Renal/Pulm FA Review

Albumin

Inulin

Inulin or creatinine

RBF= RPF/(1-hct), measure RPF using PAH

Filtered load= GFR x plasma concentration

Ch20= total urine (V) –water occupied w/ solute (Cosm); Cosm= UosmxV/Posm

0, isotonic

Ux*V… Clearance = excretion rate/Plasma concentration (note: same for drugs)

When urine glc >160-200

Deficiency in neutral AA transporter for Tryptophan in PCT. Get pellagra because Try  Niacin (used B6)

Inhbits Na/P cotransport in PCT, induces Ca/Na exchange in DCT, incr 1,25OH vit D conversion in PCT

Stimulates Aldosterone from adrenal gland, causes secretion of ADH from post pit, vasoConstricts, Constricts Efferent arteriole to preserve renal funxn in low vol state, incr PCT Na/H exchange (permits contrxn alkalosis)

more secreted. TF/P ratio is about 1.3

Decr BP in JG cells (afferent arteriole), decr Na delivery to MD cells (DCT), incr sympathetic tone (B1) to JG cells

Diarrhea, glue sniffing, RTA, hyperchloremia (acetozolamide use, diabetes)

Defect in CD ability to excrete H+, get hypokalemia and Ca containing stones. Assoc w/ autoimmune dx

Defect in PCT bicarb reabsorption. Assoc w/ hypokalemia and hypophosphatemic rickets

Hypoaldosteronism leading to hyperkalemia (cannot secrete it) and inhibition of ammonium secretion in PCT so cannot buffer urine (decr urine pH as well)

Glomerulonephritis, ischemia or malignant HTN

Tubulointersitial inflammation, acute pyelonephritis, transplant rjxn

Loop diuretics, addisons, 21-hydroxilase deficiency

Loss of protein (nephrotic syn, cirrhosis), Right sided heart failure

Decr C3 level because ICs, subepithelial, activate alternative complement cascade

Renal failure due to diffuse proliferative glomerulonephritis (DNAanti-DNA deposits and decr C4)

LM-diffuse capillary and GBM thickening. EM-Spike & dome w/ subepithelial deposits. IF granular

Captopril, gold, infxns: malaria, TB, HBV; solid tumors

Incr # of pores and incr pore size leading to subepithelial deposits, lose Ig’s so incr risk of infxn

Kids and Hodgkins patients, often post viral infxn or immune stimulus. Albumin lost in the urine, not Igs, due to GBM polyanion loss

NEG of GBM  incr permeability (microabluminuria), thickening. NEG of efferent arterioles incr GFR and leads to mesangial expansion

Caused by immune-complex (IC) deposits subendothelially and mesangial ingrowth leading to GBM regrowth ontop (tram-track). Assoc w/ HBV and HCV

Dense deposits and low C3 factor

Vit C tablets (citrate chelates Ca) or ethylene glycol (oxalate) abuse. Ethlene glycol can cause anion-gap MAcidosis

Gout, Leukemia, myeloproliferative dx such as MM

Due to decr cysteine reabsorption in PCT (also decr Ornithine, Lysine, Arg) forming cystine (2 cys molecules held together by disulfide) kidney stones if urine is acidic. Tx by alkalinizing urine (actazolamide)

EPO, ACTH, PTHrP, Prolactin

Tumor suppressor

Phenacetin Smoking (just like RCC) Aniline dyes (textiles) Cyclophosphamide

Drugs bind protein and illicit immune response (hypersensitivity), act as haptens. Diuretics, sulfonamides, NSAIDs, penicillin derives, rifampin

Acute infaction of cortices of both kidneys due to vasospasm and DIC. Assoc w/ obstetric catastrophies (abrupto placenta) and septic schock

Renal ischemia from shock or sepsis; myoglobinuria due to crush injury, fibrates, statins; toxins such as aminoglycosides or CT contrast

Uosm <350, Una >20, FeNa >2%, BUN/Cr <15

Eosinophilic casts, Ushaped cortical scars, blunted calyx

Na retension, hyperK, uremia, metabo acidosis, anemia from decr EPO prodxn, renal osteodystrophy (decr vit D)

Decr PCT absorption of glc, AA, P (Rickets), uric acid (stones), bicarb (RTA II), and electrolytes (Mg, Ca). Caused by Wilsons, glycogen storage dxs, cisplatin, expired tetracycline

Polycystic liver dx, berry aneurysms, MV prolapse

Cortex and medulla

Medullary cystic kidney dx

Secondary metabo alkalosis, hypoK, hypovolemia, incr aldosterone

Secondary non-anion gap acidosis

Decr DTRs, cardiopulm arrest, delirium

Shock, drug OD, decr ICP. SEs: pulm edema, dehydration; contraindicated in anuria and CHF

Glaucoma, urinary alkalinization, altitude sickness (causes blood to become acidic  incr ventilation and O2). SEs: hyperchloremic metabo acidosis, neuropathy, NH3 toxicity, sulfa allergy

Use: Edematous states- CHF, cirrhosis, nephrotic syn, pulm edema; HTN, hyperCa. SEs: otoxicity, hypoK, Dehyration, sulfa Allergy, interstitial nephritis, Gout

Phenoxyacetic acid derivative that blocks Na-K-Cl transporter in loop of henle. Used for patients w/ sulfa allergy or gout. SEs: ototoxicity, hypoK, dehyrdration, interstitial nephritis (all same as Furosemide except sulfa and gout)

HTN, CHF, hypercalciuria, nephrogenic DI. SEs: Hypokalemic metabo acidosis and hypoNa; hyperglycemia, hyperlipidemia, hyperuricemia, hyperCa. Sulfa allergy

Block ENaC (Na channels) in cortical collecting tubule and spare the K loss

Acetazolamide and K sparring (induces hyperkalemic state)

ACE n GRI: Angioedema (decr bradykinin block), Cough, Eating difficulties- taste change, Gestation- renal dmge, Rash, Incr rennin, hyperK

Respiratory: resp bronchioles, alveolar ducts/sacs. Conducting zone is everything else

Trachea and bronchi

Respiratory bronchioles

Terminal bronchioles

Nonciliated, columnar cells w/ granules. Secrete component of phosphatidylcholine, degrade toxins, act as reserve cells

Internal brac of superior laryngeal nerve

Recurrent laryngeal nerve

2 arteries, one to exchange gas (pulmonary) and one to feed parynchema (bronchial)

Right artery is Anterior to bronchus and Left artery is Superior to bronchus

Exercise: Rectus abs, obliques, transverses abdominus, internal intercostals. During quiet breathing, no muscles, it’s passive

Scalenes, SCM, External intercostals

RV:1.2L FRC:2.2L

0.5 L

IRV + TV + ERV

Apex of lung (air but not as much blood)

Vd = Vt (1- (PeCO2/PaCO2))

Airway=0 (none coming in, none going out) but intrapleural pressure is -5.

Increased levels of: Cl, H+, CO2, 2,3BPG, Temperature

Oxidized Fe (Fe3+) that doesn’t bind O2 as well but has HIGHER affinity for CN. Tx by giving methylene blue

Give nitrites to induce metHb, which will bind CN. Then give Thiosulfate to bind CN and be excreted renally. Can give Methylene blue to take Fe3+  Fe2+

Positive coorperativity (4 bindings sites for O2 and incr affinity w/ more binding). Mg has a plateau curve (1 binding site)

Shifted left (higher affinity)

Vgas = A/Thickness x difference in partial pressures

Pulm artery pressure >25 or >35 during exercise. Get atherosclerosis (turbulence), medial hypertrophy, intimal fibrosis of pulm arteries

INACTIVATING mutation in BMPR2 gene which usually inhibits vascular smooth muscle proliferation

COPD, mitral stenosis (pressure), LR heart shunt (incr vol and pressure), systermic scerlosis (medial hypertrophy), recurrent thromboemboli (decr cross-area), sleep apnea or high altitude (hypoxic vasoconstrxn)

(Ppulm artery – Ppulm v.)/ CO… equivalent to R = P/Q since Q is flow or CO

O2 content = (O2 binding capacity x % saturation) + dissolved O2. O2 content falls as Hb falls (note: but O2 sat and PaO2 do NOT)

>5g/dL of Deoxygenated Hb

20.1mLO2/dL

Chronic lung dx because physiological shunt decr O2 extraction ratio

PAO2 = PIO2 – (PACO2/R), usually can be estimated w/ PAO2= 150 –PACO2/0.8

V/Q mismatch, Diffusion limitation, RL shunt

High altitude, hypoventilation

Decr CO, hypoxema, Anemia, CN, CO

V/Q = 3, lots of ventilation but not as much perfusion because high alveolar pressure compresses capillaries. In other lobes of lung the Pa is > then P aveoli

Airway obstrxn. 100% O2 will not improve PO2

Blood flow obstrxn (physiological dead space-PE). 100% O2 improves O2

Oxygenation of Hb dissociates H+ which shifts carbonic anhydrase equation to form CO2 and CO2 is released from RBC (haldane)

