (IL4,5,13 and leukotrienes) can inflammation of cell and increase VCAM-1 to make infiltrate of eosinophil, neutrophil, t cell
healthy vs allergic rhinitis
healthy: th1, th17, treg –> th2 (AR)
gut dysbiosis in allergic rhinitis
increase bacteriodetes, e coli
decrease firmicutes
complications in allergic rhinitis
Eustachian tube dysfunction, chronic rhinosinusitis, adenoid hypertrophy, sleep apnea, learning delays
nasal polyps are made pf
mucus with immune cells
plasma cells, eosinophils, lymphoctytes and mucus secreting glands in stroma
chornic rhinosinusiits
sx and causes
sx: greewn yellow discharge, face pain, halitosis, fatigue, headache, polyps
causes: biofilm, osteitis (bone), bacterial superantigens (s. aureus)
non allergic rhinitis causes
viral, occupation, vasomotor, NARES (eosinophilia), rhinitis medicamentosa, rhinitis during pregnancy (estrogen increases hylaurpnic acid), vasulitide autoimmune and granulomatous disease
vasomotor rhinitis causes
nerve dysregulate, c fibers
PNS: mucus; Ach
SNS: vascular tone; NE and NPY
temp, cold, spicy, alcohol, strong odors
pharyngotonsillitis
viral or bacteria
sx
usually viral (adenovirus, rhinovirus, HIV, EBV)
sometimes bacterial (GABHS, pharyngeal diphtheria, STIs- gonorrhea, syphillis)
fungal (Candida albicans “thrush” cottage cheese plaques
sx: feverm odynophagia, dysphagia, hallitosis, airway obstruction
pharyngeal diphtheria cause and sx
corynebacterium diptheria
pseudomembrane on tonsils
GABHS suppurative and non suppurative complications
retrophayrngeal abscess (speech, neck, lymph)
peritonsillar abscess (uvula deviation)
parapharyngeal abscess (tismus, neck pain)
non suppurative (from endotoxins):::
scarlet fever (rash and strawberry tongue)
acute rheumatic fever (mycariditis, endocarditis)
post strep glomerulonephrtiits
PANDAS (kids, tics)
recurrent acute tonsillitis vs chronic tonsillitis causes
s pneumonia, s aureus, h influenza
chronic >3 months: s aureus, h influenza, bacteroides
tonsilloliths
microbial biofilms form in tonsillar crypts –> tonsiltis and halitosis
aphthous ulcer from
HHV-6 (herpes)
supra glottis / epiglottitis
cause
sx
H influenza type B
red flag
fever, drool, odynophagia, inspiratory stridor
laryngitis
cause
parainfluenza virus
bacterial if complication of virus (s pneumonia, h influenza, m catarrhalis)
non infectious i.e. GERD or vocal trauma
bacterial tracheitis
cause and sx
s aureus
airway obstruct, high fever, toxicity
spirometry in obstructive vs restrictive lung disease
obstructive (air trapped; cant exhale)
- FEV1/ FVC reduced <0.7
- increase RV, FRC (residuals)
-normal TLC
restrictive (trouble inhaling)
-physiologic FEV1/FVC
-reduced RV and FRC
-decrease TLC
extra vs intrapulmonary restrictive lung disease
and early to late sx
extra: obesity…
intra: ARDS…
early; inflammatory/ alveolitis - ground glass appearance
late; fibrosis- honeycomb lung
bronchial asthma 3 factors
inflame + hyperresponsive + reversible obstruction
hyperresponsive: narrowing via agents acting on smooth muscle i.e. histamine and increased wall thickness via edema and mucus and collagen deposits
early vs late asthma
early: bronchoconstriction, PGD2, leukotrienes, histamine
late: neutrophils (proteases), eosinophils (MBP)
key findings in asthma
Charcot leyden crystals (MBP) and curschmann spirals
spirometry in asthma
normal between exacerbations (early)
asthma exacerbations
low CO2 (hyperventilate) ==> then eventually increase CO2 and get respiratory failure
triad of sx in asthma
wheeze, dyspnea, cough
at night bad bc cortisol drops
COPD
complications
findings
complications: pulmonary hypertension, cor pulmonale
non reversible airflow limitation, proteinase damage, oxidant damage, no repair of elastin (emphysema)
risk for COPD
alpha1 antitrypsin gene
smoking #1 risk
2 types of COPD
chronic bronchitis
emphysema
blue bloater vs pink puffer
blue bloater in chronic bronchitis
-edema, RV fail, hypercapnia, productive cough
pink puffer: emphysema
- dyspnea, hypercapnia, hypoxemia, hyperventilate
chronic bronchitis vs emphysema (COPD types)
CB: large airway, mucus, blue bloater
-productive cough >3 months for 2 years
emphysema: dilated small airway, alveoli, elastin, pink puffer
-hyperinflate; air trapping
-bullae
centriacinar emphysema vs panacinar emphysema
where in lungs and causes
centriacinar: smoking - upper lobe bronchioles
panacinar: alpha1antritrypisin genes- lower lobes alveoli
bronchiectasis
irreversible airway dilation from infection (or non infectious) and obstruction
focal vs diffuse bronchiectasis
focal (localized)
-from obstruction, non infectious
-extrinsic: ie. adjacent lympahdenopathy compresses
-intrinsic: i.e. airway tumor or aspiration
diffuse (widespread)
-systemic or infectious
-viscious cycle: poor mucocillary clearance and microbe
-dilate airways, lower lobe, right side
microbial causes of diffuse bronchietasis
-psuedomonas aruginosa (colonize bronchial tree)
