Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Step 1 > Renal > Flashcards

Renal Flashcards

1
Q

Loop Diuretics (4 names)

A

Furosemide, torsemide, bumetanide, ethacrynic acid

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

Loop diuretics MOA

A

Inhibits Na-K-2Cl cotransporter in thick ascending LOH. This process is critical for maintenance of corticomedullary concentration gradient. As a result, they cannot maximally concentrate urine and those lose substantial salt and water in urine

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

Loop diuretics electrolyte abnormalities

A

HypoK
Metabolic alkalosis
Hypocalcemia

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

Loop diuretic clinical indications

A

volume overloaded states

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

Thiazide diuretics (4 names)

A

HCTZ
Chlorthalidone
Indapamide
Metolazone

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

Thiazide MOA

A

Inhibits Na-Cl cotransporter in early DCT. Have a normal corticomedullary concentration gradient and thus are able better to retain free water in response to increased ADH levels - thus they are more likely to develop hypoNa

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

Thiazide electrolyte abnormalities

A

HYPONATREMIA*
HypoK
Met alk
HYPERCAL

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

Thiazide clinical indications

A

HTN

Calcium nephrolithiasis prophylaxis

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

Carbonic anhydrase inhibitors (1 name)

A

Acetazolamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Acetazolamide MOA

A

inhibits carbonic anhydrase in PCT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Acetazolamide electrolyte abnormalities

A

HypoK

MET ACID

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

Acetazolamide indications

A

refractory metabolic alkalosis

intracranial HTN

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

Sodium channel blockers (2 names)

A

Amiloride

Triamterene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Sodium channel blockers MOA

A

Inhibits apical ENaC channel in cortical collecting duct

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

Sodium channel blocker electrolyte abnormalities

A

HyperK

Metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Indication for Na channel blockers

A

synergy w/ loop & thiazide diuretics to limit potassium loss

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

Mineralocorticoid receptor antagonists (2 names)

A

Spirinolactone

Eplenerone

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

Mineralocorticoid rec antag MOA

A

Inhibits apical ENaC channel and basolateral Na-K-ATPase pump in cortical collecting tubules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Mineralocorticoid electrolyte disturbances

A

HyperK

Met acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Mineralocorticoid receptor antag indications

A

synergy w/ loop and thiazide to limit potassium loss.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Why do thiazide and loop diuretics cause hypokalemia and metabolic alkalosis?

A

RAAS initiated due to decreased Na delivery at macula dense, which activates RAAS. Aldo then acts on collecting duct to enhance reabsorption, and promote K+ and H+ loss.

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

Chronic transplant rejection biopsy

A

Fibrous intimal thickening

consequent renal ischemia causes tubular atrophy and interstitial fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Acute cellular rejection of renal allograft

A

Dense interstitial mononuclear infiltrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

When do crescents form on biopsy?

A

mainly anti-GBM (and goodpstures), ANCA associated, or immune complex mediated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

hyper acute rejection on biopsy

A

vascular fibrinoid necrosis and neutrophil infiltration of arterioles, glomeruli, and peritubular capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

severe toxicity of mannitol?

A

pulmonary edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Primary mediators of K+ regulation

A

principal and alpha intercalated cells in late distal and cortical collecting tubule

28
Q

EPO side effect

A

hypertension, also increased risk for thromboembolic events

29
Q

What’s the difference in presentation between Wegners versus good pastures?

A

Both have hemoptysis and renal involvement; however, weg also has NASOPHARYNX (e.g., hx of sinusitis) involvement.
Also, c-ANCA w/ no IF in wegners
linear IF in goodpastures

30
Q

how to tell difference between Churgg Strauss and Microscopic polyangiitis?

A

Both have pauci immune IF, both are p-ANCA positive

CS: asthma, granulomatous inflammation, eosinophilia

31
Q

Major SE of loop diuretics

A

hypo, hypoMg, hypoCa, ototoxicity

32
Q

Major SE of thiazides

A

HypoK, hypoNa, Hyperuricemia, hyperCa

33
Q

Major SE of K+ sparing diuretics

A

hyperK

Spironolactone: gynecomastia, antiandrogen effects

34
Q

Major SE of carbonic anhydrase inhibitors

A

metabolic acidosis

35
Q

Major SE of osmotic diuretics

A

HyperNa, pulmonary edema

36
Q

Presenting signs of hyperaldo (Conn’s)

A

HTN, hypoK, metabolic alkalosis, decreased renin activity.
Aldo causes resorption of sodium and water and K wasting and H wasting at distal nephron. Renin is suppressed. First line drugs are spironolactone and eplenerone – these are Aldo antagonists

37
Q

Where is most water reabsorbed in nephron?

A

60% reads in PCT, regardless of hydration status.

38
Q

What are calcineurin inhibitors?

A

Tacrolimus, cyclosporine. Given to prevent T cells from responding to transplant and causing acute transplant rxn

39
Q

What can cause nephrotoxicity w/ calcineurin inhibitors

A

Grapefruit juice! Anything that inhibits the CYP450 enzymes in the liver or brush border of the intestine.

40
Q

Type III hypersensitivity rxn

A

immune complex mediated (like in PSGN)

41
Q

Type II hypersensitivity reaction

A

Cytotoxic (Autoantibodies), ex: goodpastures

42
Q

Type I hypersensitivity

A

Mast cells and basophils (immediate reaction), they are coated by IgE molecules which cross link upon antigen exposure and trigger release of histamine and other mediators

43
Q

Type IV reaction

A

Delayed type. Mediated by macrophages and cytotoxic T cells. Stimulated by helper Ts leading to localized inflammation, cellular destruction, and granuloma formation

44
Q

Where is lowest pH in nephron?

A

distal tubules and collecting ducts; you may see urate crystals form here

45
Q

Vasopressin (ADH) affect on urea

A

Cortical collecting duct is impermeable to urea, but vasopressin activates urea transporters in the MEDULLARY CD, increasing reabsorption and decreasing renal clearance. This significantly increases the medullary osmotic gradient which allows for production of maximally concentrated urine.

46
Q

which substance do you use to calculate GFR?

A

Inulin or creatinine clearance

Clearance = Ux * Urine flow rate / Px

47
Q

What substance do you use to measure RPF?

A

PAH

48
Q

Most common antiphospholipid antibodies

A

Lupus anticoagulant and anticardiolipin Ab

49
Q

Foscarnet

A

Antiviral, it’s an analog of pyrophosphate, Used to treat ganciclovir-resistant CMV infections. It can chelate calcium, cand cause renal wasting of Mg leading to hypocalcemia and hypomagnesemia
Can promote SEIZURES

50
Q

Cidofovir

A

Can be used for CMV retinitis - can cause nephrotoxicity

51
Q

what parts of the nephron are particularly susceptible to ischemia

A

late portion of DCT and thick ascending LOH. These are in renal medulla, are metabolically active

52
Q

Type I RTA (info and causes)

A

Urine pH >5.5
Alpha intercalated cells can’t secrete H+
HypoK
Increased risk CaPO3 renal stones (from high pH and bone turnover)
Causes: amphotericin too, analgesic nephropathy, congenital deformities of urinary tract

53
Q

Type II RTA

A

Proximal - defect in PCT bicarb reabs
hypoK, increased risk of RICKETS
urine pH <5.5 acidified by alpha intercalated cells
Causes: Fanconi, acetazolamide (carbonic anhydrase inhibitors)

54
Q

Type IV RTA

A

Hyperkalemic, hyperchloremic; from hyperaldo
Urine pH <5.5
Decreased NH3 synth in PCT, so decreased NH4 excretion
Causes: low Aldo, Aldo resistance, bacterium, ACE I/ArBs, NSAIDS< heparin, cyclosporine, adrenal insufficiency

55
Q

chloride responsive metabolic alkalosis

A
  1. Gastric fluid loss (eg, vomiting, NG drainage)
  2. Volume contraction (eg, secondary to loop or thiazide diuretics)
  3. Congenital chloride diarrhea
  4. Posthypercapnia syndrome (especially in mechanically ventilated patients with chronic lung disease)
  5. Cystic fibrosis (in toddlers)
56
Q

chloride resistant metabolic alkalosis

A
  1. Primary aldosteronism
  2. Bartter syndrome (renal sodium, potassium, and chloride wasting; often presents as failure to thrive)
  3. DOC excess syndrome (congenital adrenal hyperplasia variant)
  4. Liddle syndrome (autosomal dominant; unregulated sodium resorption in renal collecting duct)
  5. Excessive ingestion of licorice
  6. Chronic potassium depletion (eg, anorexia nervosa)
  7. Primary reninism
  8. Hyperglucocorticoidism
  9. Milk-alkali syndrome (excess calcium plus bicarbonate intake and vomiting)
57
Q

What is chloride RESPONSIVE met alk?

A 
In chloride(saline) responsive metabolic alkalosis, you initally loose both your acid and volume (eg. vomiting) 
Losing your volume will activate your normal kidney to reabsorb NaCl and water in an effort to preserve your volume. Therefore urinary Cl will be low (<10~20 mEq/L)
58
Q

oxalatee crystals in urine?

A

ethylene glycol

59
Q

what can you do to prevent kidney damage in tumor lysis?

A

pretreat w/ alopurinol; to prevent urate in kidney

60
Q

causes of renal papillary necrosis

A 
SAAD "papa" - 
Sickle cell
Acute Pyelo
Analgesic abuse (can progress from AIN)
DM
61
Q

Causes of nephrotic syndrome (5)

A
  1. Minimal change (kids, give steroids)
  2. FSGS (mcc in hispanics and AAs)
  3. Membranous nephropaty (caucasian adults; esp SLE)
  4. MPGN (mesangium prolifs and cuts deposit in 1/2 = tram track”
  5. Diabetic glomerulonephropathy
  6. Amyloidosis
    (1&2 = foot process probs)
    (3&4 = immune complex dep)
    (5&6 = systemic)
62
Q

Transitional cell carcinoma (aka urothelial carcinoma)

A

mc tumor of UT system (calyces, pelvis, ureters, and bladder)
P/w painless hematuria (no casts)
“Pee SAC”: Phenacetin, smoking , aniline dyes, and cyclophosamide

Two routes:

1) Papillary (low grade –> HG –> invasive)
2) Flat (HG–> invasive) assoc w/ early p53 mutation

63
Q

risks for bladder squamous cell

A

sdchistosoma, chronic cystitis, smoking, chronic kidney stones
p/w painless hematuria

64
Q

diffuse cortical necrosis

A

acute generalized infarct of both kidneys. likely 2/2 vasospasm and DIC
assoc w/ obstetric catastrophes (abruption) and septic shock

65
Q

adenocarcinoma of urinary tract

A

proliferation of glandular tissue - since there is no glandular tissue of bladder, arises from:

1) urachal remnant
2) cystitis glandularis (columnar metaplasia)
3) exstrophy: congenital failure to form caudal anterior abdomaial bladder wall

Step 1 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions