Unit 6A Sigs | Baamboozle - Baamboozle | The Most Fun Classroom Games!

What is the pathogenesis of interstitial lung disease?(Sigs Case 6.6b)

Lung & fibrosis + alveolar capacity membrane thickening + pulmonary remodeling -> restrictive + gas exchange decrease

Compare/contrast expected PFT findings of obstructive vs. restrictive lung diseases (Sigs Case 6.6b)

O: volumes greater than normal, ratio lower than normal, loop shifts left; R: volumes less than normal, ratio elevated, loop shifts right

What is the significance of DLCO results in interstitial lung disease? (Sigs Case 6.6b)

DLCO represents ability of lung to transfer gas from inhaled air into blood; acts as surrogate marker for extent of lung damage; may decrease in many conditions

What is the MOA and side effects of thiazide diuretics?(Sigs Case 6.6b)

Used to decrease sodium reabsorption-> decrease fluid reabsorption-> directly decrease levels of circulating sodium; AE: ion imbalance, incr. urination

What is included in the GOLD assessment and what is it used for?- (Sigs Case 6.6a)

Classification of COPD based on FEV1% of predicted value; determine severity of expiratory airflow obstruction for classification/prognosis/interventions

How does cigarette smoke cause cellular damage to the respritory tract? (Sigs Case 6.6a)

ROS & inactivation of anti-proteases-> lung inflammation-> repetitive injury to bronchial tree-> airway fibrosis & mucus trapping-> chron. bronchitis-> COPD

What are the risks and benefits of LABAs and LAMAs for treating COPD? (Sigs Case 6.6a)

LABA-deathly asthma attack when used w/out steroid = B2-adrenoceptor decrease; LAMA-arrhythmia; increased CV risk

What is the role of glucocorticoids in managing COPD? (Sigs Case 6.6a)

Steroid must be used with LABA; decrease inflammation in flare-ups (swelling, mucus production, breathlessness)

Identify confirmatory biochemical reactions for bacterial respiratory pathogens. (SIGS 6.5b)

Urease (Klebsiella is +), Catalase, Agar, Gram stain, Hemataglutination (anti-HA antibodies: HPIV)

What are the elements of the CURB-65 Scale and what is it used for? (SIGS 6.5b)

Confusion, BUN, RR, BP, age >65; criteria for inpatient vs. outpatient vs. ICU treatment of CAP

Contrast the risk factors, clinical presentation, evaluation, and complications of viral and bacterial upper respiratory infections (URIs). (SIGS 6.5b)

V: supportive care, dry cough, lower temp., bilateral +; B: antibiotics, productive cough (+mucus), acute onset, higher temp; unilateral +

What are the challenges with treating Klebsiella pneumoniae? (Sigs Case 6.5b)

facultative anaerobe (can be w/wout oxygen); resistant to ampicillin; spread from lungs = dangerous superbug; Community + Hospital acquired

Differentiate between oxyhemoglobin and carboxyhemoglobin. (SIGS 6.5a)

Carboxyhemoglobin: carbon monoxide (240x affinity vs oxygen) & hemoglobin; oxyhemoglobin: oxygen & hemoglobin

Describe the effects of CO on hemoglobin and the hemoglobin saturation curve. (SIGS 6.5a)

CO binds hemoglobin w/ 240x affinity than O2 (competitively inhibits)--> curve shift to left--> bound O2 won't release

Explain how CO2, pH, Temp., and 2,3 diphosphoglycerate (DPG) or biphosphoglycerate (BPG) would shift the hemoglobin saturation curve and how this affects tissue oxygenation.(Sigs Case 6.5a)

Right shift: tissue oxygenation increased; Left shift: holds onto oxygen

Explain how low oxygen levels can alter the electrical and mechanical functions of the heart.(Sigs Case 6.5a)

Low O2-> ischemia of heart myocardium-> decrease in contractility (LV)-> reduces CO, increased preload-> ecc. hypertrophy-> dilation-> systolic dysfunction-> HF

Describe how cor pulmonale can result in right-sided heart failure. (SIGS 6.4b)

cor pul.->RV work harder->enlargement & thickening of RV (remodeling)-> contraction decreased-> conduction path stretched-> V. arrhythmia-> Vfib-> RHF

Explain how pulmonary hypertension increases the pressure/afterload on the right side of the heart. (SIGS 6.4b)

normally very low pressure/resistance; emboli blocks flow from RV--> resistance increases--> inc. afterload on RV (needs more work to contract against resist)

What is the significance of D-dimer elevation in the formation and diagnosis of PE.(Sigs Case 6.4b)

indicates clots are forming and breaking somewhere; highly sensitive, not specific to PE/DVT (must be coupled w/ suspicion of PE)

Explain the relationship of pulmonary perfusion to ventilation. How is this altered in a PE?(SIGS 6.4b)

PP: measurement of how much blood is pumped through lungs to alveoli for gas exchange; PE blocks/reduces supply; air movement still occurs--> VQ mismatch

Explain how inhaled corticosteroids and short-acting beta 2 agonists reduce asthma symptoms. (Sigs Case 6.4a)

binds glucocorticoid receptors in lungs-> affects gene transcription (decr. inflam. genes; incr. anti-inflam. genes); B2 agonists-> incr. cAMP-> bronchodilate

Describe how the normal gross and microscopic anatomy of the airway is altered during an asthma attack. (SIGS 6.4a)

incr. mucus production, goblet cells, leukocyte infiltration (mast cell, eosinophil, lymphocyte, neutrophil), smooth cell hyperplasia/hypertrophy, thickened BM

Describe integrative approaches to asthma (Sigs 6.4a)

Avoid triggers, mindfulness, yoga, 4-7-8 breathing, meditation, Med. diet, anti-inflamm. diet

Determine common triggers and risk factors of an asthma attack. (SIGS 6.4a)

RF: family hx, allergy hx, young age; Trigger: Allergic (environmental, etc); Non-allergic (cold air, exercise, infection, Aspirin, stress)