HCP6
Describe the EKG findings of axis deviation and right ventricular hypertrophy vs left ventricular hypertrophy
Axis deviation: quick rule is Right hand Lead I left hand Lead AVF. If positive thumbs up if negative thumbs down. If both are up then it is normal, if they are going towards each other it is right axis deviation, if going away from each other then left, if both down then extreme axis deviation.
RVH: Will see large R waves over right side of heart (II, III, AvF, V1, V2), Deep S waves in V5 and V6, and usually right axis deviation.
LVH: Will see large R waves over left side of heart (I, AvL, V5, V6) and deep S waves in V1 and V2.
What are the findings in primary TB vs secondary TB?
Primary: Typically asymptomatic, may have fever, cough, chest pain, will affect middle or lower lobes on CXR
Secondary: Fever, night sweats, hemoptysis, weight loss, will affect upper lobes on CXR due to TB being obligate aerobe
Describe the EKG findings in Afib, Aflutter, and WPW
Afib: No p waves, irregularly irregular QRS
Aflutter: Sawtooth appearance
WPW: Short PR interval and delta wave (slowed upstroke of QRS)
How do FEV1/FVC, FEV1, DLCO, and AA gradient change with emphysema, chronic bronchitis, and restrictive lung diseases?
Emphysema: FEV1/FVC decreased, FEV1 greatly decreased, DLCO decreased, AA gradient increased
Chronic Bronchitis: FEV1/FVC decreased, FEV1 greatly decreased, DLCO normal, AA gradient typically increased
Restrictive lung disease: FEV1/FVC normal or increased, FEV1 decreased, DLCO typically lowered, AA gradient typically increased
Explain the pathophys of S3 and S4 heart sounds
S3: Rapid filling with large amounts of fluid, typically dilated cardiomyopathy or volume overload
S4: Atrial kick against noncompliant ventricle, typically due to ventricular hypertrophy or high pressures (HTN)
Describe some of the general gram stain and shape, buzzwords for Klebsiella, haemophilus, strep pneumo, legionella, and mycoplasma
Strep pneumo: Gram positive lancet shaped diplococci, Productive cough, lobar pneumonia, rust colored sputum
Klebsiella: Gram negative bacilli (rod), ABCDE, Aspiration pneumonia, abcess, currant jelly sputum, diabetes, and ethanol
Haemophilus: Gram negative coccobacilli, AEMOP, Arthritis, epiglotitis, meningitis, otitis media, pneumonia, will see thumbprint sign with epiglottitis
Legionella: Gram neg? coccobacilli (rod) typically use silver stain, Water sources, legionnares is respiratory invovement, diarrhea, hyponatremia, pontiac fever is just fever and malaise, urine antigen test
Mycoplasma: Atypical staining due to no cell wall, Young patient, interstitial walking pneumonia, rash (erythema multiforme), usually in dorms or barracks, IgM cold agglutination
What are methods to test for TB, how do they work, and any extra things that may affect these test results?
PPD: Due to Type 4 HSR, measure induration >15mm is positive in healthy, in immunocompromised it can be less
IFn-G Assay: Measures IFn-G released by T cells following blood sample + TB antigens, more specific for TB, can be used if pt has done BCG vaccine
Blood Culture: Will see acid fast bacilli (rod) from ziehl-nielsen (Carbol fuschin) stain, grow on lowenstein-jensen agar
CXR: Primary will have a ghon complex (ghon focus: caseating granuloma + Hilar lymphadenopathy) secondary will have caseous lesion in upper lobe or also calcifications
Describe how rheumatic fever and chronic rheumatic heart disease occurs, and what findings are found acutely vs chronic (valves)
Occurs due to a type II HSR from GAS M-protein molecular mimicry to myosin. Type II HSR occurs when antibodies bind to the surface of cells and causes destruction of them.
Acutely, it will typically cause mitral regurgitation
Chronically, it will typically cause mitral stenosis
We can tell if it is RHD by potential involvement of the aorta
What paraneoplastic syndromes occur with SCLC and how are they characterized? and how did we treat the one in our case?
SIADH:
- Euvolemic, hyponatremic state, urine osmolarity > serum osmolarity
- Treatment with Tolvaptan V2 receptor antagonist inhibits vasopressin or demeclocycline ADH antagonist
Cushings (ACTH):
- Improper ACTH, cushing syndrome -> central obesity, striae, thin limbs, hyperglycemic state
Lambert-Eaton:
- Destruction of presynaptic Ca channels -> weakness in limbs that improves with repetitive stimulation
Explain the 4 drugs in GDMT management of heart failure, their MOAs, and major side effects
These drugs improve mortality while drugs like loop diuretics and digoxin have not been shown to improve mortality but have been shown to improve symptoms.
ARNI/ACE/ARB: Valsartan/sacubitril, -pril, -sartan
- MOA: ACE/ARB prevents ATII from exerting effects on kidneys and inhibits RAAS System, Neprilysin inhibitor increases levels of ANP/BNP which increases naturiesis, diuresis, and vasodilation, NEED TO USE ARB AND NEPRILYSIN INHIBITOR TOGETHER
- Side effects: cough, angioedema, potential kidney problems (Renal artery stenosis), hypotension, hyperkalemia
Certain B-blockers (Metoprolol, carvedilol, bisoprolol):
- MOA: selectively antagonizes B1 (Metoprolol + bisoprolol) or antagonizes B1 + B2 + alpha-1 receptors. Cardioselective drugs decrease cyclic AMP which decreases intracellular calcium causing decreased heart rate and contractility. Carvediolol does this but also adds in alpha-1 antagonism which increases vasodilation.
- Side effects:
B1 selective: Bradycardia, masked hypoglycemia, hypotension
Nonselective: same + orthostatic hypotension
MRA: Spironolactone + eplerenone (K+ sparing diuretics)
- MOA: Binds to mineralocorticoid receptor and antagonizes it in the collecting duct decreasing Na reuptake and K excretion -> diuresis
- Side effects: Hyperkalemia, hyponatremia, metabolic acidosis, GI, gyno + sexual dysfunction (use eplerenone for less of these side effects)
SGLT2 Inhibitor: Empagliflozin
- MOA: Reversible inhibition of SGLT-2 in the proximal tubule -> decreased glucose reabsorption -> increased diuresis and glucose excretion
- Side effects: Dehydration, UTI
- Side Effects:
Why does chronic bronchitis or emphysema get worse with O2 therapy?
Increased O2 causes a rise in PaCO2 due to reversal of hypoxic pulmonary vasoconstriction which causes a V/Q dead space mismatch leading to hypercapnia.
Decreased ventilatory drive due to switching from Co2 sensitivity in central receptors to O2 peripheral receptors which causes a decrease in breathing due to increased O2.