-bordetella pertussis and mycoplasma pneumonia (pneumonia)
signs and sx of diffuse bronchiectaisi (airway dilate from infection or obstruction)
sx: hemoptysis, cough, dyspnea
signs: finger clubbing, pulmonary osteoarthropathy
chronic restrictive lungs disease
causes
sx
how to diagnose
inflam, fibrosis, decrease gas exhange
i.e. autoimmune, work (asbestos), drugs, pneumonia, sarcoidosis
sx: tachypnea, dyspnea, dry cough, crackles, finger clubbing, right heart failure
dx: lung biopsy
ARDS (acute respiratory distress syndrome- diffuse alveolar damage)
timing
pathophysiology
-mins to days; systemic insult i.e. sepsis, shock
-high mortality rate
-diffuse pulmonary infilitrates
-hypoxemic respiratory failure
increase vascular permeability –> protein in alveoli –> necrosis –> decrease diffusion capacity
causes and sx of ARDS
causes: infection, aspiration, sepsis, shock
sx: dyspnea, pink frothy sputum, crackles, hypoxemia
3 stages of ARDS
- exudative stage: hyaline membrane on alveoli
- proliferative
- fibrosis
acelectasis
and 3 types
atelectasis: collapse or incomplete expansion of lungs
resorption atelectasis (obstructed)
compression atelactasis
contraction atelactasis
resorption atelactasisi
obstructed airway; trapped air goes into bloodstream and vital lungs collapse
i.e. tumor, mucus plug in asthma, foreign body aspiration
alveolar collapse and decrease tidal volume
contraction atelactaisis from
fibrosis of lungs decrease compliances
compression atelastisi
compress from outside the lungs i.e. tumor, lymph, pleural effusion, pneumothorax, empyema (purulent inflammation in pleural cavity)
empyema
purulent inflammation in pleural cavity
pleural effusion causes what type of atelactaisis
compression atelactasis
dx pleural effusion
CT scan
thoracentesis - needle to remove excess fluid
pleural effusion 2 types and sx
transudative: starling force imbalance i.e. CHF
exudative: protein rich fluid build up i.e. ascites, malignancy, lupus, PE< infection
sx: chest pain, dyspnea
–> compression atelactasis
parapneumonia effusion
3 stages
exudative pleural effusion from pneumonia infection
- exudative stage
- fibropurulent stage: increase neutrophils= pus
- organized stage: fibroblasts grow exudates connecting pleural layers together; inelastic and prevent inflation
infectious pleural effusion ; 3 types
- uncomplicated: exudate with neutrophils, no microbes; antibiotics
- complicated; bacteria invade; drain
- empyema: pus; drain
influenza virulence factors
neuraminidase (bud/ spread0
hemagglutinin (binding)
RNA dependent RNA polymerase (PB protein; make viral mRNA)
cytokine storm in influenza to create which complications
TNFalpha, IL1, IL6 –> pneumonia or ARDS
types of influenza
shift or drift
unique proteins
influenza A: M2, pandemics, antigenic shift and drift
influenza B: NB, epidemics, antigenic drift
influenza C: HEF, antigenic drift
antigenic shift vs drift
shift: large change in RNA sequence, 2+ viruses swap genes, antibodies dont work
drift: point mutation in hemagglutinin and neuraminidase
complications of influenza
systemic via cytokines: myocarditis, reyes…
bacterial superinfection: severe pneumonia (strep pneumonia, s aureus)
DX of influenza
NAAT test (nose swab)
covid 19/ sars COV2 binding
spike protein binds ACE2
then TMPRSS2 (serine protease) cleaves spike protein –> viral entry –> from endosome
sx in covid 19
hypoxemia (with limited dyspnea) in acute lung injury –> ARDS
which system gets dyregulated in covid
RAAS; ACE2 cant convert ATII (vasoconstrict, Na and H2O reabsorb) into AT1-7 (vasodilate and antiinflammatory)
therefore increase AT II
late lung infection in covid 19
TNF, IL1, IL6, NO
kinins –> relax smooth muscle and increase permeability (bc ACE2 cant block kinin receptor0 =edema, leak, coagulation (micro thrombi), hyaline membrane (exudative stage of ARDS)
what cant ACE2 bind in COVID
kinins –> sx
and cant converted AT II –> AT1-7
suprarenal gland
endocrine function (top of kidney)
vessels enter/exit where in kidney
renal hilum –> renal sinus
right renal artery divides into 5 segmental arteries
renal veins –> IVC
micturition via which brain centers
pontine micturition center release from inhibitory control from cortical centres
leads to voiding and PNS switch on (detrusor contract, internal end external sphincter relax)
PAG via frontal, midcingulate, and subcortical areas= regulate voiding
umbrella cells
location, function
- make bladder wall impermeable to urine
-folds/ urothelial plaques to increase or decrease SA when fill and empty
-uroplakin plaques
-tight junctions
-aquaporin channels to reabsorb H2o
vesicouretic/ureterovesical junction
where utter enters bladder
strop back flow of urine AKA vesicoureteral reflux –> UTI and kidney infections
grade I-V
grade V= reflux to kidneys
ureteral muscle contracts when bladder fills
intravesical ureteral tunnel; 1 way flow valve
enterococci cause a UTI in which cases?
