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Renal > DIT questions > Flashcards

DIT questions Flashcards

1
Q

What segment of the renal tubule reabsorbs 67% of the fluid and electrolytes filtered by the glomerulus?

A

Proximal tubule

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2
Q

What segment of the renal tubule is responsible for concentrating urine?

A

Collecting duct

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3
Q

What segment of the renal tubule is the site of secretion of organic anions and cations?

A

Proximal tubule

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4
Q

What segment of the renal tubule is always impermeable to water?

A

Thick ascending loop

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5
Q

What segment of the renal tubule is permeable to water in the presence of ADH

A

Late distal tubule and collecting duct

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6
Q

What segment of the renal tubule is the site of the Na/2Cl/K cotransporter?

A

Thick ascending limb

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7
Q

What segment of the renal tubule is the site of isotonic fluid reabsorption?

A

Proximal tubule

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8
Q

What segment of the renal tubule is responsible for diluting urine?

A

Thick ascending limb

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9
Q

What segment of the renal tubule is the only site where glucose and AA’s are reabsorbed?

A

Proximal tubule

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10
Q

What segment of the renal tubule that does water reabsorption in the Loop of Henle?

A

Thin descending limb

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11
Q

What 3 hormones or drugs act in the proximal tubule and what do they do?

A

Ang II -> stimulates apical Na+/H+ countertransporter -> puts H+ into the tubule (allows for HCO3 reabsorption via CA)

Carbonic anhydrase (CA) inhibitors: acetazolamide inhibits CA causing NaHCO3 diuresis and a metabolic acidosis

PTH: inhibits the apical Na+/phosphate cotransporter. Causes Phosphate excretion -> PTH = phosphate trashing hormone

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12
Q

What happens in the thin descending loop?

A

Concentration of urine due to passive water reabsorption while impermeable to Na+

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13
Q

What is important to know about the Thick ascending limb?

A

1) Na2ClK cotransporter
2) Impermeable to water (dilutes urine)
3) Leak back K+ channel creates + potential for paracellular reabsorption of Mg++ and Ca++

**Blocking the transporter with loop diuretics blocks the positive potential made by K+ back leak and therefore Ca++ will not get reabsorbed. LOOPS LOSE CALCIUM

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14
Q

What is important to know about the early distal tubule?

A

1) Na+/Cl- symporter
2) Impermeable to water (makes urine dilute)
3) Ca++ reabsorption controlled by PTH (stimulates the basolateral Na+/Ca++ exchanger -> pulls calcium into interstitium to create downward gradient for Ca++ to be pulled from lumen into tubule cell via Ca++ channel).

**LOOPS LOSE CALCIUM. THIAZIDES DONT

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15
Q

What determines how much water is reabsorbed in the distal tubules and collecting ducts?

A

ADH

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16
Q

What two types of intercalated cells?

A

H+ secreting and HCO3- secreting

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17
Q

What class of diuretics directly affects principle cells?

A

Potassium sparing diuretics: Aldosterone antagonists (spironolactone, eplerenone) and ENAC blockers (amiloride, triamterine)

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18
Q

What effect does aldosterone have on principle cells and intercalated cells of the collecting duct?

A

Principle cells- increases ENAC channels and stimulates the basolateral ATPase to cause Na+ reabsorption and K+ secretion.

Intercalated cells- stimulates H+ secretion

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19
Q

What drug antagonizes aldo’s action and promotes Na+ excretion and inhibits K+ excretion?

A

Spironolactone and eplerenone

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20
Q

What does ADH do besides other than its V1 and V2 receptor actions (vessel constriction and aquaporin insertion respectively)?

A

ADH also allows the very last portion of the medullary collecting duct to be permeable to urea. This allows for extreme hypertonicity of the interstitium and concentration of urine since water is also allowed to exit the distal tubule and collecting ducts to ADH.

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21
Q

What shifts potassium OUT of cells (causing hyperkalemia)?