What is the treatment regimen for active TB (names of drugs, how long to take each), what are the MOAs of the drugs, and what are the side effects
RIPE protocol: 4 drugs for 2 months -> rifampin + isoniazid for 4 months
Rifampin:
- MOA: Inhibits DNA-dependent RNA polymerase
- Side effects: Ramps up cytochrome p450, Red-orange bodily fluids, rapid resistance if used alone
Isoniazid:
- MOA: Activated by catalase-peroxidase (KatG) and inhibits mycolic acid synthesis in the cell wall
- Side Effects: Hepatotoxicity, peripheral neuropathy (Can use pyridoxine vitB6 to prevent), CNS toxicity, high anion gap metabolic acidosis
Pyrazinamide:
- MOA: Not well known but is activated by acidic environments (inside phagolysosomes or macrophages) to pyrazinic acid which does stuff
- Side effects: Hepatotoxicity, Hyperuricemia (GOUT), athralgia, photosensitivity
Ethambutol:
- MOA: Inhibits arabinosyltransferase which thus stops carbohydrate polymerization of the mycobacterial cell wall
- Side Effects: Red-green color blindness (eyethambutol)
Describe the MOA and major side effects of Digoxin, Warfarin, dabigatran, and rivaroxaban/apixaban
Digoxin:
- MOA:
- Inhibits Na/K ATPase -> Increase intracellular Na -> reduced efficacy of Na/Ca exchanger -> increases intracellular Ca -> increases contractility, reduces heart rate
- Stimulates vagus nerve which can reduce heart rate
- Side effects: Hyperkalemia, xanthopsia, heart block, nausea, vomiting, T-wave inversion w scooped appearance (digoxin immune fab for reversal)
Warfarin:
- MOA: Inhibits hepatic vitamin K epoxide reductase -> decreases active form of vitamin K -> decreases g-carboxylation of glutamic acid residues -> decreased activation of pro-clotting factors II, VII, IX, and X as well as protein C and S, monitor with PT/INR
- Side Effects: Many interactions, increased bleeding risk, Warfarin induced skin necrosis due to decrease of protein C and S before decrease of pro-clotting factors (reversal with fresh frozen plasma, vitamin K, or correction factors), can also heparin bridge before starting therapy
Dabigatran:
- MOA: Direct thrombin (II) inhibitor
- Side Effects: Increased risk of bleeding, reverse with idarucizumab, prolonged thrombin time
Rivaroxaban/Apixaban:
- MOA: Direct factor Xa inhibitors
- Side Effects: Increased bleeding risk, reverse with adexanet alfa, prolonged PT and PTT
Describe how SCLC looks and presents and the treatment options we used + side effects
SCLC: Undifferentiated neuroendocrine (kulshitschy?) cells, hyperchromatic nuclei, centrally located, aggressive, myc-oncogene mutations, tumor markers chromogranin A, neuron specific enolase, synaptophysin, and CD56, common in smokers
Treatment:
- Durvalumab:
- MOA: Binds to PD-L1 and blocks the anti-tumor effect leading to T-cell destruction of the cancer cells
- Side effects: Cough, fatigue, diarrhea, immunostimulatory
- Cisplatin
- MOA: Crosslinks DNA throughout the cell cycle which causes decreased DNA replication and apoptosis of cells
- Side effects: NOPE (Nephrotoxicity, ototoxicity, peripheral neuropathy, emesis) and myelosuppression
- Etoposide
- MOA: Binds to topoisomerase II preventing the religation of DNA which leads to decreased DNA replication and apoptosis in S and G2 phases
- Side effects: Myelosuppression, alopecia
Describe signs and symptoms of heart failure and how right and left sided heart failure differs in presentation
Nocturia, increasing fatigue, S3/S4
Left sided: Dyspnea, orthopnea, pulmonary edema, paroxysmal nocturnal dyspnea, cardiac asthma, major cause of right sided heart failure
Right sided: Peripheral edema, hepatic congestion, JVD, hepatosplenomegaly, hepatojugular reflux
What are the clinical signs and symptoms of chronic bronchitis vs emphysema?
Common to both: Cough, dyspnea, wheezing, crackles sometimes moreso in bronchitis, barrel chest,
Chronic bronchitis: Blue bloater, productive cough for >3 months for 2 years
Emphysema: Pink puffer, dry cough, decreased BMI due to increased work of breathing,
Describe what imipenem/cilastatin does and side effects
Imipenem is a carbapenem which is a beta lactam antibiotic (binds PBP transpeptidases) but it is special in that it has resistance to beta-lactamases.