what virulence factors?
via catheter or abnormal genitalurinary tract
3 main causes of UTIS
E. coli (75%), klebseilla (15%), proteus (5%)
e coli causing UTI
what are the main virulence factors
adhesins, p fimbriae, type 1 pilus
hemolysin
operons= on/off flagella
klebseilla causing UTIS virulent factors
antibiotic resistant
LPS, polysaccharides, siderophores
fimbriae, adhesins,
biofilms
proteus causing UTIS virulence factors
ureases (make ammonium to increase ph >7)
IgA protease
hemolysin
operons (flagella on and off)
endotoxins
uncomplicated cystitis (bladder) vs complicated cystitis sx
dysuria, urinary frequency and urgency
vs back or flank pain= upper tract involved
pyelonephritis differentiation btwn cystitis
fever is present
pyelonephritis
sx
mild: low fever, CVA tenderness
severe: high fever, N/V, flank pain, rigors
diabetes - papillary necrosis and increase creatinine
types of pylenonephritis
-emphysematous pyelnophritis (gas via diabetes)
-xanthoganulomatous pyelonephritis (urinary obstruction; lipid laden macrophages)
urosepsis
sx
UTI (bladder or kidney) enters bloodstream –> sepsis (fever, chills, increase HR and RR, decrease urine output
normal vaginal flora
lactobacilli dominant –> lactic acid –> acidic pH
antimicrobials made by lactobacilli: hydrogen peroxide and bacteriocin
interstitial cystitis (bladder pain syndrome)
causes
findings
from infection (polymicrobial; dysbiosis), autoimmune, urothelial dysfunction (defects in GAGs of barrier epithelial layer)
hunner lesions (inflame)
bladder cancer
who most common in
most common type
men, older
90% urothelial malignant neoplasm (carcinoma)
bladder cancer
risks
sx
dx
risk: smoking, industrial dyes and solvents, drugs, radiation
sx: hematuria, azotemia (blood urea nitrogen and creatinine), anemia
dx: cytoscopy
urethelial papillomas vs cancer
in bladder cancer
urothelial papillomas (exophytic or inverted): non cancerous/ benign finger like outgrowth
urothelial carcinoma in situ: full thickness lesion in bladder mucosa (basement membrane in tact)
where in bladder cancer most
papillary cancer most on lateral and posterior bladder walls
high risk bladder cancer has
nuclear hyperchromazia and pleomorphism
kidney embryology
3 parts
pronephros (induction)
mesoneprhos (temporary filtration system)
metanephros (primitive proper kidney)
proneprhos
disappear wk 4, 4th-14th somites, 6-10 pairs of tubules
mesonephros
4-8 weeks
bowmans capsule and glomerulus
metanephros
ureteric bud –> renal pelvis –> collecting ducts
glomeruli by wk 36
S shaped
-distal ends: glomerulus and bowmans capsule
-proximal ends: loop of henle, distal and proximal tubules
kidney ascent
2 complications
L4 (28th somite) –> T12-L1 at birth
transient lateral splanchnic arteries
-ectopic kidney (stuck in pelvis)
-horseshoe kidney (lower poles fuse)
urine flow route
pyramids/ medulla (inner/outer zone and stripes) –> papilla –> minor calyx –> major calyx –> renal pelvis –> ureter
nephron flow
interlobular artery (get blood to filter) –> renal papilla (urine; excrete)
vascular and tubular pole of nephron
vascular pole: blood
tubular pole: filtrate enters for processing
renal corpuscle
2 cells
capillaries (glomerulus) covered by epithelial cells (bowmans capsule)
podocytes; sieve, filter
glomerular mesengial cells: remove trapped material from basement membrane, maintain filtration rate
what marks the end of the thick ascending limb
macula densa (salt sensors) in DCT
2nd 1/2 of DCT cells
principal cells: Na and H2O absorb, aquaporin channels, K+ secrete, via aldosterone
intercalated cells: acid base, pH, reabsorb K+
inner medullary collecting duct cells secrete
ADH to reabsorb H2O
juxtaglomerular apparatus is where and what cells
where thick ascending limb meets macula densa
granular cells- secrete renin
macula densa cells
extraglomerular cells
parts of kidney tubules and fucntion
PCT: absorb everything (glucose, amino acids), 80% HCO3, 65% of Na and H2O
thin descending loop of henle: H2O reabsorb only, concentrate urine
ascending loop of henle: ions reabsorb, medullary gradient
DCT: aldosterone to reabsorb ions
collecting duct: ADH to reabsorb water
trigone
bladder opening for ureters
detrusor muscle
