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USMLE/ Step ONE > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What are the gross components of the conducting zone?

A

Nose, pharynx, larynx, trachea, bronchi, and terminal bronchioles

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2
Q

What are the gross components of the respiratory zone?

A

respiratory bronchioles, alveolar ducts, and alveoli

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3
Q

Cartilage is found in what range of the resp system?

A

Trachea to bronchi

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4
Q

Describe the epithelium in the respiratory tract!

A
  • Pseudostratified ciliated columnar (ends @ terminal bronchioles)
  • Goblet cells & seromucous glands (ends @ bronchi)
  • Clara cells in terminal bronchioles
  • ciliated simple cuboidal cells (Terminal bronchioes)
  • simple squamous, Type I &II cells in alveoli
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5
Q

What is the smooth muscle content in respiratory tract?

A

between tracheal rings, then increases to highest amount bronchial tree

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6
Q

What are type I pneumocytes?

A

line 97% alveoli

thin, squamous for gas exchange

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7
Q

formula for collapsing pressure

A

CP = P [(2*Surface Tension)/Radius]

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8
Q

Which cell secretes pulmonary surfactant? What is the effect?

A
  • Type II cells- cuboidal. Also, Type I precursor.

- decreases alveolar ST and prevents alveolar collapse (atelectasis)

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9
Q

What do you do if a patient refuses life saving Tx and is competent? If not competent?

A

Respect patient’s wishes.

If not competent: Next of kin makes decision (Spouse 1st, then adult child). If none, then a judge or appointed guardian.

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10
Q

What is the adult remnant of the Umbilical vein?

A

Ligamentum teres

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11
Q

What is the adult remnant of the Ductus arteriosus?

A

Ligamentum arteriosum

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12
Q

What is the adult derivative of Ductus venosis?

A

Ligamentum venosum

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13
Q

What is the adult derivative of the Umbilical artery?

A

Medial umbilical ligament

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14
Q

Blunt abdominal trauma, think what is damaged?

Risk?

A

Spleen rupture

Spleen damage or removal leaves patient more prone to infection by encapsulated bugs

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15
Q

Liver damage has what effect on immune system?

A

Decrease complement made.
C3 defiency increase encapsulated organism infection
C5-9 def –> N. meningitidis or N. gonorrhoeae infections

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16
Q

What causes bronchocontriction?

A

Alveolar hypocapnia
Bronchial inflammation inflammation
Local mediators
Parasympathetic activity

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17
Q

What is the risk of Isoniazid monotherapy?

A

Fast emergence of TB antibiotic resistance from rapid, selective gene mutations.

Only used monotherapy for prophylaxi

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18
Q

What are Sx of TB?

A

Fever
Night sweats
Weight loss
Hemoptysis

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19
Q

What is adenopathy?

A

any disease or enlargement involving glandular tissue, especially one involving lymph nodes

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20
Q

How would you characterize Sarcoidosis?

A

Noncaseating granulomas in lungs and/or liver
Elevated ACE levels
CXR shows bilateral hilar adenopathy
Reticular opacities

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21
Q

What diseases associated w/ Sarcoidosis?

A

Erythema nodosum
Interstitial fibrosis
Bell’s Palsy
Epithelial granulomas w/ Schaumann & asteroid bodies
Uveitis
Hypercalcemia (elevated 1alpha-hydroxylase-mediated vit D activation by epithelial macropahges)

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22
Q

Sarcoidosis Tx?

A

Steroids

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23
Q

MCC of rhinitis?

A

Adenovirus

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24
Q

Allergic rhinitis caused by what immune rxn?

A

Type I Hypersensitivty

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25
Q

Who gets nasal polyps?

A

repeated rhinitis incidents

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26
Q

Child with nasal polyps, what do the then test for?

A

Cystic fibrosis

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27
Q

Aspirin-Intolerant Asthma Sx

A

Asthma
Bronchspasm (due to Aspirin)
Nasal polyps

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28
Q

What is angiofibroma and what is demographic?

A

benign tumor of nasal mucosa w/ large blood vessels and fibrous tissue

Seen in adolescent males only

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29
Q

What is key Sx of Angiofibroma

A

Profuse epistaxis in young male

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30
Q

Chinese adult w/ enlarged cervical LNs. Biopsy done, shows pleomorphic keratin-positive epi cells among lymphs. What is the condition?

A

Nasophayngeal Carcinoma

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31
Q

What are the demographics of Nasopharyngeal Carcinoma?

A

African children or Chinese adults

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32
Q

Hoarse barking cough and stridor. What is the cause? What is the condition

A

Parainfluenza virus.

Croup!

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33
Q

What is laryngeal papilloma and what causes it?

A

benign papillary tumor of vocal cord

Due to HPV 6 & 11

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34
Q

What is difference in benign papillary tumor of vocal cords in adults vs kids?

A

adults- single tumor

kids- many

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35
Q

Squamous cell carcinoma from epithelium of vocal cords risk factors? Sx?

A

Tobacco and alcohol

Cough and stridor

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36
Q

Key Sx of pneumonia?

A

Pleuritic chest pain
rusty or yellow-green sputum
Dullness on percussion

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37
Q

Which cell type is the stem cell of the alveoli?

A

Type II pneumocytes

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38
Q

Clara cell Fx?

A

Bronchiolar epithelium protection
They detoxify harmful inhalants via P450 enzymes of smooth ER
Stem cells for bronchiolar lining

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39
Q

What is secondary pneumonia?

A

Virus infection of respiratory system followed by a bacterial infection, due to inhibition of mucociliary

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40
Q

MCC of secondary pneumonia?

A

Staphylococcus aureus

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41
Q

MOA of Streptomycin?

A

Inhibits initiation of protein synthesis by binding to 30S chromosomal

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42
Q

How does silicosis lead to TB?

A

Silicosis impairs macrophage effector arm of CMI

Macrophage main defense against mycobacteria

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43
Q

Reminder slide! :)

A

Abs against Encapsulated bugs cause capsule to swell –> effect known as Quellung reaction

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44
Q

What is the hallmark test of CGD?

A

Nitroblue tetrazolium test

In CGD, Neutrophils cannot make R.O.S. due to NADPH oxidasae deficiency. CGD pts cannot reduce NBT, so Neutrophils dont turn blue.

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45
Q

What toxin Clostridium perfringens makes? What does it do?

A

Lecithinase (aka Alpha toxin, Phospholipase)

It degrades tissue/cell membrane. Can cause “gas gangrene” (myonecrosis) and hemolysis

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46
Q

How does Clostridium perfringens in lab?

A

Gram pos rods (Spore-forming), anaerobic, DOUBLE HEMOLYSIS on blood agar

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47
Q

What is mechanism of clearance of bronchioles?

A

Epithelial cilia!

There are no goblet cells & mucous secreting glands here, they end at BRONCHI

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48
Q

What are presentation w/ obstructive sleep apnea?

A
  • Obese (MBI >30)
  • Respiratory effort against obstruction –> snoring
  • System/Pulmonary HTN–>can lead to RH failure & Sudden cardiac death
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49
Q

What are presentation w/ obstructive sleep apnea?

A
  • Obese (MBI >30)
  • Respiratory effort against obstruction –> snoring
  • System/Pulmonary HTN–>can lead to RH failure & Sudden cardiac death
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50
Q

Immune system tole in Sarcoidosis?

Which cell types and cytokines play a role

A

Th1 CD4+ T-helper cells. Secrete IL-2.
IL-2 stimulates autocrine proliferation of Th1.
IFN-gamma activates macrophages–>promote granuloma formation

Increased levels of Th1, IL-2, and IFN-gamma lead to lung granulomas

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51
Q

What deficiency can Isoniazid result in? What is presentation?

A 
Vitamin Pyridoxine (B6) defiency, 
will present as peripheral neuropathy, elevated AST/ALT, convulsions, Sideroblastic anemia

Isoniazid competes w/ B6 (similar structures)–> decrease NTs (GABA, Epi, NE, Serotonin)

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52
Q

Fx of Pyridoxine?

A

Cofactor for:

  • transamination (a.a. –>alpa keto acid)
  • decarboxylation rxns
  • glycogen phosphorylase

Synthesis of:

  • Cystathionine
  • Heme
  • Niacin
  • Histamine
  • NTs (Epi, NE, 5-HT, GABA)
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53
Q

Explain sideroblastic anemia and B6 deficency

What causes B6 deficiency?

A

Pyridoxine important in heme synthesis. When B6 is low, less Hgb made leading to elevated unused iron –> sideroblastic anemia…PLUS microcytic anemia

Cause: Alcohol, Isoniazid

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54
Q

ADA deficiency is associated w/ what disease?

A

SCID

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55
Q

What bugs are a problem for neutrophils with CGD?

A

Catalase positive bacteria a problem, not killed

Catalase neg bugs still can be killed due to accumulation of H2O2 of bacteria in phagosome

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56
Q

What is a frameshift mutation?

A

Deletion or insertion of bases that are not multiples of three. Result in Non-Fx proteins.

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57
Q

What is a missense mutation?

A

Base substitutions taht result in different A.A.s to e coded for.

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58
Q

Which drugs disrupt Peptidoglycan cell wall of G+ & G- bugs?

A

Cephalosporins, vancomycin, penicillin

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59
Q

What is the MOA of Cephalosporins?

A
  • inhibit cell wall synthesis, but less susceptible to penicillinase.
  • Bactericidal
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60
Q

What are 2nd generation cephalosporins and what do they target?

A 
2nd gen: Cefoxitin, Cefaclor, Cefuroxime
Target G+C...."HEN PEcKs"
H. influenza
Enterobacter aerigebes
Neisseria spp
Proteus mirabilis
E. coli
Klebsiella pneumonia
Serratia marcescens
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61
Q

How is fetal lung maturity accessed, explain.

What is the normal values?

A

amniotic fluid L/S ration (phosphatidylcholine/ sphingomyelin)

phospholipids a key part of surfactant

mature when >2

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62
Q

Damage to the piriform recess can effect what nerve and what reflex ?

A

Internal laryngeal nerve (branch of superior laryngeal nerve…CN X). Carries only sensory; afferent limb of the COUGH reflex

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63
Q

What are the nerves of the gag reflex?

A

Sensory, afferent: CN 9

Motor: CN 10 (vagus)

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64
Q

Explain neuro of salivation

A

PANS fibers originating from glossophayngeal nerve (CN 9). They synapse on OTIC GANGLION, and postganglionic fivers travel via auricotemporal nerve to reach parotid gland

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65
Q

What is the MC type of asthma? How does it induce bronchoconstriction?

A

Atopic asthma (extopic allergies)

Inflammatory mediators: LTC4, LTD4, LTE4 (Leukotrienes) & Ach
these triggers only ones w. receptor that can be targeted by drugs

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66
Q

Are histamine blockers good for asthma? Why or why not

A

Ordinary doses of currently available antihistamines (H1-receptor antagonists) have minimal bronchodilator and bronchoprotective activity. In severe persistent asthma, H1 antagonists have no significant clinical effect.

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67
Q

Eosinophils have what key granule and what does it target? How can it damage normal tissue?

A

Major Basic Protein- Have anti-helminth Fx.

can cause bronchial epithelial damage in pts w/ atopic asthma

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68
Q

Eosinophils produce what substances?

A

MBP

Histamine, Arylsulfatase- helps limit rxn after mast cell degradulation

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69
Q

How would Coccidiodes immitis present on sample? Also, what techniques used for diagnosis?

A

Large spherule filled w/ round endospores

Use 10% KOH silver stain, will show the thick walled spherules.
Also can use serology or culture on Sabourauds agar

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70
Q

What conditions associated with Coccidiodomycosis?

A

Asymptomatic, or

Lung disease… flu-like Sx to even chronic pneumonia!

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71
Q

Where is Coccidiomycosis found?

A 
Desert areas (dust)
SW United States, California
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72
Q

What is cause of CF?

A
  • CFTR gene mutation, where Phe is deleted @ position 508.
  • mutation impairs posttranslational workup of CFTR gene–> poor protein folding–> degraded
  • Causes absence of CFTR channel from apical surface of exocrine ductal epithelial cells

thick mucus plugs

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73
Q

What systems effected by CF?

A

Lungs- chronic bronchitis, pneumonia, bronchiectasis

Pancreas- pancreatic insuffiency (malabsorbtion & steatorhea)

Liver

GI- Meconium ileus of nebworn

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74
Q

CFTR channel Fx?

A

Secretes Cl in lungs and GI, & reabsorbs Cl from sweat

If dys-Fx: thick mucus plugs in Lungs, pancreas, Liver

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75
Q

What bugs associated w/ CF respiratory infections?

