Respiratory review 2

Question 1

chemoreceptors

Answer 1

Medulla- breathing pattern generator
Pons is the inhibitor
Central chemoreceptos (PaCO2 and H+ sense 70% of chemoception)
Peripheral chemoreceptors (Paco2 and O2)
Pontine stroke: apneustic breathing breathing takes 2wice as long, with short expiratory phase, no inhibition)
Opioids and barbituates: inhibit central pattern generator, decrease depth and frequency
Medullary stroke: Ataxic breathing, disruption of pattern (both amplitude and frequency)

Question 2

Sleep

Answer 2

Children get better sleep, advanced sleep apnea (they go to bed early, delayed they go to bed late)

Parasomnias cause injury
Narcolepsy with cateplexy type 1 (sleep all the time in weird spots, vivid dreamers, no hypocretion in hypothalamus)

Question 3

Obstructive sleep apnea

Answer 3

decrease in intrathoracic pressure–> increase in right ventricle, increase in pulmonary artery resistance, decrease in left ventricle filling, septum change, increase in systemic resistance decrease in cardiac output

Cheyne-Stokes respiration: at risk people: congestive heart failure, CNS damage, ESRD, disruption/dissynchrony of neural pathway regulation respiration , sluggish, apnea/hyperpnea rythm

Question 4

Parasomnias

Answer 4

arising from sleep
Non rem: night terrors, sleep walking etc, sexomnia, confusion arousal
REM: Nightmares, REM behaviors, later in night, M>W

Question 5

Pleural anatomy

Answer 5

2 layers (visceral pleura- attached to lung, parietal pleura- attached to chest walls)
pleural space /cavity- between layers
Pleura is lined by mesothelial cells that secrete small amount of pleural fluid for lubricant

Question 6

Pneumothorax

Answer 6

AIR in the pleural space (spntaneous and tension)
Spontaneous pneumothroax: air enters from lung tissue injury, trachea deviates toward the affected side. Mainly secondary in older patients with underlying pulmonary disease, COPD. If Primary , rupture of subpleural bleb common in tall, thin young men)
Clinical presentation: sudden onset dyspnea, sometimes pleuretic chest pain, CXR: diagnosis, Treat with 100% o2 to displace the nitrogen fromm the air in the pleuritic space, if needed chest tube in air
Tension pneumothorax: usually from trauma, air enters pleural space but cannot leave, medical emergency. Emergent thoracocentesis/chest tube placement. Trachea deviates AWAY from affected side, can be solitary fibrous tumor, polypoid benign tumor

Question 7

pleural effusion

Answer 7

fluid in the pleural space, transudate (something driving fluid in pleural space, most commonly congestive heart failure, other causes- nephrotic syndrome (decrease protein), cirrhosis (decreased albumin protein), most fluid in effusion very little protein, treatment for underlying cause

Exudative: fluid leaking into pleural space, high vascular permeability has many causes–> malignancy, pneumonia, more protein, usually requires drainage. How to tell them apart- Thoracocentesis, test for protein level and LDH level, LIGHTs criteria: Exudatative: pleural protein/serum protein > .5, pleural LDH/serum LDH >.6, pleural LDH> 2/3s pf upper limits of LDH any of theses means its exudative

Question 8

Lymphatic effusion

Answer 8

chylothorax, lymphatic fluid effusion, from throacit ducts injuryt and obstruction, malignancy is most common, TRAUMA- usually surgical, milky appearing fluid with lots of TGS>100 mg/dl

Other effusions hemo, empyema, malignant

Question 9

mesothelioma

Answer 9

Pleural tumor, asbestos only known risk factor, years after asbestos exposure, imaging (pleural thickening and pleural effusion, slow onset of symptoms, poor prognosis (only 1.5 yyrs woth chemo) thickening of pleura cuboid cells

Question 10

Lung cancer

Answer 10

Risk factors (cigarette smoking, polycystic aromatic, hydrocarbons, PAH, radiation therapy: hodgkins and breast cancer survivors, environmental toxins, asbestos radon_
Bronchogenic 90-95% of lung cancer from bronchial epithelium, carcinoids 5%, sputum and cough and wright loss, benzopyreme inhibits p53

Symptoms: advanced at presentation, cough, dyspnea, with hemoptysis, CXR- pulmonary nodule and coin lesion, biopsy
Benign pulmonary nodules: granulomas (80% benign nodules), hamartomas (lung tissue and cartilage and scattered calcifaction)
Granulomas: fungi, histoplasmosis,coccoides, mycobacterium usually TB
PACK YEAR: number of packs per day times number of years smoking