A 
INsulin puts K+ back INTO cells so.......
DO low insulin LABB
Digitalis
hyperOsmolarity
low insulin
Lysis of cells
Acidosis
Beta Blockers
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22
Q

What shifts potassium into cells causing hypokalemia?

A

Insulin, hypo-osmolality, alkalosis, beta agonists, rapidly growing tumors

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23
Q

What are the normal ranges for pH, CO2, O2, and HCO3- in blood gas?

A

pH- 7.35-7.45
CO2- 35-45
O2- 75-105
HCO3- 22-28

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24
Q

How does acidosis/alkalosis affect extracellular K+ concentrations?

A

Acidosis -> incr H+/K+ pump -> hyperkalemia

Alkalosis -> pull K+ in and push H+ out -> hypokalemia

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25
Q

What things can cause a metabolic alkalosis?

A

Vomiting
Loop diuretics
Antacid use
Hyperaldosteronism

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26
Q

What causes a normal anion gap acidosis?

A 
HARD-ASSS
Hyperalimentation (overeating)
Addisons disease (not enough aldo)
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
Sniffing glue
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27
Q

What is the equation for anion gap? What is the normal anion gap?

A

Na+ - (Cl- + HCO3-)

This is normally 8-12

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28
Q

What causes an elevated anion gap metabolic acidosis

A 
MUCCKPPPIILESS
Methanol
Uremia
Cyanide
Carbon monoxide
Ketoacidosis (diabetic and alcoholic)
Propylene glycol 
Paraldehyde
Phenformin
Isoniazid (INH)
Iron tablets
Lactic acidosis
Ethylene glycol
Salicylates (late)
Shock
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29
Q

A patient with a recent kidney transplant on cyclosporin for immunosupression requires an antifungal agent for candidiasis. What drug would result in cyclosporin toxicity?

A

Ketoconazole (just need to know what drugs interfere with cytochrome P450. Ketoconazole inhibits p450)

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30
Q

What effect will a renal stone that obstructs the ureter have on GFR and filtration fraction?

A

decr GFR and decr FF

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31
Q

What is the maximal serum glucose concentration at which glucose can be absorbed at the tubules?

A

Start to spill at 160, transporters saturated at 350

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32
Q

What change in BMP might you expect in a young patient being treated for status asthmaticus?

A

What will they be taking for a drug? Beta agonist (like albuterol). These tend to shift potassium into cells -> hypokalemia.

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33
Q

A patient taking lisinopril complains of nmew onset, constant coughing. What medication class should this patient be switched to?

A

ARB -> Losartan or valsartan

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34
Q

A patient with heart failure exacerbation needs medical diuresis but has a sulfa allergy. What diuretic can be used?

A

Ethacrynic acid

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35
Q

A patient presents with hypertension, hypokalemia, metabolic acidosis, and low plasma renin. What is the diagnosis and how do you treat it?

A

Primary hyperaldosteronism (Konn syndrome). Give aldosterone antagonist (spironolactone or eplerenone).

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36
Q

Which diuretic is most useful? Acute pulmonary edema

A

Loop

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37
Q

Which diuretic is most useful? idiopathic hypercalciuria (-> calcium stones)

A

Thiazides (loops lose calcium into the urine, thiazides dont)

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38
Q

Which diuretic is most useful? glaucoma

A

Mannitol or acetazolamide

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39
Q

Which diuretic is most useful? mild to moderate CHF with expanded ECV

A

Loop

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40
Q

Which diuretic is most useful? in conjunction with loop or thiazide diuretics to retain K+

A

Spironolactone or other K+ sparing

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41
Q

Which diuretic is most useful? edema associated with nephrotic syndrome

A

Loop

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42
Q

Which diuretic is most useful? increased intracranial pressure

A

Mannitol

43
Q

Which diuretic is most useful? mild to moderate HTN

A

thiazide

44
Q

Which diuretic is most useful? hypercalcemia

A

Loop (loops lose calcium from the BLOOD)

45
Q

Which diuretic is most useful? altitude sickness

A

Acetazolamide

46
Q

Which diuretic is most useful? hyperaldosteronism

A

Spironolactone

47
Q

What is the equation for renal clearance of any substance?