A

Staph aureus and Pseudomonas

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76
Q

What is an ANOVA study?

A
  • compares means of 2 or more independent groups
  • Tests Null hypothesis- “all groups are simply random samples of same population”. If they are very different, Null is rejected.

Looking at interval variables (which can have a mean). i.e. BP, height, weight

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77
Q

What is T-test?

A

used to compare 2 group means. Looking at interval variables (which can have a mean)

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78
Q

What is Pearson correlation coefficient (r)?

A

Measure of strength of a linear relationship between 2 variables. Between -1&1, closer to 1 means stronger correlation.
r^2 usually reported

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79
Q

What is metaanalysis?

A

Pooling data from several related studies to reach an overall conclusion.
Increases statistical power
limited by study selection bias and quality of studies

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80
Q

How to define severe asthma?

A
  • Sx throughout the day and night (daily)
  • Limited activity
  • Frequent exacerbations requiring ORAL steroids
  • Decreased Lung function (pulmonary Dx tests)–> frequent use of beta-agonists
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81
Q

Best Tx for moderate to severe asthma? Describe!

A
  • Omalizumab (add-on therapy)
  • Monoclonal recombinant Abs, which are ANTI-IgE. Used in allergic asthma that is resistant to inhaled steroids and long-acting B2 agonists
  • reduces need of oral or inhaled steroids
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82
Q

What are signs of PE?

Best way to test?

A

Sudden-onset of Dyspnea, chest pain, tachypnea, obesity,prolonged immobility

CT pulmonary angiography

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83
Q

What are the types of PEs?

A

“An embolus moves like a FAT BAT”

Fat, Air, Thrombus, Bacteria, Amniotic, Tumor

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84
Q

What embolus associated w/ long-bone fractures ?

A

Fat embolus

also associated w/ liposucction

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85
Q

What embolus associated with DIC, mainly post-partum?

A

Amniotic fluid emboli

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86
Q

What is effect of PE on pulmonary value?

A

Causes V/Q imbalance–> hypoxemia–> hyperventilation–> Resp Alkalosis (high pH, low PaO2 & PaCO2)

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87
Q 
What are normal values for:
pH
PaO2
PaCO2
HCO3-
A

pH: 7.35-7.45
PaO2: 80-95 mmHg
PaCO2: 35-45 mmHg
HCO3-: 22-26 mmEq/L

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88
Q

How does influenza vaccine work?

A

Increases host Abs against viral hemagglutinin, preventing it from binding to SIALIC ACID of host cell plasma membrane’s glycoprotein RECEPTORS.

Virus cannot enter cell by receptor-mediated endocytosis

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89
Q

Which type of naked viruses are infectious?

A

SS+ (=mRNA) & purified nucleic acids of most dsDNA (exception: POX & HBV)

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90
Q

Which naked viruses are NOT infectious and why?

A

SS- and dsRNA are not, require polymerases

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91
Q

Describe the Picornaviruses? List them too

A 
Naked, SS+, linear
P.E.R.C.H.
Polio
Echo
Rhino
Coxsackie
Hepatitis (acute viral hep)
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92
Q

What lung infections are alcoholics at risk of? Best Tx?

A

KLEBSIELLA!!
Pulmonary infections and abcesses involving combinations of anaerobic oral flora: Bacteroides, Prevotella, Fusobacterium, Peptococcus
&
aerobic bacteria (i.e. Strep pneomo! MCC community acquired pneumonia)

Tx: Clindamycin [MOA: (-) 50s]

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93
Q

What is the effect of Ach on bronchi?

A

Bronchoconstriction

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94
Q

What receptors Ach acts on in Bronchi?

What drug inhibits? When is it used?

A

M1 receptors

Ipatrapium block Ach by binding to M1

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95
Q

Effects of Methylxanthines?

A

Cause bronchodilation by decreasing phoshodiesterase enzyme activity–> cAMP

Drug examples: Theophylline, Aminophylline

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96
Q

Which drugs to Tx bronchial asthma work indirectly w/ mast cells? MOA?

A

Cromolyn & Nedocromil

(-) mast cell degranulation (where they are stimulated or not on IgE side) to precent acute attacks from happening (PROPHYLAXIS!)

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97
Q

What factors are released by Mast cells?

A 
Histamine
Leukotrienes
PGs
PAFs
IL-4 & IL-5
TNF-alpha
Transforming GF-beta

“MASsive Ho’s Love Pigs & Tender Pork w/ TRANSparent colt 45.

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98
Q

How does expiration and inspiration effect pulmonary vasculature resistance?

A

Inspiration- lung and alveoli expansion

passive expiration- not much resistance

FORCED expiration- pressure from collapsing positive pressure

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99
Q

Patients w/ granulomatous diseases (Hodgkin’s, Non-Hodgkins, TB, Sarcoidosis) are prone to developing elevated levels of what ion?

A

Hypercalcemia, secondary to high levels of Vit. D

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100
Q

What is the most active form of Vit D?

A

Calcitriol

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101
Q

What are the forms of Vit D?

A

D2= ergocalciferol (from eating plants)
D3=cholecalciferol (from milk or sun expoosure to skin)
25(OH) D3= calcidol - storage form
1,25 (OH)2 D3= calcitriol (ACTIVE form)

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102
Q

Excess Vit D Sx?

A

Hypercalcemia
Hypercalciuria
loss of appetite
Stupor

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103
Q

Describe Vit D metabolism

A

1) Eat it or stand in sun
2) Bound to plasma-D- binding protein, moved to liver
3) convered to calcidol in liver by 25-hydroxylase
4) Calcidol–>Calcitrol (via kidney alpha1-hydroxylase)

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104
Q

What gives elastin it’s elastic properties?

A

Cross-linking between 4 different LYSINES on 4 different elastin chains = Desmosine cross-link
This Cross-linked due to Lysyl hydroxylase

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105
Q

What protects Elastin from elastase?

