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Flashcards in Anatomy to Micro, plus Physiology Deck (31)
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What is Winter's formula?

predicted compensatory PaCO2 = (1.5 * HCO3) + 8 +/- 2

If actual PaCO2 is greater than predicted = concurrent respiratory acidosis

If actual PaCO2 is less than predicted = concurrent respiratory alkalosis


Pt with painless hematuria, right-sided renal mass, malignant cells with chromosome 3p deletion? Associated conditions?

Renal cell carcinoma as part of Von Hippel-Lindau disease
gene deletion on chr.3 of VHL tumor suppressor (autosomal dominant)

- cerebellar hemangioblastomas
- clear cell renal carcinomas
- pheochromocytomas


What embryological structure gives rise to the glomerulus through to the distal convoluted tubule? Which gives rise to the collecting duct?

Bowman's and glomeruli to the DCT
= metaneprhic mesoderm/mesenchyme/blastema

Collecting tubules and duct, calyces, renal pelvis, and ureters
= ureteric bud / metanephric diverticulum


Where is the tubular fluid most concentrated and most dilute in the nephron in the absence of ADH?

most concentrated in the bottom of the loop of Henle (between the descending and ascending limbs)

most dilute in the collecting ducts


Mechanism of graft rejection one week after transplant? Treatment/prevention of all rejection?

Acute - host T cells activated against donor MHCs, antibodies can also be formed against donor

- calcineurin inhibitors - inhibit activation and proliferation of the Th subset of T cells by inhibiting calcineurin within these cells, leading to a failure to synthesize cytokines
- systemic corticosteroids


Ceramide trihexoside accumulation? Risk for what complication?

Fabry disease

leads to renal failure


What is Filtration Fraction (FF)? In severe hypovolemia, what is GFR, RPF, and FF?

FF = GFR / RPF (normally around 20%)

Severe hypovolemia:
- decreased RPF due to decline in circulating blood volume
- less pronounced decreased in GFR (renin activation leads to AngII-mediated constriction of the efferent glomerular arteriole to increase hydrostatic P in the glomerular capillaries to try and maintain GFR)
- FF is thus increased (low GFR / very low RPF)


What is GFR and RPF? Clearance of what molecules are used to calculate each?

GFR = volume of fluid filtered from renal glomerular capillaries into Bowman's space per unit time
Clearance of inulin (filtered but not secreted or reabsorbed) used to calculate; creatinine clearance used as an approximate measure of GFR (slightly overestimates because some secretion)

RPF = volume of plasma delivered to kidney per unit time
Clearance of PAH (filtered and secreted, but not reabsorbed)


What selectively constricts the efferent arteriole? What happens to GFR, RPF, and FF with vasoconstriction of the efferent arteriole?

Angiotensin II

GFR increases with selective vasoconstriction of the efferent arteriole due to increased hydrostatic pressure in the glom. capillaries. At very high constriction, GFR starts to decrease.

RPF decreases due to reduced flow.

FF thus increases (always increases with increasing efferent arteriole constriction).


Where in the nephron is K+ concentration in the urine regulated? What part of the nephron is responsible for most of the K+ reabsorption?

The principal and alpha-intercalated cells of the cortical collecting tubules (as well as the late distal tubule) are the primary mediators of K+ regulation!

2/3s of freely filtered K+ load is reabsored in the proximal tubule and the TAL of the loop of Henle further reabsorbs 25-30% more via the Na/K/Cl transporter.


Woman with bilateral renal masses of fat, smooth muscle, and blood vessels?

Renal angiomyolipoma,
associated with tuberous sclerosis -- autosomal dominant condition characterized by cortical tubers and subependymal hamartomas in the brain, with consequent seizures and mental retardation

Hamartomas in CNS and skin (tissue normally found at the site, but growing in a disorganized mass)
Mitral regurgitation
Ash-leaf spots
cardiac Rhabdomyoma
(Tuberous sclerosis)
autosomal dOminant
Mental retardation
renal Angiomyolipoma


Which part of the nephron is impermeable to water regardless of ADH levels?

thick and thin ascending limb
Na+/K+/Cl- transporter here reabsorbs electrolytes and contributes to the formation of the corticomedullary concentration gradient

Before the ascending limb, permeability HIGH
After the ascending limb and proximal DCT, permeability VARIABLE and dependent on ADH


How do you convert between renal blood flow (RBF) and renal plasma flow (RPF)?

