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Renal Cram Deck > Additional Cards > Flashcards

Additional Cards Flashcards

1
Q

Which syndrome is most correlated with Hep C

A

MPGN

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2
Q

Difference between HCO3 movement in PT and TAL

A

PT - basolateral membrane has a HCO3 Cl symporter

TAL - HCO3 and Cl transporter is an exchanger

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3
Q

Say whether the following stimulate or reduce bicarbonate reabsorption/acid excretion: aldosterone/AII, volume expansion, hypokalemia

A

Aldosterone/AII = stimulates acid excretion
Volume expansion = reduces acid excretion
Hypokalemia = stimulates acid excretion

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4
Q

Winter’s formula

A

pCO2 = (1.5*HCO3) + 8

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5
Q

An acute change in pCO2 of 10 should align with a pH change of:

A

0.08

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6
Q

How to get the proteinuria in a day

A

Divide urine protein by urine creatinine -> g/day

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7
Q

Creatinine clearance equation

A

UcrV/Pcr

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8
Q

What is a middle-of-the-road specific gravity

A

1.010 - 1.015 -> 250-300 serum osm

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9
Q

Two main ethical principles that come up in transplant

A

Truth-telling for the blameless medical excuse

Non-maleficence for the harm you are inflicting on the living donor

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10
Q

Main things that cause a metabolic acidosis through loss of bicarbonate

A

Diarrhea, and proximal (Type II) RTA

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11
Q

Main mechanisms of metabolic acidosis that do not include losing bicarbonate

A

Kidneys not excreting acid - CKD, distal RTA (Type I, which can lead to kidney stones)
H+ intoxication
Lactic or ketoacidosis

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12
Q

What DURHAM stands for

A 
Diarrhea
Ureteral diversions
RTA (Type 2/proximal)
Hypocapnia
Acetazolamide/Ampho B
Mineralocorticoid deficiency (RTA Type 4)
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13
Q

What offsets what in different types of metabolic acidosis (if just one)

A

Elevated anion gap -> bicarbonate is smaller and unmeasured anion is larger in equal amount

Non-elevated -> bicarbonate smaller and chloride higher to compensate

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14
Q

What is a normal body temperature in Celcius

A

36.1-37.2

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15
Q

Main types of RTA

A
  • Type II first - proximal - patient not fully reclaiming all the bicarbonate -> so you have a systemic acidosis. Common causes are multiple myeloma and medications. Hypokalemia.
  • Type I - distal - defect in pumping out hydrogen effectively - also going to make you acidotic. Hypokalemia
  • Type IV RTA - systemic acidosis with hyperkalemia - not enough aldosterone - diabetic patients
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16
Q

Definition of high value prescribing

A

providing simplest medication regimen that minimizes physical and financial risk while achieving the best outcome

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17
Q

How to decrease out of pocket costs for prescribing

A

“GOT MeDS”
GENERICS: prescribe when possible; educate patients on safety/efficacy
ORDERING IN BULK: 3-month supplies of drugs from pharmacy or by mail
THERAPEUTIC ALTERNATIVES: OTC meds; cheaper meds in same class
MEDICATION REVIEW: regularly review med list; remove unnecessary meds
DISCOUNT DRUGS: $4 drugs (Walmart, Target, etc); discount cards
SPLITTING PILLS: prescribe higher dose and advise patients to split pills

18
Q

Difference between tonicity and osmolality

A

Tonicity excludes ineffective osmols, while osmolality includes them

19
Q

Listed approach to hyponatremia and treatment decision criteria

A

1) Osmolar status (2Na + Gl/18 + BUN/2.8)
2) volume status (clinical)
3) ADH present (Uosm > 100)
4) ADH appropriate (yes if serum osm high, secondarily low effective circ volume)
5) Treatment:
Volume depletion -> Saline
Hypoosmolarity with euvolemia or hypervolemia -> water restriction
Other things to do with hypervolemia -> diuretic
If having symptoms -> hypotonic saline