Defiency results in…

A

alpha-1 antitrypsin

Defiency of a1-antitripsin cause excessive elastin degradation in
Lungs–> PANACINAR emphysema
Liver–> cirrhosis (misfolded proteins build up)

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106
Q

Compare elastin to collagen

A
  • Rich in proline and glycine, but NOT hydroxylated
  • no triple helix in elastin
  • collagen made w/ hydroxylation, glycosylation, and disulfide bridges @ C-terminus of procollagen. Processes not in elastin
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107
Q

Explain elastin production

A
  • precursor TROPOELASTIN secreted into ECF and interacts w/ fibrilin to make scaffolding structure
  • In ECF, interacts w/ lysine –>Desmosome crosslink
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108
Q

What is an alternate name for apical lung tumors?

A

Pancoast tumor

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109
Q

Pancoast tumor invade other tissues and present w/ distinque Sx. Examples!

A

Invasion of:

  • Parietal pleura, ribs, vertebrae–> shoulder pain
  • brachial plexus->weakness or parathesia
  • SVC compression-> SVC syndrome
  • recurrent laryngeal nerve ->Hoarseness
  • paravertebral SANS chain-> Horner’s
110
Q

What are key Sx of Apical tumors?

A 
Horner syndrome
Shoulder pain
SVC syndrome
arm weakness
arm parathesias
Hoarseness
111
Q

In terms of Lab testing, how do you determine if erythrocytosis (polycythemia) is present?

A

HCT levels
Men: >52%
Women: >48%

112
Q

Differentiate Absolute vs relative erythrocytosis

A

in relative, there is significantly less plasma (example, significant diuretic therapy for CHF), giving misleadingly high HCT levels.

Test RBC mass to see. If normal, RELATIVE.
If high, ABSOLUTE

113
Q

Differentiate Primary vs Secondary erythrocytosis

A

Use EPO levels
Low: Primary (Polycythemia Vera- all 3 lines)

High: Secondary.

114
Q

Causes of Primary erythrocytosis

A

myeloproliferative diseases (i.e. PV)

115
Q

Causes of Secondary erythrocytosis

A

Hypoxia from high altitudes, smoking, COPD, abnormal secretion from tumors

To be sure of

116
Q

Pulse Ox; SaO2 s state?

A

Hypoxic

117
Q

Blood gas PaO2 <65mmHg means

A

Hypoxemia.

Cannot determine hypoxemia by SaO2!!!

118
Q

What is the time-frame for erythrocytosis types?

A

If HCT increase acutely (few days), it is sign of relative erythrocytosis.

Absolute (Primary-PV, & Secondary) take months to develop.

119
Q

What is elastase and where is it found?

A

Neutral PROTEASE from neutrophils and alveolar macrophages that infiltrate alveolar fluid

Released during inflammation

120
Q

How is excess elastase kept under control? What happens to lungs if not?

A

Balanced w/ alpha1-anti-trypsin

excess: centriacinar & panacinar emphysema

121
Q

Fx of CCSP of Clara cells?

A

(–) turning ON and RECRUITING Neutrophils

122
Q

How to calculate Absolyte Risk Reductions

A

ARR = Event Rate(control) - Event Rate(Tx)

123
Q

WHen should advance care planning for end of life issues take place? Give examples of issues

A

Best: Outpatient visits 1st

Then, during admission

Exs: mechanical ventilation, intubation, tube feeding, parenteral feeding, CPR, cardioversion

124
Q

When do you see Cheyene-Stokes?

A

Cardiac and neurological disease

***Advanced CHF***
Stroke
Brain tumor; injury
Syncope
Coma
CO poisoning
125
Q

Explain Pathophysiology of Cheyene-Stokes

A

Characterized as cyclic breathing with increasing tidal volumes, then decreasing tidal volumes, then followed by periods of apnea.

This state results due to decreased respiratory feedback loop w/ increased CO2 sensitivity. CO2 levels rise, but decreased feedback loop leaves patient in apnea state. When levels become very high, respiratory system abruptly responds with heavy breathing (increasing TV), followed with decreasing TV. However, CO2 drops so much that patient enters apnea state. Cycle continues.

126
Q

Describe Candida albicans (medium, temperature, presentation)

Where are they found?

A

True hyphae = “germ tubes”, incubated for 37C

In tissue: single cells w/ pseudohyphae

Normal flora on skin, mouth, vagina, GI

127
Q

Candida albican infections occur when?

A 
Antibiotic use
Corticosteroid use
DM
HIV, immunosuppresion 
neonates
128
Q

How is Candida albicans treated?

A

Topical azole for vaginal

Fluconazole or caspofungin for oral/esophageal or system (plus amphotericin B for systemic)

129
Q

Best indicator of alveolar hyperventilation?

A

Low Arterial PaCO2; HYPOCAPNIA

PaCO2 = BMR/ alveoalr ventilation
inverse relationship

130
Q

Causes of hypercapnia

A

Upper airway obstruction
Reduced Ventilatory drive
Respiratory Muscle Fatigue
Decreased Chest wall Compliance

131
Q

What is required for degrandulation during an allergic rxn (Type I HS)?

A

Cross-linking of two IgE molecule on cell surface by one mollecule of allergin

(mast cells & basophils)

132
Q

Which cell has key role in targeting TB?

A

CD4+ Th1 cells of the CMI. They stimulate macrophages, which kill M. tuberculosis

133
Q

What are Langhans giant cells?

A

Large cells found in granulomatous conditions.
They are formed by the fusion of epithelioid cells (macrophages), and contain nuclei arranged in a horseshoe-shaped pattern in the cell periphery.

134
Q

What drug (-) mycolic acids, thus, stopping proliferation of Acid Fast bug?

A

Isoniazid

135
Q

What sized particles can reach alveoli?

A

< 2 um

136
Q

What drug class inhibits beta-glucan (polysaccharude part of fungal wall)?

A

Echinocandins:
CASPOFUNGIN

MICAFUNGIN

137
Q

What is clinical use for caspofungin & Micafungin?

A

Candida & Invasive Aspergillosis

138
Q

What is presentation of Potter syndrome? Cause

A

Fetus has hypoplastic lungs, absent kidneys, and abnormal face features: suborbital crease, depressed nasal tip, retrognathia, low-set ears.

cause is OLIGOHYRADMNIOS, due to renal agenesis

139
Q

Define and differentiate Anti-fingal drugs

A

FA, pg 184

140
Q

During exercise, what processes increase?

A

Increase:

  • Cardiac Output 5L/min –> 20L/min
  • skeletal muscle CO2 made–> higher PCO2 in mixed venous blood
  • Oxidative metabolism of GLU & FAs in SkM
  • Increase CO2 & SkM perfussion & ventilation to balance increase CO2, and higher consumption of O2.
  • Increase preload
  • Increase blodo to working muscle
  • MAP increase only 20-40mmHg (TPR drops)
141
Q

What decreases in exercise?

A

Decrease:

  • venous blood O2.
  • Venous blood pH
  • TPR
  • decrease blood flow tissues other than musles (artery contriction)
142
Q

What causes sputum to turn green when sick?

A

MPO

  • It’s from azurophilic granules in Neutrophils
  • a heme-containing blue/green pigmented molecule
  • produces hypochlorous acid (HOCl) from Cl & H2O2
143
Q

Does a high bacterial load discolor sputum?

A

Bacteria directly does not change body secretion color

Increased bacteria in respiratory trigger increased MPO release into sputum, and that is direct cause of sputum becoming green

144
Q

What is a normal Alveolar-arterial O2 gradient? What is this indicative of V/Q

A

(PA- Pa), normal between 10-15mmHg

Therefore, no V/Q mismatch.

145
Q

Hypoxemia w/ normal PA-Pa gradient causes?

A
  • Alveolar hypoventilation
  • inspiration of air w/ low pO2 (i.e. high altitude)
  • decrease inspiratory capacity: Obesity, MG
146
Q

Main causes of hypoxemia

A

Increase PA-Pa gradient:

  • V/Q mismatch
  • Diffusion limitation
  • R–>L shunt

Normal PA-Pa gradient

  • Hyporventilation
  • low pO2 in air (high altitude)
  • Decrease inspiration capacity
147
Q

Reminder slide!

Genetics

A

When pedigrees are given, do punnet square ALWAYS. You may assume one proportion while forgetting to exclude a genetic possibility

Ex: Healthy person w/ CF sibling. Patients healthy, must be carriers. Tempting to say healthy person has 1/2 chance to have the gene. Look at pedigree results:
FF, Ff, Ff, ff –> you forgot to eliminate ff, since subject doesn’t have CF. Therefore, subject probability of having CF gene is 2/3 [(Ff,Ff)/(FF,Ff,Ff)]

148
Q

What are cold agglutinin illnesses? Be specific to diseases

A

Diseases that result in Cold Abs, IgM, in immune response to condition

CLL
Mycoplasma pneuomonia
EBV (infectious mononucleosis)

“Cold ice-cream, yuMMM)

149
Q

Which encapsulated bugs have vaccines, and how are they made (list components)?

A

Strep pneuomo
Neisseria meningitidis
H. influenza

Polysaccharide capsule (portion) + protein carriers

protein carriers=
diphteria toxin (mutant)
N. meningitis outer membrane complex,
& tetanus toxoid

150
Q

Key Sx of acute epiglottis?

Which bug main cause?

A

Sx:

  • Cherry-red epiglottis
  • airway obstruction.
  • “thumb-sign” on xray
  • Possibly stridor.

H. influenza!!!

151
Q

What is SaO2? How is it effected in cyanide poisoning?

A

% Hgb saturation w/ O2

Increase in cyanide poisoning, due to failure of O2 unloading in tissues

152
Q

What are factors for TOTAL O2 content of blood?

A

1) [Hgb]
2) SaO2
3) PaP2- partial pressure of O2 dissolved in blood

153
Q

What explains:
Normal PaO2 & SaO2, but
low O2 content (aka total O2)

A

Chronic blood loss!

* type of ANEMIA*

154
Q

compare breathing (resp. rate, tidal volume, etc) in patients w/ Increased ELASTIC resistance Vs. increased AIRFLOW resistance

A

Increased elastic resistance (i.e. Pulmobary fibrosis): Respiratory rate high w/ low tidal volume (Fast, shallow breaths)

Increased Airflow resistance (asthma, COPD) breath at lower rate, higher TV (slow, deep breaths) to minimize breathing work.

155
Q

What is cause of walking pneumonia?

A

Mycoplasma pneumoniae

156
Q

Which respiratory bug can also cause anemia?

A

Mycoplasma pneumoniae

Shares Ag’s w/ RBCs, so the immune response (w/ cold agglutins) will also cause blood lysis

157
Q

List catalase positive organisms

A 
Listeria
Aspergillus, Candida
Enterobacteriaceae, Pseudomonas
TB
Staph aureus
Nocardia (weakly G-stains), TB (no G-stain)
Cryptococcus
158
Q

MOA of Azoles

A

(-)P450 enzyme, which converts lanosterol to ergosterol in fungi

159
Q

Azoles S/E

A

w/ ketoconazole mostly: (-) Testosterone synthesis –> gynecomastia

Liver dysfunction,due to P450 (-)

Increase serum concentration of drugs metabolized by liver P450–> drug toxicity

160
Q

Best drug combo for Cryptococcal meningitis

A

Flucytosine & Amphotericin B

161
Q

Causes of congenital absence of vas deferens –> azoospermia

A

Cystic Fibrosis

Unilateral Renal agenesis

162
Q

Cause of PKU?

A

Mutations–>misfolded protein–>
Decrease in liver enzyme Phenylalanine Hydroxylase or decrease THB (cofactor)

AR disease

163
Q

Key Sx of PKU

A 
Mental Retardation
Growth Retardation
Seizures
Fair skin
Eczema
Musty body odor

Pleitropic disease (one gene, multiple phenotypic presentation)

164
Q

Cause of Friedeich’s ataxia?

A

Trinucleotide repeat: GAA–>

mutation of frataxin gene

165
Q

Sx of Friedeich’s ataxia?

A

Staggering, falling a lot
Hypertrophic cardiomyopathy (C.O.D.)
as a kid, Sx kyphoscoliosis

166
Q

Nucleolus main site for what? What enzyme is prominent here then?

A

Site of ribosomal subunit maturation and assembly

RNA polymerase I makes most of rRNA (18S, 5.8S, & 28S)

167
Q

Fx of RNA polymerase II?

What inhibits it and S/E?

A

makes mRNA (largest RNA, Massive)

-) by alpha-amanitin from Amanita phalloiedes (death cap mushrooms
S/E: liver toxicity

168
Q

RNA polymerase III Fx?

A 
Makes rRNA (smallest RNA, Tiny) & 5S rRNA
**5S rRNA located outside nucleolus**
169
Q

Alternate name for Lecithin?

When do levels increase significantly?

A

Phosphatidylcholine!

