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First Aid: Behavioral Science/ Renal Flashcards

1
Q

What does a cross sectional test tell you?

A

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
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2
Q

Is a cohort study prospective or retrospective?

(a) Result

A

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

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3
Q

Which of the 4 core ethical principles do the following protect

(a) Informed consent
(b) Triage
(c) Confidentiality

A

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

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4
Q

Explain sensitivity vs. specificity

A

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

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5
Q

Differentiate the 4 phases of a clinical trial?

A

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

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6
Q

Is a case control study prospective or retrospective?

(a) Result

A

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)

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7
Q

Define low birth wt

(a) Associated conditions

A

Low birth wt = under 2500 g

(a) Neonatal respiratory distress, necrotizing enterocolitis, interventricular hemorrhage

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8
Q

Which: positive predictive value or sensitivity/specificity- are fixed properties of a test

A

Sensitivity/specificity are fixed properties of a test

-while PPV and NPV vary depending on the disease prevalence

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9
Q

Name the 5 components of the APGAR score

A 
APGAR score: (get 2 pts for each)
appearance
pulses
grimace
activity 
respiration
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10
Q

Differentiate incidence and prevalence

A

Incidence = over a period of time

Prevalence = current cases at a single point in time

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11
Q

Which observational study gives you

(a) Odds ratio
(b) Relative risk

A

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

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12
Q

Describe number needed to treat

(a) Formula

A

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

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13
Q

Differentiate primary, secondary, and tertiary prevention

(a) Give example of each

A

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

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14
Q

Differentiate null and alternative hypothesis

A

H0 (null) hypothesis = no association btwn variables

H1 (alternative) hypothesis = association exists

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15
Q

Is a sensitive or specific test better as a screening test?

A

As a screening test you want a sensitive test b/c high sensitivity means high false negative rate (you won’t miss ppl)

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16
Q

Examples of when confidentiality can be broken

A
  • 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
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17
Q

Differentiate statistical tests

(a) T-test
(b) ANOVA
(c) Chi squares

A

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)

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18
Q

Explain PPV vs. NPV

A

PPV = probability of pt having disease is test is positive

NPV = probability of pt being disease free if a test is negative

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19
Q

Give the term for the following

(a) True negative rate of a test
(b) True positive rate of a test

A

(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

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20
Q

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

(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

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21
Q

Formula for

(a) Sensitivity
(b) Specificity

based on the classic 2x2 table

A

(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)

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22
Q

Name a noninherited caused of cystic kidney disease

(a) Mechanism of disease

A

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

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23
Q

Mesonephros vs. metanephros

A

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

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24
Q

Ureteric bud gives rise to what structures?

(a) Needs differentiation signal from what?

A

Ureteric bud => collecting ducts, calyces, pelvis, ureters (collection systme)

(a) Requires interplay/differentiation from metanephric mesenchyme (forms nephrons)

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25
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
26
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)
27
Which kidney is taken for donor transplant?
Take the left b/c it has a longer renal vein
28
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
29
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) ```
30
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)
31
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
32
Formula for filtration fraction using substituted clearance values
FF = GFR / RPF = (Creatinine clearance) / (PAH clearance)
33
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
34
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
35
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
36
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
37
Where does ATII act on the nephron?
Angiotensin II 1. Constricts efferent arteriole to increased GFR and FF 2. Stimulates Na/H exchange at the PCT to increase Na/H2O/HCO3 reabsorption
38
In what 2 parts of the nephron does urine get concentrated?
Gets concentrated as it goes down 1. In thin descending loop- impermeable to Na+ so water reasborbed and filtrate is concentrated 2. In collecting duct
39
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
40
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
41
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
42
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
43
3 stimulants of renin release
1. reduced BP sensed by JG cells 2. Reduced Na concentration delivery to macula densa 3. beta adrenergic (beta1) tone stimulates JG cells directly
44
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
45
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
46
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
47
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
48
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
49
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
50
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
51
Metabolic abnormality seen in renal tubular acidosis
Normal anion gap (hyperchloremic) metabolic acidosis
52
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
53
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
54
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
55
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
56
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
57
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
58
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
59
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
60
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
61
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
62
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
63
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
64
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
65
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 1. Diffuse proliferative glomerulonephritis (ex: SLE) 2. Membranoproliferative glomerulonephritis (IC deposition, either intramembranous or subendothelial)
66
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
67
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
68
Goodpasture syndrome (a) Immunoflorescence pattern (b) Tx
Goodpasture syndrome = anti-basement membrane antibodies (a) IF pattern = linear (b) Tx = emergent plasmaphoresis
69
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
70
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
71
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
72
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
73
Name some conditions associated w/ secondary renal amyloidosis
Secondary amyloid = amyloid light chain deposition Associated w/ multiple myeloma, TB, RA
74
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
75
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
76
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
77
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
78
How to visualize uric acid kidney stones
Uric acid stones are radiolucent => not visible on Xray But they are visible on CT or ultrasound
79
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
80
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
81
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)
82
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
83
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
84
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
85
pH disturbance seen from acetazolamide toxicity
Acetazolamide decreases HCO3- reabsorption = urine alkalinization => hyperchloremic metabolic acidosis
86
'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) ```
87
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
88
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
89
Name of direct renin inhibitor
Direct renin inhibitor = Aliskiren | -used in tx of HTN but not really used over ACEi
90
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 ```
91
Name some ACEi
ACEi = Catalopril, Lisinopril, Enalapril, Ramipril

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