Renal

Front 1

components of autoregulation

Back 1

1. intrinsic pressure sensitive myogenic mechanisms of afferent arteriole 2. renin release from JG apparatus and ang mediated efferent arteriol vasoconstriction

Front 2

increase plasma renin activity

Back 2

1. hemmorrhage 2. diuresis 3. salt depletion (low salt) 4. ecv volumue depletion 5. adrenal insufficiency (renin and ang increased but aldosterone decreased b/c adrenal gland unable to make it)? 6. upright posture 7. nephrotic syndrome 8. heart failure 9. cirrhosis with ascites (in 7-8 total fluid high but blood flow to kidney decreased)

Front 3

hyponatremia

Back 3

water excess

Front 4

hypernatremia

Back 4

water deficiency

Front 5

hyponatremia + high osmolality

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hyperglycemia, mannnitol infusion called pseudohyponatremia

Front 6

hyponatremia + normal osmalality

Back 6

high lipid, high protein

Front 7

hyponatremia with hypovolemia

Back 7

1. extrarenal diarrhea/vomiting/3rd spacing/burns 2 renal: diuretics/osmotic diuresis

Front 8

hyponatremia with euvolemia

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1. SIADH 2. hypothyrodism 3. adrenal insuffiency 4. glucorticoid deficiency 5. primary polydypsia

Front 9

hyponatremia with hypervolemia

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1. renal failure (AKI/CKD), CHF, liver failure (cirrhosis), nephrotic syndrome

Front 10

SIADH disorders

Back 10

think: too much water! Hyponatremia. 1. malignancy 2. pulmonary disorder 3. CNS 4. endocrine addison/hypothyroidsm 5. protein malnutrition 6. surgery

Front 11

hypernatremia + hypovaolemia

Back 11

1. gi loss (vomiting/diarrhea) 2. burns/excess sweat 3. loop diuretics/renal disease

Front 12

hypernatremia + euvolemia

Back 12

1. DI 2. reset osmotstat 3. fever, sweat

Front 13

hypernatremia + hypervolemia

Back 13

1. hypertonic fluid administer, minderalcorticoid excess

Front 14

causes of central DI

Back 14

not producing ADH. congential, trauma, neurosurg, malignancy, granuloma (TB or sarcoid), idiopathic

Front 15

cause of nephrogenic DI

Back 15

kidney doesn't respond to ADH. inhereted (X link), acquired with renal disease (PCKD, Medullary cysic kidney, sickle cell, medulalry sponge, amyloid/multiple myeloma), tempoary (post obstructive, hypokalemia, hypercalcemia, pyelonephritis, lithium toxicity)

Front 16

sweating you lose…

Back 16

hypotonic sweat (mostly water, some NaCl) treat with 0.45% half normal saline

Front 17

1. polyuria 2. oliguria 3. anuria

Back 17

1. > 3 L 2. <0.5L 3. <50 ml a day

Front 18

increase ADH secretion

Back 18

1. increase in extracellular fluid osmolality (hypothalamic osmoreceptors). 2. decrease in actual effective intravascular fluid volume (carotid sinus) 3. SIADH 4. nausea

Front 19

inhibit ADH secretion

Back 19

1. increase in anp 2. alcohol

Front 20

proximal tubule

Back 20

Na/H exchanger (ang 2 stimulates)

Front 21

fanconi syndrome

Back 21

proximal tubule doesn't work, won't absorb things

Front 22

distal convoluted tubule

Back 22

Na/Cl transporter, Ca (apical ca channel, vitamin d depending ca binding protein)

Front 23

cortical collecting duct

Back 23

1. principle cells aldosterone works 2. type a secrete H through luminal h/k channel 2. type b secrete bicarb by Cl/bicarb exchange (luminal)

Front 24

medullary collecting duct

Back 24

adh determines reabsorption of fluid

Front 25

creatinine clearance innaccurate when

Back 25

decreased muscle mass, severe malnutrition, patients who don't eat meat

Front 26

causes of polyuria

Back 26

1. DI 2. psychogenic polydypsia (drinking excess fluid) 3. uncontrolled DM (glucose in urine) 4. exogenous substance (mannitol) 4. use of excessive diuretics (also see Na, K, cl in urine)

