Spirometry

1. Total Lung Capacity

2. Vital Capacity

3. Inspiratory Capacity

4. Functional Residual Capacity

*when is pulmonary vascular resistance lowest?

1. TLC = IRV + VT + ERV + RV

2. VC = IRV + VT + ERV

3. IC = IRV + VT

4. FRC = ERV + RV

*PVR at lowest*

FRC

1. Obstructive Lung Disease

2. Restrictive Lung Disease

1. Higher FRC 

lung compliance increased

Expansive > Collapsing

2. Lower FRC

lung compliance decreased

Collapsing > Expanding

HbA = a2b2

HbF = a2y2

HbF affinity for oxygen bc it doesn't effectively bind 2,3-DPG

a.  this is how the fetus extracts oxygen from maternal hemoglobin in placenta

Cyanide Poisoning

1. features?

2. treatment

3. treatment*

CN- Binds cytochrome a-a3 complex of ETC, block aerobic metabolism and result in rapid cell death

Features

a. rapidly-progressing flushing, tachypnea, HA, tachycardia, N/V

b. lab: Lactic Acidosis with lessened arterial and venous 02 difference 

i.e., venous blood still highly oxygenated

Treatment: Nitrates 

a. induce met-Hb formation (Fe 3+ form; high CN- affinity)

b. binds CN- so it can't reach ETC

Excretion: Sodium Thiosulfate

a. binds CN- forming thiocynate : urine

Bronchial circulation in response to hypoxia

complication of chronic hypoxia?

Vasoconstiction

a. shunt blood toward oxygenated regions for more efficient gas exchange

chronic hypoxia

a. Pulmonary HTN -> cor pulmonale (Side HF due to lung disease)

R-side HF= JVD, hepatomegaly, Edema

Pulmonary Hypertension

1. Primary

2. Secondary

3. pulmonary circuit pressures

Primary Pulmonary HTN

*BMPR2 gene inactivation

a. normally inhibits vascular smooth muscle proliferaiton

b. *plexiform lesions (tuft of capillaries)

c. medial hypertrophy of arteries + laminar intimal fibrosis

Secondary Pulmonary HTN

a. any pathologic state that raises pressure in pulmonary ciruit

a. ex., mitral stenosis, COPD, L-R shunts, Sleep apnea

Normal: 10-14 mmHg

HTN: >25 mmHG (rest) or >35 mmhg (exercise)

A-a gradient

1. equation + normal values

2. Equation for alveoli

3. what is it's importance

4. Normal A-a 

5. High A-a

A-a gradient: PA02 - Pa02

normal: 10-15 mmHg

a. difference in P02 in alveoli and oxygenated blood

b. normal PA02 : 100mmHg

c. normal Pa02: > 92 mmHg

Alveolar Gas Equation: PA02  =  150 - (PaC02/0.8)

Importance of A-a: determine cause of Hypoxemia 

Normal A-a:

1. High Altitude

2. Hypoventilation

Increased A-a (>15):

1. Diffusion Defect (Emphysema/CO/Fibrosis)

2. V/Q defect:

3. R->L shunt: 

V/Q ratio

1. High Vq?

2. Low Vq?

3. V/Q = 0

4. V/Q = infinity

Ventilation/perfusion ratio (V/Q = 1 is ideal for gas exchange)

1. Apex(V/Q)= 3

(wasted ventilation- can't get into blood)

2. Base (V/Q)= .6

*ventilation and perfusion are greater at base (hence, lower ratio) than apex

3. Airway obstruction (shunt)

*no improvement with 100%02

4. Blood Flow obstruction (Dead space)

*Improves w/ 100% O2 

C02 transport

1. mechanism

2. Cloride shift

3. main transport form

Hb responsible to carrying 02 to tissues & C02 to lung

Mechanism:

1. C02 enters RBC & Carbonic Anyhdrase converts it to H+ & HC03-

2. H+ is Buffered in RBC by deoxy-Hb

3. HC03- diffuse out of RBC into plasma in exchange for Cl- entry

*Cloride Shift* (maintain electroneutrality)

*reason for high RBC Cl- in venous blood

4. Enter lungs: process reversed & C02 is exhaled

HC03 = main C02 transport

 Nasal polyp

1. Child?

2. Adult?

child = test of Cystic Fibrosis

Adult = Asprin-intollerant asthma

*triad:

1. Asthma

2. aspirin-induced bronchospasms

3. Nasal polyps

Nasopharyngeal carcinoma 

1. associated

1. EBV infection

2. Posterior LN enlargement

Biopsy: Pleomorphic, Keratin (+) cells with lymphocytes

Acute Epiglottitis

1. who?

2. due to?

3. symptoms?

4. avoid?

Inflammation of epiglotis

a. H. influenza (b)

b. non-immunized child

Present:

1. Drooling with dysphagia

2. Muffled voice

3. inspiratory stidor

*Don't mess with airway, risk it closing.

Laryngeal papilloma

1. adults?

2. children?

presentation: hoarseness with mass on vocal cord

a. Adult = Singular tumor

b. child = multiple tumors

Due to: HPV 6,11

Lobar pneumonia

1. microbes?

2. Four Stages

a. timing

b. macro

c. Alveolar

consolidation in entire lobe of lung

Microbes:

1. S.pneumonia (#1 CAP)

2. Klebsiella

a. Currant jelly a. Elderly, Nursing Homes, Diabetics

Stages

1. Congestion (24 hrs)

micro: Vascular dilation

Alveolar contains bacteria

2. Red Hepatization (2-3 d)

macro: Red, Firm lobe (liver-like)

Alveolar: erythrocytes, neutrophils, fibrin

3. Grey Hepatization (4-6d)

macro: Gray-firm nodule

Alveolar: RBC degredation

4. Resolution (via type II pneumocytes)

macro; normal architecture restored

Alveolar:  Enzymatic digestion of exudate

Bronchopneumonia on CXR?

1. Superimposed on Viral?

2. Superimposed on COPD?

3. Cystic Fibrosis

4. IC pts, CAP, or COPD superimposed?

Patchy Consolidation around Bronchioles

a. multi-lobular and Bi-lateral

1. Staph. Aureus

2. H. Influenza

a. Moraxella Cararrhalis

3. Pseudomonas

4. Legionella

a. water-source

b. silver stain

Interstitial (Atypical) pneumonia on CXR?

histology?

Diffuse interstitial infiltrates

a. Increased lung markings

Histology:

a. inflammatory cells within cell walls lining air sac

b. No consolidation

primary TB lung location?

secondary TB lung location?

Primary = Lower lobes

a. Caseating Necrosis

b. Hilar LN undergo Fibrosis + Calcification

* A + B = Gohn Complex

Secondary: Apex (high 02)

a. IC state or TNF-a inhibitor

b. Caseating Granuloma

c. Fever, Night sweats, Cough with Hemoptysis, weight loss

1. Meninges (base of brain)

2. kidney (sterile pyuria)

3. Lumbars (Potts disease)

Spiromety: COPD

FVC?

FEV1?

FEV1/FVC?

TLC?

FVC: Down

FEV1: DOWN DOWN

FEV1:FVC: Down

TLC: Increased

(Air Trapping ; total amount of air in lung)

Reid Index: Ratio of Mucus gland layer of bronchial wall submucosa to thickness of entire wall 

a. not including cartilage

normal: 40%

Chronic Bronchitis: > 50%

"Blue Bloaters" = Cyanosis

a. Inc. PA02 in alveoli takes away from Pa02 which results in dec. perfusion

Chronic Bronchitis presenting symptoms?

association?

Productive Cough for 3+ months over past 2 years

a. Tons of mucus

b. Blue Bloater (Inc. PaCo2 -> dec. Pa02)

associated: Smoking!

Emphysema 

1. due to?

2. PE

3. Types

Destruction of alveolar air sacs and diminished elastic recoil

a.  results in "air-trapping"

Etiologies:

1. Smoking (excess protease activity)

2. A1AT deficiency (anti-protease) 

PE:

1. Barrel-Chest

2. Pink-Puffer: prolonged expiration of pursed lips 

*inc. backpressure to keep alveolar open so air can exit

3. Cough with minimal sput (vs. Chronic Bronchitis)

Types:

1. Centri-acinar (smoking)

2. Panacinar (A1AT) 

Emphysema Subtypes

1. Centriacinar

2. Panacinar

Centriacinar Emphysema (Smoking)

a. Pollutants damage to bronchioles & cause inflammatory reaction

b. release Proteases (esp. elastase) from infiltrating neutrophils & alveolar MO

*imbalance between Proteases / Anti-proteases

location: Upper lobes

Panacinar Emphysema (A1AT deficiency)

A1AT inhibits proteolytic Enzymes & produced by liver

a. A1AT accumulates in liver & lead to hepatic problems

liver stain : PAS (+)

Location: Lower Lobes 

*Early onset of COPD & history of liver disease should highten suspicious of A1AT def

Panacinar emphysema at risk for?

