Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Concepts / Lists > Nephrology > Flashcards

Nephrology Flashcards

(60 cards)

Start Studying
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

kidney functions

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

parathyroid hormone acts on kidneys where?

A

distal convoluted tubule to increase Ca reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

aldosterone affects

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

hyperaldosteronism sx

A

hypoK and metabolic alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

increased antidiuretic hormone (ADH) leads to?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

aldosterone and ADH act where?

A

collecting duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

acute glomerulonephritis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

major differences btw nephrotic and nephritic syndrome

A

nephrotic - proteinuria >3.5g/day

nephritic - proteinuria and hematuria (+ immune mediated)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

mc type of AKI

A

prerenal (result from hypovolemia, reduced perfusion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

postrenal AKI cause

A

obstruction (ex. BPH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

intrinsic AKI basic cause

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

acute tubulointerstitial nephritis (AIN)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
extrarenal sx of adult polycystic kidney disease
- cerebral "berry" aneurysms - hepatic cysts - mitral valve prolapse - colonic diverticula
26
HYPOphosphatemia causes/sx
-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
HYPERphosphatemia causes/sx
-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
chronic kidney disease sx:
- 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
pt at risk for CKD
DM, HTN, chronic NSAID use, AA/Hisp/Asian, age >60, sLE, s/p kidney transplant, fam hx
30
CKD staging
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
complications of CKD
- anemia of CD (tx w/ iron and erythropoietin if persists) - coagulopathy (platelet dysfx --> petechiae) - renal osteodystrophy (Ca/PO4 dysregulation) - metabolic acidosis
32
syndrome of inappropriate ADH (SIADH)
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
2 normal stimuli to increase ADH secretion
HYPOvolemia or HYPERosmolarity
34
etiologies for SIADH
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
diabetes insipidus
-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
2 normal stimuli to increase Aldosterone release
HYPOvolemia and/or HYPERkalemia
37
low BP --> RAAS
hypovolemia (decrease arterial volume) causes juxtaglomerular cells in kidney to release renin, activating Renin-Angiotensin-Aldosterone System --> increased aldosterone promotes Na retention
38
ADH vs aldosterone
ADH determines water homeostasis | Aldosterone determines Na+ homeostasis
39
normal serum osmolality
285 - 295
40
abnormal serum Na concentration is due to problems with
``` water control (primarily by ADH) (i.e. dehydration --> decreased free water = increased serum [Na] = hypernatremia ```
41
abnormal extracellular fluid volume size is due to problems with...
total body Na control (determines ECFV) ECFV = interstitial fluid vol and intravascular space vol (i.e. hypervolemia = inc total body Na)
42
normal serum creatinine level
1.0
43
hypertonic hyponatremia
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
isotonic hyponatremia
NOT true hyponatremia (free water normal) | -lab artifact/error due to hypertriglyceridemia or hyperproteinemia
45
hypotonic hyponatremia
TRUE hyponatremia - kidney unable to excrete free water (make dilute urine, increased ADH) - volume status gives clue to cause (hypovolemic, euvolemic, hypervolemic)
46
hypovolemic hyponatremia
- decreased volume (Na + water) and increased free water | - causes: renal volume loss (diuretics/thiazides), extrarenal volume loss like bleeding, D/V
47
euvolemic hyponatremia
- normal volume (Na + water) and increased free water | - SIADH, hypothyroidism, adrenal insufficiency, primary polydipsia (water intox), MDMA
48
hypervolemic hyponatremia
- increased volume (Na + water) AND increased free water | - edematous states: CHF, nephrotic syndrome, cirrhosis
49
hypernatremia
MC caused by net water loss | -CNS dysfunction (shrinkage of brain cells)
50
hypomagnesemia common causes
malabsorption (esp alcoholics) renal losses (diuretics) PPIs
51
hypomagnesemia symptoms
``` inc DTR tetany hypoCa (Mg needed to make parathyroid hormone) palpitations (due to associated hypoK) prolonged PR + QT interval TORSADES ```
52
hypokalemia common causes
diuretic therapy V/D metabolic alkalosis hypomagnesemia
53
hypokalemia symptoms
``` muscle weakness / rhabdo nephrogenic - polyuria dec DTR palpitations, arrhythmias T-wave flattening (early) --> prominent U wave (+/- hypomagnesemia changes) ```
54
hyperkalemia causes
- decreased renal excretion, decreased aldosterone (adrenal insufficiency) - ACEI/ARBs, digoxin, B-blockers, NSAIDs, K sparing diuretics - metabolic acidosis (DKA)
55
MC side effect of hyperparathyroidism
kidney stones (due to excess Ca)
56
most common solid renal tumor of childhood
Nephroblastoma, or Wilms tumor
57
What drug must be withheld for 48 hours after the administration of a contrast agent? (Intravascular administration of iodinated contrast media)
metformin - can result in lactic acidosis
58
MC cause of AKI in children
Hemolytic-Uremic Syndrome (E. coli 0157:H7 - shiga-like toxin, strep. pneumo, drug toxicity)
59
Hemolytic-Uremic Syndrome Triad
hemolytic anemia (schistocytes) thrombocytopenia renal insufficiency
60
renovascular HTN (renal artery stenosis)
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions