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Boards - Step 1 > First Aid: Behavioral Science/ Renal > Flashcards

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
Q

D/o that arises from abnormal interaction btwn the ureteric bud and the metanpehric mesenchyme

A

Abnormal communication => multicystic dysplastic kidney = noninherited congenital abnormal renal parenchyma w/ cysts and cartilage

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26
Q

Name some etiologies of Potter sequence

A

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)
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27
Q

Which kidney is taken for donor transplant?

A

Take the left b/c it has a longer renal vein

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28
Q

What percent of total body water is intra vs. extra cellular?

A

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

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29
Q

Formula for renal clearance of a substance

A

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)
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30
Q

What do the following best predict

(a) Renal inulin clearance
(b) Renal PAH clearance
(c) Renal creatinine clearance

A

(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)

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31
Q

Formula for filtration fraction

(a) Normal value

A

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

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32
Q

Formula for filtration fraction using substituted clearance values

A

FF = GFR / RPF = (Creatinine clearance) / (PAH clearance)

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33
Q

Change in filtration fraction due to

(a) Dilation of afferent arteriole
(b) Constriction of efferent arteriole
(c) Increase in plasma protein concentration

A

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

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34
Q

At what level of serum glucose does glucosuria begin?

A

Above serum glucose of 200 (threshold), glucose excreted in urine

Then TM of receptors is about 375, above which no glucose can be reabsorbed

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35
Q

How does Hartnup disease result in features of pellagra?

A

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

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36
Q

2 places where PTH acts on the nephron

A

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

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37
Q

Where does ATII act on the nephron?

A

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
Q

In what 2 parts of the nephron does urine get concentrated?

A

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
Q

Mechanism of ADH action at the collecting duct

A

ADH binds to V2 (vasopressin) receptors to upregulate aquaporin channels on the collecting duct’s apical membrane => increases reabsorption of water

40
Q

Fanconi syndrome

(a) Causes
(b) Primary clinical symptom

A

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
Q

Differentiate Barter and Gitelman syndrome

(a) Location of defect at nephron
(b) Metabolic abnormalities

A

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
Q

Which diuretic is best to tx Liddle disease?

A

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
Q

3 stimulants of renin release

A
  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
Q

Ppl w/ Bartter syndrome look like they’re on what diuretic?

A

Bartter syndrome = defect in NKCC channel which is inhibited by loop diuretics, so Bartter syndrome mimics furoside overdose

45
Q

Which substance is net secreted by the kidneys?

(a) Net secretion = net reabsorption

A

PAH is net secreted

(a) Net secretion = net absorption for creatinine and inulin

46
Q

Fxn of ANP and BNP

A

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
Q

What part of the kidney can beta-blockers directly work on to decrease BP

A

Beta-blockers can inhibit beta-1 receptors of the JGA to directly decrease renin release

48
Q

Do the following push K+ into or out of cells?

(a) Digitalis
(b) Beta agonist
(c) Acidosis

A

(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
Q

Electrolyte disturbance that can manifest as

(a) Tetany
(b) U waves on ECG
(c) Torsades

A

(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
Q

Electrolyte disturbance that manifests as

(a) Muscle weakness
(b) Reduced DTRs
(c) Renal stones

A

(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
Q

Metabolic abnormality seen in renal tubular acidosis

A

Normal anion gap (hyperchloremic) metabolic acidosis

52
Q

Type of renal tubular acidosis caused by

(a) Amphotericin B toxicity
(b) Bactrim toxicity
(c) ACEi

A

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
Q

Type of renal tubular acidosis caused by

(a) Fanconi syndrome
(b) Adrenal insufficiency
(c) Acetazolamide

A

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
Q

Differentiate the three types of renal tubular acidosis

(a) Urine pH over 5.5
(b) Hyperkalemia

A

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
Q

Which type of renal tubular acidosis increases risk for calcium phosphate kidney stones?

A

Type I (distal) RTA: can’t properly acidify urine, urine pH above 5.5 which increases risk of calcium phospphate kidney stones

56
Q

What do the following on UA indicate

(a) RBC casts
(b) WBC casts

A

(a) RBC casts = glomerulonephritis (more nephritic syndrome), malignant HTN
(b) WBC casts = AIN (acute interstitial nephritis), acute pyelonephritis, transplant rejection

57
Q

What do the following on UA indicate

(a) Fatty casts
(b) Granular casts

A

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
Q

What do the following on UA indicate

(a) Oval fat bodies
(b) Muddy brown casts

A

(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
Q

What do the following on UA indicate

(a) Waxy casts
(b) Hyaline casts

A

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
Q

UA findings indicative of

(a) ESRD
(b) Acute pyelo
(c) Malignant HTN

A

UA finding of

(a) ESRD and CRF = waxy casts
(b) Acute pyelo = WBC casts
(c) Malignant HTN = RBC casts

