BMS test 2 Flashcards

1
Q

sneezing and rhinorrhea (mucus) from what in allergic rhinitis

A

histamine –> trigeminal nerve –> sneeze

histamine, leukotrienes, prostagladings –> mucus

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2
Q

early and late phase of allergic rhinitis

A

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

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3
Q

healthy vs allergic rhinitis

A

healthy: th1, th17, treg –> th2 (AR)

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4
Q

gut dysbiosis in allergic rhinitis

A

increase bacteriodetes, e coli

decrease firmicutes

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5
Q

complications in allergic rhinitis

A

Eustachian tube dysfunction, chronic rhinosinusitis, adenoid hypertrophy, sleep apnea, learning delays

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6
Q

nasal polyps are made pf

A

mucus with immune cells

plasma cells, eosinophils, lymphoctytes and mucus secreting glands in stroma

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7
Q

chornic rhinosinusiits

sx and causes

A

sx: greewn yellow discharge, face pain, halitosis, fatigue, headache, polyps

causes: biofilm, osteitis (bone), bacterial superantigens (s. aureus)

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8
Q

non allergic rhinitis causes

A

viral, occupation, vasomotor, NARES (eosinophilia), rhinitis medicamentosa, rhinitis during pregnancy (estrogen increases hylaurpnic acid), vasulitide autoimmune and granulomatous disease

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9
Q

vasomotor rhinitis causes

A

nerve dysregulate, c fibers
PNS: mucus; Ach
SNS: vascular tone; NE and NPY

temp, cold, spicy, alcohol, strong odors

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10
Q

pharyngotonsillitis

viral or bacteria

sx

A

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

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11
Q

pharyngeal diphtheria cause and sx

A

corynebacterium diptheria

pseudomembrane on tonsils

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12
Q

GABHS suppurative and non suppurative complications

A

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)

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13
Q

recurrent acute tonsillitis vs chronic tonsillitis causes

A

s pneumonia, s aureus, h influenza

chronic >3 months: s aureus, h influenza, bacteroides

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14
Q

tonsilloliths

A

microbial biofilms form in tonsillar crypts –> tonsiltis and halitosis

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15
Q

aphthous ulcer from

A

HHV-6 (herpes)

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16
Q

supra glottis / epiglottitis

cause
sx

A

H influenza type B

red flag

fever, drool, odynophagia, inspiratory stridor

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17
Q

laryngitis

cause

A

parainfluenza virus

bacterial if complication of virus (s pneumonia, h influenza, m catarrhalis)

non infectious i.e. GERD or vocal trauma

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18
Q

bacterial tracheitis

cause and sx

A

s aureus

airway obstruct, high fever, toxicity

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19
Q

spirometry in obstructive vs restrictive lung disease

A

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

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20
Q

extra vs intrapulmonary restrictive lung disease

and early to late sx

A

extra: obesity…
intra: ARDS…

early; inflammatory/ alveolitis - ground glass appearance

late; fibrosis- honeycomb lung

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21
Q

bronchial asthma 3 factors

A

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

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22
Q

early vs late asthma

A

early: bronchoconstriction, PGD2, leukotrienes, histamine

late: neutrophils (proteases), eosinophils (MBP)

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23
Q

key findings in asthma

A

Charcot leyden crystals (MBP) and curschmann spirals

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24
Q

spirometry in asthma

A

normal between exacerbations (early)