internal and external urethral sphincter when peeing
PNS contracts detrusor
PNS relaxes internal sphincter
External is voluntary control via skeletal muscle and pudendal nerve
then bulbospongious to get last drop out
cortical nephrons vs juxtamedullary nephrons
cortical: LOH not into medulla, no thin ascending limb
juxtamedullary nephrons: LOH deep into medulla, has thin ascending limb
3 functions of kidneys
- filtration: (GFR) dissolves substances from blood into bowmans space (via starling forces adn permeability)
- ultrafiltration –> form urine
-via glomerulus fenestrations and filtration slit (btwn pedicels of podocytes)
-proteins and RBCs dont fit (ions, glucose, amino acids, h2o and positive charges do) - secretion: active transport from blood into tubules
- reabsorption: active transport from tubules into blood
starling forces
hydrostatic out
oncotic in
afferent vs effect arteriole
constrict and dilate impact on GFR
afferent
- constrict: decrease GFR
-dilate: increase GFR
efferent
-constrict: increase GFR
-dilate: decrease GFR
as fluid moves along capillaries, the net filtration pressure decreases why
because increase in oncotic pressure in blood because protein free fluid (low oncotic) goes into bowman (proteins to big to be filtered)
lots of protein in blood that want water to come in increases oncotic pressure
autoregualtion of GFR
myogenic: smooth muscle in afferent arterial contract/ relax bc BP changes
tubuloglomerula feedback (alter filtration rate) via macula densa and granular cells (renin)
too much solute (NaCl) into macula densa
MD releases ATP or adenosine –> decrease ATII
less renin from granular cells
less dilation of afferent and less constriction of effernt
decreases GFR
too little solute in macula densa
MD releases prostaglandin to prevent excess constriction from ATII
increase renin; vasodilate afferent arterial
macula dense releases
ATP or adenosine who too much solute (decrease ATII and GFR)
prostagalndins and NO when too little solute (increase ATII and GFR)t
tubular flow via macula dense
NO released with increased tubular flow to decrease GFR
ATII impact on GFR
constrict affront a bit, constrict efferent a lot–> increase reabsoprtion and increase GFR
decrease in afferent pressure; granular cells release renin
NE and epinephrine impact on GFR
NE: increase renin release (RAAS –> ATII –> increase GFR)
epinephrine: constrict afferent and efferent –> decrease RBF and GFR
endothelia and natriuretic peptide (ANP, BNP) impact on GFR
endothelin causes vasoconstriction in vascular damage –> decrease RBF and GFR
ANP.,BNP: via heart if volume overload; inhibit renin, relax afferent and increase GFR and fluid excretion/urine
azotemia (low filtration at glomerulus, build up waste in blood)
3 types
pre renal azotmeia (low blood flow to kidneys) i.e. CHF, shock, dehydration
renal azotemia (kidney damage)
post-renal azotemia (urine flow blockage) i.e. ureters, bladder, urethra blocked
substances that are only filtered (eGFR)
inulin
creatinine
cystitis C
–> glucose clearance= O because all reabsorbed (unless diabetes and transporters saturated)
types of transports
passive diffusion: water, lipid soluble I,e urea
facilitated diffusion: amino acids, glucose
active transport: NAKpump basolateral
secondary active transport: symport, antiport
ECF and ICF
what ions in which
ECF
-100 Na+
-100 Cl-
-30 HCO3-
ICF
-100 K+
transceullar vs paracellualr
para= tight junctions
water and Na rules
water always reabsorbed, never secreted
na+ absorption in loop of henle is always greater than water
water transport via
tight junctions and aquaporins
what the fuck is going on in the PCT
HCO3 and H+ –> CO2 and H2O via carbonic anhydrase, also exhange Cl- via Na+ HCO3- cotrasnporter (NBC)
SGLT1 and 2 (apical) GLUT2 and 1 (basolatersl)
amino acids, phosphate via Na+ cotrasnportes
water via osmosisi
K+ and Cl- paracellular
Na via glucose, phosphate, bicarbonate, then naKpump
2 methods of Na reabsorption in PCT
method 1: NaK ATPase basolateral , many apical transporter, h2o and Cl- follow it
method 2: HCo3 and H+ into Co2 via carbonic anhydrase to diffuse into cell
-H+ exhanged for Na at apex (cycled into and out of cell)
-HCO3 cotrasnport w Na basolateral
–>increased by ATII
organic solutes in PCT
organic solutes (glucose adn amino acids) are only reabsorbed in PCT, dont want lost in urine
proteins in PCT
proteins (albumin, inulin, GF) are degraded and use amino acids into PCT via pinocytosis
organic solute secretion (blood –> PCT cell)
oct and oat
cations; NE, serotonin, Ach…
anions: fatty acids, biles salts…
OCT: via negative membrane potential
OAT: countertrasnport via alpha ketoglutarate
what powers OAT trasnporter
alpha ketoglutarate
principal cells in the DCT
Na+ reabsorb: ENaC channels are unregulated via aldosterone binding mineralocorticoid receptors
-aldosterone increase na reabsorb
h2o reabsorb via aquapoin 2, aldosterone indirectly helps via Na and osmosis
K+ secretion: na/k atpase –> into lumen via apical K+ channels
loop of henle mechanims
countercurrent exchanger: h20 descending and ions ascending loop
multiplier: amplify [ ] gradient in medulla via NKCC channel (sodium, potassium chloride cotrasnporter)
-high osmolarity in medullar
-h2o reabsorb in collecting ducts
hypothalamus secreted what into kidneys and impact one urine
secrete ADH from posterior pituitary
when blood osmolarity increases (dehydration) then secrete ADH fro water reabsorb = concentrated urine
ADH adds aquaporin channels in collecting duct to increase h20 permeability
urea trasnporters in where in kidney and what transportsers and impact on urine
diffuse out of thin ascending limb into interstitium
UT-A1 and UT-A3 for urea reabsorption in collecting duct= concentrate urine
NKCC where
thick ascending limb –> intersitium
hairpin loop structure of henle for countercurrent and multipiler
closer proximity of asciedng and descending = exchange ions and h2o
also vasa rectae (peritubular capillaries)
RAAS pathwya
angiotensiongen (liver ) –> AT I (via renin) –> ATII (via ACE)
then ATII can vasoconstrict, Na reabsorb, increase aldosterone
impact of renin
renin –> aldosterone –> H2o and Na retention –> increase BP and perfusion
what happens to renin in low vs high sodium diet
low: increase renin (for na retention)
high: decrease renin
impact of SNS on renin
Ne on beta-adrenergic receptors on JG cells –> cAMP –> increase renin
low vascular volume increase renin
high pressure decrease renin
JG/granular cells (renin)
afferent arterial pressure decreases causes renin to increase
macula densa cells release ATP and adenosine in high Na –> decrease renin and GFR and increase calcium
low Na–> macular densa release PGDs and NO –> cAMP –> increase renin and increase GFR
ATII impacts
vasoconstrict: decrease RBF and GFR and decrease Na+ load filtered
Na+ reabsorbed more via
-NHE3 Na/H+ antiporter (apical) and NA/Katpase (basolateral) in PCT
-NCC Na/Cl- symporter and ENaC in DCT and collecting duct
aldosterone impacts
in DCT to increase Na+ reabsorb and increase BP and volume
aldosterone binds mineralocorticoid receptors
principal cells: ENaC and Na/K pump
if ATII high then also increase NCC symporters
how does aldosterone cross kidney
lipid. freely cross; bind mineralocorticoid receptor –> transcribe genees
Ca2+ and phosphate through the kidney
PCT: majority of Ca2+ (paracellular and trans cellular)
-Na+phopshate cotrasnporter
thick ascending loop: Ca2+ minimal paracellular, no phosphate
–> this is for NKCC2
DCT: PTH to increase Ca2+ reabsorption via adding channels, minimal phospahte
collecting duct: PTH and calcitonin for Ca2+ (minimal), minimal phosphate (PTH and GFG23 for phosphate excretion)
what increase ca2_ in collection duct and DCT
PTH and calcitonin
what helps with phosphate excreting in collecting duct
(PTH and GFG23 for phosphate excretion)
buffer systems
-carobinc acid-bicarbonate buffer system: ECF
-protein buffer system: hemoglobin and albumin in ECF and ICF via amino acid acidic and basic side groups
-phospahte buffer system: ICF and tubule
-ammonia buffer system: NH3 (ammonia)- NH4+ (ammonium) in tubule and urine
-bone buffer system: calcium salts (calcium carbonate and calcium phso[hate
highest acid/base in blood
bicarbonate (reabsorb in PCT)
-carbonic anhydrase and H+ –> H-ATPase
-Na/HCO3 symptom, NHE3 (Na-H+) antiport
type A and B intercalated cells
type A (in acidosis): H-ATPase and H-K ATPase put H+ into lumen and remove excess acid, HCO3- across basolateral via AE1 antiporter
type B (in alkalosis): secrete HCO3- via pendrin into lumen adn H+ into blood
type A vs B intercalated cells
type A if acidic then out H+ into lumen and reabsorb bicarbonate
type B if alkalosis; then secrete HCO3 into lumens dn H+ into blood
high hydrostatic pressure in peritubular capillaries facilitates reabsorption of
h20 and na+ into bloodstream
sources of acids and bases
-carb metabolism make pyruvic and lactic acid
weak acids from citrus are alkalizing when oxidize (CO2 and H2O)
fat metabolism: beta oxidation makes CO2 and H20, if imcomplete then ketone bodies are acidic
protein: amino acids with sulfur groups –> sulphuric acid or ketoacid intermediates
GI: stomach acid vs bicarbonate in pancreas
renal/metaolic and respiratory acidosis and alkalosis
renal is slow via bicarb
respiratory is rapid via pCO2
renal acidosis: increase HCO3 reabsorption and increase H+ into urine (i.e. kidney failure)
respiratory acidosis: hyperventilate to decrease CO2 and shift carbonic acid bicarb system left to increase pH (i.e COPD)
respiratory alkalosis: hypoventilate to increase CO2 –> decrease pH
respiratory acidosis vs alkalosis
hyperventilate to increase or decrease CO2
decrease
acidosis: hyperventilate to decrease CO2
respiratory alkalosis: hypoventilate to increase CO2 –> decrease pH
most common lung cancer
non small cell; adenocarcinoma
types of non small cell lung cancer and who they are most in
adenocarcinoma: women, nonsmoker, peripheral
squamous cell carcinoma: men, smoke, central
large cell carcinoma: smoke, peripheral
key findings in the 3 non small cell lung cancers
adenocarcinoma: mucosal glands
squamous: keratin pearls and hypercalcemia
large cell: NEITHER
who is small cell lung cancer in most and which cells effected
women, smoking, central or hilum, neuroendocrine
prognosis of lung cancer and staging
T:tumor size
N: lymph nodes
M: metastases
stage 1- small tumor
stage 2 and 3= regional lymph
sage IV- metastasis
sx of lung cancer
cough
central tumor: cough, dyspnea, hemoptysis, wheeze, atelactaiss, pneumonia
peripheral tumor: pain if infiltrate pleura and chest wall, pleural effusion, cough, dyspnea
central vs peripheral lung cancer
central: squamous and small cell
peripheral: adenocarcinoma and large cell
smoker vs non smoking for lung cancers
nonsmoker: adenocarcinoma
smoke: squamous, large cell, small cell
pancoast tumors and Horner syndrome and pacnoast sydrome
Horner syndrome; sympathetic nerve plexus –> Ipsilateral miosis, ptosis, anhidrosis
pan coast syndrome: arm and shoulder pain (C8, T1, T2), atrophy hand muscles, Horners syndrome (brachial nerve)
what type of cancer and where is pan coast tumor
squamous cell in apex of lung
loco regional spread of lung cancer
hoarse voice (laryngeal nerve)
dysphagia (esophageal compress)
superior vena cava syndrome (face edema, headaches, dysphagia, venous distention)
distant metastasis from lung cancer and sx
weight loss cachexia
bone: spinal impingement (constipation, erectile dysfunction, paralysis, muscle cramp, bone pain)
brain: headache, seizure, N/V, ataxia
liver: anorexia, jaundice, hepatomegaly
paraneoplastic syndrome
nonmetastatic systemic effects from cancer or substances from cancer (i.e. hormones, cytokines) –> alter immune (antibodies cross react)
which type of lung cancer usually has paraneoplastic syndrome
small cell
paraneoplastic syndrome examples
hypercalcemia (ectopic PTH) –> muscle weak, ab pain…
syndrome of inappropriate ADH –> hyponatreamia, thirst, depress
distal clubbing, hypertrophic pulmonary osteoarthropathy
ACTH, cushing syndrome –> increase cortisol and hypokalemia
risk for lung cancer
smoking
asbestos (mesothelioma)
radon
air pollution
genetic risk for lung cancer
K-ras gene (adenocarcinoma) correlated with smoking
EGFR (tyrosine kinase); female, nonsmoker, east asian
EML4- ALK trasnlocation: nonsmoker, adenocarcinoma
K-ras and EML4-ALK translocation from genetic mutation cause which type of lung cancer
adenocarcinoma
carcinoid (lung cancer)
which cells,
rare
neuroendocrine cells, but no paraneoplastic syndrome
nonsmokers
slow growing, good prognosis
mesothelioma effects where in the lung? cause?