Front 27

diarrhea

Back 27

lose isotonic fluid, ECF decreased ICF same

Front 28

cellular uptake of K stimulated by

Back 28

plasma K, insuline, catecholamines

Front 29

kidney excretion of stimulated by

Back 29

plasma K, aldosterone, distal Na delivery (and flow rate), poorly reabosrbable anions, met alkalosis

Front 30

causes of hypokalemia

Back 30

1. transcellular shift of K (alkalosis, insulin, catecholamines, hypokalemic periodic pararlysis) 2. GI (reduced intake, vomiting, diarrhea), 3. skin (sweating, burns) 4. kidney loss (increased distal Na delivery - thiazide and loop diuretics, minearlcorticoid excess - primary or secondary hyperaldosteronosim, poorly reabsorbable anions/alkaline anions - RTA type I and II, met alkalsos, diabetic ketoacidosis

Front 31

Bartter syndrome

Back 31

mutation in the Na/K/2Cl cotransporter at TAL - hypokalemia

Front 32

Gitelman syndrome

Back 32

mutation in Na/Cl cotransporter at distal convoluted tubule - hypokalemia

Front 33

consequence of hypokalemia

Back 33

1. NM weakenss, paroalysis, rhabdo 2. ST depression, flattened T waves, U waves, v arrythmias 3. metabolic (carb intolderance, growth retardation, low aldosterone, stimulate RAAS 4. kidney - thirst, polydipsyis, nehrogenic DI, met alkalosis. Can cause vacuolization of the tubule and chronic progress kidney disease

Front 34

fractional excretion of K determining hypokalemia

Back 34

FEK > 10% kidney loss, FEK less than 6% non kidney loss

Front 35

tx hypokalemia

Back 35

dietary, K salts (hypokalemia + met alkalsos KCl, hypokalemia w/metabolic acidosis K bicarb, citrat), IV rate of KCL up to 10-20 moniture EKG

Front 36

causes of hyperkalemia

Back 36

1. pseduohyperkalemia 2. transcellular shifts (acidosis, hyperglycemis, beta blocker, severe exercise/tissue breakdown, hyperkalemic periodic paryalisis) 3. increased K intake (dietary, IV) 4. K retention (kidney failure, hypoaldosternoism, adrenal insufficenscy (addison), hyporeninemic hypodaldosterinism typ 4 rta, K retaining drugs)

Front 37

consequence of hyperkalemia

Back 37

1. NM function wekaness, parayslys 2. peaked T wave, flattening/loss P waves, wide QRS, v tac/v fib, cardiac arrist 5. NAGMA type 4 rta

Front 38

treatment of hyperkalemia

Back 38

1. ecg monitoring 2. IV calcium gluconate or chloride 3. insulin with glucose 4. sodium bicarb (correct metabolic acidosis) 5. beta agonist 6. cation exchange resin with sorbitol 7. dialysis for kidney failure

Front 39

low urine chloride with high urine K concentration

Back 39

vomiting! Mechanism of hypokalemia not from loss of K in gastric jucice but from kidney loss of K as a result of development of metabolic alkalosis

Front 40

factors that increase urine H excrection

Back 40

PACK 1. decreased EVC 2. decreased plasma pH 3. decreased plasma K 4. increased aldosterone

Front 41

early phase of vomiting/gastric suction

Back 41

bicarb increased, urine bicarb increased, urine na increased, urine k increased, urine cl increased, urine ph increased, URINE CL DECREASED

Front 42

late phase of vomiting/gastric suction (3 or more days)

Back 42

bicarb increased, urine bicarb decreased, urine na decreased, urine K decreased, urine cl decreased, urine pH DECREASED (paradoxic aciduria) b/c want to maintain volume

Front 43

met alkalosis + urine Cl less than 15

Back 43

chloride responsive: gastric fluid loss, stool, diuretic, post hyperkapneis, severe K depleation: treat volume expansion (NaCl), K replacement