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25
asthma exacerbations
low CO2 (hyperventilate) ==> then eventually increase CO2 and get respiratory failure
26
triad of sx in asthma
wheeze, dyspnea, cough at night bad bc cortisol drops
27
COPD complications findings
complications: pulmonary hypertension, cor pulmonale non reversible airflow limitation, proteinase damage, oxidant damage, no repair of elastin (emphysema)
28
risk for COPD
alpha1 antitrypsin gene smoking #1 risk
29
2 types of COPD
chronic bronchitis emphysema
30
blue bloater vs pink puffer
blue bloater in chronic bronchitis -edema, RV fail, hypercapnia, productive cough pink puffer: emphysema - dyspnea, hypercapnia, hypoxemia, hyperventilate
31
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
32
centriacinar emphysema vs panacinar emphysema where in lungs and causes
centriacinar: smoking - upper lobe bronchioles panacinar: alpha1antritrypisin genes- lower lobes alveoli
33
bronchiectasis
irreversible airway dilation from infection (or non infectious) and obstruction
34
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
35
microbial causes of diffuse bronchietasis
-psuedomonas aruginosa (colonize bronchial tree) -bordetella pertussis and mycoplasma pneumonia (pneumonia)
36
signs and sx of diffuse bronchiectaisi (airway dilate from infection or obstruction)
sx: hemoptysis, cough, dyspnea signs: finger clubbing, pulmonary osteoarthropathy
37
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
38
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
39
causes and sx of ARDS
causes: infection, aspiration, sepsis, shock sx: dyspnea, pink frothy sputum, crackles, hypoxemia
40
3 stages of ARDS
1. exudative stage: hyaline membrane on alveoli 2. proliferative 3. fibrosis
41
acelectasis and 3 types
atelectasis: collapse or incomplete expansion of lungs resorption atelectasis (obstructed) compression atelactasis contraction atelactasis
42
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
43
contraction atelactaisis from
fibrosis of lungs decrease compliances
44
compression atelastisi
compress from outside the lungs i.e. tumor, lymph, pleural effusion, pneumothorax, empyema (purulent inflammation in pleural cavity)
45
empyema
purulent inflammation in pleural cavity
46
pleural effusion causes what type of atelactaisis
compression atelactasis
47
dx pleural effusion
CT scan thoracentesis - needle to remove excess fluid
48
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
49
parapneumonia effusion 3 stages
exudative pleural effusion from pneumonia infection 1. exudative stage 2. fibropurulent stage: increase neutrophils= pus 3. organized stage: fibroblasts grow exudates connecting pleural layers together; inelastic and prevent inflation
50
infectious pleural effusion ; 3 types
1. uncomplicated: exudate with neutrophils, no microbes; antibiotics 2. complicated; bacteria invade; drain 3. empyema: pus; drain
51
influenza virulence factors
neuraminidase (bud/ spread0 hemagglutinin (binding) RNA dependent RNA polymerase (PB protein; make viral mRNA)
52
cytokine storm in influenza to create which complications
TNFalpha, IL1, IL6 --> pneumonia or ARDS
53
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
54
antigenic shift vs drift
shift: large change in RNA sequence, 2+ viruses swap genes, antibodies dont work drift: point mutation in hemagglutinin and neuraminidase
55
complications of influenza
systemic via cytokines: myocarditis, reyes... bacterial superinfection: severe pneumonia (strep pneumonia, s aureus)
56
DX of influenza
NAAT test (nose swab)
57
covid 19/ sars COV2 binding
spike protein binds ACE2 then TMPRSS2 (serine protease) cleaves spike protein --> viral entry --> from endosome
58
sx in covid 19
hypoxemia (with limited dyspnea) in acute lung injury --> ARDS
59
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
60
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)
61
what cant ACE2 bind in COVID
kinins --> sx and cant converted AT II --> AT1-7
62
suprarenal gland
endocrine function (top of kidney)
63
vessels enter/exit where in kidney
renal hilum --> renal sinus right renal artery divides into 5 segmental arteries renal veins --> IVC
64
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
65
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
66
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
67
enterococci cause a UTI in which cases? what virulence factors?
via catheter or abnormal genitalurinary tract
68
3 main causes of UTIS
E. coli (75%), klebseilla (15%), proteus (5%)
69
e coli causing UTI what are the main virulence factors
adhesins, p fimbriae, type 1 pilus hemolysin operons= on/off flagella
70
klebseilla causing UTIS virulent factors
antibiotic resistant LPS, polysaccharides, siderophores fimbriae, adhesins, biofilms
71
proteus causing UTIS virulence factors
ureases (make ammonium to increase ph >7) IgA protease hemolysin operons (flagella on and off) endotoxins
72
uncomplicated cystitis (bladder) vs complicated cystitis sx
dysuria, urinary frequency and urgency vs back or flank pain= upper tract involved
73
pyelonephritis differentiation btwn cystitis
fever is present
74
pyelonephritis sx
mild: low fever, CVA tenderness severe: high fever, N/V, flank pain, rigors diabetes - papillary necrosis and increase creatinine
75
types of pylenonephritis
