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Question 1

what 3 substances can cause overestimation of GFR by serum creatinine levels?

Answer 1

ketoacids
cimetidine
trimethoprim

these competitively inhibit tubular Cr secretion

Question 2

what 4 meds can cause prerenal aki by decreasing renal blood flow

Answer 2

NSAIDs
ACEI
ARBs
cyclosporine

Question 3

is urine Na and bun/cr ratio high or low in prerenal AKI? why?

Answer 3

Na is low (<20). ratio is high aka >20:1. both bc RAAS

Question 4

is urine Na and bun/cr ratio high or low in ischemic ATN? why?

Answer 4

Urine Na is high >40. ratio is normal. both bc damaged tubules are unable to reabsorb properly.

Question 5

3 general mechanisms that contrast induces AKI

Answer 5

1. constrict afferent arteriole and vasa recta -> lower GFR and blood flow to blood vessels
2. high osmolality so kidney has to work harder -> raise O2 demand of kidney
3. increase ROS, decrease antioxidants -> oxidative stress/damage

Question 6

what do you give to patients before contrast to reduce risk of ATN AKI?

Answer 6

N-acetylcystine (antioxidant properties, promotes renal vasodilation) and isotonic saline (dehydration/low ECF is a risk factor)

Question 7

in pigment nephropathy, filtered myoglobin precipitates with _____. causing tubular obstruction. what is the treatment for this?

Answer 7

precipitates with Tamm-Horsfall protein
.
treat by alkalinizing urine. it decreases precipitation

Question 8

rhabdomyolysis is what causes pigment nephropathy (the myoglobin and hemoglobin come out into blood from muscles). but what are causes of rhabdomyolysis that aren’t obvious? (2)

Answer 8

1. hmg coa reductase inhibitor aka statins

2. alcohol and drugs (like cocaine)

Question 9

whats that thing that you have coke/tea colored urine and strip test is positive for blood. but if you do microscopy there’s no red blood cells?

Answer 9

pigment nephropathy. it’s bc of the myoglobin/hemoglobin.

Question 10

Serum creatinine peaks within how many days of contrast induced AKI? returns to normal by when?

Answer 10

peaks in 5 days. normal in 7-10 days

Question 11

what can cause AKI without oliguria

Answer 11

aminoglycosides nephrotoxicity. it’s bc afferent arteriole constriction is not a major player in this pathophysiology so GFR isn’t as decreased as in other AKIs. but AGs do constrict mesangial cells which causes mild decrease in GFR

Question 12

2 main mechanisms of AG nephrotoxicity

Answer 12

1. constrict mesangial cells -> mildly lower GFR
2. principal cells take up AGs very concentrated. reduces ability to concentrate urine -> urine osmolalitly 300-350 (same as in glomerulus/plasma basically)

Question 13

what casts do you see or not see in PRERENAL AKI?

Answer 13

ONLY see hyaline casts! which are NORMAL. made of Tamm Horsfall proteins (which precipitate with myoglobin in pigment nephropathy btw)

Question 14

what casts in urine for ischemic ATN?

Answer 14

muddy brown granular casts and tubular cell casts

Question 15

what things and casts in urine for glomerulonephritis?

Answer 15

proteinuria, RBCs, and RBC casts

Question 16

serum phosphate is regulated by renal reabsorption or secretion?

Answer 16

reabsorbtion

Question 17

serum K+ is regulated by renal reabsorption or secretion?

Answer 17

secretiooonnnn. can increase secretion if hyperkalemia.

Question 18

kidney dz patient on ACEI or ARB or K+ sparing diuretic is bad news -> hyperkalemia
.
heart failure or liver failure pt on NSAID or ACEI or ARBs is bad news -> acute kidney injury
.
these are some important “pt has underlying condition and you put them on this drug and bad things happen” examples

Answer 18

moving on

Question 19

synthesis of what amino acid by intact nephrons maintains elevated NH4+ urinary excretion in compensated CKD?

Answer 19

glutamine synthesis. idk why

Question 20

which 2 mediators cause unregulated/fixed Na excretion in CKD? pg 432

Answer 20

NPs and PGE2
.
so if Na excretion > intake, pt will have orthostatic hypotension (hypovolemic state). if intake >excretion, pt will have edema and hypertension (hypervolemic state)
.
THIS IS NOT WHAT CAUSES HYPER OR HYPONATREMIA BC REMEMBER THAT’S A WATER BALANCE ISSUE, NOT NA+ even tho its all related what the heck

Question 21

why does CKD continue to progress even if you remove initial insult/offender?