Question 11

Small cell carcinoma (15%)

Answer 11

Fast growing, early metastastis, cant fix surgically, happens in smokers, very responsive, treated with chemotherapy poor prognosis, CMYC gene oncogene
Poorly differentiated small cells, “oat cells” male smokers, classic in male smokers, neuroendocrine tumor, central hilar tumors, sometimes makes hormones aka PARANEOPLASTIC syndromes (cushings, ACTH, SIADH, carcinoid, MG)
ACTH: cushing syndrome, progressive obesity, hyperglycemia
ADH: SIADH, hyponatremia, dilute plasama–> confusion
Abs: against pre synaptic ca channels in neurons, block release of Ach, lambert eaton syndrome, main syptom is weakness

Question 12

non-small cell (85%)

Answer 12

can sometimes be resected, better surgical prognosisi, usually peripheral SMokers, and non smokers, Squamous cell carcinoma, adenocarcinoma, Large cell carcinoma, Bronchioalveolar carcinoma, carcinoid tumor

Question 13

Squamous cell carcinoma

Answer 13

hilar mass arising from bronchus, key patholgy (keratin production (pearls) by tumor cells, intercellular desmosomes (intercellular bridges), male smokers
Can produce PTH rP–> hypercalcemia, strones, bones, psychiactric overtones

Adenosqamous cell carcinoma- like adenocarcinoma, but in scar

Question 14

Adenocarcinoma

Answer 14

can form in scars, glandular tumors, most common llung cancer for non smokers and women, a peripheral gene

all the genes but Cmyc make it (kys ets),

Bronchoalveolar carcinoma- a subtype of adenocarcinoma, similar to adenocarcinoma, happens in non smokers, peripheral, MUCINOUS type- derived from goblet cells, non-mucinous type (Clara cells/type 2 pneumocytes), Looks like DNA on CXR, lobar consolidation excellent prognisis (surgery radiotherapy adjuvant chemo
Lepidoic spread- in the alveolar

Question 15

Large cell carcinoma

Answer 15

poorly differentiated, lacks glandular or squamous differentiation, lacks small cells, smokers cancer, central or peripheral, poor prognosis

Question 16

Carcinoid syndrome

Answer 16

neuroendocrine, well differentiated, chromogranin positive, non smokers, rarely causes carcinoid syndrome, non smokers, IHC and hemoptysis, diarrhea

Question 17

Complications of lung tumors

Answer 17

pleural effusions (tap fluid, cytology) Phrenic nerve compression (diaphragm paralysis, dyspnea, hemidiaphragm elevated on SXR), Recurrent laryngeal nerce compression- hoarseness

Question 18

SVC syndrome

Answer 18

obstruction of blood flow thru SVC
Can be caused compression from tumor (lung NSCLC and SCLL) if in mediastinum (lymphoma)
Thrombosis (indwelling catheters, pacemaker wires, facial swelling/head fullness, arm swelling, can cause increased ICP, headaches confusion, coma, cranial artery rupture
CXR diagnosis, anti coagulation, steroids (lymphoma, chemo/radiation/stenting

Question 19

Pancoast tumor

Answer 19

carcinoma at the apex of lung, involves superior sulcus (groove fro subclavian vessles) arm edema on same side, shoulder pain–> axilla scapula, arm parestheis, can compress sympathetic nerves–>hoarsenesss, miosis, ptosis anhydrosis

Question 20

Mets to and from lung

Answer 20

mets from lung cancer: to adrenals (usually found on imaging without symptoms), to brain (headache, neuro deficits, seizures) to bone (pathologic fractures), to liver (hepatomegaly, jaudice)

Mets to lungs, much more common than primary, from breast or collon usually in multiple places

Question 21

Pulmonary embolism

Answer 21

usually lower lobe
thrombus in pulmonary artery, rarely formed in heart or pulmonary vasculature, majority come from femoral vein or deep leg veins, travels to lung via IVC–> RA–> RV
can be unprovoked, secondary to hypercoagulable state 2econdary malignancy, surgery, primary protein C/ S deficiency, AT2 deficiency
Chest pain worse qith deep breath
Respiratory distress- dyspnea, hypoxemia, tachypnea, massive PE–> sudden death, obstruction thru PAs (PVR increases) small chronic PEs –> pulmonary HTN

