Cardio/Renal Flashcards
Drug added to regimen for stable angina (with atenolol and aspirin) causes hypotension and bradycardia. What drug was it?
Non-hydropyridine CCB (verabamil, diltiazam) –> additive negative chronotropic effects (slows HR) when combined w/ b blocker
5 groups of drugs w/ negative chronotropic effects (slow HR)
b blockers non-hydropyridine CCB cardiac glycoside (digoxin) amiodarone and sotalol cholinergic agonists
Graph showing dissociation of described class I antiarrhythmics being faster than quinidine. What could that antiarrhythmics be?
Class IB so lidocaine or mexiletine This is because Na+ channel binding strength for class I antiarrhythmics is IC > IA > IB, so IB dissociates fastest IC dissociates slowest, so it demonstrates most "use dependence" (higher rates of depolarization leads to increased Na+ channel blockade)
What’s a coronary steal? What drugs do this? And what do you wanna chieve instead?
In ischemia, collateral circulation maintains perfusion to areas distal to occluded vessel
Drugs that cause CORONARY ARTERIOLAR dilation exacerbate ischemia by causing the already well-perfused vessels (nonischemic) to dilate and steal blood from that collateral circulation
Adenosine and dipyridamole (selective vasodilators) do this
What you wanna achieve instead in this scenario is systemic venous & arterial dilation
Microelectrodes placed in cardiac muscle cells detect rapid decrease in cytoplasmic calcium level immediately preceding relaxation. What mediates this?
Na+/Ca2+ exchange mechanism (sarcolemmal, doesn’t need ATP)
The answer is NOT calmodulin, which stimulates plasma membrane Ca2+-ATPase (indirect contributor of efflux)
NE administered to correct hypotension. What’s the cellular/messenger changes?
Increase in cAMP in CARDIAC MUSCLE CELL (B1 receptors work thru increase in cAMP)
NOT cAMP increase in vascular smooth muscle cell, whose a1 receptors work thru increase in IP3 (and DAG)
NOT cAMP increase in bronchial smooth muscle cell, whose b2 receptors aren’t stimulated by NE
a2 receptor works thru decrease in cAMP (decreases NE release and insulin release)
Where are the 3 leads of biventricular pacemakers?
1) RA (from -> SVC -> RA)
2) RV (same as 1)
3) Left ventricular coronary sinus, which lies in the artrioventricular groove in the posterior aspect of the heart (from left subclavian -> SVC -> RA -> coronary sinus ostium -> left ventricular coronary sinus -> lateral tributaries to regulate LV)
What class of drugs is CI in low level C1 esterase inhibitor?
ACEi (side effect of angioedema from bradykinin accumulation)
Low level of C1 esterase inhibitor -> hereditary angioedema (AD condition)
C1 esterase inhibitor normally inhibits classical complement pathway and kallikrein (normally kallikrein increases bradykinin level by converting it from kininogen)
Pt w/ preexisting atherosclerotic plaque. What increased intraplaque activity will predispose to MI?
Metalloproteinases (destabilizes fibrous cap by degrading collagen)
Get a rise in creatinine after starting ACEi. What structure is involved?
Efferent arteriole
B/c ACEi reduces Ang II, which normally constricts efferent arteriole and thus increases GFR
If less Ang II, GFR decreases
What are the 4 components of crescent formation in RPGN?
1) Fibrin - essential pathologic step, shows up on IF
2) Plasma protein (C3b, NO C4)
3) Parietal cells
4) Monocytes & macrophages
A substance inhibits glucose carrier in proximal tubule. Glucose clearance will now resemble the clearance of what substance?
Inulin, because its filtered amount is now equal to the excretion amount (glucose is not reabsorbed or secreted anywhere else)
Inulin is freely filtered and neither reabsorbed nor secreted = so approximate GFR
What heart sounds are you trying to listen to in LLD position?
S3, S4, MS
What maneuvers make S3 easier to hear?
Make pt fully exhale while lying LLD -> heart closer to chest wall b/c of decreased lung volume
What does use-dependence mean in the context of antiarrhythmics? What’s reverse use-dependence?