-emphysematous pyelnophritis (gas via diabetes) -xanthoganulomatous pyelonephritis (urinary obstruction; lipid laden macrophages)
76
urosepsis sx
UTI (bladder or kidney) enters bloodstream --> sepsis (fever, chills, increase HR and RR, decrease urine output
77
normal vaginal flora
lactobacilli dominant --> lactic acid --> acidic pH antimicrobials made by lactobacilli: hydrogen peroxide and bacteriocin
78
interstitial cystitis (bladder pain syndrome) causes findings
from infection (polymicrobial; dysbiosis), autoimmune, urothelial dysfunction (defects in GAGs of barrier epithelial layer) hunner lesions (inflame)
79
bladder cancer who most common in most common type
men, older 90% urothelial malignant neoplasm (carcinoma)
80
bladder cancer risks sx dx
risk: smoking, industrial dyes and solvents, drugs, radiation sx: **hematuria**, azotemia (blood urea nitrogen and creatinine), anemia dx: cytoscopy
81
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)
82
where in bladder cancer most
papillary cancer most on lateral and posterior bladder walls
83
high risk bladder cancer has
nuclear hyperchromazia and pleomorphism
84
kidney embryology 3 parts
pronephros (induction) mesoneprhos (temporary filtration system) metanephros (primitive proper kidney)
85
proneprhos
disappear wk 4, 4th-14th somites, 6-10 pairs of tubules
86
mesonephros
4-8 weeks bowmans capsule and glomerulus
87
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
88
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)
89
urine flow route
pyramids/ medulla (inner/outer zone and stripes) --> papilla --> minor calyx --> major calyx --> renal pelvis --> ureter
90
nephron flow
interlobular artery (get blood to filter) --> renal papilla (urine; excrete)
91
vascular and tubular pole of nephron
vascular pole: blood tubular pole: filtrate enters for processing
92
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
93
what marks the end of the thick ascending limb
macula densa (salt sensors) in DCT
94
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+
95
inner medullary collecting duct cells secrete
ADH to reabsorb H2O
96
juxtaglomerular apparatus is where and what cells
where thick ascending limb meets macula densa granular cells- secrete renin macula densa cells extraglomerular cells
97
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
98
trigone
bladder opening for ureters
99
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
100
cortical nephrons vs juxtamedullary nephrons
cortical: LOH not into medulla, no thin ascending limb juxtamedullary nephrons: LOH deep into medulla, has thin ascending limb
101
clearance formula
amount from blood into urine half lives = [x](urine) * flow(urine) / [x](blood)
102
3 functions of kidneys
1. 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) 2. secretion: active transport from blood into tubules 3. reabsorption: active transport from tubules into blood
103
starling forces
hydrostatic out oncotic in
104
afferent vs effect arteriole constrict and dilate impact on GFR
afferent - constrict: decrease GFR -dilate: increase GFR efferent -constrict: increase GFR -dilate: decrease GFR
105
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
106
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)
107
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
108
too little solute in macula densa
MD releases prostaglandin to prevent excess constriction from ATII increase renin; vasodilate afferent arterial
109
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
110
tubular flow via macula dense
NO released with increased tubular flow to decrease GFR
111
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
112
NE and epinephrine impact on GFR
NE: increase renin release (RAAS --> ATII --> increase GFR) epinephrine: constrict afferent and efferent --> decrease RBF and GFR
113
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
114
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
115
substances that are only filtered (eGFR)
inulin creatinine cystitis C --> glucose clearance= O because all reabsorbed (unless diabetes and transporters saturated)
116
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
117
ECF and ICF what ions in which
ECF -100 Na+ -100 Cl- -30 HCO3- ICF -100 K+
118
transceullar vs paracellualr
para= tight junctions
119
water and Na rules
water always reabsorbed, never secreted na+ absorption in loop of henle is always greater than water
120
water transport via
tight junctions and aquaporins
121
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
122
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
123
organic solutes in PCT
organic solutes (glucose adn amino acids) are only reabsorbed in PCT, dont want lost in urine
124
proteins in PCT
proteins (albumin, inulin, GF) are degraded and use amino acids into PCT via pinocytosis
125
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
126
what powers OAT trasnporter
alpha ketoglutarate
127
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
128
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
129
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
130
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
131
NKCC where
thick ascending limb --> intersitium
132
hairpin loop structure of henle for countercurrent and multipiler
closer proximity of asciedng and descending = exchange ions and h2o also vasa rectae (peritubular capillaries)
133
RAAS pathwya
angiotensiongen (liver ) --> AT I (via renin) --> ATII (via ACE) then ATII can vasoconstrict, Na reabsorb, increase aldosterone
134
impact of renin
renin --> aldosterone --> H2o and Na retention --> increase BP and perfusion
135
what happens to renin in low vs high sodium diet
low: increase renin (for na retention) high: decrease renin
136
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
137
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
138
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
139
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
140
how does aldosterone cross kidney
lipid. freely cross; bind mineralocorticoid receptor --> transcribe genees
141
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)
142
what increase ca2_ in collection duct and DCT
PTH and calcitonin
143
what helps with phosphate excreting in collecting duct
(PTH and GFG23 for phosphate excretion)
144
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
145
highest acid/base in blood
bicarbonate (reabsorb in PCT) -carbonic anhydrase and H+ --> H-ATPase -Na/HCO3 symptom, NHE3 (Na-H+) antiport
146
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
147
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
148
high hydrostatic pressure in peritubular capillaries facilitates reabsorption of
h20 and na+ into bloodstream
149
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
150
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
151
respiratory acidosis vs alkalosis hyperventilate to increase or decrease CO2
decrease acidosis: hyperventilate to decrease CO2 respiratory alkalosis: hypoventilate to increase CO2 --> decrease pH
152
most common lung cancer
non small cell; adenocarcinoma
153
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
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key findings in the 3 non small cell lung cancers
adenocarcinoma: mucosal glands squamous: keratin pearls and hypercalcemia large cell: NEITHER
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who is small cell lung cancer in most and which cells effected
women, smoking, central or hilum, neuroendocrine
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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
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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
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central vs peripheral lung cancer
central: squamous and small cell peripheral: adenocarcinoma and large cell
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smoker vs non smoking for lung cancers
nonsmoker: adenocarcinoma smoke: squamous, large cell, small cell
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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)
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what type of cancer and where is pan coast tumor
squamous cell in apex of lung
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loco regional spread of lung cancer
hoarse voice (laryngeal nerve) dysphagia (esophageal compress) superior vena cava syndrome (face edema, headaches, dysphagia, venous distention)
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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
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paraneoplastic syndrome
nonmetastatic systemic effects from cancer or substances from cancer (i.e. hormones, cytokines) --> alter immune (antibodies cross react)
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which type of lung cancer usually has paraneoplastic syndrome
small cell
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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
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risk for lung cancer
smoking asbestos (mesothelioma) radon air pollution
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genetic risk for lung cancer
K-ras gene (adenocarcinoma) correlated with smoking EGFR (tyrosine kinase); female, nonsmoker, east asian EML4- ALK trasnlocation: nonsmoker, adenocarcinoma
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K-ras and EML4-ALK translocation from genetic mutation cause which type of lung cancer
adenocarcinoma
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carcinoid (lung cancer) which cells,
rare neuroendocrine cells, but no paraneoplastic syndrome nonsmokers slow growing, good prognosis
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mesothelioma effects where in the lung? cause?
pleural lining --> pleural effusion asbestos rare poor prognosis
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metastasized cancers will go where into lung
edges adn lower lobes i.e bladder, breast, kidney ...
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mPAP of pulmonary hypertesnion
>20mmHg
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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
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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
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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...
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left heart disease causes
pulmonary edema
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pulmonary edema pressures and sx