RBF is the volume of blood that flows through the kidney per unit time and can be calculated by dividing RPF flow by (1 - hematocrit)


What is actively reabsorbed in the proximal tubule? What about other ions?

glucose, amino acids, and HCO3-

other ions are absorbed isotonically with water


What is furosemide and how does it work? Name two factors.

loop diuretic that works by:

1) inhibiting Na/K/2Cl transporters in the ascending limb -- blocks Na and Cl transport to result in increased Na, Cl, and fluid excretion

2) stimulates prostaglandin release (vasodilation of afferent arteriole) leading to increased renal blood flow, increased GFR, and enhanced drug delivery


What effects do NSAIDs have on loop diuretics?

NSAIDs block prostaglandin synthesis and thus result in a decreased diuretic response (prostaglandins normally increase blood flow and enhance drug delivery)


120 out of 400 with ACE inhibitor has acute coronary event.
100 out of 300 without ACE inhibitor has acute coronary event.

Relative risk?

risk of developing disease in exposed group divided by risk in the unexposed group
typically used in cohort studies

(120/400) / (100/300)

Construct a 2x2 table! (x-axis: event vs. no event; y-axis: tx vs. no tx)
Relative risk = [a/(a+b)] / [c/(c+d)]


Constriction of what vessel leads to decreased RPF and increased FF?

efferent arteriole constriction

impedes blood flow through the kidney = decreased RPF
increases glomerular capillary hydrostatic pressure as fluid backs up = increased GFR -> increased FF


What is hyperacute rejection? What type of hypersensitivity reaction is it?

happens within minutes with preformed recipient antibodies reacting to antigens on donor organ
Type II hypersensitivity


Where in the nephron is fluid most dilute (100-110mOsm/L)?

Distal convoluted tubule


Pt in DKA - what are his pH, HCO3-, and H2PO4- levels in urine?

pH low (acidosis)
HCO3- low (increased recycling, decreased secretion)
H2PO4- high (acid excretion in urine in the form of titratable acids)

Limit to the amount of free H+ that can be excreted in urine, so H2PO4- and NH4+ also excreted.


Two effects of Vasopressin acting on V2 receptor (regulation of serum osmolarity)?

permeability to water AND urea at medullary collecting duct

1) increases number of aquaporins in principal cells of collecting duct
2) increases number of passive urea transporters int he inner medullary collecting duct, allowing a substantial fraction of high concentrated urea to diffuse down its concentration gradient into the medullary interstitium (enhances water-absorbing capacity of the nephron)


9yo with red urine, periorbital edema, mild pedal edema. History of asthma, atopic dermatitis, and recently treated for impetigo. Type of hypersensitivity, and mechanism?

Post-Streptococcal glomerulonephritis
Type III hypersensitivity
immune complex deposition in glomerular BM


Salicylate/aspirin intoxication - acid/base disturbances?

1) FIRST causes an acute respiratory alkalosis
Directly stimulate medullary respiratory center resulting in hyperventilation, increased loss of CO2, and respiratory alkalosis

2) Few hours later, anion gap metabolic acidosis due to organic acid accumulation

Mixed acid-base disturbance that can result in normal or close to normal pH


What are the findings in secondary hyperaldosteronism? What are potential causes?

high renin, high aldosterone

potential causes:
- renal artery stenosis
- diuretic use
- malignant HTN
- renin-secreting tumors (rare, small, solitary, benign juxtaglomerular cell neoplasms; strongly considered in pts with marked hyperreninemia and HTN who clearly do not have renovascular disease)


Where does the majority of free water absorption take place in the nephron?

Regardless of hydration status, majority of free water reabsorption in the nephron occurs in the proximal tubule passively with the reabsorption of solutes.


PAH: Can filtration be saturated? Can secretion be saturated?

Filtration is not a process that can be saturated.

Secretion of PAH is a carrier enzyme-mediated process and therefore is able to be saturated.


How to calculate GFR from creatinine urine and serum concentration?

(urine concentration x urine flow) / serum concentration


Pt with end stage renal disease, diabetes, HTN - ESRD puts her at greatest risk for?


Renal failure:
- decreased synthesis of active vitD
- retention of phosphorous (binds calcium and exacerbates hypocalcemia; complexes also deposit in various organs)

Hypocalcemia and hyperphosphatemia can cause secondary hyperparathyroidism -- PTH increases bone turnover and cause cause resorptive bone lesions (osteitis fibrosa cystica)


What happens to calcium levels in renal failure? Phosphate levels?
What is osteitis fibrosa cystica?

Low calcium (low vitaminD)
High phosphate (increased retention)

Osteitis fibrosa cystica - high bone turnover rate seen in hyperparathyroidism (can be due to ESRD)