Use-dependence: effects exaggerated with increased HR -> Na+ channel blockers, esp class IC (flecainide and propafenone) -> QRS interval more prolonged w/ increased HR Reverse use-depdendence: effects exaggerated with decreased HR -> class III antiarrhythmics (K+ channel blockers - amiodarone, ibutilide, dofetilide, sotalol) -> QT interval more prolonged w/ slower HR
What antiarrhythmic drug prolongs QRS interval during immediate recovery period after stress test?
Flecainide and propafenone (class IC aniarrhythmics) -> strongest use-dependence (the higher the HR, like immediately after exercise test, the more prolonged QRS)
What nitrate agent has the highest bioavailability PO?
Isosorbide mononitrate (metabolite of isosorbide dinitrate) Both nitroglycerin and isosorbide dinitrate undergo extensive 1st pass in liver
Tamponade triad?
Severe hypotension
Muffled heart sounds
Elevated JVP
32-yo healthy male passed a stone in his urine. What abnormalities are you likely to find in his blood and urine?
Normocalcemia and hypercalciuria -> bc calcium stone is the most common kidney stone and it’s idiopathic hypercalciuria half the time
3 ways to get normocalcemia and hyperoxaluria?
Diets high in oxalate such as chocolate, nuts, spinach
Diets low in calcium (so more free oxalate around)
Crohns and other intestinal malabsorptions
How do you get normouricemia w/ hyperuricosuria? How about hyperuricemia w/ hyperuricosuria?
High protein diet
If high both in blood and urine, it’s something more systemic (tumor lysis, myeloproliferative disorders, gout, lesch-nyhan, etc)
What are the characteristics of PSGN deposits under EM?
subEPITHELIAL deposits of immune complex -> lumpy bumpy IgG, IgM, C3 along GBM and mesangium
How do you prevent paradoxical increase in MVO2 demand when using nitrates?
Prescribe B-blocker w/ it (prevents reflex tachycardia) -> prevents catecholamine from stimulating B1 receptors on myocardium -> slows conduction thru AV node & cardiac conduction system in general
How does chronic kidney disease result in increased bone resorption?
By decreasing phosphate excretion -> more phosphates complex w/ calcium -> body thinks you’re low on serum calcium and starts producing more PTH -> “renal osteodystrophy” -> bone pain/osteopenia/sign of soft tissue calcification on X-ray
Also by decreasing calcitriol (less a1 conversion of vit D)
What’s Kussmaul’s sign? What 5 conditions do you see this?
Paradoxical increase in jugular venous distension/pressure during inspiration (normally would decrease it)
Seen in chronic pericarditis, restrictive CM, right sided HF, tricuspid stenosis, cardiac tamponade
What’s pulsus paradoxus? What 5 conditions do you see this?
Drop of systolic BP of more than 10 mmHg during inspiration -> this is because inspiration increases venous blood return resulting in increased right heart volume, which normally doesn’t affect the left heart much because your RV can expand into pericardium; in certain diseases (below) where pericardium can’t expand, increasing RV volume results in interventricular septum being pushed towards the left and reducing left heart diastolic volume & SV -> so get exaggerated decrease in BP during inspiration
Seen in cor pulmonale, constrictive (chronic) pericardial disease, cardiac tamponade, severe obstructive lung disease (incl acute asthmatic episode!), restrictrive cardiomyopathy
What setting do you see acute cor pulmonale? Chronic?
Asthma - acute
COPD - chronic
What’s pericardial knock? What 1 condition do you see this ?
Brief diastolic sound right after S2 (may be confused w/ the opening snap of MS)
Seen in constrictive (chronic) pericarditis
Give characteristics of multicystic kidney dysplasia
Multiple cysts of varying sizes + absence of normal pelvocaliceal system (atresia)
So can dx this in newborns
Give formula for MAP, CO and SV
MAP = CO x SVR CO = HR x SV SV = EDV (preload) - ESV
Compensatory mechanisms in acute and chronic AR to maintain CO
AR is the state of volume overload
So to fix this, initially, body increases HR (tachycardia; CO = HR x SV)
Sustained response however is increase in preload (thus increase in SV)
Tx of acute severe AR?
Nitroprusside (vasodilator)
Dopamine or dobutamine (IV inotropic agent)
Pt w/ isolated systolic HTN was put on med that resulted in peripheral edema and flushing. What’s the med?
Dihydropyridine CCB (so amlodipine) 1st line drugs for isolated systolic BP are dihydropyridine CCB (so NOT verapamil, etc), and thiazides, but thiazides don't create flushing and edema
What do you prescribe with niacin (nicotinic acid) to prevent facial flushing and warmth?
Aspirin
What molecules play the most significant role in regulating coronary blood flow?
NO (from arginine + O2) - major regulator of flow-mediated vasodilation in large arteries and pre-arteriolar arteries Adenosine (from ATP metab) - major vasoconstrictor in small coronary arterioles Nervous input (NE and ACh) has very little effect on coronary blood flow
Triad found in cardiac tamponade
Beck’s triad: JVD (distended neck vein), hypotension, muffled heart sound
In addition, might find pulsus paradoxus and tachycardia
Came into hospital for muscle pain, fatigue, and dark urine. Current meds are metoprolol, atorvastatin, aspirin. Now having kidney failure. What was prescribed?
Erythromycin (or any other macrolides except azithromycin) b/c macrolides inhibit P450, leading to increased statin level -> increased risk of rhabdomyolysis -> kidney failure
Differentiate between 4 causes of hematuria post-infection
1) HUS: follows diarrheal infection (E. coli) -> additional sx of conjunctival pallor from microangiopathic hemolytic anemia
2) PSGN: follows pharyngeal/skin infection (strep) -> additional sx of edema, HTN, proteinuria, low C3, but no anemia
3) HSP (IgA deposition vasculitis, see increased IgA): follows URI -> additional sx of palpable purpura , athralgia
4) Berger disease (IgA nephropathy): HSP without extra-renal sx, distinguish from PSGN by IgA MESANGIAL deposits, normal C3 level, and the fact that it takes 2-3 days to develop rather than 2 weeks like PSGN
What’s a Korotkoff sound? In what context might you see this used?
Blood flow sound when taking blood pressure
Used in the context of pulsus paradoxus
Take down BP when you first hear this sound during expiration as the cuff pressure is gradually reduced from above systolic BP
Then take down BP when you hear this sound during all phases of respiration
If the difference between the 2 values is > 10 mmHg -> “pulsus paradoxus”
Unequal pulse strength in extremities. What do you have to suspect?
Acute aortic dissection (impaired blood flow past dissection) -> widened mediastinum and abnormal cardiac contour in the setting of HTN or Marfan
What 2 pressure values should be equal during normal diastole?
LA end diastolic pressure and LV end diastolic pressure (if unobstructed mitral valve)
What 2 pressure elevations would you get in dilated & restrictive cardiomyopathy & cardiac tamponade?
PCWP (LA end diastolic pressure), LVEDP (LV end diastolic pressure)
Both values will be approximately equal
How do you decrease RPF and increase FF?
Constricts EFFERENT arteriole
FF = GFR/RPF
What molec estimates RPF? How do you calculate RBF if you know RPF?
PAH clearance (both filtered and actively secreted) RBF = (PAH clearance) / (1 - hematocrit)
What molec estimates GFR?
Inulin clearance (freely filtered and neither reabsorbed nor secreted)
What parameter is equal between the systemic and pulmonary circulations? What parameters are different?
Equal: blood flow per minute -> both at rest and exercise -> b/c we always have LV output equaling RV at all times!
Parameters that are higher in systemic than pulmonary: MAP, diastolic arterial pressure, systolic arterial pressure (aka “driving pressure for blood flow”)
3 antiarrhythmics that can cause AV block?
Drugs that prolong PR interval! B-blockers CCBs (verapamil, diltiazam) Digoxin So if picking between these two given the side effect, pick CCBs in pts w/ COPD or asthma (b/c we know those pts can't use nonselective B-blockers due to potential exacerbation)
Lymph drainage for bladder?
Upper half -> internal iliac nodes
Lower half -> external iliac nodes
Most common cause of death due to MI during pre-hospital phase? In-hospital phase?
Pre-hospital: SCD (sudden cardiac death = w/in 1 hr) from ventricular arrhythmias
In-hospital: ventricular failure (cardiogenic shock)
What would MI look like on CO (y) vs. right atrial pressure (x) graph and venous return (y) vs. end diastolic volume (x) graph?
It would cause isolated decrease in CO w/out any changes in venous return
What would anaphylaxis look like on CO (y) vs. right atrial pressure (x) graph and venous return (y) vs. end diastolic volume (x) graph?
Significant drop in venous return graph b/c of widespread venous and arteriolar vasodilatation + increased capillary permeability
How do you explain the fact that PAH extraction ratio decreases progressively as the PAH plasma conc goes up beyond a certain threshold value?
PAH gets into urine thru 2 processes:
Filtration: as a general rule, NOT a process that can be saturated b/c it’s not enzyme/protein mediated, so if this were the only process involved, extraction will linearly go up as plasma conc goes up
Secretion (in PCT): CAN be saturated b/c there’s a transport maximum of secretion enzyme -> above this secretion plateaus
So at conc above this transport maximum, any increase in urine PAH conc (which will go up more slowly than before) is due to increased filtration alone
Can excretion be saturated?
No, excretion is Filtration + Secretion - Reabsorption -> filtration can’t be saturated (not enzyme/protein mediated) so excretion can’t be saturated either
Both secretion and reabsorption can be saturated tho
Started on new med for HTN that causes increase in creatinine and potassium. What’s the med?
ACEi (“-pril”)
Increase in creatinine comes from decrease in GFR (because now there’s less Ang II around to constrict efferent arteriole and cause increase in GFR)
What does chronic renal failure do to the level of phosphate?
Hyperphosphatemia
DON’T think of it as losing vit D means losing phosphate reabsorption ability, instead think of it as renal failure impairs excretion of phosphorus (so totally separate from what happens to vit D level)
Where’s the receptor for aldosterone? What are the channels it upregulates?
Cytosol (aldos freely crosses cell membrane to bind the receptor)
Increases # of Na+/K+-ATPase and Na+ channels in principal cells (collecting duct)
Promotes H+ secretion from intercalated cells (collecting duct)
What’s the mechanism behind podocyte damage in MCD?
Primary defect in immunologic fx -> overproduction of cytokine (possibly IL-13) -> direct damage to podocyte
What’s the mechanism behind podocyte damage in MCD?
Primary defect in immunologic fx -> overproduction of cytokine (possibly IL-13) -> direct damage to podocyte
Hearing loss + ocular abnormalities + hematuria?
Alport syndrome: defect in formation of type 4 collagen -> thinning of GBM
Differences of urinary protein loss in MCD and other nephrotic syndromes (membranous nephropathy, FSGS)
MCD: selective loss of albumin (small molecs)
Others: nonselective
Sign that you have upper UTI rather than lower UTI?
WBC casts (only formed in tubules, where they're precipitated by Tamm-Horsfall protein secreted by tubular epithelial cells) -> pathognomonic for acute pyelonephritis (unless it's presented w/ low-grade fever and NO painful urination -> then consider acute interstitial nephritis) Suprapubic pressure more specific to cystitis than urethritis
Principle behind normal anion gap metabolic acidosis?
Loss of bicarb (prolonged diarrhea, etc)
Primary cause of isolated systolic HTN?
Age-related decrease in compliance of aorta and its major branches
Things you can derive from shape changes in pressure-volume loop?
Contractility: slope of line drawn from 0,0 to left upper corner of new graph (steeper -> higher contractility)
Afterload change: peak bump of new graph minus peak bump of old graph
Preload change: how far to the right the new graph is
SV change: width of the graph
LV compliance: unchanged if the bottom lines of the graphs line up
What does nitroprusside do to afterload, preload, contractility, and SV?
Decrease both afterload and preload (it’s a vasodilator of both veins and arteries)
Doesn’t change contractility or SV
What metabolic abnormality does overuse of diuretics produce? What’s the mechanism behind that?
Metabolic alkalosis (contraction alkalosis) This is b/c vol contraction is sensed by macula densa -> renin and aldosterone out -> low K+ and low H+ now
When do you see HTN and hypokalemic pts w/ low renin and low aldos (4)? Low renin and high aldos (2)? High renin and high aldos?