A

Clearance = (Urine concentration x Urine flow rate) / Plasma concentration

48
Q

A 40 year old patient of yours weight 100kg. What is her estimated plasma volume?

A

60 40 20 rule. 100kg -> 60 kg body water. 40kg intracellular. 20 kg extracellular -> 3/4 (x20kg) is interstitial = 15 kg. 1/4 (x20kg) is plasma volume = 5 kg or 5L.

49
Q

What are the actions of angiotensin II?

A

1) “Tense angio” = vasoconstriction.
2) Aldosterone release from the adrenal gland (incr K+ excretion, H+ excretion, Na+ and H20 reabsorption)
3) Constrict the efferent arteriole causing increased GFR and decreased RPF = incr FF.

50
Q

What is the site of action of mannitol?

A

Proximal tubule

51
Q

what is the site of action of the thiazides?

A

Early distal tubule

52
Q

What substances can be used to estimate GFR?

A

Inulin and creatinine

53
Q

What substance can be used to estimate RPF?

A

PAH

54
Q

What is the WAGR complex

A

Wilms tumor, Aniridia (lack of an iris), Genitourinary malfomations, and retardation (MR)

55
Q

What is Beckwith-Wiedemann syndrome

A

Wilms tumor, neonatal hypoglycemia, muscular hemihypertrophy (muscles on one side of body larger than on the other side), and organomegally (esp the tongue)

56
Q

Which glomerular disease? IF: granular pattern of immune complex deposition; LM: diffuse capillary thickening

A

Membranous nephropathy

57
Q

Which glomerular disease? IF: granular pattern of immune complex deposition; LM: hypercellular glomeruli

A

Acute poststreptococcal glomerulonephritis

58
Q

Which glomerular disease? IF: linear pattern of immune complex deposition

A

Goodpastures (causes Rapidly progressive (crescentic) glomerulonephritis)

59
Q

Which glomerular disease? IF: deposition of IgG, IgM, IgA and C3 in MESANGIUM

A

IgA nephropathy (Burgers disease)

60
Q

Which glomerular disease? EM: subendothelial humps and tramtrack appearance

A

Mebrano-proliferative glomerulonephritis type I (MPGN type I)

61
Q

Which glomerular disease? Nephritis, deafness, cataracts

A

Alports syndrome

62
Q

Which glomerular disease? LM: Crescent formation in the glomeruli

A

Rapidly progressive (crescentic) glomerulonephritis (RPGN)

63
Q

Which glomerular disease? LM: segmental sclerosis and hyalinosis

A

Focal segmental glomerulosclerosis (FSGS)

64
Q

Which glomerular disease? purpura on back of arms and legs, abdominal pain, IgA nephropathy

A

Henloch Schonlein purpura

65
Q

Which glomerular disease? EM: spiking of the basement membrane due to electron dense subepithelial deposits

A

Membranous nephropathy (Gotta be a member of the spike and dome club to have a mercede’s SLE)

66
Q

What are the risk factors for transitional cell carcinoma?

A 
Pee SAC
Phenacetin (acetaminophen)
Smoking
Aniline dyes
Cyclophosphamide
67
Q

What changes will be seen in a basic metabolic panel in a patient with renal failure?

A

elevated potassium and phosphate, elevated BUN and creatinine, low calcium

68
Q

A CT scan reveals massively enlarged kidneys bilaterally. What is the diagnosis

A

Autosomal dominant polycystic kidney disease

69
Q

A CT scan reveals cysts in shrunken kidneys bilaterally. What is the diagnosis

A

Medullary cystic disease

70
Q

Which electrolyte disturbance? correcting too rapidly may result in central pontine myelinosis

A

Hyponatremia (low to high the brain will die, high to low the brain will blow)

71
Q

Which electrolyte disturbance? peaked T wave

A

Hyperkalemia

72
Q

Which electrolyte disturbance? tetany

A

Hypocalcemia

73
Q

Which electrolyte disturbance? arrhythmias

A

hypo or hyperkalemia, or low Mg++

74
Q

Which electrolyte disturbance? decreased deep tendon reflexes

A

High Mg++

75
Q

Which electrolyte disturbance? flattened T waves, U waves on EKG

A

hypokalemia

76
Q

Most common tumor of the urinary tract system?

A

Transitional cell carcinoma

77
Q

Most common renal malignancy of childhood

A

Wilms tumore

78
Q

Histological appearance of renal cell carcinoma

A

Clear cell carcinoma (polygonal clear cells)

79
Q

Histological appearance of chronic pyelonephritis

A

Eosinophilic casts (thyroidization of the kidney -> looks like the colloid in the thyroid)

80
Q

Fever + rash + hematuria + eosinophilia

A

Acute interstitial nephritis

81
Q

Cancer associated with Schistosoma haematobium

A

Squamous cell carcinoma of the bladder

82
Q

Treatment for cystine kidney stones

A

Alkalinization of the urine

83
Q

Which glomerular disease? Kimmelstiel Wilson nodules (nodular glomerulosclerosis)

A

Diabetic glomerulonephropathy

84
Q

Which glomerular disease? EM: loss of podocyte foot processes

A

Minimal change disease (could also be focal segmental glomerulosclerosis)

85
Q

Which glomerular disease? most common nephrotic syndrome in AA’s and hispanics adults?

A

Focal segmental glomerulosclerosis

86
Q

Which glomerular disease? most common nephrotic syndrome in caucasian adults?

A

Membranous nephropathy

87
Q

Which glomerular disease? nephrotic syndrome a/w Hep B

A

Membrano-proliferative glomerulonephritis type I

88
Q

Which glomerular disease? nephrotic syndrome a/w HIV

A

Focal segmental glomerulosclerosis (FSGS) -> also associated with HIV and Sickle cell

89
Q

Which glomerular disease? anti-GBM antibodies, hematuria, hemoptysis

A

Goodpastures (Rapidly progressive (crescentic) glomerulonephritis)

90
Q

Which glomerular disease? LM: Wire loop appearance

A

Diffuse proliferative glomerulonephritis

91
Q

Which glomerular disease? nephrotic syndrome with apple green birefringence with Congo red stain under polarized light

A

Amyloidosis

92
Q

When would you see RBC casts?

A

Acute glomerular nephritis

93
Q

When would you see WBC casts?

A

Classic for Acute pyelonephritis
-> can see pyuria (WBCs in the urine) with acute interstitial nephritis (AIN) but this tends to be eosinophils and not casts!!

94
Q

When would you see bacterial casts?

A

acute pyelonephritis

95
Q

When would you see epithelial cell casts?

A

renal tubular damage

96
Q

When would you see waxy casts?

A

CKD, renal failure

97
Q

When would you see fatty casts?

A

nephrotic syndrome

98
Q

When would you see granular casts?

A

Granular = muddy brown casts. Acute tubular necrosis (ATN)

99
Q

Glomerular histology reveals multiple mesangial nodules. This lesion is indicative of what disease?

A

Diabetic glomerulonephropathy (Kimmelstiel-Wilson nodules)

100
Q

A teenager preseents with nephrotic syndrome and hearing loss. What is the disease?

A

Alport’s syndrome

101
Q

A 4 year old boy presents with facial edema and proteinuria. What is the appropriate treatment?

A

If acute prostreptococcal glomerulonephritis -> will resolve spontaneously.

If minimal change disease-> give corticosteroids.

102
Q

UTI caused by proteus vulgaris. What type of renal stone is this patient at risk for?

A

AMP stone (ammonium magnesium phosphate stone) -> predisposing to staghorn calculi.

Proteus has urease that makes ammonia.

103
Q

A patient reports long term acetaminophen use. What renal pathology is she at risk for?

A

Renal papillary necrosis

104
Q

What artery prevents a horseshoe kidney from ascending in the abdomen?

A

IMA

Renal (1 decks)

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