pleural lining –> pleural effusion
asbestos
rare
poor prognosis
metastasized cancers will go where into lung
edges adn lower lobes
i.e bladder, breast, kidney …
mPAP of pulmonary hypertesnion
> 20mmHg
PAWP (pressure in left atrium) for pulmonary hypertension from left heart disease vs all other causes of PH
PH from left heart disease: >15mmHg
<15mmHg from all other causes
mild vs sever pulmonary hypertesnion
mild: media thickens
severe: fibrosis and muscle thicekns
grade 4 is not reversible, 1-3 are
teloangietatic dilations in pulmonary artery
pulmonary arterial hypertesnion
pre capillary
leads to right sided heart failure –> cor pulmonale
women
increase pulmonary vascular resistnace
increase right venticle work to preserve cardiac output (decrease CO in end stage and decrease mPAP)
extra pulmonary sx: kidney disease, increase ATII adn aldosterone…
left heart disease causes
pulmonary edema
pulmonary edema pressures and sx
increase hydrostatic pressure and permeability, decrease osmotic pressure
sx: dyspnea, suffocate, palpitation, anxiety, cold
interstitial (early) vs alveolar (late) pulmonary edema
interdigital: overloaded lymph spill into alveoli, little effect on pulmonary fucntion
alveolar: protein and red cells, alveoli collapse bc pressure, cant breath, hypoxemia
lung disease
pulmonary hypertesnion is usually modest, i.e. 90% of COPD have mPAP >20 but only 5% have mPAP >35 mmHg
venous thromboembolism
DVT or PE
PE: venous or nonthrombotic emboli (fat or air)
PE: deep veins of legs and migrate to venous system
virchows triad for venous thromboembolism
stasis of blood, vessel wall injury, hypercoagulability
hyper coagulable: gene mutation; factor V leiden, prothormbin, deficient antithrombin, protein C and S
venous thrombolism effect on heart
increase RV pressure and dysfunction –> LV preload and CO decreased –> decreases systemic pressure
3 catgeogires of PE
- massive PE: systemic arterial hypotension, shock
- submassive: RV dysfunction, normal systemic arterial pressure
- low risk
cor pulmonale
right ventricle fails from excessive high pulmonary artery pressure
i.e. COPD, pulmonary emobli
RV: hypertrophied and dilated
sarcoidosis
granulomas in lungs
schistosomiasitis
parasitic infection –> granulomas in lung; hypertesnion and hepatosplenmegaly
vascultiis
inflamed blood vessels, ischemia of tissues
granulomas, eosinophils, neutrophils
large: aorta
medium: visceral arteries
small: capillaries, venules, arterioles
which vasculitis sully has lung involvemnt
small
-microscopic polyangitis
-churg strauss (allergic granulomatosis)
wegners granulomatosis (granulomatosis with polyangitis)
-churg strauss (allergic granulomatosis): from vasculitis
-churg strauss (allergic granulomatosis): kids with asthma, granuloma + eosinophil, tx: corticosteroid
wegners granulomatosis (granulomatosis with polyangitis) from vasculitis
necrotizing vasculitis, + ANCA, nodular infiltrates with cavitation, systemic i.e. eyes, kidneys, ears, skin
lupus pernio: lesions on face
maculopapular lesions on trunk
increase spleen, rib and spine activity
AV block (cardiac sarcoidosis), ventricular tachycardia
sarcoidosis
restrictive lung disease
noncaseating granulomas, systemic esp lung and lymph
cause of sarcoidosisi
myobacteria, malignancy, envo, cigarettes, insecticides
risk for sarcoidosis
geese, 40-55yrs, black, twins
restrictive impacts of sarcoidosis
decrease FVC adn FEV, hypoxemia, pulmonary hypertension
and obstructive in fibrocystic stage
4 stages of sarcoidosis
stage 1: granuloma in lymph –> lofgren’s syndrome: erythema nodosum (painful skin bumps), hilar adenopathy (enlarged lymphs in lung hilum), arthritis
stage 2: granulomas in lymph and lung –> hilar nodes, paratracheal adenopahty, reticulonodular infiltrates
stage 3: granulomas in lung
stage 4: pulmonary fibrosis, –> fibrocystic sarcoidosis, bulbous, scarring, parenchymal infiltrates
lofgren syndrome in stage 1 of sarcoidosis
lofgren’s syndrome: erythema nodosum (painful skin bumps), hilar adenopathy (enlarged lymphs in lung hilum), arthritis
progressive systemic sclerosis (scleroderma)
pulmonary fibrosis, pulmonary hypertension
connective tissue disease; skin and organs overproduce collagen
systemic lupus ertyhematosus
pleuritis, pulmonary infiltrates, fibrosis, PAH
rheumatoid arthritis impacts lungs
pleuritis, fibroses, PH
occupactional lung disorders
inorganic: asbestos, silica, coal, beryllium –< fibrosis, cancer, COPD
organic: cotton, grain, agriculture –> asthma , bronchitis, COPD
asbestos related lung diseas
asbestosis, mesothelioma (cancer)
initial macrophage alveolitis –> fibrosis
asbestosis: interstitial pneumonitis and fibrosis (diffuse)
-restrictive, bibasilar rales, dyspnea
silicosis (lung from silica)
alveolitis, calcify hilar nodes, RA, mycobacterium tuberculosis, mesothelioma (cancer)
ground glass appearnace
massive: obstructive and restrictive
coal workers pneumoconiosis (CWP)
COPD, chronic bronchitis
Caplan syndrome (complicated CWP): RA
coal macule, centriacinar emphysema
obstructive and restircitve
PAH, hypxemia