Low renin & aldos: non-aldosterone causes -> CAH, adrenal tumor producing deoxycorticosterone, Cushing syndrome, exogenous mineralocorticoids
Low renin & high aldos: primary aldosteronism -> Conn’s syndrome, bilateral adrenal hyperplasia
High renin & aldos: 2ndary aldosteronism -> things that full kidney into secreting renin -> renovascular HTN (renal artery stenosis assc. w/ fibromuscular dysplasia or atherosclerosis), diuretic use, malignant HTN (leading to microvascular damage and ischemia), renin-secreting tumors (juxtaglomerular cell neoplasm)
Mtral regurg (character, maneuvers, presenting sx)
Character: holosystolic, high-pitched blowing, radiates to axilla
Maneuvers that enhance: handgrip (increases SVR), squatting (increases venous return)
Presenting sx: dysphagia (blood pools in LA)
Tricuspid regurg (character, maneuvers)
Character: holosystolic, high-pitched blowing, radiates to right sternal border
Maneuvers that enhance: inspiration
Aortic stenosis (character, maneuvers, presenting sx)
Character: crescendo, decrescendo systolic, radiates to neck, pulsus parvus et tardus (small and slow rise in carotid pulse during systole) -> listen at cardiac “base”
Maneuvers that enhance: rapid squatting (increases venous return)
Presenting sx: syncope, angina, dyspnea on exertion -> can feel systolic vibrations or carotid shudder (thrill)
VSD (character, maneuvers)
Character: holosystolic, harsh-sounding at tricuspid area
Maneuvers that enhance: handgrip (increases SVR)
Mitral valve prolapse (character, maneuvers)
Character: late systolic crescendo after midsystolic click (sudden tensing of chordae tendineae)
Maneuvers that enhance: intensity increases w/ handgrip and rapid squatting, midsystolic click happens earlier w/ valsava and standing
Aortic regurg (character, maneuvers, presenting sx)
Character: high-pitched blowing early diastolic decrescendo, HEAR AT LSB, wide pulse pressure
Maneuvers that enhance: handgrip (increases SVR) -> vasodilators decrease intensity
Presenting sx: head bobbing, bounding pulses (“water-hammer pulses”)
Mitral stenosis (character, maneuvers, presenting sx)
Character: delayed rumbling diastolic murmur after opening snap (from abrupt half in leaflet motion) -> the earlier the OS, the worse the condition
Maneuvers that enhance: expiration
Presenting sx: dysphagia, hoarseness
PDA (murmur character)
Continuous machine-like murmur loudest at S2
Phase 0-4 of ventricular AP and ion channels involved?
Phase 0: rapid depol from incoming Na+
Phase 1: initial repol from outgoing K+
Phase 2: plateau from incoming Ca2+ balancing outgoing K+
Phase 3: rapid repol from outgoing K+
Phase 4: resting potential from leak currents (dominated by K+ permeability)
Phase 0, 3, 4 of pacemaker AP and ion channels involved?
Phase 0: rapid depol from incoming Ca2+
Phase 3: rapid repol from outgoing K+
Phase 4: slow diastolic depol from incoming Na+ (funny current) -> slope of this phase determines HR (ACh and adenosine decrease this whereas catecholamines increase it)
What does P wave on ECG correspond to?
Atrial depol
What does PR interval on ECG correspond to? What’s the normal value?
Conduction delay thru AV node
Normal < 200 msec (< 1 large box) (longer than this is considered 1st degree AV block)
Prolonged by B-blocker and nondihydropiridine CCBs
Shortened in WPW syndrome (from delta wave)
What does QRS complex on ECG correspond to? What’s the normal value?
Ventricular depol (masking atrial repol) -> phase 0 of ventricular myocyte AP
(so prolonged w/ abnormal foci, LBBB/RBBB, fascicular block, pacemakers)
Bundle branch conductivity determines duration of QRS complex!
Normal < 120 msec (< 3 small boxes)
What does QT interval on ECG correspond to? What does it approximate?
Mechanical contraction of ventricles Approximate AP duration -> this is why class IA and III antiarrhythmics predispose you to QT prolongation (they both increase APD)
What does T wave on ECG correspond to?
Ventricular depol
Inversion - recent MI
What does U wave on ECG signify?
Hypokalemia, bradycardia
2 congenital long QT syndrome? What does it involve?
Romano-Ward syndrome: AD, no deafness
Jervell and Lange-Nielsen syndrome: AR, + sensorineural deafness
Both involve mutations in K+ channel proteins
Cushing rxn triad?
HTN, bradycardia, resp depression
From increased ICP constricting arterioles -> reflex sympa increase in perfusion pressure -> HTN -> increased stretch -> reflex baroreceptor induced-bradycardia
What would RPF, GFR, and FF look like in pt who lost a lot of fluid thru diarrhea and vomiting?
Losing fluid would result in decreased RPF and GRF, but GFR decreases to a lesser degree b/c your body can actually compensate thru making Ang II to constrict efferent arteriole -> so you end up having increased FF (b/c FF = GRF/RPF)
Differences in complications and causes of chronic mitral regurg vs. acute mitral regurg?
Chronic MR (from myxomatous degeneration or MVP): increased LA compliance, prone to A-fib and mural thromboembolism Acute MR (from infective endocarditis, chordae tendineae rupture, ischemia, papillary m. rupture, prosthetic valve failure): near-normal LA compliance, prone to marked pulm HTN and pulm edema
What does TdP look like on ECG?
polymorphic QRS complex of varying amplitude and cycle length -> looks like it twists around ECG baseline
What’s the most common predisposition to native valve bacterial endocarditis? And what’s one way bacterial endocarditis can present?
MVP (esp in 15-60 yo)
If older than 60, consider calcification of mitral annulus (esp w/ prior myxomatous degeneration and chronically elevated LV pressure)
Can present as sign of stroke (throwing clots up the brain) + fever
3 embryonic vein systems and what they become in adults
- umbilical vein: degenerates (ligamentum teres hepatis)
- vitelline vein: portal vein system
- cardinal vein: systemic circulation (SVC)
What is ascending aorta derived from? Descending aorta?
Asc. aorta: truncus arteriosus
Desc. aorta: fusion of right and left dorsal aorta
3 things on ECG in WPW syndrome
Delta wave
Shortened PR
Wider QRS complex -> later converted to narrow QRS during tachyarrhythmia b/c accessory pathway no longer pre-excites ventricles but instead forms re-entrant circuit back to atria
4 cardio/resp things that exercise affect?
- Increases CO
- Increases preload: from increasing contraction of venous system -> increased venous return
- Increases contraction of arterioles in all tissues except actively working muscles
- Decreases afterload: adaptive decrease in SVR (so decreases LV end SYStolic volume) -> why exercising results in only minor increase in BP (should have been a more drastic increase if based on 1-3 alone)
- LV end-diastolic pressure remains unchanged (increased CO cancels out decreased SVR)
What’s the cell of origin of clear cell renal carcinoma? Where does it like to met?
“Hypernephroma” = renal cell carcinoma
Proximal renal tubular epithelium -> golden-yellow grossly from lots of glycogen and lipid
Most common site for mets is lung
What is renal oncocytoma and what’s the cell of origin?
Renal oncocytoma: large, well-differentiated, contains numerous mitochondria
Collecting duct cells
Dx of multifocal renal papillary tumors composed of urothelium supported by thin fibrovascular stalk?
Transitional cell carcinoma
3 cardiac abnormalities assc. w/ DiGeorge?
Think of things involving outflow tract. Examples are
Tetralogy of Fallot
Interrupted aortic arch (more extreme version of coarctation of the aorta)
Truncus arteriosus
Common cause of hypersensitivity myocarditis? What do you see under microscope?
Starting a new drug -> see perivascular infiltrate w/ abundant eosinophils
What 2 conditions cause increase in serum osmolarity and decrease in both ICF and ECF (“hyperosmotic vol contraction”)?
DI, profuse sweating
What 2 conditions cause decrease in ECF and no change in ICF and serum osmolarity (“isosmotic volume contraction”)?
Acute GI hemorrhage, diarrhea
What condition causes decrease in ECF and serum osmolarity and increase in ICF (“hyposmotic volume contraction”)?
Adrenal insufficiency
What condition causes increase in ECF and serum osmolarity and decrease in ICF (“hypertonic volume expansion”)?
Infusion of large amount of hypertonic saline
What 2 conditions cause increase in ECF and ICF and decrease in serum osmolarity (“hyposmotic volume expansion”)?
SIADH, primary polydipsia
% of K+ along the length of kidney tubule
Glomerulus: 100% (all K+ filtered)
PCT: 65% reabsorbed, leaving 35% in tubule -> fixed
Thick asc limb of loop of Henle: another 25-30% reabsorbed (thru NKCC2), leaving 5-10% in tubule -> fixed
Collecting tubules: where regulations of K+ occurs -> principal and a-intercalated cells have final say in how much K+ ends up in pee (can actually excrete more K+ than what’s filtered in high dietary intake state)
4 things that increase K+ excretion
High extracellular K+
Increased aldosterone
Alkalosis
Things that cause increased fluid flow -> vol expansion, high Na+ intake, diuretic use (thiazide and loop)
4 things that can result in renal papillary necrosis? What causes the sx?