*histology of that organ?

Asthma 

1. mechanism

2. Histology

Reversible Airway constriction

a. TYPE 1 HSR

b. FAMILY HX of ALLERGIC DISORDERS

Mechanism:

1. First exposure: Sensitized Th2

2. Second Exposure: IgE-mediated cross-linking (HSR I)

 a. Histamine

b. Eosinophils : Major Basic Protein -> damage

c. Leukotrienes: bronchoconstriction

Histology: Curschman spirals w/ charcot-leyden crystals

Kartagener Syndrome

1. specific defect?

2. triad?

*Dynein arm dysfunction (ciliary movement)

1. recurrent sinusitis

2. infertility

3. situs inversus (vs. cystic fibrosis)

Coal Workers' Pneumoconiosis 

1. exposure?

2. findings?

3. complication?

1. Inhale coal dust

 2. Black Lung covered with coal

a. shrunken and fibrotic

3. Rheumatoid Arthritis (Caplan Syndrome)

Silicosis

1. exposure?

2. *pathology?

3. Findings?

1. Silica

a. Sandblasters, Silca miners

2. Impairs Phagolysosome formation in MO to kill particles

*INC. RISK FOR RB Reactivation

3. Eggshell calcification of hilar lymph nodes surrounded by fibrotic tissue

Berylliosis

1. exposure?

2. *findings?

3. complication?

1. Aerospace industry, Berrylium miners

2. Noncaseating granulomas in Lung, Hilar LN, and systemic organs

*Mimics Sarcoidosis 

Asbestosis

1. exposure?

2. findings?

3. complication?

1. Construction workers/ shipyard, plummer

2. Calcified pleural plaques in mid-lung zones

a. Asbestos Bodies* (Long, golden-brown fibers with iron)

3. Lung Carcinoma and Mesothelioma

a. CANCER > Mesothelioma

Idiopathic pulmonary fibrosis

1. drives damage

2. drugs

Insidious onset of extertional dyspnea with Restrictive-profile Pulmonary function tests

a. interstitial fibrosis

b. Honeycomb lung (cystic airspace enlargement

*TGF-B drives Fibrosis

Bleomysin

Busulfan

Amiodarone

Sarcoidosis 

1. common pt

2. classic finding

3. Ratio

4. Elevated in serum?

1. African American Females

2. *noncaseating granulomas in multiple organs (Lung + Hilar LN)

a. Asteroid body (stellate inclusions) inside giant cells

3. High CD4:CD8 ratio

*Sarcoidosis is disease of disordeed immune regulation

4. *Elevated ACE

1. Dysnpea or cough

2. elevated serum Ace

3. hypercalcemia

a. alpha1 hydroxylase activity of epitheliod histiocytes convert Vit d to acive form)

*non-caseating granulomas in lungs, Hilar LN, other parts of body

Treatment

1. small cell lung carcinoma?

2. Non-small cell carcinoma

1. Chemotherapy!

*cant be surgically resected

"cells so small that surgeon cant see them"

2. Sugery

Rules of thumb

: Lung Cancers staring with "S" (3)

Small Cell Carcinoma

Squamous cell carcinoma

1. Male Smokers

2. Centrally located

3. Paraneoplastic syndromes

a. Small Cell: ADH, ACTH, Lambert-Eaton

b. Squamous cell: PTHrp

Small Cell Carcinoma

1. Histology

2. association?

3. location?

4. other?

1. Neuroendocrine (Kulchitsky) cells

a. POORLY-differentiated

b. (+) Chromogranin

2. Male Smokers

3. Central

4. Paraneoplastic Syndrome

a. ADH: SIADH

b. ACTH: Cushing's

c. Lambert-Eaton

Trachea shift

1. spontaneous pneumothorax?