61
Q

UA findings indicative of

(a) Transplant rejection
(b) ATN
(c) Nephrotic syndrome

A

UA

(a) Transplant rejection = WBC casts
(b) ATN = granular/muddy brown casts
(c) Nephrotic syndrome = fatty casts = oval fat bodies

62
Q

UA findings indicative of

(a) Acute cystitis
(b) Bladder cancer
(c) Kidney stones

A

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
Q

Focal vs. diffuse glomerular disease

A

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
Q

Proliferative vs. membranous glomerular disease

A

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
Q

Name 2 MC causes of nephritic-nephrotic syndrome

A

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
Q

Post strep glomerulonephritis

(a) Clinical findings
(b) Type of hypersensitivity
(c) Lab results

A

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
Q

Goodpasture syndrome

(a) Type of nephritic or nephrotic syndrome?
(b) Type of hypersensitivity rxn

A

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
Q

Goodpasture syndrome

(a) Immunoflorescence pattern
(b) Tx

A

Goodpasture syndrome = anti-basement membrane antibodies

(a) IF pattern = linear
(b) Tx = emergent plasmaphoresis

69
Q

MC cause of death in lupus pts

A

MC cause of death in lupus pts = diffuse proliferative glomerulonephritis = subtype of rapidly progressive glomerulonephritis nephritic-nephrotic syndrome

70
Q

Diffuse proliferative glomerulonephritis

(a) Type of nephritic or nephrotic syndrome?
(b) LM finding

A

Diffuse proliferative glomerulonephritis = MC cause of death in lupus pts

(a) Nephritic, its a subclass of rapidly progressive (crescentic) glomerulonephritis

71
Q

Renal pathology of Henoch-Schonlein purpura

(a) LM finding
(b) Nephrotic or nephritic?

A

HSP = IgA nephropathy

a) LM: mesangial proliferation (typical of nephritic
(b) Nephritic

72
Q

What abnormality may be seen on light microscopy of minimal change disease

A

Overall light microscopy will show normal glomeruli, but may see lipid in the PCT

73
Q

Name some conditions associated w/ secondary renal amyloidosis

A

Secondary amyloid = amyloid light chain deposition

Associated w/ multiple myeloma, TB, RA

74
Q

Mechanism of the following in diabetic nephropathy

(a) Increased glomerular permeability
(b) Increased GFR

A

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
Q

Way to differentiate calcium phosphate and calcium oxalate kidney stones

A

Calcium phosphate stones precipitate at high pH
-hence why giving citrate is protective here

Calcium oxalate stones precipitate in low pH

76
Q

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

(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
Q

Name 3 bugs indicated in struvite stone formation

A

Struvite kidney stones = ammonium magnesium phosphate stones that precipitate in urine pH, from infection w/ urease positive bugs

  • Proteus mirabilis
  • Staph saprophyticus
  • Klebsiella
78
Q

How to visualize uric acid kidney stones

A

Uric acid stones are radiolucent => not visible on Xray

But they are visible on CT or ultrasound

79
Q

Which two types of kidney stones can form staghorn calculi?

A

MC in adults = struvite stones (ammonium magnesium phosphate) from infection w/ urease positive organism

In children = cysteine stones can cause staghorn calculi formation

80
Q

When would hydronephrosis cause elevated serum creatinine?

A

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
Q

Location of gene responsible for RCC

A

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
Q

Does AD or AR PKD have the potential to present w/ Potter sequence?

A

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
Q

Some imaging characteristics of complex vs. simple renal cyst

A

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
Q

Explain the use of acetazolamide in glaucoma and pseudotumor cerebri

A

Acetazolamide increases HCO3- excretion, so reduces total body bicarb and fluid- draining fluid out of the eye and intracranial space

NaHCO3 diuresis

85
Q

pH disturbance seen from acetazolamide toxicity

A

Acetazolamide decreases HCO3- reabsorption = urine alkalinization => hyperchloremic metabolic acidosis

86
Q

‘OH DANG’ mnemonic for loop diuretic toxicity

A

Loop diuretic toxicity: inhibits KNCC in ascending loop

Ototoxicity 
Hypokalemia 
Dehydration
Allergy (they're sulfa drugs)
Nephritis (interstitial)
Gout (by reducing urate excretion)
87
Q

Name two diuretics that

(a) Increase blood pH
(b) Decrease blood pH

A

(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
Q

Explain the concept of contraction alkalosis 2/2 loop diuretics

A

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
Q

Name of direct renin inhibitor

A

Direct renin inhibitor = Aliskiren

-used in tx of HTN but not really used over ACEi

90
Q

CATCHH mnemonic for ACEi toxicity

A

ACEi toxicity

Cough (dry) 
Angioedema
Teratogen (fetal renal malformation) 
Creatinine boost (2/2 reduction in GFR from dilation of efferent arteriole) 
Hypotension
Hyperkalemia
91
Q

Name some ACEi

A

ACEi = Catalopril, Lisinopril, Enalapril, Ramipril

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