Answer 21

high SNGFR of intact nephrons = intraglomerular hypertension. this leads to hyperfiltration injury -> proteins deposited in mesangium and tubules (also NH4+, which activates alternative complement pathway, furthering inflammation and injury) -> glomerular sclerosis and tubular fibrosis = irreversible changes. GG.
bts this makes kidneys shrink so small shrunken kidneys are end stage CKD kidneys even tho in the beginning you have hypertrophic intact nephrons

Question 22

in CKD you get LVH. which 2 things predisposes you to eccentric LVH? which one for concentric LVH?

Answer 22

eccentric: chronic anemia and volume overload (which you can both get from CKD)
.
concentric: CKD related Hypertension. obvis, from CKD.
.
its a never ending cycle gah

Question 23

bad things hyper PTH does.

Answer 23

1. arterio/atherosclerosis
2. neuro calcium overload -> polyneuropathy and encephalopathy
3. bone bone disorders (osteitis fibrosa cystica)

Question 24

guy has CKD, comes in with FEVER and PRECORDIAL CHEST PAIN that’s worse with breathing and laying down. what is it??

Answer 24

uremic pericarditis. +- pericardial friction rub +- cardiac tamponade (will then have pulsus and electrical alternans where QRS goes up and down, inverted, right way up again, back and forth)