H+ produced from tissues shifts oxygen dissoc curve to right, causing O2 unloading. Secondary mechanism: CO2 produced by tissues binds to Hb amino terminus favoring T form  O2 unloading

Incr ventilation causes metabo alkalosis  induces PFK to make more 1,3BPG which is converted to 2,3BPG right shift

Incr ventilation, incr EPO, incr 2,3BPG, incr mitochondria, incr renal excretion of bicarb acidosis and right shift, chronic pulm vasoconstrxn

No change in PaCO2 nor PaO2 but venous CO2 does elevate

Airways close prematurely at high lung volumes

Pulmonary embolus, CoPD

Gland depth/total thickness of bronchial wall. >50% means COPD/chronic bronchitis

Productive cough for >3 consecutive months in > or = 2years

Small airways, esp terminal bronchioles. Wheezing, early onset cyanosis (shunting) and late onset dyspnea (blue bloater)

Terminal bronchiole collapses. Pancacinar emphysema occurs when entire repiratory unit is distended while in centriacinar emphysema only the respiratory bronchiole is distended

Bronchial hyperresponsiveness, smooth mscle hypertrophy and Curshmann Spirals (shed epithelium from mucous plugs, due to MBP)

Chronic necrotizing infxn of bronchi leading to permanently dilated airways, purulent sputum, infxns, hemopytysis. Assoc w/ bronchial obstrxn, CF, Kartageners. Can develop aspergillosis

ARDS, nARDS, Pneumoconiosis, Sarcoidosis, Idiopathic pulm fibrosis, Goodpastures syn, Wegener’s granulomatosis, Eosinophilic granuoloma, Drugs: Bleo, Amio, Busulfan

Affects upper lobes, can cause Caplan syndrome w/ Rheumatoid nodules in lung; can cause cor pulmonale

Macros respond to silica & release fibrogenic factors leading to fibrosis. Affects upper lobes and get egg shell calcifications of hilar lymphs. Silica may also disrupt phagolysosomes and impair macros funxning w/ TB

Diffuse alveolar damage from PMNs and coagulation cascade causing incr alveolar capillary permeability  leakage of protein rich fluid making hyaline membranes. PMNs can damage type II pneumos also

Absent or decr breath sounds, decr resonance, decr fremitus, and tracheal deviation toward side of lesion (being pushed by normal lung)

Decr breath sounds over effusion, dullness, decr fremitus, no trach deviation

Maybe bronchial breath sounds, dullness, INCR fremitus, no trach deviation

Decr breath sounds, hyperresonant, absent fremitus, tracheal deviation away from lesion (affected lung cavity filling w/ air)

SVC syndrome, Pancoast, Horners, Endocrine neoplasias, Recurrent laryngeal probs, Effusions

Central arising from bronchus, cavitates, linked to smoking, PTHrP release. On histo has Kertin pearls and intercellular bridges

Peripheral tumor developing in sites of prior inflammation. Clara cells become type II pneumos and CXR has multiple densities

Mucin producing cells. Not linked to smoking and grows along airways. Can result in osteoarthropathy (clubbing, periositis). Clara cells become type II pneumos and there are multiple densities on chest.

Peripheral tumor that is anaplastic and undifferentiated. Removed surgically and is less responsive to chemo (unlike small cell). Histo shows pleomorphic giant cells w/ leukocyte frags in cytoplasm

Adrenals, brain(seizure), bone (fracture), liver

S Pneumonia, Klebsiella (alcoholics)

S aureus, Hflu, Klebsiella, S pyogenes

RSV, adenovirus, Mycoplasma, Legionella, Chlamydia

CHF, nephrotic syn, hepatic cirrhosis (decr protein)

Malignancy, pneumonia, collagen vascular dx, trauma

Diphenhydramine, dimenhydrinate, chlorpheniramine, hydroxazine promethazine. Can also be used for motion sickness. SEs: sedation, antimuscarinic, anti-alpha (post dizziness)

Loratadine, fexofenadine, desloratadine, cetirizine. Less sedating then 1st gen because decr entry into CNS

Isoproterenol is nonspecific beta blocker used for asthma. SE-tachycardia

Tremor and arrhythmia

Blocks phosphodiesterases thus incr cAMP levels causing bronchodilation. SEs: cardiotoxicity and neurotoxicity (the O is CardiO and NeurOtoxic) and blocks action of adenosine. Metabolized by p450

Beta blockers or benzos

Inactivate NF-kB thus decr cytokines