Front 44

met alkalosis + urine Cl > 20

Back 44

chloride resistant: primary hyperaldosteronism, sterois, bartter, cushing, hypokalemia. Treat cause, NaCl ineffective

Front 45

generate met alkalosis

Back 45

1. plasma H loss (gi, urine, movement of H into cells) 2. bicarb gain 3. volume contraction

Front 46

maintain met alkalosis

Back 46

1. ecv depletion 2. hypokalemia 3. hypochloremia

Front 47

high serum osmolality

Back 47

methanol, ethanol, ethylene glycol

Front 48

examples of unmeasured anions

Back 48

SOAP: sulfate, organic acids, keto acid/lactic acid, low albumin, phosphate

Front 49

NAGMA

Back 49

diarrhea, RTA, aldosterone deficiency

Front 50

AGMA

Back 50

high acid input: ingestion of alcohol, methaon, ethylene glycol, ASA or production of acid by shock, lactic acidosis, ketoacidosis (DM, starvation, diabetic) or low acid output: kidney failure

Front 51

type 1 RTA

Back 51

failure of distal H/ATPpse luminal pump. Amp B/lithium. Bicarb low. K low. Urine ph greater 5.6

Front 52

type 2 RTA

Back 52

proximal RTA unable to reabsorb bicarb. Bicarb 12-20 (lowish), low K, urine pH may be low

Front 53

type 4 RTA

Back 53

distal hyperkalemic RTA. Lack of ammoniogensis secondary to low aldosterone. Cause HIGH K

Front 54

stepwise approach to acid base

Back 54

1.25 0.7 0.2 0.4

Front 55

nephrotic syndrome

Back 55

1. massive protein 2. hypoalbumin 3. edema 4. hyperlipidemia

Front 56

nephritic syndreom

Back 56

1. oliguria + hematuria 2. hypertension 3. active urine sediment (dysmorib RBC, RBC cast)

Front 57

minimal change mechanism

Back 57

loss of net neg charge associated with podocyte foot process - break down glomerular cap barrier

Front 58

DKA major form of volume contraction? ICF and ECF?

Back 58

yes! Low ECF due to osmotic diuretics, low ICF due to hyperosmolality

Front 59

DKA and K

Back 59

K high due to acidosis, total body K low because she is peeing out Na and K. lack of insulin, normally brings it inside of cell but since you don't have it stays outside. That is why you see hyperkalemia but low total body stores

Front 60

ECV depletion leading to metabolic alkalosis

Back 60

ECV depleted --> RAAS activation --> HCO3 and Cl reabsorbed --> maintain metabolic alkalosis

Front 61

CKD due to urinary obstruction from enlarged prostate

Back 61

high BUN and create, NAGMA due to decreased ammoniogensis b/c of renal failure (Type 4 RTA)

Front 62

persistend diarrhea

Back 62

NAGMA

Front 63

primary hyperaldosteronism

Back 63

Conn's syndrome - hypokalemia/met alkalosis

Front 64

type 1 RTA

Back 64

high urine pH, NAGMA, hypokalemia

Front 65

antifreeze ingestion

Back 65

AGMA

Front 66

mortality of AKI due to

Back 66

1. infection 2. cardiovascascular problems

Front 67

3 kinds of ketoacidosis

Back 67

diabetic, alcoholic, starvation

Front 68

which one causes high bicarb: vomiting, hypovolemia, furosemide?

Back 68

they all do!

Front 69

urine specific gravity of 1.035 think:

Back 69

this is high: CHF, SIADH, hemorrhagic shock, liver cirhossis

Front 70

urine specific gravity fo 1.000

Back 70

this is low: think DI

Front 71

low complement

Back 71

MEPPS: MPGN, endocartditis, post strep, post infectious, SLE

Front 72

history of miscarriage

Back 72

SLE! Antiphospholipid antibodies are pro-coagulants, clot off, can get thrombo embolic events.