Question 25

``` what does CKD do to blood lipids? VLDL TAGs HDL LDL ```

Answer 25

VLDL and TAGs increase HDL decreases LDL IS UNCHANGED. unless nephrotic proteinuria present

Question 26

what happens to sex hormones CKD? clinical presentation?

Answer 26

estrogen and progesterone and testosterone are low thus, LH and FSH are high (but in women no LH spike so no ovulation) both genders have hypogonadism and are infertile

Question 27

which serum biomarkers are elevated in 2ndry hyperPTH osteitis fibrosa cystica?

Answer 27

osteoblasts -> alkaline phosphatase and osteocalcin | osteoclasts -> tartrate resistant acid phophatase (TRAP)

Question 28

what is the threshold of (serum Ca2+) X (serum phophate) when tissue calcification starts happening?

Answer 28

> 55 mg2/dL2

Question 29

the 4 mechanisms causing pruritus in CKD

Answer 29

1. inflammatory cytokines 2. excess beta endorphins 3. increased mast cells, they release histamine 4. dermal calcifications from excess PTH irritate sensory nerve endings

Question 30

the 3 pulmonary manifestations of CKD and their mechanisms

Answer 30

1. restrictive lung dz from pulmonary calcification and fibrosis 2. uremic penumonitis = cytokine mediated permeability lung edema. PAWP IS NORMAL TO LOW 3. serosanguinous pleural effusions in stage 4 and 5

Question 31

which variables in starling forces equation does inflammation alter?

Answer 31

Kf (fluid permeability) S - surface area of capillary sigma (protein permeability) OPis - interstitial osmotic pressure (bc its affected by permeability)

Question 32

in nephrotic syndrome, the pathogensis for edema differs if serum albumin is above or below 2.0 g/dL. if it's >2, what is stimulating increase in Na reabsorption and where in the nephron is it happening? what about for <2?

Answer 32

>2: proteolytic enzymes like plasminogen/plasmin stimulate ENaC in cortical collecting duct -> Na reabsorption increases -> increased HPc . <2: decreased capillary oncotic pressure. then, hypovolemia -> RAAS -> aldosterone -> stimulate ENaC in CCD

Question 33

hemodynamic findings (increased, decreased, or normal) during acute exacerbation of COPD (which will cause edema): ECV, CO, JVP, SVR/BP, PaCO2

Answer 33

ECV decreased (bc edema and its acute so body doesn't have time to adjust) CO high (to compensate) JVP normal to low SVR/BP: decreased (b/c CO2 is increased which is a vasodilator). btw this is vasodilation theory/mechanism that initiates edema in this case paCO2 increased just think of it ias paCO2 is the primary increase and everything is following or compensating for that.

Question 34

so far i 've only come across one thing that causes edema that doesn't involve increased RAAS. what is it.

Answer 34

nephrotic syndrome where serum albumin >2 g/dL

Question 35

3 theories/mechanisms by which hepatic cirrhosis causes decreased Na excretion. remember theyre named by the INITIATING EVENT that caused the decrease in Na excretion

Answer 35

1. vascular underfill: hepatic venous obstruction -> edema -> hypovolemia -> RAAS 2. vasodilation theory: lots of vasodilators in cirrhosis for some reason -> decrease ECV -> activate RAAS 3. hepatic venous outflow obstruction -> activate intra sinusoidal baroreceptors -> activate SNS -> activate RAAS ->

Question 36

drug of choice for edema caused by hepatic cirrhosis and why

Answer 36

spironolactone. bc its an aldosterone inhibitor. bc RAAS is the major factor. btw this is what you need in idiopathic edema. other diuretics will only increase aldosterone and thats bad

Question 37

4 mechanisms of hypothyroidism caused edema (myxedema)

Answer 37

1. decreased albumin synthesis. lowers plasma oncotic pressure. OPc and OPis difference increases 2. decreased sigma (increased protein permeability) 3. lymphatic flow is sluggish 4. mucopolysaccharides bind water, prevent removal by lymphatics and makes it nonpitting

Question 38

mechanism of idiopathic edema

Answer 38

1. dilation of precapillary sphincters | 2. decrease in sigma (increased protein permeability) -> edema -> VASCULAR UNDERFILLING -> RAAS

Question 39

is vascular overfilling or underfilling responsible for NSAID induced edema?

Answer 39

overfilling

Question 40

which nuclei are responsible for regulating plasma osmolality and volume?

Answer 40

osmolality: supraoptic nucleus volume: periventricular nucleus

Question 41

what senses change in ECF tonicity? what senses change ECF volume?

Answer 41

tonicity: hypothalamic osmoreceptors volume: arterial baroreceptors, JG baroreceptors, atrial volume receptors

Question 42

what drugs can cause SIADH | what category of hyponatremia does it fall under

Answer 42

cancer drugs (vincristine, cyclophophamide), psychoactive drugs (SSRIs, amitriptyline, phenothiazines), other drugs (NSAIDs, opioids, carbamazepine) . hypotonic isovolemic hyponatremia. .

Question 43

acute and refractory treatments for SIADH.

Answer 43

acute: h20 restriction, furosemide + NaCl refractory: tolvaptan (v2 antagonist, aquaretic), and Demeclocycline (causes ADH resistance aka diabetes insipidus in a normal person)

Question 44

dominant clinical presentation in hyponatremia | ECG findings?

Answer 44

the main problem is brain cells are swelling so you get neuro and neuromuscular symptoms like asterixis, confusion, seizures, muscle fasciculations, dilated pupils, Babiski signs. cns swelling also causes anorexia, nausea, vomiting, and tentorial cerebral herniation! can also have cheyne-stokes respirations if severe/very acute no ECG findings,

Question 45

