First Aid: Behavioral Science/ Renal Flashcards
What does a cross sectional test tell you?
Cross sectional study = observational study that looks at group of ppl at a particular point in time (one point in time, not longitudinal)
- can give disease prevalence
- can tell you associated risk factors, but not causality
Is a cohort study prospective or retrospective?
(a) Result
Cohort study can be either prospective (take exposure and look forward to see who has disease) or retrospective (take disease and look back to see who had exposure)
-compares group w/ exposure vs. w/o exposure
(a) Relative risk
ex: Prospective asks who will develop disease, retrospective asks who developed the disease
Which of the 4 core ethical principles do the following protect
(a) Informed consent
(b) Triage
(c) Confidentiality
4 core ethical principles: autonomy, beneficence (what’s in the pt’s best interest), nonmalificence (do no harm), justice (fair and equitable)
(a) Informed consent to respect the pt’s ability to chose = autonomy
(b) Triage = justice, fairness
(c) Confidentiality = autonomy
Explain sensitivity vs. specificity
Sensitivity = true positive rate = probability that test will be positive in a pt w/ the disease
SNNOUT- negative result rules out disease
Specificity = true negative rate = probability that test will be negative in pt w/o the disease
SPPIN- positive result rules disease in
Differentiate the 4 phases of a clinical trial?
Clinical trial phases
I- small group of healthy subjects to assess safety
II- small group of diseased subjects to assess efficacy/dosing/side effects
III- large group of randomly assigned pts to compare tx to standard of care
IV- postmarket surveillance after approval to assess for rare or long term side effects
Is a case control study prospective or retrospective?
(a) Result
Case control = observational study that is retrospective (looking back) comparing group of ppl w/ disease to group of ppl w/o
-to look at prior exposure to a risk factor
(a) Odds ratio
ex: pts w/ COPD had a higher odds of a history of smoking than those w/o COPD
- take disease (COPD) and look back at RF (smoking)
Define low birth wt
(a) Associated conditions
Low birth wt = under 2500 g
(a) Neonatal respiratory distress, necrotizing enterocolitis, interventricular hemorrhage
Which: positive predictive value or sensitivity/specificity- are fixed properties of a test
Sensitivity/specificity are fixed properties of a test
-while PPV and NPV vary depending on the disease prevalence
Name the 5 components of the APGAR score
APGAR score: (get 2 pts for each) appearance pulses grimace activity respiration
Differentiate incidence and prevalence
Incidence = over a period of time
Prevalence = current cases at a single point in time
Which observational study gives you
(a) Odds ratio
(b) Relative risk
Observation study that gives
(a) Odds ratio = case control = retrospective study comparing group w/ and w/o disease
(b) Relative risk = cohort study = compares group w/ and w/o given exposure
Describe number needed to treat
(a) Formula
NNT = number of pts who need to be treated for one patient to benefit
(a) NNT = 1 / ARR
- ARR = absolute risk reduction (difference in risk attributable to the intervention)
Ex: Flu vaccine: 2% who get vaccine get the flu, 8% who don’t develop flu
ARR = 8-2 = 6%
NNT = 1/6
Differentiate primary, secondary, and tertiary prevention
(a) Give example of each
Primary prevention = prevent disease before it occurs
(a) Gardasil (HPV) vaccine
Secondary prevention = preventing morbidity after pt has clinical disease, catch and treat early
(a) Pap smear screening
Tertiary = preventing symptoms from already apparent clinical disease, reduce disability from disease
(a) Chemotherapy for diagnosed cancer
Differentiate null and alternative hypothesis
H0 (null) hypothesis = no association btwn variables
H1 (alternative) hypothesis = association exists
Is a sensitive or specific test better as a screening test?