Front 73

treatment for SLE + lupus nephritis

Back 73

prednisone, cyclophosphamide, mycophenolate mofetil

Front 74

microscopic hematuria

Back 74

1. IgA nephropathy 2. alport/thin basement membrane

Front 75

gross hematuria

Back 75

1. IgA nephropathy 2. anti GBM/Good pasture 3. MPGN 4. post -infections GN 5. vasculitis (wegners) 6. lupus 7. ADPKD

Front 76

lung/sinus problems

Back 76

1. good pasture (pulmonary hemorrhagee) 2. wegners (granulomas in lungs) 3. SLE 4. post infectious strep (right away) 5. IgA (few weeks later)

Front 77

RPGN

Back 77

1. good pasture/anti-GBM 2. immune complex (SLE), wegners (C-ANCA), Churg strauss (P-ANCA) pauci-immune 5. non glomerular - PCKD

Front 78

treat IgA

Back 78

fish oil/ACEi + RAAS blockade

Front 79

single most important factor of developing overt kidney disease in diabetics

Back 79

microalbumineriua!

Front 80

does high K occur in early or late CKD?

Back 80

in late CKD. Remaining nephrons work really hard to excrete K

Front 81

3 things to know for hyperaldosteronism

Back 81

1. retain Na (HTN) 2. low K 3. retain HCO3 (metabolic alkalosis)

Front 82

BUN/Cr ratio

Back 82

BUN normally excrete 30% so if fractional excretion of BUN > 40 - prerenal azotemia

Front 83

causes of primary hyperaldosteronism

Back 83

conn's adenoma, renal secreting tumor. High aldo low renin.

Front 84

causes of secondary hyperaldosteronism

Back 84

renal artery stenosis/renin producing tumor, low ECV. High renin high aldo

Front 85

causes of third hyperaldosteronism

Back 85

pseudo - licorice. Low aldo low renin

Front 86

CKD

Back 86

decrease Vit D, decreased serum ca, increased PTH, renal osteodystrophy

Front 87

mechanism for renal osteodystrophy

Back 87

decreased alpha hydroxylation leads to Vit D. increased serum phosphate (renal damage can excrete phophsate) leads to decreased serum ca (metasttic Ca P deposition), causing decreased serum calcium causing increased PTH

Front 88

gold standard for renal anatomy

Back 88

1. renal arteiogram/angiography (gold standard) 2. mra: negative galodineum cause nephrogenic systemic fibrosis 3. ct angiograph - non invasve. Contrast can caause renal toxicity

Front 89

gold standard for renal blood flow

Back 89

1. renal angiogrphay. Can also du duplex ultrasound, nucleiar imaging with captopril

Front 90

hypertensive disorders associated with hyperkalemia

Back 90

1. hyperaldosteronism 2. cushings (too much cortisol acts like aldo) 3. pheochromyctoma (beta agonist put K back in cells)

Front 91

imaging for stones

Back 91

non-constrast helical CT scan (spiral CT)

Front 92

normal GFR

Back 92

minimal change, FSGS (can progress usually doesn't) IgA thin basement membrane alport

Front 93

measure adequacy of dialaysis

Back 93

"URR = Urea reduction ratio (optimal URR>70%) Kt/V (optimal Kt/V>1.3)

Front 94

INDICATIONS FOR STARTING CHRONIC DIALYSIS

Back 94

Symptomatic Uremia Fluid (salt and water) Overload not responsive to diuretics Hyperkalemia not controlled with diet GFR < 10 cc/min, <15 cc/min if diabetic

Front 95

ppl on dialysis die of

Back 95

cardiovascular disease, infection

Front 96

phase 1 of host response

Back 96

innate inflammation – innate immune response. Have neutrophils and macrophages that activate complement, cyotine, adhesion molecules, antigen INDEPENDENT. Phase 1 results in ATN (acute tubular necrosis) if injury too strong. Occurs 0-72 hrs. symptoms called delayed graft function. Takes a few days for the kidneys to recover.

Front 97

phase 2 of host response

Back 97

immune specific response. T cells, antibodies get ready, direct response against tissue antigens. Occurs in 0-10 days but can be at any course during transplant if you stop immune suppresion. Acute rejection

Front 98

phase 3 of host response

Back 98

" phase 3: fibroblast producing fibrogen, collagen, scarring molecules. Mechanism antigen dependent and independent. Htn with dm. months-years