beryllium disease
acute pneumonitis, chronic granulomatous disease (looks like sarcoidosis)
sensitization phase 1st
viral causes of community acquired pneumonia (CAP)
coronavirus; sars cov2
influenza virus
adenovirus
parainfluenza virus
test for community acquired pneumonia (CAP)
- sputum gram stain
- urinary antigen (legionella and s pneumonia)
- viruses
1st line of defnse against respirator infection
cough reflex, IgA, mucus, neutrophils, complement, spleen…
acquired immunity for respiratory infections
via exposure develop IgG antibodies
high risk in infants and agammaglobulinemia
pneumonia Dx
1 of: fever, altered mental status if >70yoa, leukopenia/leukocytosis
2 of: cough, dyspnea, tachypnea, sputum, worse gas exchange, rales or bronchial breath sounds
tuberculosis causes
features
exogenous vs endogenous
mycobacteriacase; m. tuberculosis (m. bovid and m. africanum)
acid fast bacilli
exogenous; poor ventilation
endogenous: HIV, cancer, immunosuppressive drugs
primary TB vs postprimary/reactivate TB
primary: kids, immunocompromised, sx right after infection, disseminated milady tuberculosis, less transmissible
post primary: adults, cavitation, more infectious, higher risk if HIV or immunocompreised
sx of tuberculosis
none or fatigue, weight loss, cough, hemoptysis
sx of pulmonary abscess
productive cough, fever, sweat, weight loss
anaerobic bacteria and can cause…
bactericides, fusobacterium…
pulmonary abscess, botulism, food poison, gangrene, tetanus
pulmonary abscess
necrotizing lung infection via pus fulled cavitary lesion
pulmonary abscess from
oral secretion aspiration (common), endobrachial obstruction, anaerobic infection
aspiration risks: depressed consciousness, impaired deglutination, periodontal disease
nosocomial pneumonia tx
empiric antibiotics
HAP vs VAP (nosocomial pneumonia)
-causes
HAP: >48 hrs after hospital admission
-s. aureus, MRSA. strep, p. aeruginosa, gram negative
–> early: e coli, k. pneumonia, h influenza, s aureus, s pneumonia
–>late: MRSA, acineotbacteria
VAP: >48 hrs after intubation or ventilation
-acinetobacter, s. maltophilis, anaerobic (bactericides)
2 types/ parts of lungs for typical CAP
lobar pneumonia: uniform consolidation of entire lobe from s. pneumonia
bronchopneumonia: in alveoli, incomplete consolidation
klebsiella pneumonia can cause
necrotizing lobar pneumonia if alcohol, diabetes, COPD,
UTI
pseudomonas aeruginosa infects
eye, ear, skin, GI, respiratory (pneumonia if chronic lung disease or CHF)
bordetella pertussis and parapertussis
whooping cough
H influenza can casues
otitis media, sinusitis, meningitis, septic arthritis, pneumonia (if HIV or immunocompromised)
atypical pneumonia
x ray doesnt correspond to clinical findings on physical exam
3 causes of atypical pneumonia
chlamydia
mycoplasma pneumonia
legionella
chlamydia
chylamydia pneumonia: pharyngitis, larnyngitis, bronchitis, interstitial pneumonia
legionella:
from contaminated water
legionnaires disease: atypical, acute lobar pneumonia with multisystem sx
virulence factors in strep . pneumonia
polysaccharide capsule (interfere w phagocytosis)
c substances (react with CRP)
pneumocystis (alpha hemolysis)
IgA protease
predisposing factors for strep pneumonia
cerebral impaired, splenectomy, pulmonary congestion, abnormal respiratory tract
most common type of CAP
s. pneumonia
pyogenic effects of s. penumonia
pneumonia, otitis media, sinusitis, mastoiditis, meningitis
when reach alveoli it increase WBC and RBC –> consolidation
strep agalactiae
group B
neonatal sepsis and meningitis
strep viridans
subacute bacterial endocarditis
strep pyogenes (group A strep) is the #1 cause of
pharyngitis
1# cause of phayrngitis
strep pyogenes
effects of strep pyogenes
pyogenic: cellulitis, impetigo
toxigenic: scarlet fever, toxic shock
immunologic (antibodies cross react and form immune complexes): rheumatic fever and acute glomeruloneprhtitis
alpha vs beta hemolytic streptococci and example
alpha hemolytic: incomplete lysis of RBC (i.e. s. pneumonia)
beta hemolytic: complete lysis of RBC via hemolysin (streptolysin O and S) (i.e. s. pyogenes)
virulence factors in staph aureus
catalase
coagulase
beta lactamase
exotoxins
- enterotoxin (food poisoning)
-toxic shock
-exfoliatin (scalded skin, bulls impetigo)
pyogenic (pus) from staph aureus
abscess, folliculitis, impetigo
local: skin
disseminated: sepsis, endocarditis
types of CAP
typical: s pneumonia (50%) (also s aureus and h influenza)
atypical: mycoplasma, chlamydia, legionella
gram + vs -
+ = blue; peptidoglycan cell wall
- = red
nosocomial pneumonia
gram negative
klebsiella pneumonia
e coli
pseudomonas argionas
anaerobes
HAP: s aureus (empyema, caviation)
REFER TO OTHER SLIDE FOR OTHER CAUSES
gram positive: strep vs staph
staph: grapelike, make catalase (degrade hydrogen peroxide)
–> s. aureus makes coagulase (differ from other staph)
step: chains, no catalase
location of staph and strep
staph: nose
strep: skin, throat, intestines
gram negative
h influenza
bodetella pertussis
klebseilla penumonia
pseudomonas aeruginosa