Sickle cell disease
Analgesic nephropathy (phenacytin, NSAIDs)
DM
Acute pyelonephritis and UTO -> compresses medullary vasculature and predisposing to ischemia
What’s causing the sx is sloughed papillae obstructing ureter
What vasculitis do you see transmural inflammation of arterial wall w/ fibrinoid necrosis? What’s the disease assc.?
PAN (polyarteritis nodosa) -> assc. w/ HBV
Can see this in vessels of any tissues but lungs!
What cell is DIRECTLY responsible for intimal thickening in atherosclerosis?
Medial SMC -> summoned to intima and is directly responsible for reactive intimal hyperplasia and collagen deposition
Cutoff value for micro/macroalbuminemia? When can you detect with dipstick urinalysis?
Microalbuminuria: 30-300 mg/day
Macroalbuminuria: > 300 mg/day -> detected by dipstick urinalysis
4 diseases that can cause myocardial fibrosis?
Dermatomyositis
Muscular dystrophy
Sarcoidosis
Scleroderma
What’s the pathogenesis of vegetations assc. w/ bacterial endocarditis?
Fibrin and platelet deposition
NOT WBC infiltration (even if it’s staph aureus)!
Auscultatory indicator of how bad mitral stenosis is?
A2-OS interval -> the narrower, the more severe
Will also hear diastolic rumbling and presystolic accentuation (from LA contraction) -> but these correlate poorly w/ severity
The ABSENCE of presystolic accentuation might signify that MS becomes severe enough to precipitate A-fib (b/c atrial contraction is what causes pre-systolic accentuation in MS)
What 2 info should you gather in metabolic alkalosis?
Urine chloride and volume status
If low urine chloride -> think vomiting, nasogastric aspiration, PRIOR diuretic use -> these are saline-responsive
If high urine chloride -> assess volume status ->
If hypervolemia, consider excess mineralocorticoid activity (Conn syndrome, Cushing disease, ectopic ACTH) -> NOT saline responsive
If hypovolemia or euvolemia, consider CURRENT diuretic use (saline-responsive), or Bartter&Gitelman syndromes
What class of anti-lipid drug should you always think about starting when pt had previous atherosclerotic cardiovascular disease regardless of lipid levels?
Statins! Don't care if low HDL, high TG, etc -> this is the only class that proves beneficial to this pt population
2 pathways HDL delivers cholesterol to liver?
Direct: uses SCARB1 (scavenger receptor) on hepatocytes
Indirect: cholesteryl ester transfer protein transfers cholesterol from HDL to LDL and VLDL
CXR finding on acute LV failure?
Cardiomegaly, pleural effusion, Kerley B lines (represent edema of interlobular septa), increased vascular shadowing
What kind of heart dysfx do viral myocarditis and cardiotoxic agents (incl alcohol and chemo agents) cause?
Dilated cardiomyopathy -> predominant systolic dysfx -> so get increase in both end-diastolic volume (preload) and end-systolic volume
What does Wilms tumor resemble under LM?
Primitive metanephric tissue
Given inulin clearance and substance’s plasma conc and tubular reabsorption rate, how do you calculate excretion rate?
Excretion = Filtration - Reabsorption
Reabsorption rate given, so calculate filtration rate by multiplying inulin clearance (representing GRF) by substance’s plasma conc, then plug that into the equation
Most common cause of aortic stenosis in older pts and its pathogenesis?
Age-related calcific aortic stenosis (the benign version of this is called “aortic sclerosis”)
From cell necrosis (2ndary to chronic hemodynamic stress or atherosclerotic inflammation) -> dystrophic calcification
What nephron segment responds to ADH by increasing absorption of ammonia to maintain high medullary conc gradient?
Medullary collecting duct -> ADH increases # of passive urea transporter -> urea go reabsorbed and go to the thin asc. loop of Henle -> urea allowed to recirculate and further concentrate
Urea also reabsorbed at PCT, but here ADH doesn’t play any role
How do you prevent acyclovir-assc. crystalluria?