PE V/Q–> ventilation without perfusion, mismathc shunting hyperventilation, blood gas finding variable, classic findings: decrease PaO2 and PCO2

Question 22

DVT and PE

Answer 22

Thrombus within a deep vein, usually in calf or thigh, commonly femoral/popliteal veins, can extend or grows, precedes PE, often 2 hyper coagulable state

Asymptomatic until PE–> calf pain, palpable cord (thrombosed vein), unilateral edema, warmth, tenderness, erythema, homans sign: calf pain with dorsiflexion of foot, lower extremitiy US

Treatment: similar to pe, venous thromboembolism, prevent in hospital pts, prophylaaxis- SQ heparin,

Question 23

Fat embolism

Answer 23

often after long bone fracture, Fat crosses lungs–> small artery infarcts, fat embolism syndrome: pulmonary neuro and skin, dyspnea hypoxemia, capillary leak–> ARDS, neuro (confusion focal deficits petichiae

Question 24

Amniotic fluid embolism

Answer 24

during labor, amniotic fluid, fetal cells and fetal debris–> mom, inflammatory RXN, FATAL

Phase 1: pulmonary artery vasospasm–> pulmonary HTN–> RHF, hypoxia, myocardial capillary damage–> left hearrt failure, pulmonary capillary damage–> ARDS

Phase 2: hemorrhagic bleeding DIC, bleeding and seizures

Question 25

Atelectasis

Answer 25

collapsed lung, Resorptive, loss of surfactant, contraction
Resorption atelectasis: due to complete airway obstruction, air is resorbed via pres of kohn, mucus plug, aspiration, bronchial asthma, bronchitis, bronchiectasis, neoplasms, Fever, dyspnea, trachea deviation toward affected side, and diphragm elevation

Compression atelectasis: usually due to pleural effusion or pneumothorax, trachea and mediastinum move away from the messed up lung

Neonatal atelectasis: loss of surfactant, synthesized by type 2 pneumocytes, RDS (via maternal diabetes, hyaline membranes)

Contraction atelectasis: fribrotic in lung, no expansion

Question 26

Acute lung injury

Answer 26

Endothelial/epithelial injury, initiated by numourous factors, Non herited or herited. Mediators: Cytokines, oxidants, GFs- TNF, IL1 IL6 IL10, IGF, manifestations (PE, diffuse alveolar damage), Edema due to alterations in starling pressure, increased hydrostatic pressure in capillaries or decreased oncotic pressure–> transudate

Question 27

ARDS

Answer 27

non cardiogenic pulmonary edema from a capillary damage, direct or indirect lung damage, infection (sepsis, diffuse lung infections) gastric aspirations, physical injury/trauma, alveolar macrophages–> cytokines–> hyaline membrane–> diffuse alveolar damage

Question 28

Defense barriers against bacterial infections, bacterial strategies to overcome HOST barriers

Answer 28

Defense mechanisms: ability to filter particles based on size, mechanical restriction (epiglottis and cough reflex, mucociliary escalator, RT secretion-immune

Bacterial strategies to overcome defense: Adherence and invasion of RT tissue (pili, fimbrae, adhesins), secretion of tissue damaging enzymes (lysins, proteases, elastases). Inhibitors or neutralizing agents (proteases and capsule, toxins (EF2, super Ags and biofilms)

Question 29

Bordetella pertusis

Answer 29

gram negative coccobacillus, aerobe, adheres to cilia of respiratory epithelium, produces pertussis toxin (PTx). Adhesins- FHA, pertactin, pili
very infectious, transmitted to young and adults often asymptomatic
Whooping cough: catarrhal, paroxysmal, connvalesscence, vaccine available, acellular attack on PTx, bacteria binds to ciliated epithelium-> increased secretion and mucus production–> damage to mucociliary escalator

Question 30

cornyebacterium diptheria

Answer 30

gram positive, pallisades *, diptheria toxin (DTx) ADP ribosylates EF2–> produces pili (bacterial colonization of upper RT)
vaccines–> psuedomembrane, toxin has systemic effects (fever, sorethroat and malaise), diptheria toxin- vaccine and carrier function

Question 31

Neisseria meningitidis

Answer 31

gram negative diplococci, oxidase positive, catalase positive, polysaccaride capsule, produce pili–> nasopharynx–> pharyngitis and pneumonia
MOA: capsule prevents phagocytosis and complement fixation Type 4 pili colonization of nasopharynx
LOS endotoxin in activity, vaccine against polysaccharide capsule

Question 32

Streptococcus pyogenes (GROUP A)

Answer 32

gram positive in chains, beta hemolytic, processes M proteins, and hylauronic acid capsule, catalase negative pharyngitis (strep throat)- redness and edema of mucous membranes
Scarlet fever (strep and erythmea rash)- due to pyogenic exotoxin
Surface proteins (M FLTA) tissue destruction

Question 33

staphylococcus aureus

Answer 33

Gram positive in clusters, catalase positive, polysaccaride capsule, coatein with protein A, many tumors and cytopathic enzymes
Pneumonia: aspiration of oral secretion –> hematogenous spread
Pulmonary tissue destruction fue to secreted enzymes

Question 34

Streptococcus pneumoniae

Answer 34

gram positive cocci, diplocci, alpha hemolytic, poly saccharide capsule–> lobar pneumonia, oits media
Pneumolysin- destroys lung tissue–> over activation of immune response–> fluid in lung
Aduts at risk (23V capsule vaccine), Kinds under 2- 13 V conjugated vaccine

Question 35

Haemophilus influenza

Answer 35

Small gram negative rods, grows on chocolate agar (Needs heme and NAD to survive) Polysacchraide capsule–> pili and OMPS
Pneumonia otitis, non encapsulated stains–> upper RT, increased proinflammatory response, systemic infection and CNS involvement

Question 36

Mycoplasma pneumoniae

Answer 36

Fried egg appearance no cell wall, coccoid, pleomoirphic bound by triple layerd membrane (sterols) obligate aerobe, PI adhesions, tracheobronchits and atypical pneumonia

Question 37

Pseudomonas Aeruginosa

Answer 37

gram negative rod, single flagella, oxidase positive, biofilme, sticks on catheters, opportunistic, lung infections for cystic fibrosis, produces pilins and adhesins

Question 38

Legionalla pneumophilia

Answer 38

Gram negative rod, opportunistic pathogen, flagella, water supplies and or amoeba, disease associated with infection C, legionnaires disease, severe pneumonia- like symptoms, pontiac fever- self limiting flu like symptoms

Survives inside alveolar macrophage within lungs, various enzymes (phosphatase, lipase, nuclease) kills infected host cells

Question 39

Mycobacterium TB

Answer 39

Acid fast rods, thick waxy cell wall, mycolic reids and lipoarabinous mannan, granulomas–> acute or latent infection TB reactives, PPD test mantoux test, CXR

Question 40

Rhinovirus

Answer 40

Ageent with lots of diversity, grows at 33 C, transmission by respiratory secretion (directly from person to person) via fomites, Prevention via handwash, and disinfectants causes common cold–> symptoms of immune system

Question 41

Enterovirus

Answer 41

D68 and C version, common cold symtoms, complication (Serious RD and systemic disease) no vaccine or antiviral therapy, acute flacid myelitis, weakness, loss of muscle tone, facial droop, difficulty swallowing, slurred speech, paralysis

Question 42

Corona virus

Answer 42

common cold second to rhinovirus, no vaccine availabel

Question 43

MERS

Answer 43

camels transmit, nosocomial transmission in hospitals in MId East ARF, lower respiratory tract

Question 44

parainfluenza

Answer 44

lower RT tract, croup, types 1 and 2–> croup, Type 3–> RSV, type 4 mild, no vaccine

Question 45

Respiratory syncitial virus

Answer 45

no systemic spread, blocks airways in kids–> bronchitis, pneumonia both cold, treatment supportive, ribaviren and RSVIg no vaccine

Question 46

Metapneumovirus

Answer 46

clinical spectrum of disease, similar to RSV but milder, IDendtified by RC PCR, no vaccine antiviral

Question 47

Influenza

Answer 47

ARD, virus infects upper RT- inhibits respiratory epithelium, cell damage, viremia, not major problem

Question 48

adenovirus

Answer 48

leads to ARD and pneumonia

Question 49

Serum prlactonis

Answer 49

Amino acid that increases with bacterial infections

Question 50

Risk factors for otitis media

Answer 50

6-24 months prior incidence, indigenous people, acute infections (strep pneumo 50%, H flu 45%) chroniclly (staph aureus, psuedomonas)
Treatment: younger for 6 moths, or sever pain for >48 hours or febrile, treat with amoxicillan 90 or augmentin
Chronic–> tube placement

Question 51

Acute rhinusitis

Answer 51

W>M viral usually clear, bacterial usually discolored, bacterial (streptococcal pneumonia, H FLU, moraxella dental infection, Treatment Augmentin or amoxicillin)

Question 52

tonsilitis/ peritonsillar abcess

Answer 52

Group A strep, –> acute rheumatic fever, abcess,

Bactrim blood agar (S pneumonia), blood agar (strep pyogenes), mannitol (Staph aureus)- only use one colony

Question 53

Herpes

Answer 53

Herpes Stomatitis (HSV1), trasmits person to persom, virus persists in formant state (asymptomatic) reactivates vesicles (cold sores), intraepithelial edema ( clear fluid, ruptures, ulcer multinucleated cells, tzank smear

Question 54

Candidiasis

Answer 54

Thrush, most common fungal infection, causes (dentures, diabetes, steroids, immunosuppresed)
Fungal hyphae on GMS STAIN

Question 55

Cancers of oral cavity and larynx

Answer 55

95 of cancers, are squamous cell carcinoma, M>F, tobacco alcohol, Fam Hx, HPV16 and 18 leukoplakia (rare), erythroplakia (common)

Question 56

Precancerous lesions

Answer 56

leukoplakia- white patch epidermal thickening or hyperkeratosis, cant be scraped, ocassionally associated with epithlial dysplasia (5-25% malignancy)
Erythroplakia- clinical not pathologic RED, Glandular, poorly differentiated borders 50% malignancy)

Epithelial dysplasia: loss of polarity, increased number of mitotic nuclear, size and shape, hyper chromasia. displasia carcinoma in situ invasion

Question 57

Squamous cell carcinoma of the moutch

Answer 57

weyders ring, tongue and floor, and glottis (vocal cords), supra infra glottic, asymptomatic, hemoptysis, dysphagia, classic keratinizing, HPC associates non keratinizing

Question 58

HPV- squamous cell carcinoma

Answer 58

Oropharynx, waldeyers ring (tonsillar adenoids, neck and lymph nodes, no keratinization

Question 59

rhinosinusitis

Answer 59

viral, allergic, obstructive process, edematous nasal turbinates enlarged,
microscopy infiltrative, edema, thickend basement membrane, nasyl polyps
nasal cavity paranasal sinus, malignant olfactory neuroblastoma, nasopharyngeal carcinoma

Question 60

olfactory neuroblastoma

Answer 60

arises in superior and lateral mucosa of nose 50 years, symptoms- epistaxis, nasal obstruction, headache, uniform cells with round nuclei, scant cytoplasm chromatin, locally invasive

Question 61

NAsopharyngeal carcinoma

Answer 61

north africans and china, EBV virus, salt fish and smoking
2 types keratinizing and non keratinizing
Prognosis silent until unresectable

Question 62

Sjorgren syndrome

Answer 62

autoimmune disease (serology Anti SSP, sicca dry mouth and eyes in association), pathology (lymphocytic infiltration of salivary and lacrimal glands with eventual gland destruction

Question 63

Salivary gland neoplasms

Answer 63

Parotid gland mainly: benign (Pleomorphic adenoma, warthin tumor), MAlignant (Mucoepidermal, adenoid cystic carcinoma)

pleomorphic adenoma: most common salivary gland tumor, wide age range, 75-85%, occur in the parotid glands, bengin mixed tumor, painless rarely mets

Warthin tumor: parotid glands, m>F, smoking, bilateral salivary, papillary cystic , bilateral pink ce;;s and lymphocytes

Mucoepidermal carcinoma: most common malignant tumor of salivary gland usually in parotids some in salivary glands, Mix of squamous, mucusm and others, low grade tumors

Adenoid cystic carcinoma : perineural invasion cribriform arctecture, local occurence

Question 64

thyroglossal duct cysts

Answer 64

midline, presents 4th decade, connected to hyoid bone moves with swallowing thyroid tissue in wall cysts

Question 65

Brachial cleft cyst

Answer 65

75%, young adults, lateral neck, prone to infection, essentially a huge pimle of squamous lining, lymphoid tissue

Question 66

associations of cancers

Answer 66

HPV balls in large neck mass, EBV nasal oropharynx keratin and sheets, alcohol tobacco squamous keratin, adenoid cystic balls around cribriform, pleomorphic lots of chromatin