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DIT questions Flashcards

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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
What things can cause a metabolic alkalosis?
Vomiting Loop diuretics Antacid use Hyperaldosteronism
26
What causes a normal anion gap acidosis?
``` HARD-ASSS Hyperalimentation (overeating) Addisons disease (not enough aldo) Renal tubular acidosis Diarrhea Acetazolamide Spironolactone Saline infusion Sniffing glue ```
27
What is the equation for anion gap? What is the normal anion gap?
Na+ - (Cl- + HCO3-) | This is normally 8-12
28
What causes an elevated anion gap metabolic acidosis
``` 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 ```
29
A patient with a recent kidney transplant on cyclosporin for immunosupression requires an antifungal agent for candidiasis. What drug would result in cyclosporin toxicity?
Ketoconazole (just need to know what drugs interfere with cytochrome P450. Ketoconazole inhibits p450)
30
What effect will a renal stone that obstructs the ureter have on GFR and filtration fraction?
decr GFR and decr FF
31
What is the maximal serum glucose concentration at which glucose can be absorbed at the tubules?
Start to spill at 160, transporters saturated at 350
32
What change in BMP might you expect in a young patient being treated for status asthmaticus?
What will they be taking for a drug? Beta agonist (like albuterol). These tend to shift potassium into cells -> hypokalemia.
33
A patient taking lisinopril complains of nmew onset, constant coughing. What medication class should this patient be switched to?
ARB -> Losartan or valsartan
34
A patient with heart failure exacerbation needs medical diuresis but has a sulfa allergy. What diuretic can be used?
Ethacrynic acid
35
A patient presents with hypertension, hypokalemia, metabolic acidosis, and low plasma renin. What is the diagnosis and how do you treat it?
Primary hyperaldosteronism (Konn syndrome). Give aldosterone antagonist (spironolactone or eplerenone).
36
Which diuretic is most useful? Acute pulmonary edema
Loop
37
Which diuretic is most useful? idiopathic hypercalciuria (-> calcium stones)
Thiazides (loops lose calcium into the urine, thiazides dont)
38
Which diuretic is most useful? glaucoma
Mannitol or acetazolamide
39
Which diuretic is most useful? mild to moderate CHF with expanded ECV
Loop
40
Which diuretic is most useful? in conjunction with loop or thiazide diuretics to retain K+
Spironolactone or other K+ sparing
41
Which diuretic is most useful? edema associated with nephrotic syndrome
Loop
42
Which diuretic is most useful? increased intracranial pressure
Mannitol
43
Which diuretic is most useful? mild to moderate HTN
thiazide
44
Which diuretic is most useful? hypercalcemia
Loop (loops lose calcium from the BLOOD)
45
Which diuretic is most useful? altitude sickness
Acetazolamide
46
Which diuretic is most useful? hyperaldosteronism
Spironolactone
47
What is the equation for renal clearance of any substance?
Clearance = (Urine concentration x Urine flow rate) / Plasma concentration
48
A 40 year old patient of yours weight 100kg. What is her estimated plasma volume?
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
What are the actions of angiotensin II?
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
What is the site of action of mannitol?
Proximal tubule
51
what is the site of action of the thiazides?
Early distal tubule
52
What substances can be used to estimate GFR?
Inulin and creatinine
53
What substance can be used to estimate RPF?
PAH
54
What is the WAGR complex
Wilms tumor, Aniridia (lack of an iris), Genitourinary malfomations, and retardation (MR)
55
What is Beckwith-Wiedemann syndrome
Wilms tumor, neonatal hypoglycemia, muscular hemihypertrophy (muscles on one side of body larger than on the other side), and organomegally (esp the tongue)
56
Which glomerular disease? IF: granular pattern of immune complex deposition; LM: diffuse capillary thickening
Membranous nephropathy
57
Which glomerular disease? IF: granular pattern of immune complex deposition; LM: hypercellular glomeruli
Acute poststreptococcal glomerulonephritis
58
Which glomerular disease? IF: linear pattern of immune complex deposition
Goodpastures (causes Rapidly progressive (crescentic) glomerulonephritis)
59
Which glomerular disease? IF: deposition of IgG, IgM, IgA and C3 in MESANGIUM
IgA nephropathy (Burgers disease)
60
Which glomerular disease? EM: subendothelial humps and tramtrack appearance
Mebrano-proliferative glomerulonephritis type I (MPGN type I)
61
Which glomerular disease? Nephritis, deafness, cataracts
Alports syndrome
62
Which glomerular disease? LM: Crescent formation in the glomeruli
Rapidly progressive (crescentic) glomerulonephritis (RPGN)
63
Which glomerular disease? LM: segmental sclerosis and hyalinosis
Focal segmental glomerulosclerosis (FSGS)
64
Which glomerular disease? purpura on back of arms and legs, abdominal pain, IgA nephropathy
Henloch Schonlein purpura
65
Which glomerular disease? EM: spiking of the basement membrane due to electron dense subepithelial deposits
Membranous nephropathy (Gotta be a member of the spike and dome club to have a mercede's SLE)
66
What are the risk factors for transitional cell carcinoma?