2. Tension Pneumothorax

1. *Side of collapse

a. rupture of emphysematous bleb causes transient lung collapse 

2. Away from collapse

a. air buildup on side of penetrating energy

*surgical emergency

Hypersensitivity pneumonitis

a. *granuloma w/ eosinophils right after exposure indicates HSR *

removal of exposure leads to recovery

Cancer of Pleura

associated: asbestosis 

Hemorrhagic pleural effusions 

*Psammoma bodies

It INCREASES

Cheyne Strokes respirations?

Associations?

pathophysio

Cyclin breathing in which apnea is followed by gradually increasing Tidal volumes and then decreasing tidal volumes until next apneic period.

Associated:  CHF or Neurologic Disease

Problem: Slow resp. feedback loop with enhanced response to PaC02

apnea: PaC02 levels rise, but delay in loop allows higher than normal PaC02

This causess and overcompensitory respiratory response to lower PaC02

*Cycle of Apnea and Hyperventilation

Cystic fibrosis most common mutation?

Resulting in?

CF can develop due to ________ (another mutation)?

Codon deletion coding for PHE at 508

Non-functional CFTR protein -- does not even reach cell surface.

Frameshift mutation

Left pirform recess associated with what nerve?

Common site of?

If damaged, what reflex will be affected?

1. Internal laryngeal nerve (CN IX)

2. Lodged foreign bodies (chicken/fish bones)

3. Cough reflex

Internal laryngeal nerve mediates afferent limb of the cough reflex.

Perfusion Limited vs. Diffusion Limited Gas exchange

etiologies?

equation?

Perfusion Limited Gas Exchange

a. normally physiologic resting state

b. equilibrium of blood & alveolar gas occurs early along capillary length

c. 02, C02, N20

Diffusion limited Gas Exchange

a. pathologic state (COPD/Restrictive, ARDS, etc)

b. blood p02 doesn't equilibrate with alveolar p02 by capillary length

Diffusion = A/T x  D(P1-P2)

Emphysea: decrease SA

Fibrosis: Thicken membrane

Pulmonary: Exercise 

1. what increases?

2. decreases

3. remain same

4. V/Q

Increased:

1. C02 production

2. 02 consumption

3. pulmonary blood flow

4. ventilation rate

Decreased:

1. pH (lactic acidosis)

Not Change

*Pa02 & PaC02 

*but inc. in venous C02 content

V/Q Apex to Base becomes uniform

Atypical Pneumonia Etiologies

1. Dormatory / Military Recruits / Young adults

2. Infants

3. Posttransplant immunosuppressive therapy

4. Elderly, Pre-existing lung diseases

5. Farmers / Veterinarians

1. Mycoplasma Pneumonia

a. complications: Cold Auto-immune hemolytic Anemia (IgM)

2. RSV

3. CMV

4. Influenza

a. Risk superimposed: S. aureus / H. Influe

5. Coxiella Burnetii

Acute Respiratory Distress Syndrome (ARDS)

1. Hallmark?

2. Features

3. CXR

Damaged Alveolar capillary interface

a. leakage of protein-rich fluids, edema

1. Hallmark: Hyaline Membrane Alveoli

2. Hypoxemia and cyanosis WITH respiratory distress

a. thickened diffusion barrier / collapse of air sacs

3. CXR: White out

Type I pneumoncytes

2. Type II Pneumocytes

2. clara cells

Type I

a. Gas Exchange (squamous)

Type II

1. Surfactant production

2. Regenerate lining after injury

 Clara cells

Nonciliated columnar cells (deeper than terminal bronchioles)

degrade toxins

Airway Histology

1. Trachea to Bronchi

2. Terminal Bronchioles

 3. how long do ciliated cells persist in respiratory tree

4. what clears infiltrate if it gets passed the terminal bronchioles

Trachea to bronchi

Ciliated Psuedostratified columnar epithelium

a. Cartilage & smooth muscle

b. Goblet cells

c. Glands: Submucousal, mucoserous

*Extend only to bronchi*

Terminal Bronchioles

Ciliated simple cuboidal epithelium

lack: cartilage, goblet cells, glands, smooth muscle

3. Persist from trachea to Terminal bronchioles

a. sweep mucous/particles toward pharynx (Mucocilliary Clearance)