Aggressive IV hydration and dosage adjustment (infuse slower)
Main compensatory mechanism responsible for why you don’t get peripheral edema w/ some ppl w/ right HF?
Increased lymphatic drainage -> compensates for increase in interstitial fluid up to a point
What abnormalities would you see w/ drug-induced acute interstitial nephritis? What 4 drugs commonly cause this?
High serum eosinophils and IgE, granuloma formation
Beta lactams, diuretics, NSAIDs, anticonvulsants
What does bulbus cordis become?
Ventricular outflow tract -> smooth part of ventricles adjacent to pulm artery/aorta
What does sinus venosus become?
Smooth part of RA (sinus venarum) -> receives blood from vena cavae
What structure is ductus arteriosus derived from?
6th aortic arch
What’s the pathogenesis of supine hypotension syndrome in pregnant women > 20 wks?
Compression of IVC by gravid uterus during supine -> so less venous return -> less CO -> hypotension and syncope
What happens to pressure-volume loop w/ AVM?
You’re bypassing arterioles (source of greatest resistance) -> decreases TPR -> so get lower afterload
Also get increased preload
So high volume shunt can cause high-output cardiac failure
Diff bet. xanthoma and xanthelasma?
Xanthoma: benign foamy macrophages (containing TG, cholesterol, phospholipids) surrounded by inflammatory cells and fibrotic stroma
Xanthelasma: no inflammatory cells or fibrotic stroma
Most common cause of unilateral fetal hydronephrosis?
Obstruction at ureteropelvic jx (so bet. kidney and ureter) -> metanephros begin producing urine before ureteric bud canalization is complete (the jx is the last segment of ureter to canalize)
3 precipitating factors for isolated episodes of AF?
Binge alcohol consumption (holiday heart syndrome)
Increased cardiac sympathetic tone
Pericarditis
EKG for A-fib?
Absent p waves
Variable R-R interval (irregularly spaced ventricular contractions)
What is high QRS voltage in precordial leads a sign of?
Ventricular hypertrophy
What does prolonged QRS complex mean?
Ventricular dyssynchrony or slowed intraventricular impulse conduction -> BBB is a common cause
2 sx of Conn’s syndrome (too much aldos) precipitated by hypokalemia?
Muscle weakness (from hypokalemic paresis) and paresthesias (from hypokalemic alkalosis)
What can vesicoureteral reflex be a complication of? What 2 things does it predispose to?
Prostatectomy or bladder surgery
Predisposes to pyelonephritis and hydroureteronephrosis
Besides inhibiting NKCC2, what else does loop diuretics do?
Stimulate prostaglandin release -> increases renal blood flow -> increased GFR and enhanced drug delivery
So decreased response is assc. w/ NSAIDs use
What cells produce endothelin?
Smooth muscles
What happens to renin, Ang I, Ang II, aldos, and bradykinin after starting ARB?
No ARB stimulation means decreased aldosterone w/ no change on bradykinin
Starting ARB also means less AT-1 receptor (Ang II receptor) stimulation -> less negative feedback regulating RAAS -> increases renin -> increases Ang I -> increases Ang II
What does positive urinary cyanide-nitroprusside test dx of?
AR defect of renal PCT and intestinal AA transporter for COLA (Cysteine, Ornithine, Lysine, Arginine) -> cystine stones
Risk factors of transitional cell carcinoma? What do you see on cystoscopy?
Risk factors: smokers, occupational exposure to rubber, plastics, aromatic amine-containing dyes, textiles, leather
On cystoscopy: see multifocal sessile or papillary tumors
What sign indicates glomerular bleeding source besides RBC cast?
Acathocytes
What vessel has the highest O2 extraction?
Coronary vessels -> so see the most difference bet. the arterial and venous side
This means blood oxygen content here will differ most from aorta (don’t even see that degree of difference in pulm artery b/c even the deoxygenated systemic blood returning via SVC and IVC has more O2 content than coronary venous blood)
Why are you more prone to hyponatremia w/ thiazide diuretics compared to loop diuretics?
Loop inhibits solute absorption in thick asc limb of Henle -> this portion is important to corticomedullary conc gradient -> so can’t concentrate urine in loop and lose lots of BOTH salt and water in urine
Thiazide inhibits at a diff place -> so normal corticomedullar conc gradient -> better able to retain water in response to increased ADH -> so lose more salt than water -> hyponatremia