30wks big increase

170
Q

What is Lead-time Bias? What’s a potential clue for it?

A

artificial increase in survival time among tested patients who didnt have prognosis change. Disease simply detected earlier

think of Lead-time basis w/ “new screening test” for poor prognosis diseases like lung of pancreatic!

171
Q

How far up are the lung apices? What can happen with penetrating injury?

A

extends above the level of clavicle & 1st rib through superior thoracic aperture

Pneumothorax

172
Q

What structures make of the posterior neck triangle?

If stabbed here, what nerve damaged?

A

SCM, Trapezius muscle, & clavicle

Accessory nerve (CN 11)

173
Q

Where are carotid bodies?

A

bifurcation of common carotid artery, inferior to hyoid bone

174
Q

penetrating trauma to neck superior to the cricoid cartilage can damage what nerve?

A

Ansa cervicalis (C1, C2, C3)

175
Q

Sx of walking pneumonia?

A

nagging nonproductive dry cough
Malaise
low-grade fever

176
Q

What do mycoplasma need for medium growth?

A

Cholesterol

177
Q

Compare severity of Sx with CXR for walking pneumonia

A

Sx are not very severe (low-grade fever, malaise, nagging dry cough), but CXR looks WORSE

178
Q

What can increase risk for panacina emphysema in alpha1-antitrypsin deficiency?

A

Smoking

179
Q

Cause of alpha1-antitrypsn deficiency?

presentation?

A

Misfolded protein which builds up in liver cell ER, (genetics: PiMM normal, PiZZ abnormal, PiMz hetero)

Cirrhosis w/ pink PAS-positive globules in liver (a1AT misfolded and build up)
Panacinar emphysema

180
Q

What parts of immune system affected by SCID?

A

SCID shows combined T- & B-cell dysfunction

181
Q

What type of infections can present w/ SCID?

Important Sx?

A

Frequent viral, bacterial, fungal & protozoal infections.

Sx: absence of thymic shadow (hypoplasia), hypogammaglobulinemia, chronic diarrhea, failure to thrive

182
Q

Does H. influenza vaccine target all H influenza? Why or why not?

A

vaccine for type b H. influenza

90% of strains from middle ear (otitis media infection) are “Nontypable” and lack a capsule, thus, vaccine wont work on them.

Vaccine ONLY against type b strains (not other capsule types or nontypable)

183
Q

Describe the MC type of Hodgkins lymphoma?

A

Nodular sclerosis- nodular growth pattern w/ surrounding fibrous bands & lacunar-varient Reed Sternberg cells

184
Q

What are cancer risks associated w/ asbestos exposure?

A

Bronchogenic carcinoma occurs 1/4 in asbestos exposure, is MCC of death amongst this group

2nd cancer risk is Mesothelioma

185
Q

How those smoking play a role in cancer risks w/ chronic asbestos exposure?

A

Asbestos exposure can lead to Bronchogenic carcinoma

Among exposed to asbestos, smokers have 90X risk of B.C. vs. population

Nonsmokers: 5x risk vs population

186
Q

characterization of Asbestos exposure?

describe microscopic exposure

A

Calcified plaque on parietal pleura
pleural thickening
fibrosis of lower lung lobes (restrictive lung disease)

Micro: Asbestos bodies (golden-brown fusiform rods like dumbbells)

187
Q

What pathogen can present in steroid-dependent asthmatic patients and have recurrent Transient pulmonary infiltrates & Proximal bronchiectasis. Eosinophilia will take place.

A 
Aspergillus fumigatus
causes ABPA (allergic bronchopulmonary aspergillos)
188
Q

What is bronchiectasis?

A

Chronic necrotizing infection of bronchi, causing:
permanently dilated airways (–>decrease tone–> AIR TRAPPING),
purulent sputum
recurrent infections
hemoptysis

189
Q

What drug is used to diagnose asthma? describe

A

Methacholine- Muscarinic cholingeric agonist that increase bronchial mucus made and bronchial contraction

Tested w/ spirometry

190
Q

Explain use of Bosentan drug

A

competitive antagonist of endothelium receptors

used to Tx primary (idiopathic) pulmonary arterial HTN

191
Q

Pulmonary HTN w/o any any underlying heart or lung disease, and family history of this

A

Primary Idiopathic HTN

192
Q

most potent cerebral vasodilator?

A

pCO2, specifically, hypercapnia. Leads to decrease cerebral vascular resistance

193
Q

What blood pressure affects cerebral blood flow?

A

BP >150 mmHg –> increased blood flow and increased pressure

BP hypoperfusion –>brain ischemia

194
Q

What levels of pO2 affect brain perfusion

A

Goes up when <50 mm Hg

195
Q

What are physiological presentations of restrictive lung disease?protein

A

decrease lung volume (decrease FVC & TLC)
increase in FEV1/FVC ratio
increased expiratory flow rate

196
Q

what is component of physiological dead space?

A

Anatomic dead space + alveolar dead space

Anatomic dead space = air in conducting airways
alveolar dead space= air that doesnt participate in gas exchange due to insufficient blood flow

197
Q

Which type of virus can produce multiple proteins from a single mRNA transcript?

A

SS+, linear, nonsegmented RNA

198
Q

Which fungus has a polysaccharide capsule?

Appearance w/ india ink?

A

Cryptococcus neoformans

Clear zone w/ india ink

199
Q

Organism capsule appears red on mucicarmine stain. What tissues does it infect? Sx?

A

Cryptococcus neoformans

infects lungs. Usually no-Sx, but can have pneumonia like Sx

200
Q

What medium does H. influenza need for growth?

A

Chocolate agar w/ Factor X (hematin) & factor V (NAD+)

201
Q

What enzyme is needed to make INH an active metaboliteand potent for Mycobacterium? How can Mycobacterium become resistant to INH?

A

Bacterial catalase-peroxidase (KatG)

resistance to drug through non-expression of KatG

202
Q

How does pyrazinamide target TB? Can resistance develop?

A

Drug lowers pH in environment to target TB

Drug becomes active by mycobacterial pyrazinamidase; mutation of enzyme can leave drug ineffective

203
Q

increase arabinosyl transferase production in mycobacteria leads to resistance for what drug?

A

Ethambutol

enzyme mentioned increases production of mycobacterial wall components

204
Q

Leading cause of chronic bronchitis?

Sx?

A

Smoking

Sx:
Productive cough, wheezing, crackles
Cyanosis, “blue bloaters”
Mucous gland hypertrophy (reid index >50%)
Patchy squamous metaplasia of bronchial mucosa
Neutrophil infiltration
Cor pulmonale

205
Q

Recurrent sinopulmonary & GI tract infections, and anaphylactic response to blood products, are presentations in what deficiency?

A

Selective IgA deficiency- absense of secretory IgA

IgA w/n transfused blood product leads to allergic response, w/ body thinks is foreign.

206
Q

How to calculate PAO2 (alveolar O2 levels)

A

PAO2 = 150 - (PaCO2/ 0.8)

207
Q

When does diffusion capacity in lungs decrease?

A

Alveoalr walls are thickened (i.e. PF, hyaline membrane disease)

or, when alveolar membrane destroyed (i.e. emphysema..like in smokers)

208
Q

Which TB drug S/E is visual disturbances?

Which specific disturbances?

A

Ethambutol

S/E: Optic neuropathy (red-green color blindness) & liver toxicity.
Removing drug from regimen will improve vision.

209
Q

Which lung cancer is surgery not part of Tx?

A

Small-cell carcinoma
Disease is rapid growthing and spreading, and surgery ineffective. Main Tx is radiation.

Also, it has low survival is 5-years

210
Q

MCC of SVC syndrome?

A

Mediastinal tumor, specifically, Bronchogenic carcinoma

211
Q

Differentiate MC cause of SVC syndrome

A 
#1- Bronchogenic carcinoma
#2- Pancoast tumors
#1 associated w/ smoking, and presents w/ hempotysis
#2 more commonly presents w/ shoulder pain & Horners syndrome
212
Q

How does pulmonary fibrosis appear on Xray

A

bilaterial reticulonodualr pattern of opacities

look up!

213
Q

What is lung biopsy of PF?

A

pathcy interstitial lymphocytic inflammation of alveolar walls

214
Q

W/ persistent bronchial asthma, what is the best anti-inflammatory agent?

A

Inhaled glucocorticoids (i.e. Fluticasone)

215
Q

Glucocorticoids effect on inflammation

A

Anti-inflammatory

(-) pro-inflammatory cytokines
Apoptosis of inflammatory cells: macrophages, lymps, Eos
reduce hyperresponsiveness

216
Q

What effect does beta-2 agonists & Ach (-) on bronchial inflammation?

A

Minimal. Inhaled glucocorticoids used instead

so, drugs like Ipatropium or albuterol not effective for anti-inflammation

217
Q

Effect of using protein conjugation when making vaccines (for bugs w/ capsules)?

A

conjugate becomes a Tcell dependent Ag. leading to a Tcell immune response –>Ab class switching

218
Q

For blood gas levels to be biggest influence on cranial vessel resistance, what must BP be?

A

60-140 mmHg

219
Q

Hypoxia effect on cerebral blood flow

Increased CO2?

A

sever hypoxia ( rapid increase in cerebral blood flow and intracranial pressure

also increases flow (25-100)

220
Q

Panic attacks have what changes in blood gas levels?

A

Decrease pCO2

221
Q

Tx for cerebral edema?

A

Hyperventilation

222
Q

Describe Cl- levels in venous blood Vs. arterial blood. Why is Cl- higher in one.

A

CO2 in blood enters RBCs. CA w/ RBCs forms Bicarb from CO2 & H2O. Bicarb diffuses out of RBC into plasma. TO maintain electrical balance, Cl- from plasma goes into RBC, aka “Chloride shift”. This why high Cl- content in venous blood

draw this out!`

223
Q

PFT presentation in low anti-protease levels

A

Likely alpha1-antitrypsin deficiency and associated early onset emphysema (if worsening exertional dyspnea)

decreased FEV1/FVC, increased TLC. decreased diffusing capacity

224
Q

Insufficient surfactant can lead to what condition?

A

alveolar collapse (atelectasis)

225
Q

Define COPD

A

group of diseases w/ airway obstruction, anatomical or physiological, where the lung does not empty & air is trapped

226
Q

COPD lungs function tests (spirometry)

desribe them

A

decreased FEV1/FVC ratio (more decrease in FEV1),
FVC- air to blow out candles, FEV1- air expired in 1 sec

TLC higher, >7L (due to air trapping)

227
Q

What is time-frame diagnostic criteria for chronic bronchitis?
What is Reid index requirement?

A

Productive cough >months a year (doesn’t have to be consecutive) for >2 yrs.

Reid index: >50%

228
Q

Explain the pathophys for chronic bronchitis, CYANOSIS

A

Heavy mucus content picks up CO2 from smoking–> elevated PA-CO2. Extra pressure from CO2 –> decrease PA-O2–> decrease Pa-O2

229
Q

How is emphysema an air obstructive disease?

A

Alveoli loose elastic recoil, and cannot push much air out (“balloons to shopping bags”)

lack of elasticity–> airway collapse

physiologic airway obstruction

230
Q

MCC of emphysema?

explain path

A

SMOKING!

This COPD disease due to imbalance of elastase & a1-antitrypsin (protease & antiprotease). Smoking –> inflammation–> elevated elastase levels.

alpha1-antritrypsin deficiency another cause, but not as common

231
Q

differentiate types of emphysema

A

Centriacinar- smoking cause. more severe in upper lobes ($ “smoke rises” $)

panacinar- a1AT deficiency. Lower lobes.

232
Q

Sx oh emphysema?

A
  • prolonged expiration w/ pursed-lips “PINK-PUFFER”
  • dyspnea & cough w/ minimal sputum
  • weight loss (pressing lips alway a workout)
  • Barrel chest
233
Q

Explain chest shape in emphysema

A

normally, chest wall and lungs in “tug-of-war” w/ each other, @ balance @ FRC

loss of recoil, chest wall winning and expands out–> AP diameter of chest

***FRC is reset in emphysema, higher”
(in fibrosis, lungs win and FRC reset to lower value)

234
Q

hypoexmia in emphsema

A

1) CYANOSIS (explained in other slide)

2) decreased alveoli surface area for gas exchange

235
Q

explain pathogenesis (immuno) of asthma (ILs, Ab)

A

allergin induces Th2 (of CD4+ Tcells) to release
IL-4: (plasma cell class switch to IgE)
IL-5: recruits Eos
IL-10: (-) Th1 cell, promotes Th2 subtype

Crosslinking of IgE on mast to an Ag–> Hist release
MPO by Eos

236
Q

SIte of histamine induced vasodilation?

leakiness of vessels?

A

arterioles

leakinf of fluid @ post-capillary venule

237
Q

What is released during reexposure of Ag in asthma? Early phase vs late phase?

A

Mast cells: Histamine, C4,D4, E4 (early)

Late phase: MPO, Eos

238
Q

Microscopic ID of asthma?

A 
Charcoat-Leyden crystals (from Eos)
Curschmann spirals (spiral shaped mucus plugs)
239
Q

Adult w/ nasal polyps, what are causes?

A

repeated rhinitis

** aspirin-induced asthma**

240
Q

Causes of Bronchiectasis?

A 
*necrotizing inflammation of airway*
CF
Kartagener syndrome 
Aspergillosis (CF & asthmatics)
necrotizing infection
Tumor, foreign body
241
Q

What are Sx of Kartagener syndrome?

A

Infertility
Sinusitis

LOOK UP!! edit

242
Q

clinical features of bronchiectasis?

A

foul-smelling sputum
secondary amyloidosis
cor-pulmonale, cough, dyspnea

243
Q

What is primary amyloidosis?

A

Amyloid light chain deposition (plasma cell problem)

244
Q

Secondary amyloidosis?

A

chronic inflammation. SAA overmade. SAA–» AA

245
Q

What are body cavities lined w/?

A

Mesothelium

246
Q

Where is asbestos exposure seen?

A

Insulation work & shipyards

247
Q

Sx of mesothelioma?

In Xray & EM?

A

hemorrhagic pleural effusions
X-ray: pleural thickening
EM: tumor cellls; multiple, long, thin microvilli & lots of tonofilaments

248
Q

How to distinguish Mesothelioma from Adenocarcinoma by EM?

A

Adenocarcinoma cells: short, plump microvilli

Mesothelioma: long, thin microvilli

249
Q

What is adenocarcinoma?

A

Peripheral lung cancer, MC in nonsmokers & women

Associated w/ hypertrophic osteoarthropathy (clubbing)

250
Q

Describe adenocarcinoma on CXR & Histo

A

CXR:(Bronchioalveolar subtype) hazy infiltrates like pneomonia

Histo: “thickening” of alveolar walls

251
Q

Patient has MI. What effect can this have on lungs. Explain.

A

decreased lung compliance

MI affects LV most. Less LV output-> increase LV endsystolic pressure-> elevated pressure in pulmonary vessels

Increase Pulmonary pressure-> increase fluid pushed into lung interstitium-> decreases lung compliance

252
Q

Left heart failure Sx

A 
Dyspnea
Bibasilar crackles
S3 sounds
recent MI
Pulmonary edema, PND
Orthopnea
253
Q

Signs of Fragile X?

10 points!

A
  • long face, big jaw, large ears, cleft palate
  • Mild-moderate mental retardation
  • eXtra large balls; macroorchidism
  • MV prolapse
  • pes cavus
  • double-jointed thumbs
  • single palmar crease
254
Q

Output of VPL?

A

Somatosensory cortex (brodmann area 3,1,2)

255
Q

What is Fragile-X syndrome?

A

Defect affecting methylation and expression of FMR1 gene

  • 2nd MC mental retardation
  • a trinucleotide repeat disorder of CGG
256
Q

Explain sensitivity of a test ?

A

(# of true positives)/(# pts w/ disease)

important to have high sensitivity for screening tests

257
Q

Use of positive predictive value?

A

TPs/ (#TPs + # FPs)

Test’s ability to correctly ID those w/ disease from those w/ positive results
depends of disease prevalence

258
Q

Bacteria that are able to take up free DNA called?

Examples?

A

Competent

Strep pneumo, H. influenza, N. meningitidis

259
Q

What is conjugation?

A

Pilus mediated transfer of DNA

260
Q

What is transposon-mediated DNA transfer?

A

DNA from plasmids or phage transfered w/n a genome or between plasmids.

261
Q

Difference in primary and secondary TB?

A

Primary: focal, caseating necrosis in LOWER lobe of lung & hilar lymph nodes. Will calcify and fibrose–> Ghon complex

Secondary: Reactivation of infection of M. tuberculosis. Occurs @ lung APEX. Cavitarys made. Classic TB Sx: hemoptysis, weight loss, fever.

262
Q

What tissues affected by spread of TB?

A
  • lumbar vertebra: POTT disease
  • Kidneys- sterile pyuria
  • Cervical LNs
  • Meninges
263
Q

How is Histoplasma capsulatum seen in lung tissue?

What does it target?

A

Ovoid cells w/n macrophages

the fungus uptaken by macrophages. Granulomas formed, like TB.

Targets Histiocytes and RES system–> lymphadenopathy & hepatosplenomegaly.

264
Q

How does one get H. capsulatum

A
  • go to a cave
  • sniff bat or bird poop from cave
  • travel to Mississippi & Ohio river for the heck of it
265
Q

How does perfussion change in lungs in upright position?

Supine?

A

Perfussion increases from apex->base (much higher in base). Look at is as zones for pressures:
Zone 1: alveolar > venous >arterial. No flow! Occurs in hemorrhage, high Alv pressure. Dead space
Zone 2: Arteriole > alveolar > venous. Pulsatile flow by arteriole end. Top of lungs
Zone 3: Arteriole> venous > alveolar. Continuous flow.

Lungs become all Zone 3 @ supine

266
Q

V/Q, V, & Q changes apex to base:

A

Perfussion (Q=flow) very low at apex, very high at base
Ventillation goes up from apex to base (not as much as Q)

V/Q goes down (apex to base)

267
Q

MC renal malignancy? Histo presentation?

A

Clear cell carcinoma

From renal tubular cells. Abundant clear cytoplasm, filled w/ glycogen and lipids..”clear”

268
Q

What are Lung function tests presentation in emphysema?

A

Increased: TLC, RV, & FRC due to decreased lung elastic recoil

Air trapping increases exploratory reserve volume-> increase FRC

269
Q

explain Sx of hyperventillation: sever anxiety, dizziness, weakness, blurred vision

A

Hypocapnia causes vasocontriction, thus, less cerebral blood flow

270
Q

Compression of SVC has what Sx?

A

Facial edema, dyspnea, dialted collateral veins in upper trunk

USMLE/ Step ONE (20 decks)

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