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Concepts / Lists > Nephrology > Flashcards

Nephrology Flashcards

1
Q

parasympathetic = cholinergic (use acetylecholine) what effects?

A

constrict pupils, constrict bronchioles (inc secretions), decrease HR, dilate BV, increase GI mvmt and salivation, bladder contraction

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2
Q

kidney functions

A

regulate BP, volume, excrete waste, regulate solute conc (Na, K, Ca, Mg), regulate extracellular pH, erythropoietin, synthesize vit D

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3
Q

most active secretion (to be excreted) site in kidney?

A

distal convoluted tubule - uric acid, K, H, drugs, foreign substances, creatinine (from muscle activity), bile salts

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4
Q

most reabsorption (to keep) occurs where in kidney?

A

proximal tubule (reabsorb organic nutrients like glucose and a.acids, most bicarb, Na (75%), Cl, 75%-90% of H20

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5
Q

parathyroid hormone acts on kidneys where?

A

distal convoluted tubule to increase Ca reabsorption

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6
Q

aldosterone affects

A

inc aldosterone –> inc Na reabsorption (in exchange for inc secretion of K + H+) in collecting duct

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7
Q

hyperaldosteronism sx

A

hypoK and metabolic alkalosis

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8
Q

increased antidiuretic hormone (ADH) leads to?

A

production of concentrated urine when hypovolemia, hyperosmolarity and inc RAAS activation in collecting duct

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9
Q

aldosterone and ADH act where?

A

collecting duct

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10
Q

path through nephron

A

afferent art / efferent art –> glom in bowman’s –> proximal convoluted –> loop of henle (thin descend, thin ascend, thick ascend) –> distal convoluted –> collecting duct

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11
Q

minimal change disease

A

80% of nephrotic syndrome in children (20 adults)

  • glomerular damage causes protein loss in urine
  • associated w/ viral infx, allergies (insect, NSAIDS)
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12
Q

acute glomerulonephritis

A

immunologic inflam of glomeruli causing protein and RBC leakage in urine; often after URI, GI infx or GABHS

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13
Q

major differences btw nephrotic and nephritic syndrome

A

nephrotic - proteinuria >3.5g/day

nephritic - proteinuria and hematuria (+ immune mediated)

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14
Q

phases of AKI

A
  1. oliguric (maintenance phase) (dec output <400ml/d, azotemia, hyperK, metabolic acidosis
  2. diuretic phase (inc output, hypotension, hypoK)
  3. recovery
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15
Q

mc type of AKI

A

prerenal (result from hypovolemia, reduced perfusion)

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16
Q

prerenal AKI cause

A

reduced renal perfusion (hypovolemia) - nephrons intact (can lead to intrinsic if not corrected)
-can also be afferent constriction (NSAIDS, IV contrast) and efferent dilation (ACEI/ARB)

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17
Q

postrenal AKI cause

A

obstruction (ex. BPH)

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18
Q

intrinsic AKI basic cause

A

direct kidney damage - nephrotoxic, cytotoxic, prolonged ischemic, inflammatory insults
-cellular cast formation - hallmark of intrinsic

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19
Q

types of intrinsic AKI

A
  1. acute tubular necrosis (ATN) - MC
  2. acute tubulointerstitial nephritis (AIN)
  3. Glomerular (acute glomerulonephritis - AGN)
  4. Vascular
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20
Q

acute tubular necrosis (ATN)

A

acute destruction/necrosis of renal tubules of nephron

  • ischemic - prolonged prerenal, hypoTN, hypovolemia
  • nephrotoxic - AMINOGLYCOSIDES, contrast dye, meds, crystal precipitation (gout), myoglobinuria (rhabdo), lymphoma/leukemia, bence-jones (MM)
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21
Q

UA signs of acute tubular necrosis

A
  • epithelial, muddy brown +/- waxy casts (formed in damaged tubules)
  • low specific gravity (unable to concentrate urine due to damaged cells)
  • hyperK, inc phosphatemia
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22
Q

acute tubulointerstitial nephritis (AIN)

A

inflammatory or allergic response in interstitium (spares glom and BV)
-MC drug hypersensitivity, then infections, autoimmune

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23
Q

causes of vascular AKI (intrinsic)

A

micro: TTP, HELLP syndrome, DIC
macro: aortic aneurysm, renal artery dissection, renal artery/vein thrombosis, malignant HTN

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24
Q

adult polycystic kidney disease

A
  • autosomal dominant (genes PKD1 mc or PKD2)
  • formation + enlargement of kidney cysts and cysts in other organs (LIVER, spleen, pancreas)
  • vasopressin stimulates cystogenesis –> ESRD
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25
Q

extrarenal sx of adult polycystic kidney disease

A
  • cerebral “berry” aneurysms
  • hepatic cysts
  • mitral valve prolapse
  • colonic diverticula
26
Q

HYPOphosphatemia causes/sx

A

-inc urinary PO4 excretion (primary hyperparathyroid, vitamin D deficiency)
-internal PO4 redistribution (insulin can shift PO4 intracellularly)
-decreased intestinal absorption (antacids)
SX: diffuse muscle weakness, flaccid paralysis (dec ATP)

27
Q

HYPERphosphatemia causes/sx

A

-renal failure MC (dec Ca, inc Phos, inc iPTH)
-primary hypoparathyroid (dec Ca, inc Phos, inc iPTH)
-vitamin D intoxication (inc Ca, inc Phos, dec iPTH)
SX: soft tissue calcifications, heart block

28
Q

chronic kidney disease sx:

A
  • progressive fx decline >3 mo
  • proteinuria
  • abnormal urine sediment, serum/urine chemistries, imaging
  • inability to buffer pH, make urine, excrete nitrogenous waste
  • decreased synthesis vit D / erythropoietin
29
Q

pt at risk for CKD

A

DM, HTN, chronic NSAID use, AA/Hisp/Asian, age >60, sLE, s/p kidney transplant, fam hx

30
Q

CKD staging

A

Normal GFR 120-130

  1. kidney damage w/ normal GFR >90
  2. GFR 89-60
  3. GFR 59-30
  4. GFR 29-15
  5. GFR <15 ESRD - requires dialysis or transplant if <10 or sCR >8 (<15 and >6 for DM)

Albuminiruia
A1: ACR <30 mg/g
A2: ACR 30-300
A3: ACR >300

31
Q

complications of CKD

A
  • anemia of CD (tx w/ iron and erythropoietin if persists)
  • coagulopathy (platelet dysfx –> petechiae)
  • renal osteodystrophy (Ca/PO4 dysregulation)
  • metabolic acidosis
32
Q

syndrome of inappropriate ADH (SIADH)

A

non-physiological excess of inc ADH from pituitary or ectopic source –> free water retention and impaired water excretion –> hypoNa and inability of kidney to dilute urine

33
Q

2 normal stimuli to increase ADH secretion

A

HYPOvolemia or HYPERosmolarity

34
Q

etiologies for SIADH

A

CNS: stroke (SAH) MC, head trauma, meningitis, CNS tumors, post-op, HIV
Pulm: small cell lung cancer, infx/pneumonia
Drugs: narcotics, NSAIDs, anticonvulsants, carbamazepine, cyclophosphamide, SSRIs/TCA, hydroclorothiazide, ecstasy
Endo: hypothyroid, Conn syndrome

35
Q

diabetes insipidus

A

-ADH/vasopressin deficiency MC (posterior pituitary)

  • insensitivity to ADH (nephrogenic) –>inability of kidneys to concentrate urine –> produce large amounts of dilute urine
    - hyperCa, hypoK
36
Q

2 normal stimuli to increase Aldosterone release

A

HYPOvolemia and/or HYPERkalemia

37
Q

low BP –> RAAS

A

hypovolemia (decrease arterial volume) causes juxtaglomerular cells in kidney to release renin, activating Renin-Angiotensin-Aldosterone System –> increased aldosterone promotes Na retention