As a screening test you want a sensitive test b/c high sensitivity means high false negative rate (you won’t miss ppl)
Examples of when confidentiality can be broken
- reportable diseases (STI, TB, hepatitis, food poisoning): physician warns public officials who can then warn ppl at risk
- Tarasoff decision = physicians required to inform and protect potential victims
- child/elder abuse
- suicidal/homicidal pts
Differentiate statistical tests
(a) T-test
(b) ANOVA
(c) Chi squares
Statsssss
(a) T-test compares the means of two groups
(b) ANOVA compares the means of 3 or more groups = analysis of variance (called by UWORLD…poopheads)
(c) Chi-squared compares the percentage or proportions (not the mean) of two or more groups
ex: Comparing the percent of members of 3 different ethnic groups who have essential HTN (not comparing the numbers of BP, just the proportion of population w/ HTN)
Explain PPV vs. NPV
PPV = probability of pt having disease is test is positive
NPV = probability of pt being disease free if a test is negative
Give the term for the following
(a) True negative rate of a test
(b) True positive rate of a test
(a) True negative rate = specificity = probability that test will be negative given pt is disease free
(b) True positive rate = sensitivity = probability that test will positive in pt w/ disease
Ex] Study showed 21% of smokers developed lung cancer while only 1% of non-smokers developed LC
(a) What is the relative risk?
(b) What is the attributable risk?
(a) Relative risk = 21/1 = 21, risk of developing disease in exposed group / risk in unexposed group
(b) Attributable risk = 21 - 1 = 21, proportion of disease attributable to the exposure
Formula for
(a) Sensitivity
(b) Specificity
based on the classic 2x2 table
(a) Sensitivity (true positive rate) = (TP) / (TP + FN)
- probability test will detect disease when disease is present
(b) Specificity = probability test will be negative in disease free pt = (TN) / (TN + FP)
Name a noninherited caused of cystic kidney disease
(a) Mechanism of disease
Multicystic dysplastic kidney = noninherited but congenital malformation of the renal parenchyma leading to cysts w/ abnormal tissue (typically cartilage)
(a) Due to abnormal interaction btwn the ureteric bud and metanephric mesenchyme during embryologic development
Mesonephros vs. metanephros
Mesonephros acts as the primitive kidney during the first trimester, later contributes to the male GU system
While metanephros is the permanent structure that begins development around 5th week of gestation
-contains the ureteric bud and metanephric mesenchyme
Ureteric bud gives rise to what structures?
(a) Needs differentiation signal from what?
Ureteric bud => collecting ducts, calyces, pelvis, ureters (collection systme)
(a) Requires interplay/differentiation from metanephric mesenchyme (forms nephrons)
D/o that arises from abnormal interaction btwn the ureteric bud and the metanpehric mesenchyme
Abnormal communication => multicystic dysplastic kidney = noninherited congenital abnormal renal parenchyma w/ cysts and cartilage
Name some etiologies of Potter sequence
Potter sequence 2/2 oligohydramnios: flat facies, low set ears, limb/extremity hypoplasia, pulmonary hypoplasia
Etiologies of oligohydramnios = when the fetus can’t produce urine
- b/l renal agenesis
- ARPKD (aut recessive polycystic kidney disease)
- obstructive uropathy (ex: posterior urethral valves)
Which kidney is taken for donor transplant?
Take the left b/c it has a longer renal vein
What percent of total body water is intra vs. extra cellular?
60% of our body is water, then 1/3 of that water is extracellular while the other 2/3 is intracellular
So 40% of total body mass is intracellular water, while 20% is extracellular water
Formula for renal clearance of a substance
C = (U x V) / P
C = clearance U = urine concentration of substrate (mg/ml) V = urine flow rate (ml/min) P = plasma concentration of substrate (mg/ml)
What do the following best predict
(a) Renal inulin clearance
(b) Renal PAH clearance
(c) Renal creatinine clearance
(a) Inulin is used as a predictor of GFR b/c there is no net secretion or reabsorption, so amount filtered is what gets excreted
(b) PAH gets both filtered and secreted, so basically all of it in serum gets excreted, so PAH clearance predicts renal plasma flow
(c) Creatinine clearance estimates GFR (a bit overestimated bc bit of Cr secretion)
Formula for filtration fraction
(a) Normal value
FF = GFR / RRF (renal plasma flow)
RPF = RBF / (1 - Hct)
(a) FF normally 20%
- so about 20% of the blood thru the afferent arteriole gets filtered
Formula for filtration fraction using substituted clearance values
FF = GFR / RPF = (Creatinine clearance) / (PAH clearance)
Change in filtration fraction due to
(a) Dilation of afferent arteriole
(b) Constriction of efferent arteriole
(c) Increase in plasma protein concentration
FF = GFR / RPF
(a) Stays the same when prostaglandins dilate the afferent arteriole, b/c both GFR and RPF are increased
(b) FF increases when ATII constricts the efferent arteriole b/c RPF decreases but GFR increases
(c) Increased plasma protein decreases GFR => decreases FF
At what level of serum glucose does glucosuria begin?