20
Q

Speed to increase SNa

A

Not more than 8 Meq/L/day

21
Q

What urine osm can tell you about hypernatremia

A

If low - DI

If high - likely losing more water through insensible losses and GI than you are taking in (decreased H20 intake)

22
Q

Main categories of hypertonic hypernatremia

A
  • Hypertonic Na gain (drinking sea water)
  • Polyuric (increase in clearance of free water) - solute diuresis (glucose) or pure H20 diuresis (DI)
  • non-polyuric (decrease in clearance of free water) - hypodipsia, fever, sweating, GI losses
23
Q

Differences between solute and water diuresis

A

Solute diuresis starts with a high Uosm at a low flow rate, and gets lower as it speeds up because there is less time to reabsorb water - end at about 300-350 uOsm

Water diuresis starts low and gets higher as urine flow speeds up because there is less time to remove solutes - ends at about 150-200

24
Q

Postural/orthostatic proteinuria

A

Proteinuria in upright position but not supine, more common in adolescents

25
Q

Isolated proteinuria

A

Without hematuria or reduction in GFR

26
Q

Glomerular vs. tubular proteinuira

A

Glomerular is often albumin
Tubular is excretion of low molecular weight proteins due to damage to tubules - might see low albumin-creatinine ratio with high protein-creatinine ratio

27
Q

Overflow proteinuria

A

Due to overproduction of immunoglobulin light chains in multiple myeloma. Increased excretion of low molecular weight proteins.

28
Q

Post-renal proteinuria

A

inflammation in urinary tract

29
Q

Prevalence of CKD

A

14%/30 million, mostly stage 1-3

30
Q

What gov’t vs. private usually funds for types of research

A

NIH - basic

Private - clinical

31
Q

Exclusivity lengths of drugs

A

Exclusivity - period of time when brand-name drugs are protected from generic drug competition. Granted once the drug is approved.
New chemical entity exclusivity - 5 year exclusivity for drug with new active moiety
Orphan drug exclusivity - 7 year exclusivity for a drug that treats a disease/condition that affects less than 200,000 people in the US. incentive to make a new drug for rare conditions.
New clinical investigation exclusivity - 3 year exclusivity added in certain circumstances when brand name drug is already approved (i.e. found new way of delivering active ingredient. Tablet form instead of liquid).
Biologics get 12 year exclusivity before biosimilars can enter
Even with patents/exclusivity, entities can license for drugs to be manufactured by other companies

32
Q

What does APOL1 Gene do

A

The APOL1 gene has been linked to increased risk of non-diabetic CKD and ESRD development among patients with West African ancestry.

33
Q

Names of different regions of abdomen

A
34
Q

Where the kidneys, ureters, bladder, and urethra derive from

A

Kidneys and ureter - intermediate mesoderm

Bladder and urethra - endoderm

35
Q

The two mains parts of the kidney coming from the intermediate mesoderm

A

Excretory portion of kidney: metanephros -> metanephric blastema -> nephron tubules

Collecting portions of kidney/ureters: mesonephric duct -> ureteric bud

36
Q

Pronephros vs. mesonephros vs. metanephros

A

Pronephros: most cranial, 3-4 weeks, vestigial/regress completely

Mesonephros - develop caudally, briefly functional and then degrade by week 8. Mesonephric duct just caudal becomes the ureteric bud though.

Metanephros - start around week 5 and continue, the “true kidneys”

37
Q

Renal agenisis

A

No formation of kidney, usually associated with oligohydraminos (too little amniotic fluid

38
Q

How the bladder develops

A

Endoderm-derived cloaca -> divides into rectum and urogenital sinus (separated by urorectal septum, which is mesoderm derived)

39
Q

Exstrophy of the bladder

A

Bladder develops outside of fetus because of thin cloacal membrane

40
Q

Allantosis and issues it may cause

A

It is a connection from the gut to support tissues of the embryo. It degenerates to form the urachus (permanent fibrous cord). It’s lumen may persist as a cyst, sinus, or fistula.

41
Q

Metanephric diverticulum

A

Also known as ureteric bud, comes off of the mesonephric duct

Renal Cram Deck (24 decks)

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