chronic hyponatremia causes increased risk of hip fractures, especially in elderly. why?

Answer 45

CNS impairment causes confusion and unsteady gait so they fall more . chronic hyponatremia also causes osteoporosis. so bones break more easily when they do fall

Question 46

meds that cause nephrogenic diabetes insipidus

Answer 46

lithium | demeclocyline (treats SIADH remember)

Question 47

how do cells adapt to hypernatremia, given a couple of days

Answer 47

they make idiogenic osmoles: glutamine and nyoinositol. they increase intracell tonicity and minimize cell shrinkage

Question 48

if you correct hyponatremia or hypernatremi too fast what are the consequences.

Answer 48

correct hyponatremia too fast: osmotic demyelination syndrome (seen in acute severe hypernatremia) . correct hypernatremia too fast: cerebral edema (seen in hyponatremia)

Question 49

where in nephron is 90% of filtered K+ load reabsorbed?

Answer 49

proximal tubules and TAL. this part is not really regulatable. the part you can change is amt of K+ excretion in principal cells (basolateral Na/K ATPase) of cortical connecting tubules and CCD

Question 50

what are the 2 feed forward mechanisms to protect against hyperkalemia when you eat. these work in 3-5 minutes BEFORE serum K+ increases

Answer 50

1. portal hepatic GI sensors -> increase K+ secretion 2. proteins stimulate pancreas to release glucagon -> stimulates liver to make cAMP -> cAMP increases GFR -> increase K+ secretion

Question 51

how does high tubular flow rate (caused by diuretics and osmotic diuresis) stimulate K+ secretion?

Answer 51

high flow rate -> primary cilium bends -> raises intracellular calcium -> activate BK channels -> increased K+ secretion

Question 52

which 4 meds cause hypER kalemia and how?

Answer 52

1. digoxin -> inhibits Na/K ATPase 2. aldosterone antagonists (Spironolactone, ACEI's) 3. beta antagonists - inhibit SNS stimulation of RAAS, and remember beta stimulation causes K uptake into cells 4. NSAIDs - decrease RAAS. especially if used with ACEIs or ARBs

Question 53

what is the triad that SAME and Liddle syndrome present with?

Answer 53

1. hypokalemia 2. metabolic alkalosis 3. HTN

Question 54

what is the mutation in Liddle syndrome causing?

Answer 54

gain in function of ENaC in principal cells -> increase Na reabsorption and thus increase K+ and H+ secretion

Question 55

Gitelman syndrome. I was born with a ______ diuretic . Bartter syndrome. I was born with a _______ diuretic. how do they present?

Answer 55

Gitelman = thiazide diuretic. LOF of NaCl cotransport in DCT Bartter syndrome = loop diuretic. LOF of Na/K/Cl in TAL both present with hypokalemia, metabolic alkalsosis, and hypOtension (unlike Liddles which has htn but same other 2 signs)

Question 56

(remember K+ is a vasodilator, naturally comes out of cells during exercise to increase blood flow to muscles). so during hypokalemia, K+ vasodilating effect is not there -> rhabdomyolysis -> pigment nephropathy AKI

Answer 56

GG

Question 57

hypokalemia decreases phase __a___ current. __b__(inc/dec) Na conductance in Purkinje cells. both cause __c___

Answer 57

a. phase 4 repolarizing current (reduced Na/K atpase activity) b. increase Na conductance c. enhanced automaticity/excitability -> tachyarrhythmias

Question 58

hypokalemia reduces Na/K atpase activity, but it also destroys protein for which other channel? what's the result of this?

Answer 58

for Kir channel. slows repol -> prolong QT interval -> EAD triggered torsades de pointes. SEE ACTION POTENTIAL GRAPH PICTURE

Question 59

ECG findings in hypokalemia

Answer 59

ST depression (meh can't rlly see it though) low T wave amplitude (bc slower repol) increased U wave amplitude long QT interval (bc slower repol) later on T wave will invert so don't get U wave confused as T wave, which will still be upright

Question 60

don't forget about that Atrial tachycardia w/ 2:1 AV block, caused by digoxin toxicity, which youre more prone to when you have hypokalemia bc it increases affinity of cardiac for digoxin.

Answer 60

the atrial tachy w/ av block is due to DAD TRIGGERED ACTIVITY

Question 61

hyperkalemia: a. causes depol or hyperpol? b. leads to increased or decreased membrane excitability?

Answer 61

a. depol b. constant depol -> inactivates fast Na channels -> decreased excitability -> muscle weakness but it can also just depol and increase excitability -> enhanced automaticity in cardiac cells -> tachyarrhythmias ALSO acute severe hyperkalemia messes up cardiac conduction of fast action potentials -> ventricles can't be excitated -> asystole -> SCD

Question 62

what does hyperkalemia do to ECG

Answer 62

rapid repol -> tall T waves . decreased cardiac conduction and slower phase 0 depol -> prolong QRS complex, P wave, and PR interval . reduced Ikr current -> shorten QT interval . but..ecg is not a sensitive indicator of hyperkalemia so...normal ECG doesn't exclude hyperkalemia

Question 63

treatment of acute hyperkalemia. 3 steps

Answer 63

1. calcium gluconate - limit cardiac toxicity 2. nebulized B2 agonist + insulin and glucose -> shift K+ into cells 3. loop diuretic and resin (patiromer or sodium polystyrene sulfate) to increase renal and fecal k+ excretion

Question 64

treatment of CHRONIC hyperkalemia. 2 steps

Answer 64

1. dietary K+ restriction, discontinue K+ retaining meds | 2. loop and thiazide diuretics, and resin to increase renal and fecal K+ excretion

Question 65

rhabdo causes what 3 things?

Answer 65

AKI hypERkalemia hypOcalcemia (damaged muscles uptake calcium)