Above serum glucose of 200 (threshold), glucose excreted in urine
Then TM of receptors is about 375, above which no glucose can be reabsorbed
How does Hartnup disease result in features of pellagra?
Hartnup disease = autosomal recessive defect in neutral amino acid transporter in the proximal convoluted tubule (AA reabsorbed actively) and enterocytes
=> tryptophan (neutral AA) can’t be reabsorbed by kidney or reabsorbed in gut => decreased tryptophan available to make niacin (B3) => pellagra-like symptoms
2 places where PTH acts on the nephron
PTH activity on the nephron: ‘phosphorus trashing hormone’
PTH acts on PCT to inhibit Na/PO4 cotransport => increase PO4 excretion (decrease phosphate reabsorption)
PTH also acts on the DCT to increase Ca/Na exchange to increase Ca reabsorption
Where does ATII act on the nephron?
Angiotensin II
- Constricts efferent arteriole to increased GFR and FF
- Stimulates Na/H exchange at the PCT to increase Na/H2O/HCO3 reabsorption
In what 2 parts of the nephron does urine get concentrated?
Gets concentrated as it goes down
- In thin descending loop- impermeable to Na+ so water reasborbed and filtrate is concentrated
- In collecting duct
Mechanism of ADH action at the collecting duct
ADH binds to V2 (vasopressin) receptors to upregulate aquaporin channels on the collecting duct’s apical membrane => increases reabsorption of water
Fanconi syndrome
(a) Causes
(b) Primary clinical symptom
Fanconi syndrome = defective PCT reabsorption => urinary loss of amino acids, glucose, HCO3, and PO4
- loss of HCO3 => type II (proximal) renal tubular acidosis
- loss of PO4 => rickets or osteomalacia
(a) Hereditary, from certain drugs (expired tetracyclines), lead poisoning
(b) Bone demineralization 2/2 PO4 wasting
Differentiate Barter and Gitelman syndrome
(a) Location of defect at nephron
(b) Metabolic abnormalities
Bartter and Gitelman syndromes are renal tubular defects
Bartter is more severe- defect in the NaKCC at thick ascending loop => hypokalemia, metabolic acidosis w/ hypercalcuria (high Ca in urine) so hypocalcemia
Gitelman less severe- 2/2 resorptive defect in DCT => hypokalemia, hypomagnesemia, metabolic alkalosis, hypocalciuria
Which diuretic is best to tx Liddle disease?
Liddle disease = gain of function in ENac channel => too much Na reabsorption => HTN, hypokalemia, metabolic alkalosis, hypoaldo
Tx w/ Amiloride which directly inhibits ENac channel
3 stimulants of renin release
- reduced BP sensed by JG cells
- Reduced Na concentration delivery to macula densa
- beta adrenergic (beta1) tone stimulates JG cells directly
Ppl w/ Bartter syndrome look like they’re on what diuretic?
Bartter syndrome = defect in NKCC channel which is inhibited by loop diuretics, so Bartter syndrome mimics furoside overdose
Which substance is net secreted by the kidneys?
(a) Net secretion = net reabsorption
PAH is net secreted
(a) Net secretion = net absorption for creatinine and inulin
Fxn of ANP and BNP
Released by atria and ventricles respectively to act as a check on the RAAS system, decreases renin secretion and relaxes vascular smooth muscle via cGMP to increase GFR
What part of the kidney can beta-blockers directly work on to decrease BP
Beta-blockers can inhibit beta-1 receptors of the JGA to directly decrease renin release
Do the following push K+ into or out of cells?