``` Pee SAC Phenacetin (acetaminophen) Smoking Aniline dyes Cyclophosphamide ```
67
What changes will be seen in a basic metabolic panel in a patient with renal failure?
elevated potassium and phosphate, elevated BUN and creatinine, low calcium
68
A CT scan reveals massively enlarged kidneys bilaterally. What is the diagnosis
Autosomal dominant polycystic kidney disease
69
A CT scan reveals cysts in shrunken kidneys bilaterally. What is the diagnosis
Medullary cystic disease
70
Which electrolyte disturbance? correcting too rapidly may result in central pontine myelinosis
Hyponatremia (low to high the brain will die, high to low the brain will blow)
71
Which electrolyte disturbance? peaked T wave
Hyperkalemia
72
Which electrolyte disturbance? tetany
Hypocalcemia
73
Which electrolyte disturbance? arrhythmias
hypo or hyperkalemia, or low Mg++
74
Which electrolyte disturbance? decreased deep tendon reflexes
High Mg++
75
Which electrolyte disturbance? flattened T waves, U waves on EKG
hypokalemia
76
Most common tumor of the urinary tract system?
Transitional cell carcinoma
77
Most common renal malignancy of childhood
Wilms tumore
78
Histological appearance of renal cell carcinoma
Clear cell carcinoma (polygonal clear cells)
79
Histological appearance of chronic pyelonephritis
Eosinophilic casts (thyroidization of the kidney -> looks like the colloid in the thyroid)
80
Fever + rash + hematuria + eosinophilia
Acute interstitial nephritis
81
Cancer associated with Schistosoma haematobium
Squamous cell carcinoma of the bladder
82
Treatment for cystine kidney stones
Alkalinization of the urine
83
Which glomerular disease? Kimmelstiel Wilson nodules (nodular glomerulosclerosis)
Diabetic glomerulonephropathy
84
Which glomerular disease? EM: loss of podocyte foot processes
Minimal change disease (could also be focal segmental glomerulosclerosis)
85
Which glomerular disease? most common nephrotic syndrome in AA's and hispanics adults?
Focal segmental glomerulosclerosis
86
Which glomerular disease? most common nephrotic syndrome in caucasian adults?
Membranous nephropathy
87
Which glomerular disease? nephrotic syndrome a/w Hep B
Membrano-proliferative glomerulonephritis type I
88
Which glomerular disease? nephrotic syndrome a/w HIV
Focal segmental glomerulosclerosis (FSGS) -> also associated with HIV and Sickle cell
89
Which glomerular disease? anti-GBM antibodies, hematuria, hemoptysis
Goodpastures (Rapidly progressive (crescentic) glomerulonephritis)
90
Which glomerular disease? LM: Wire loop appearance
Diffuse proliferative glomerulonephritis
91
Which glomerular disease? nephrotic syndrome with apple green birefringence with Congo red stain under polarized light
Amyloidosis
92
When would you see RBC casts?
Acute glomerular nephritis
93
When would you see WBC casts?
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
When would you see bacterial casts?
acute pyelonephritis
95
When would you see epithelial cell casts?
renal tubular damage
96
When would you see waxy casts?
CKD, renal failure
97
When would you see fatty casts?
nephrotic syndrome
98
When would you see granular casts?
Granular = muddy brown casts. Acute tubular necrosis (ATN)
99
Glomerular histology reveals multiple mesangial nodules. This lesion is indicative of what disease?
Diabetic glomerulonephropathy (Kimmelstiel-Wilson nodules)
100
A teenager preseents with nephrotic syndrome and hearing loss. What is the disease?
Alport's syndrome
101
A 4 year old boy presents with facial edema and proteinuria. What is the appropriate treatment?
If acute prostreptococcal glomerulonephritis -> will resolve spontaneously. If minimal change disease-> give corticosteroids.
102
UTI caused by proteus vulgaris. What type of renal stone is this patient at risk for?
AMP stone (ammonium magnesium phosphate stone) -> predisposing to staghorn calculi. Proteus has urease that makes ammonia.
103
A patient reports long term acetaminophen use. What renal pathology is she at risk for?
Renal papillary necrosis
104
What artery prevents a horseshoe kidney from ascending in the abdomen?
IMA

Renal (1 decks)

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