increase hydrostatic pressure and permeability, decrease osmotic pressure sx: dyspnea, suffocate, palpitation, anxiety, cold
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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
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lung disease
pulmonary hypertesnion is usually modest, i.e. 90% of COPD have mPAP >20 but only 5% have mPAP >35 mmHg
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venous thromboembolism
DVT or PE PE: venous or nonthrombotic emboli (fat or air) PE: deep veins of legs and migrate to venous system
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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
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venous thrombolism effect on heart
increase RV pressure and dysfunction --> LV preload and CO decreased --> decreases systemic pressure
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3 catgeogires of PE
1. massive PE: systemic arterial hypotension, shock 2. submassive: RV dysfunction, normal systemic arterial pressure 3. low risk
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cor pulmonale
right ventricle fails from excessive high pulmonary artery pressure i.e. COPD, pulmonary emobli RV: hypertrophied and dilated
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sarcoidosis
granulomas in lungs
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schistosomiasitis
parasitic infection --> granulomas in lung; hypertesnion and hepatosplenmegaly
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vascultiis
inflamed blood vessels, ischemia of tissues granulomas, eosinophils, neutrophils large: aorta medium: visceral arteries small: capillaries, venules, arterioles
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which vasculitis sully has lung involvemnt
small -microscopic polyangitis -churg strauss (allergic granulomatosis) wegners granulomatosis (granulomatosis with polyangitis)
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-churg strauss (allergic granulomatosis): from vasculitis
-churg strauss (allergic granulomatosis): kids with asthma, granuloma + eosinophil, tx: corticosteroid
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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
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sarcoidosis
restrictive lung disease noncaseating granulomas, systemic esp lung and lymph
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cause of sarcoidosisi
myobacteria, malignancy, envo, cigarettes, insecticides
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risk for sarcoidosis
geese, 40-55yrs, black, twins
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restrictive impacts of sarcoidosis
decrease FVC adn FEV, hypoxemia, pulmonary hypertension and obstructive in fibrocystic stage
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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
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lofgren syndrome in stage 1 of sarcoidosis
lofgren's syndrome: erythema nodosum (painful skin bumps), hilar adenopathy (enlarged lymphs in lung hilum), arthritis
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progressive systemic sclerosis (scleroderma)
pulmonary fibrosis, pulmonary hypertension connective tissue disease; skin and organs overproduce collagen
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systemic lupus ertyhematosus
pleuritis, pulmonary infiltrates, fibrosis, PAH
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rheumatoid arthritis impacts lungs
pleuritis, fibroses, PH
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occupactional lung disorders
inorganic: asbestos, silica, coal, beryllium --< fibrosis, cancer, COPD organic: cotton, grain, agriculture --> asthma , bronchitis, COPD
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asbestos related lung diseas
asbestosis, mesothelioma (cancer) initial macrophage alveolitis --> fibrosis asbestosis: interstitial pneumonitis and fibrosis (diffuse) -restrictive, bibasilar rales, dyspnea
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silicosis (lung from silica)
alveolitis, calcify hilar nodes, RA, mycobacterium tuberculosis, mesothelioma (cancer) ground glass appearnace massive: obstructive and restrictive
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coal workers pneumoconiosis (CWP)
COPD, chronic bronchitis Caplan syndrome (complicated CWP): RA coal macule, centriacinar emphysema obstructive and restircitve PAH, hypxemia
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beryllium disease
acute pneumonitis, chronic granulomatous disease (looks like sarcoidosis) sensitization phase 1st
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viral causes of community acquired pneumonia (CAP)
coronavirus; sars cov2 influenza virus adenovirus parainfluenza virus
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test for community acquired pneumonia (CAP)
1. sputum gram stain 2. urinary antigen (legionella and s pneumonia) 3. viruses
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1st line of defnse against respirator infection
cough reflex, IgA, mucus, neutrophils, complement, spleen...
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acquired immunity for respiratory infections
via exposure develop IgG antibodies high risk in infants and agammaglobulinemia