38
Q

ADH vs aldosterone

A

ADH determines water homeostasis

Aldosterone determines Na+ homeostasis

39
Q

normal serum osmolality

A

285 - 295

40
Q

abnormal serum Na concentration is due to problems with

A 
water control (primarily by ADH)
(i.e. dehydration --> decreased free water = increased serum [Na] = hypernatremia
41
Q

abnormal extracellular fluid volume size is due to problems with…

A

total body Na control (determines ECFV)
ECFV = interstitial fluid vol and intravascular space vol
(i.e. hypervolemia = inc total body Na)

42
Q

normal serum creatinine level

A

1.0

43
Q

hypertonic hyponatremia

A

NOT true hyponatremia (not assoc w/ free water)

  • dilutional drop in serum [Na] due to presence of osmotically active molecules (glucose or mannitol infusion)
  • hyperosmotic causes water to shift from intracellular to extracellular space
44
Q

isotonic hyponatremia

A

NOT true hyponatremia (free water normal)

-lab artifact/error due to hypertriglyceridemia or hyperproteinemia

45
Q

hypotonic hyponatremia

A

TRUE hyponatremia

  • kidney unable to excrete free water (make dilute urine, increased ADH)
  • volume status gives clue to cause (hypovolemic, euvolemic, hypervolemic)
46
Q

hypovolemic hyponatremia

A
  • decreased volume (Na + water) and increased free water

- causes: renal volume loss (diuretics/thiazides), extrarenal volume loss like bleeding, D/V

47
Q

euvolemic hyponatremia

A
  • normal volume (Na + water) and increased free water

- SIADH, hypothyroidism, adrenal insufficiency, primary polydipsia (water intox), MDMA

48
Q

hypervolemic hyponatremia

A
  • increased volume (Na + water) AND increased free water

- edematous states: CHF, nephrotic syndrome, cirrhosis

49
Q

hypernatremia

A

MC caused by net water loss

-CNS dysfunction (shrinkage of brain cells)

50
Q

hypomagnesemia common causes

A

malabsorption (esp alcoholics)
renal losses (diuretics)
PPIs

51
Q

hypomagnesemia symptoms

A 
inc DTR
tetany
hypoCa (Mg needed to make parathyroid hormone)
palpitations (due to associated hypoK)
prolonged PR + QT interval
TORSADES
52
Q

hypokalemia common causes

A

diuretic therapy
V/D
metabolic alkalosis
hypomagnesemia

53
Q

hypokalemia symptoms

A 
muscle weakness / rhabdo
nephrogenic - polyuria
dec DTR
palpitations, arrhythmias
T-wave flattening (early) --> prominent U wave (+/- hypomagnesemia changes)
54
Q

hyperkalemia causes

A
  • decreased renal excretion, decreased aldosterone (adrenal insufficiency)
  • ACEI/ARBs, digoxin, B-blockers, NSAIDs, K sparing diuretics
  • metabolic acidosis (DKA)
55
Q

MC side effect of hyperparathyroidism

A

kidney stones (due to excess Ca)

56
Q

most common solid renal tumor of childhood

A

Nephroblastoma, or Wilms tumor

57
Q

What drug must be withheld for 48 hours after the administration of a contrast agent? (Intravascular administration of iodinated contrast media)

A

metformin - can result in lactic acidosis

58
Q

MC cause of AKI in children

A

Hemolytic-Uremic Syndrome (E. coli 0157:H7 - shiga-like toxin, strep. pneumo, drug toxicity)

59
Q

Hemolytic-Uremic Syndrome Triad

A

hemolytic anemia (schistocytes)
thrombocytopenia
renal insufficiency

60
Q

renovascular HTN (renal artery stenosis)

A

HTN due to renal artery stenosis (1 or both) –> inc RAAS
MC cause of secondary HTN
-suspect if HTN onset <20 or >50, HTN resistant to 3 drugs, abdominal bruit or if PT DEVO AKI AFTER INITIATION OF ACEI

-etiology: atherosclerosis mc in elderly, fibromuscular dysplasia mc women <50

Concepts / Lists (16 decks)

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