4. Alveolar Marcophages

Anatomy

1. Pulmonary Artery relation to lungs

2. Aspiration locations

3. Thoracocentesis levels

1. "RALS"

a. Right Anterior

b. Left Superior

2. Right main bronchus (wider, more verticle angle)

3. Thoracocentesis

a. miclavicular: above 7th rib

b. Midaxillary: above 9th rib

c. Posterior scapular line: above 11th rib

*If done lower = penetrate abdominal structures

*if done higher = penetrate lungs

Lung / Chest wall compliance

1. FRC values

2. Penetrating Injury

Compliance = Volume / Pressure

*Inverse to elastance

Chest wall (expanding): (-) transmural Pressure

Lung (collapsing): (+) alveolar transmural Pressure

FRC

Airway Pressure : 0 cm H20

Intrapleural Pressure: - 5 cm H20 

*keep lungs inflated

Penetrating Injury

*puncture pleura: allow intrapleural communication w/ atmostphere (0cmH20)

a. (-) intrapleural pressure equilibriates w/ atmosphere via air entering intrapleural space

*Pneumothorax

1. Cabon Monoxide Poisoning

2. Methemoglobin

a.  problem

b.  affect on Hb

c. 02-dissociation shift

d. treatment

1. Carboxyhemoglobin

a. CO has 200x affinity for Hb vs. Oxygen

b. Prevents 02 release from Hb = Bright Red Skin

c. left shift on 02-dissociation curve

d. Tx: 100% 02

2. Methemoglobin Poisoing

a. Ferrous (II) oxidized to Ferric (III) which can't bind 02

b. 02 can't bind Hb = Cyanosis (functional anemia)

c. Left-shift on 02-dissociation curve

d. Tx: Methemoglobin Blue

*both will have normal Partial Pressure of 02 in arterial blood

bc it's a measure of 02 dissolve in plasma, not related to Hb function

02-dissociation Curve

1. shape

2. p50

3. shifts

relationship bw Partial pressure of 02 (x-axis) and 02-hb saturation (y-axis)

a. sigmoid: as each 02 binds, the 02 affinity increases

2. P50: 50% of Hb is saturated

decrease: inc. 02 affinity (vise versa)

Right Shift: Tissues

*lower affinity; higher P50*

a. C02

b. BPG affinity

c. Exercise

d. Acid/Altitidue

e. Temp

Left Shift: lungs

*higher affinity ; lower P50*

*opposite + C0 & Met-Hb poisoining*

Pulmonary Circulation

1. description

a. relation to systemic circulation

2. Low Oxygen

Low Resistance, High-compliance 

a. rate of flow must equal systemic cirulation

if slower: LV would soon be empty

if faster: LV would be overloaded

Hypoxic conditions: vasoconstrict regions

a. shunt blood toward better ventilated regions for efficent gas exchange

*this increases resistance in the pulmonary circuit, possibly leading to pulmonary HTN and cor pulmonale

Reactive Polycythemia

1. Absolute vs. Relative

2. Primary vs. Secondary

3. Hypoxis vs. other 

a. what do you measure for each differential?

Polycythemia: Increase in Hct level 

a. men > 52%

b women > 48%

Absolute vs. Relative Erythrocytosis

*measure Hct Levels

Absolute: True Increase in RBC mass

Relative: Normal RBC mass

Primary vs. Secondary Erythrocytosis

*Measure EPO levels

Primary: Low EPO

a. Myeloproliferative disorders (ex. Vera) 

Secondary: increased EPO

a. Pathologic Hypoxia or EPO secreting tumor

Hypoxic vs. other secondary causes

*measures arterial oxygen saturation (Sa02)

Secondary Polycythemia: Sa02< 92% (Pa02 < 65 mmHG)

Sa02 normal: tumor?

Don't confuse Sa02 vs. Pa02

*Sa02 measured as Percentage

*Pa02 measured has partial pressure in mmHG* 

What 3 factors affect total blood oxygen?

1. Anemia

2. CO poison

3. CN poison

4. Obesity

3 Components of total blood oxygen

1. Sa02 = % 02 saturation of hb

2. Pa02 = partial pressure of 02 in blood

3. Hemoglobin [ ] 

Anemia

a. Low Hb & 02 content

b. normal Pa02 + Sa02

CO poisoning

a. Low Sa02 & 02 Content

b. normal Pa02

CN- poison

a. Sa02 increased in venous blood (Failure of unloading)

Obesity

a. Low Pa02 (hypoventilation & Hypoxia)