(a) Digitalis
(b) Beta agonist
(c) Acidosis
(a) Digitalis (cardiac glycoside) pushes K+ out of cells => can cause hyperkalemia
(b) Beta-agonist (ex: albuterol) pushes K+ into cells
(c) Acidosis pushes K+ out of cells (b/c H+ rushes into cells, kicking out a positive ion) => acidosis can cause hyperkalemia and alkalosis can cause hypokalemia
Electrolyte disturbance that can manifest as
(a) Tetany
(b) U waves on ECG
(c) Torsades
(a) Tetany due to low calcium or low Mg
(b) U waves on ECG seen in hypokalemia
(c) Torsades can be caused by hypomagnesemia
Electrolyte disturbance that manifests as
(a) Muscle weakness
(b) Reduced DTRs
(c) Renal stones
(a) Muscle weakness 2/2 hyperkalemia
- vs. tetany seen from hypocalcemia and hypo-Mg
(b) Reduced DTRs from hypomag
(c) Renal stones from hyperphosphatemia and hypercalcemia
Metabolic abnormality seen in renal tubular acidosis
Normal anion gap (hyperchloremic) metabolic acidosis
Type of renal tubular acidosis caused by
(a) Amphotericin B toxicity
(b) Bactrim toxicity
(c) ACEi
RTA
(a) Amphotericin B can cause type I (distal) RTA where there is defective proton secretion by alpha intercalated cells of the collecting duct
(b) Bactrum toxicity is associated w/ type IV hyperkalemia RTA
(c) ACEi also associated w/ type IV hyperkalemic RTA b/c ACEi reduces aldo secretion
Type of renal tubular acidosis caused by
(a) Fanconi syndrome
(b) Adrenal insufficiency
(c) Acetazolamide
RTA
(a) Fanconi syndrome => type II (proximal) RTA where PCT can’t reabsorb bicarb
(b) Adrenal insufficiency => low aldo secretion => type IV (hyperkalemic) RTA
(c) Acetazolamide inhibits carbonic anhydrase in PCT => type II (proximal) RTA
Differentiate the three types of renal tubular acidosis
(a) Urine pH over 5.5
(b) Hyperkalemia
RTA: distal type I where alpha intercalated can’t secrete protons properly, proximal type II where PCT can’t properly reabsorb bicarb, type IV 2/2 hypoaldo
(a) Urine pH over 5.5 in type I distal RTA b/c can’t pump out enough protons to acidify the urine
- urine pH below 5.5 in both type II and IV
(b) Hyperkalemia seen in type IV
- hypokalemia seen in both type I and II
Which type of renal tubular acidosis increases risk for calcium phosphate kidney stones?
Type I (distal) RTA: can’t properly acidify urine, urine pH above 5.5 which increases risk of calcium phospphate kidney stones
What do the following on UA indicate
(a) RBC casts
(b) WBC casts
(a) RBC casts = glomerulonephritis (more nephritic syndrome), malignant HTN
(b) WBC casts = AIN (acute interstitial nephritis), acute pyelonephritis, transplant rejection
What do the following on UA indicate
(a) Fatty casts
(b) Granular casts
UA
(a) Fatty casts = oval fat bodies = nephrotic syndrome
- liver responds to very thin (no protein) blood by pumping out lipids => hyperlipidemia
(b) Granular casts = muddy bron casts seen in ATN
What do the following on UA indicate
(a) Oval fat bodies
(b) Muddy brown casts
(a) Oval fat bodies = fatty casts = nephrotic syndrome
- liver responds to very thin (no protein) blood by pumping out lipids => hyperlipidemia
(b) Muddy brown casts = granular casts seen in ATN
What do the following on UA indicate
(a) Waxy casts
(b) Hyaline casts
UA
(a) Waxy casts indicative of ESRD or CRF (end stage renal disease or chronic renal failure)
(b) Hyaline casts are a very nonspecific finding, can even be normal
UA findings indicative of
(a) ESRD
(b) Acute pyelo
(c) Malignant HTN
UA finding of
(a) ESRD and CRF = waxy casts
(b) Acute pyelo = WBC casts
(c) Malignant HTN = RBC casts
UA findings indicative of
(a) Transplant rejection
(b) ATN
(c) Nephrotic syndrome
UA
(a) Transplant rejection = WBC casts
(b) ATN = granular/muddy brown casts
(c) Nephrotic syndrome = fatty casts = oval fat bodies
UA findings indicative of
(a) Acute cystitis
