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*First Aid in Brainscape* > AAW - renal/acid base > Flashcards

AAW - renal/acid base Flashcards

1
Q

6 months old presents with FTT, oliguria, recurrent UTIs, enlarged unilateral renal pelvis, normal ureters, and uremia.

what you think

A

ureteropelvic junction obstruction - most common site of obstruction in young ones because it is the last to canalize

common in males

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2
Q

where do sickle cells damage the kidney

A

in the vasa recta, the arteries that follow the loop of henle

they damage here because the blood osmolarity is very high here

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3
Q

What does furosemide do to the GFR and how

A

it increases the GFR:

blocks NKCC

NKCC is present in ascending limb AND macula densa

Macula densa gets less sodium into the cells because NKCC is blocked

kidney thinks that there is low sodium and high water because no sodium gets into the cell

macula densa secretes renin to constrict efferent arteriole to increase GFR to get rid of what it thinks is excess water

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4
Q

how does acetazolomide cause an increase in Na secretion in the proximal tubule

A

it stops the hydrogen ion from being made inside the proximal tubule cell, which is normally antiported for the sodium that is in the lumen

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5
Q

what is the only diuretic that acts totally upstream of the macula densa

A

carbonic anhydrase inhibitor - acetazolamide

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6
Q

why do you get acidotic on acetazolomide

A

because you cannot convert the bicarb in the lumen to CO2 in order for it to be reabsorbed by the proximal tubule cell, so the bicarb gets peed out

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7
Q

what does Captopril do to potassium levels

A

they could cause hyperkalemia because of decreased RAAS

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8
Q

RAS vs RAAS

A

RAS - renal artery stenosis

RAAS - renin-angiotensin-aldosterone system

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9
Q

what hypertensive drugs are contraindicated in renal artery stenosis and why

A

lisinopril, catalopril, other ACEs

because when the body isn’t able to perfuse the kidneys because of stenosis, the normal response of the kidney is to actiave RAAS so that the efferent arteriole constricts, PRESERVING kidney flow

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10
Q

someone’s urine output is lets say 150ml/min and you give ADH and it doesn’t change. why

A

type 2 DM

hyperglycemia prevents proximal tubule reabsorption of glucose, increases delivery of fluid to loop of henle, overloading the loop and reducing it’s gradient, which causes ADH resistance.

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11
Q

how does proteus increase the pH in the urine

A

splits urea into ammonia using urease

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12
Q

what do you kidneys do to bicarb if you chronically live at high altitude

A

your kidney responds to your chronic respiratory alkalosis by secreting more bicarb

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13
Q

What is the molecule in the basement membrane of the glomerulus that has a negative charge

A

Heparan Sulfate

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14
Q

Hartnup Disease

A

Autosomal recessive
Deficiency of neutral amino acid (tryptophan) transporters in proximal tubule and in enterocytes
Get pellegra like symptoms
treat with high protein diet and nicotinic acid

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15
Q

what diuretic can cause hypercacemia/hypocalcuria and why

A

thiazide

works on distal convoluted by blocking Na Cl contransporter on luminal side

this causes a decrease in sodium in the cell

Na/Ca antiporter on the basalateral side is upregulated to get more sodium back into the cell, which throws Ca out into the blood

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16
Q

Where do you find carbonic anhydrase enzyme in the proximal tubule?

A

In the proximal tubule cell cytoplasm and in the luminal brush boarder.

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17
Q

what diuretic can cause hypocalcemia/hypercalcuria and why

A

loop

loops increase sodium in distal lumen

Na/Cl activity increases

more Na in tubular cell

no need to use Na/Ca transporter on basolateral side

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18
Q

chlorthalidone

A

blocks NaCl cotransporter

thiazide

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19
Q

Hydrochlorothiazide

A

blocks NaCl cotransporter`

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20
Q

what is the “only other time” that your body is making activated vitamin D if the kidneys aren’t doing it?

