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)

Explain the role of metoprolol in the management of HCM.(Sigs Case 6.3b)

antagonizes catecholamine binding at Beta1 adren. receptors (card. nodal cells)-> decrease HR; antagonize B1-adren. recept. on card. myocytes-> decr. contract

Explain the relationship of HCM and heart failure with preserved ejection fraction (HFpEF)(Sigs Case 6.3b)

diastolic dysfunction (early diastolic relaxation) + LV hypertrophy (concentric)- thick wall = pressure overload + less volume (EDV-ESV/EDV) = up EF

Contrast normal systolic and diastolic function in a healthy heart with the systolic and diastolic function of HCM.(Sigs Case 6.3b)

may have average systolic funct. but poor diastolic funct.; diastolic dysf. will have preserved EF; systolic dysf will have reduced EF

Describe the potential benefits and precautions for the use of CoQ10 and L-carnitine for cardiac function. (SIGS 6.3b)

CoQ10: facilitates ATP production via ETC in mitochondria; body can become dependant- do not stop abruptly; L-Carn.: "shuttle" for FA to mitochondria in L vent.

Describe the alterations in vascular reactivity that result from endothelial damage. (SIGS 6.3a)

damage to endothelium--> dysfunction (inability to react to vasodilation)--> structural remodeling--> alters function

Characterize specific dietary modifications, medicinal foods, and lifestyle modifications for ASCVD.  (SIGS 6.3a)

Med. diet, Ornish Undo It, DASH, olive oil, nuts, cocoa, red wine, whole grains, fiber, B vitamins

Correlate hyperlipidemia with the development of atherosclerotic plaques in blood vessels. (SIGS 6.3a) 

lipids/lipoproteins->cross endothelial barrier to artery intima-> retention & endo.dysfunct.-> inflam.-> macroph-> foam cells-> calcification-> rupture

Contrast how the distal arterioles compensate for the stenosis in their respective coronary arteries.(Sigs 6.3a)

MILD: dilation --> meet met. need; MOD: dil.--> meet met. need @ rest; exertion: max blood flow low despite dil. --> can't meet met. need;COMPLETE OCCUL: unable

Describe how cardiac chamber dilation results in global hypokinesis and systolic dysfunction.(Sigs Case 6.2b)

constant backup fluid-> dilation chambers-> decrease ability to contract & overstretching-> impaired contraction-> less EF-> systolic dysfunct-> systolic fail

Explain the mechanism of action of amiodarone and the rationale for its use in dysrhythmias. (SIGS 6.2b)

Class III anti-arryth; MOA: blocks VG K+ channels --> inhibit Phase 3 repol--> prolong cardiac action potential & refractoriness--> decr. SA node firing rate

Describe how ventricular preload and contractility are altered in DCM and their effects on cardiac output. (SIGS 6.2b)

myocyte damage-> enlargement of chamber-> incr. preload (filing); enlarged chamber w/ decr. contract. d/t eccentric fibrosis

Discuss the effects of alcohol on the heart. How can alcoholism lead to thiamine deficiency and exacerbate DCM? (SIGS 6.2b)

myocyte damage/necrosis, mitochon. degeneration, fibrosis, chamber dilation; deficiency d/t poor nutrition & poor vitamin absorption

Define the characteristic histopathologic features of acute viral myocarditis.(Sigs Case 6.2a)

lymphohistocytic; infiltration of lymphocytes that bring about T lymphocytes; myocyte is elongated w/ nuclei

Describe the pathogenesis of coxsackievirus type B and how it relates to viral myocarditis. (Sigs Case 6.2a)

GI tract (stable at low gI pH)→infects mucosal epithelial cells→viremia→infects + lyse heart/pleural surfaces

What is the MOA of Colchicine and how does it relate to the management of pericarditis?(Sigs Case 6.2a)

used as a theoretical anti-inflamm. agent; inhibits IL-1 from cascading, interferes w/ NFK-B; binds to microtubular tubulin in neutrophils-> inhibits mitosis

Discuss the use of ACE-inhibitors and beta-blockers to slow or reverse cardiac remodeling. (Sigs Case 6.2a)

ACE-inh.: allows heart to get more blood flow & decrease LV filing & decreases peripheral resistance; BB: decreases demand on heart and lowers BP

Describe integrative approaches to atrial fibrillation. (SIGS 6.1b)

Med. diet, stress reduction, no alcohol or caffeine, diet high in magnesium, fish oil, CoQ10

Explain how atropine alters conduction. (SIGS 6.1b)

M2 muscarinic antagonist--> block muscarinic receptor--> decrease parasympathetic response--> increase HR, decrease phase 4 of nodal cells

Distinguish between cardiac conduction blocks (sinus block; bundle branch block; hemiblock) on an EKG. (SIGS 6.1b)

A: Sinus block; B: LBBB; C: RBBB; D: Hemi/fascicular (Left posterior hemiblock is associated with a frontal plane QRS axis more positive than +120°)

Identify the AV blocks, rhythm, and atrial and ventricular rates on the ECGs.(SIGS 6.1b)

1st: Prolonged PR; 2nd Type I: Prolong PR, drop P; 2nd Type II: Drop QRS w/out PR prolong; 3rd: No association between P and QRS constant R-R interval

Explain the effects of electrolyte imbalance on cardiac conduction and the impact erythromycin would have. (SIGS 6.1a)

alter depol/ pol/ repol; macrolide antibiotic w/ AE prolonged QT intv. d/t blockage of K+ channels--> delays phase 3 repolariz.--> more intracellular K+--> EADs

Describe the role of INR monitoring in anticoagulation therapy and explain the need for bridge therapy with warfarin. (SIGS 6.1a)

monitor coagulability (maintain optimal level- not too low or too high); Bridge therapy for warfarin due to taking several days to achieve therapeutic effects

Describe the mechanism(s) of action of diltiazem and its effect on cardiac conductivity (SIGS 6.1a)

MOA: inhibits inflow Ca2+ ions into cardiac smooth muscle (SM) during depolarization; Decr. intracellular Ca2+ --> incr. SM relaxation/vasodilation--> decr. BP

Explain how multiple wandering re-entrance circuits can result in atrial fibrillation. (SIGS 6.1a)

Wandering re-entrance circuits able to continuously find excitable tissue--> depolarization of atria--> fibrillatory contractions in atrial myocytes