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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
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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
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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
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sx of tuberculosis
none or fatigue, weight loss, cough, hemoptysis
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sx of pulmonary abscess
productive cough, fever, sweat, weight loss
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anaerobic bacteria and can cause...
bactericides, fusobacterium... pulmonary abscess, botulism, food poison, gangrene, tetanus
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pulmonary abscess
necrotizing lung infection via pus fulled cavitary lesion
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pulmonary abscess from
oral secretion aspiration (common), endobrachial obstruction, anaerobic infection aspiration risks: depressed consciousness, impaired deglutination, periodontal disease
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nosocomial pneumonia tx
empiric antibiotics
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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)
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2 types/ parts of lungs for typical CAP
lobar pneumonia: uniform consolidation of entire lobe from s. pneumonia bronchopneumonia: in alveoli, incomplete consolidation
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klebsiella pneumonia can cause
necrotizing lobar pneumonia if alcohol, diabetes, COPD, UTI
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pseudomonas aeruginosa infects
eye, ear, skin, GI, respiratory (pneumonia if chronic lung disease or CHF)
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bordetella pertussis and parapertussis
whooping cough
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H influenza can casues
otitis media, sinusitis, meningitis, septic arthritis, pneumonia (if HIV or immunocompromised)
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atypical pneumonia
x ray doesnt correspond to clinical findings on physical exam
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3 causes of atypical pneumonia
chlamydia mycoplasma pneumonia legionella
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chlamydia
chylamydia pneumonia: pharyngitis, larnyngitis, bronchitis, interstitial pneumonia
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legionella:
from contaminated water legionnaires disease: atypical, acute lobar pneumonia with multisystem sx
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virulence factors in strep . pneumonia
polysaccharide capsule (interfere w phagocytosis) c substances (react with CRP) pneumocystis (alpha hemolysis) IgA protease
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predisposing factors for strep pneumonia
cerebral impaired, splenectomy, pulmonary congestion, abnormal respiratory tract
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most common type of CAP
s. pneumonia
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pyogenic effects of s. penumonia
pneumonia, otitis media, sinusitis, mastoiditis, meningitis when reach alveoli it increase WBC and RBC --> consolidation
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strep agalactiae
group B neonatal sepsis and meningitis
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strep viridans
subacute bacterial endocarditis
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strep pyogenes (group A strep) is the #1 cause of
pharyngitis
236
1# cause of phayrngitis
strep pyogenes
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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
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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)
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virulence factors in staph aureus
catalase coagulase beta lactamase exotoxins - enterotoxin (food poisoning) -toxic shock -exfoliatin (scalded skin, bulls impetigo)
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pyogenic (pus) from staph aureus
abscess, folliculitis, impetigo local: skin disseminated: sepsis, endocarditis
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types of CAP
typical: s pneumonia (50%) (also s aureus and h influenza) atypical: mycoplasma, chlamydia, legionella
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gram + vs -
+ = blue; peptidoglycan cell wall - = red
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nosocomial pneumonia
gram negative klebsiella pneumonia e coli pseudomonas argionas anaerobes HAP: s aureus (empyema, caviation) REFER TO OTHER SLIDE FOR OTHER CAUSES
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gram positive: strep vs staph
staph: grapelike, make catalase (degrade hydrogen peroxide) --> s. aureus makes coagulase (differ from other staph) step: chains, no catalase
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location of staph and strep
staph: nose strep: skin, throat, intestines
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gram negative
h influenza bodetella pertussis klebseilla penumonia pseudomonas aeruginosa
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