A

granulomatous disease like sarcoid or wegeners

can cause hypercalcemia

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21
Q

contraction _______

(alkalosis or acidosis)?
explain how it could happen

A

alkalosis

Volume contraction -> aldosterone ->H+ secretion at collecting duct

volume contraction -> AT II -> HCO3− reabsorption at proximal convoluted tubule

could happen from a diuretic (like thiazide) or other loss of fluid

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22
Q

Tx for nephrogenic DI

A

Thiazides (paridoxical)
Amiloride (paridoxical)
Indomethacin (constricts afferent arteriole reducing renal flow)

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23
Q

why do people with kidney dysfunction get secondary hyperparathyroidism

A

usually in ESRD

get decreased secretion of PO4 and decreased activation of vit D

(the parathyroids are trying to compensate for the low serum Ca and the high serum PO4, but usually they can’t quite return the levels to normal)

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24
Q

Causes of metabolic alkalosis

Mech

A

–Vomiting
–Loop diuretics (and sometimes thiazides)
–Antacid use
–Hyperaldosteronism (primary, cushing, bartter)

You go “BLAH” when you vomit

“VLAH”

loops cause alkalosis because you get more Na in the collecting tubule, causing an upregulation of aldosterone -> Na is exchanged for K in the principle cell, then you resorb the K by excreting H in the intercalated cell

Hyperaldosteronism causes alkalosis because of the same mech.

if there is no change in volume status (like in primary hyperaldosteronism, cushing, bartters) then the alkalosis with be (saline unresponsive) - treat with potassium

if they are hypovolemic, treat with saline

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25
Q

what makes a metabolic alkalosis (chloride responsive) or (saline responsive)

list causes

A

it occurs when you are hypovolemic
you see low Cl in the urine because the body is reuptaking ions to combat the hypovolemia
Tx is normal saline.

Vomiting or nasogastric suction
Diuretics
Posthypercapnia
Cystic Fibrosis
Low chloride intake
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26
Q

what does your blood glucose have to get to in order to see glucoseuria

A

about 200mg/dlL

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27
Q

WAGR

A

wilms tumor
Anirida
Genital abnormalities
mental and motor Retardation

assc with deletion of chromosome 11

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28
Q

when do you see abundant clear cells in the kidney

A

renal cell carcinoma

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29
Q

kidney condition assc with asbestosis

A

RCC

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30
Q

von hippel lindau disease

A

Assc with mutant tumor suppressor gene VHL, resulting in constitutive expression of HIF 1a

Normally functioning VHL aids in ubiquitin apoptosis

autosomal dominant

Assc cancers: *BILATERAL RCC, Cavernous hemangiomas in skin, mucosa, organs;
hemangioblastoma (high vascularity with hyperchromatic nuclei) in retina, brain stem,
cerebellum; and pheochromocytomas

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31
Q

a bunch of eosinophillic cells packed with mitochondria, you think:

A

oncocytoma (mitochondria are present because the name of the tumor!) (a prof said this, and we still can’t figure out why)

often benign

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32
Q

hamartomatous blood vessels in the kidney mean what

A

angiomyolipoma, benign tumor

assc with tuberous sclerosis

33
Q

in the kidney, when would you see circular grouping of dark tumor cells surrounding pale neutrofibrils

A

these are called homer-wright bodies, and they are found in neuroblastoma, a tumor of the medulary adrenal

34
Q

if you take a biopsy of the kidney and see embryonic glomerular structures, what is it

A

Wilms tumor

35
Q

IgA nephropathy diseases

A

HSP

Bergers

36
Q

DDx for hypercalcemia

A

cancer (squamous cell lung producing PTHrP)

hyperparathyroid

thiazide

37
Q

dipstick is positive for blood but you see no blood in a high power field. what is it

A

myoglobinurea

usually occurs after intense physical activity/rhabdo

38
Q

miliary

A

(of a disease) accompanied by a rash with lesions resembling millet seed.

i.e. in miliary TB
it means that the TB has spread (happens in immunocompromized patients)

39
Q

Ziehl-neelsen is used to look for what

A

acid fast bacteria

like TB - an bacillus

40
Q

fungal lung infection from latin america

what is a characteristic finding of the yeist

A

paracoccidioidomycosis

see “multiply budding” or “pilot’s wheel” yeast forms

41
Q

how to calculate the GFR from a 24 hour urine collection

A 
V = urine flow (mL/min)
Uc = urine creatinine (mg/ml)
Pc = plasma creatinine (mg/ml)
CCr = clearance of creatinine ~= GFR