(b) Bladder cancer
(c) Kidney stones
UA
(a) Acute cystitis = pyuria (pus in urine) w/o casts
(b,c) Bladder cancer and kidney stones = hematuria w/o casts
-painless hematuria w/ no casts suggests bladder cancer, w/ casts would lean more towards nephritic syndrome
Focal vs. diffuse glomerular disease
Focal- involves less than 50% of the glomeruli
ex: Focal segmental glomerulosclerosis where less than 50% of glomeruli have segmental sclerosis
Diffuse- more than 50% of glomeruli are involved
ex: Diffuse proliferative glomerulonephritis in SLE
Proliferative vs. membranous glomerular disease
Proliferative = hypercellular glomeruli
ex: membranoproliferative glomerulonephritis = nephritic syndrome that often copresents w/ nephrotic syndrome
Membraneous = thickening of glomerular basement membrane
ex: membranous nephropathy where filtration barrier thickened by subepithelial immune complexes
Name 2 MC causes of nephritic-nephrotic syndrome
Nephritic-nephrotic syndrome = such severe nephritic syndrome (GBM destruction) that the glomerular filtration chrage barrier is damaged causing nephrotic-range proteinuria
- Diffuse proliferative glomerulonephritis (ex: SLE)
- Membranoproliferative glomerulonephritis (IC deposition, either intramembranous or subendothelial)
Post strep glomerulonephritis
(a) Clinical findings
(b) Type of hypersensitivity
(c) Lab results
PSGN about 2-3 wks after GAS pharyngitis or impetigo
(a) Peripheral/periorbital edema, cola-colored urine, HTN
(b) Type III (immune complex)
(c) Elevated anti-DNase B titers (GAS Ab), low C3
Goodpasture syndrome
(a) Type of nephritic or nephrotic syndrome?
(b) Type of hypersensitivity rxn
Goodpastures
(a) Nephritic, subtype of rapidly progressive (crescentic) glomerulonephritis = type of nephritic syndrome that quickly (weeks to months) progresses to renal failure
(b) Type II hypersensitivity: where IgG attack self, other examples = myasthenia gravis, ABO incompatibility
Goodpasture syndrome
(a) Immunoflorescence pattern
(b) Tx
Goodpasture syndrome = anti-basement membrane antibodies
(a) IF pattern = linear
(b) Tx = emergent plasmaphoresis
MC cause of death in lupus pts
MC cause of death in lupus pts = diffuse proliferative glomerulonephritis = subtype of rapidly progressive glomerulonephritis nephritic-nephrotic syndrome
Diffuse proliferative glomerulonephritis
(a) Type of nephritic or nephrotic syndrome?
(b) LM finding
Diffuse proliferative glomerulonephritis = MC cause of death in lupus pts
(a) Nephritic, its a subclass of rapidly progressive (crescentic) glomerulonephritis
Renal pathology of Henoch-Schonlein purpura
(a) LM finding
(b) Nephrotic or nephritic?
HSP = IgA nephropathy
a) LM: mesangial proliferation (typical of nephritic
(b) Nephritic
What abnormality may be seen on light microscopy of minimal change disease
Overall light microscopy will show normal glomeruli, but may see lipid in the PCT
Name some conditions associated w/ secondary renal amyloidosis
Secondary amyloid = amyloid light chain deposition
Associated w/ multiple myeloma, TB, RA
Mechanism of the following in diabetic nephropathy
(a) Increased glomerular permeability
(b) Increased GFR
Diabetic nephropathy 2/2 nonenzymatic glycosylation eventually leading to hyaline arteriolosclerosis
(a) Glomerular permeability increased 2/2 nonenyzmatic glycosylation of the glomerular basement membrane
(b) GFR increased by preferential nonenyzmatic glycosylation of the efferent arteriole => eventually leads to hyperfiltration injury
Way to differentiate calcium phosphate and calcium oxalate kidney stones
Calcium phosphate stones precipitate at high pH
-hence why giving citrate is protective here
Calcium oxalate stones precipitate in low pH
Urine crystals shaped as the following are indicative of what kind of kidney stone?