Cilastatin is needed because it inhibits dehydropeptidase I in the kidneys that breaks down imipenem
Side effects: Seizures, GI upset, rash
Describe the Fick equation, PCWP, Cardiac output, cardiac index, Mixed venous O2, and CHADS-VASC
Fick Equation: Cardiac output = oxygen consumption (VO2)/(Arterial O2-venous O2)
PCWP: Left atrial pressure
Cardiac Output: Volume of blood heart pumps per minute, CO = HR x SV
Cardiac Index: Cardiac output in relation to body surface area
Mixed Venous O2: Measures the oxygen level in the blood returning to the heart from the whole body, indicates how much oxygen the body is using. Low = tissues extract more O2 due to low CO, high = tissues are extracting less oxygen
CHADS-VASC:
- CHF, Hypertension, Age, Diabetes, Stroke or TIA, Vascular disease
Describe the staging of SCLC
Staging can be done with TNM or with limited and extensive stage
TNM:
- Tumor size: Bigger = worse
- Lymph node involvement: If big tumor + lymph node involvement worse, if small tumor and lymph node involvement not as bad
- Metastasis: Automatic stage 4
Staging:
- Limited Stage: Confined to ipsilateral hemithorax
- Extensive Stage: Beyond ipsilateral hemithorax
Explain the pathophysiology of HFrEF vs HFpEF and also how this changes systolic vs distolic function
HFrEF: Reduced stroke volume and reduced EF (<40%) Typically caused by volume overload (Dilated cardiomyopathy) or damage and loss of myocytes. Will cause a systolic function decreasing cardiac output.
HFpEF: Reduced stroke volume and normal or reduced EDV, preserved EF (>50%). Typically caused by hypertension or hypertrophy/stiffness. Will cause diastolic dysfunction decreasing cardiac output while EF stays normal.
Describe MOA + Side effects of cephalosporins, fluoroquinolones, macrolides, and clindamycin.
Cephalosporins: Cef
- MOA: beta lactam antibiotics, Bind to Penicilin binding protein transpeptidases, less susceptible to penicilinases
- Side Effects: Penicilin allergy anaphylaxis, neurotoxicity, not too much bad stuff
Fluoroquinolones: -floxacin
- MOA: Inhibits Topoisomerase II and IV, causes double stranded breaks, inhibits DNA replication and transcription
- Side effects: GI upset, neurological symptoms, QT prolongation, photosensitivity, rash, cartilage degradation
Macrolides: mycin (NOT CLINDAMYCIN THOUGH)
- MOA: Binds to the 23s R RNA subunit of the 50S ribosomal subunit which inhibits translocation and production of proteins
- Side effects: MACRO: GI motility, arrhythmia, C not important now, Rash, eosinophilia
Clindamycin: Clindamycin is a lincosamide not a macrolide
- MOA: Binds to 50S subunit inhibiting translocation -> decreased protein synthesis
- Side effects: GI upset, C diff, teratogen
Describe the formation of a granuloma in TB and what can happen if TB is not treated
1: Mycobacteria are recognized as PAMPs and are phagocytosed by macrophages
2: Sulfatides from mycobacteria inhibit phagolysosome formation thus allowing the bacteria to live inside the macrophages
3: Cord factor is released which induces TNF-alpha release from macrophages to form granulomas
4: Th1 cells are activated and release IFN-g to activate macrophages to secrete TNF-a thus causing formation of the granuloma
5: TB can go into the blood and go to other places in the body
Describe the pathogenesis and pathophysiology of Afib in this patient and what this can lead to. Also how to control it.
Mitral stenosis -> increased LA Volume and pressure -> Cardiac remodeling -> increased risk of areas which trigger bursts of electircal activity or pre-excitation.
Afib causes rapid innefective contraction of the atria -> stasis of blood -> thromboembolism and stroke
Manage with rate control FIRST (B-blocker/Non-dihydropyridine CCB first line, digoxin and amiodarone second line) or rhythm control Cardioversion
Describe GOLD classifications and GOLD management of COPD
GOLD Classification: Classify by looking at postbronchodilator FEV1% of the predicted
- Mild: >80%
- Moderate: 50-79%
- Severe: 30-49%
- Very severe: <30%
Treatment:
- Group A: Not too bad, LABA or LAMA
- Group B: More exacerbations but still not too bad, LABA + LAMA
- Group E: LABA + LAMA + ICS
Tell me something about heart failure that has not been mentioned already
You are so smart and will do great on the exam.