(a) Coffin lid
(b) Dumbbell shaped
(c) Rhomboid
(d) Envelope shaped
(e) Hexagonal
(a) Coffin lid = ammonium magnesium phosphate stone
(b, d) Dumbbell or envelope shaped = calcium phosphate/oxalate stones
(c) Rhomboid stone = uric acid stone
(e) Hexagonal stone = cysteine stone (child w/ cystinuria), cystine “sixtene” for hexagon
Name 3 bugs indicated in struvite stone formation
Struvite kidney stones = ammonium magnesium phosphate stones that precipitate in urine pH, from infection w/ urease positive bugs
- Proteus mirabilis
- Staph saprophyticus
- Klebsiella
How to visualize uric acid kidney stones
Uric acid stones are radiolucent => not visible on Xray
But they are visible on CT or ultrasound
Which two types of kidney stones can form staghorn calculi?
MC in adults = struvite stones (ammonium magnesium phosphate) from infection w/ urease positive organism
In children = cysteine stones can cause staghorn calculi formation
When would hydronephrosis cause elevated serum creatinine?
Hydronephrosis = distention/dilation of the renal collecting system (renal pelvis and calyces)
But only causes elevated creatinine if pt only has one kidney or the hydronephrosis is bilateral
Location of gene responsible for RCC
3 letters in RCC: VHL gene (tsg) responsible for RCC on chromosome 3
VHL mutation can either be acquired or inherited (hemangioblastoma of CNS, RCC)
Does AD or AR PKD have the potential to present w/ Potter sequence?
ARPKD can present w/ Potter sequence (flat facies, low set ears, extremity abnormalities) 2/2 oligohydramnios
While ADPKD the cysts aren’t present in utero, develop over time and pts present in early adulthood
Some imaging characteristics of complex vs. simple renal cyst
Simple cysts- anechoic (black) on ultrasound, super common incidental finding
Complex cyst- septated, enhanced, or any solid components on imaging => f/u or remove 2/2 risk of RCC
Explain the use of acetazolamide in glaucoma and pseudotumor cerebri
Acetazolamide increases HCO3- excretion, so reduces total body bicarb and fluid- draining fluid out of the eye and intracranial space
NaHCO3 diuresis
pH disturbance seen from acetazolamide toxicity
Acetazolamide decreases HCO3- reabsorption = urine alkalinization => hyperchloremic metabolic acidosis
‘OH DANG’ mnemonic for loop diuretic toxicity
Loop diuretic toxicity: inhibits KNCC in ascending loop
Ototoxicity Hypokalemia Dehydration Allergy (they're sulfa drugs) Nephritis (interstitial) Gout (by reducing urate excretion)
Name two diuretics that
(a) Increase blood pH
(b) Decrease blood pH
(a) Increase blood pH from loop diuretics and thiazides: reduced volume increases ATII which activates NaH exchange in the PCT => increased HCO3- reabsorption
(b) Decrease blood pH w/ carbonic anhydrase inhibitor and K+ sparing (spironolactone): acetazolamide decreases bicarb reabsor, while spironolactone decreases K and H secretion
Explain the concept of contraction alkalosis 2/2 loop diuretics
Loop diuretics and thiazides reduce blood volume, causing JG cells to increase renin => increased ATII which stimulates NaH exchanger on the PCT
More H+ pumped out => more HCO3= reabsorbed
Name of direct renin inhibitor
Direct renin inhibitor = Aliskiren
-used in tx of HTN but not really used over ACEi
CATCHH mnemonic for ACEi toxicity
ACEi toxicity
Cough (dry) Angioedema Teratogen (fetal renal malformation) Creatinine boost (2/2 reduction in GFR from dilation of efferent arteriole) Hypotension Hyperkalemia
Name some ACEi
ACEi = Catalopril, Lisinopril, Enalapril, Ramipril