CCr = V * Uc / Pc

42
Q

alveolar gas equation

A

PA02 = PI02 - PACO2/R

43
Q

oxybutynin

A

muscarinic antagonist

inhibits urination

44
Q

muscarinic antagonists that help you not wet your pants

A

oxybutynin
darifenacin
solfenacin
tolterodine

they only help with urge incontenance, not stress incontinence

45
Q

bethanechol

A

cholinergic agonist

helps incontinence by contracting the detrusor muscle

46
Q

bumetanide

A

loop diuretic

used when furosemide doesnt work

47
Q

neostigmine

A

anticholinesterase

would treat incontinence by increasing cholinergic activity and contracting the detrusor

48
Q

individuals with defiviencies in the alternative complement pathway are at increased risk of disease from what

A

neisseria

49
Q

lambert eaton syndrome

A

anto-antibodies against calcium channels, which produce muscle weakness

50
Q

Coughing and peeing blood with no Hx of infection

What is the most likely diagnosis

A

Goodpasture’s

see linear deposits of IgG in the glomeruli

51
Q

what embryologic structure forms the adult kidney

A

Ureteric bud induces the development of the metanephros, which becomes the kidney

52
Q

What does DIC do to the kidneys

A

causes diffuse cortical necrosis

53
Q

head injury and polyurea

what are you thinking

A

damage to the pituitary decreases the amount of vasopressin getting to the kidney

diabetes insipidus

54
Q

what causes type 1 renal tubular acidosis

how can you tell its type 1

what happens physiologically

A

“distal tubular acidosis”

amphotericin B, analgesic nephropathy, congenital abnormalities

only renal tubular acidosis where urine pH is >5.5
assc with hypokalemia

defect in alpha intercalated cells -> cannot secrete H+ into the lumen

55
Q

what causes type 2 renal tubular acidosis

how can you tell its type 2

what happens physiologically

A

“proximal tubular acidosis”

fanconi syndrome, carbonic anhydrase inhibitors (“close that gap, #2!”)

type 2 because you have urine pH is less than 5.5 and you get hypokalemia

you get decreased absorption of bicarb in the proximal tubule, but the alpha intercalated respond by secreting acid so your urine pH is actually low

56
Q

what does urate do to the kidney

how can you stop it from doing what it does

A

causes an acute tubular necrosis (nephrotoxic)

urate is a salt of uric acid seen in things like tumor lysis syndrome

allopurinol before chemo

57
Q

what nephropathy is associated with lupus

A

membranous nephropathy

spike and dome depostits next to the podocytes

hep b,c, solid tumors, SLE, or drugs like NSAIDS

58
Q

C3 nephritic factor in the blood is assc with what kidney things

what does it do

A

type two membranoproliferative glomerulonephritis
AKA dense deposit disease

it stabilizes C3 convertase which causes the overactivation of complement which can cause inflammation and drive the glomerulonephritis

59
Q

nitrites in the urine

what does it mean

A

bacteria are there

bacteria convert nitrates into nitrites

60
Q

atrophic tubules with eosinophilic material resembling thyroid tissue in the kidney

A

chronic pyelonephritis

61
Q

hemangioblastomas in the cerebellum and cysts in the kidney

what is the genetic defect specifically

A

loss of the VHL tumor suppressor gene, which leads to increased IGF-1 (promotes growth) and increased HIF transcription factor (increases VEGF and PDGF)

62
Q

when do you see blastema cells

A

in a wilms tumor

they are immature kidney mesenchyme

63
Q

kidney tumor, hypoglycemia, muscular hemihypertrophy, organomegaly

A

beckwith-wiedemann syndrome

assc with mutations in WT2 gene cluster, particularly IGF-2

64
Q

7 year old girl with what looks like she is on a huge dose of a loop diuretic, with family history of kidney problems

A

bartter’s syndrome

defective NKCC

65
Q

what does PTH do to phosphate levels and where in the kidney does it work to do this

What does PTH do to Ca levels and where in the kidney does it work to do this

A

decreases them by inhibiting resorption in the PROXIMAL convoluted tubule

(it causes calcium resorption in the distal convoluted tubule)

66
Q

tryptophan gets converted into niacin with the help of what other vitamin

A

B6, pyridoxine

67
Q

what type of diabetes insipidus does lithium produce

A

nephrogenic DI

68
Q

mech of sulfamethoxazole

A

inhibition of dihydropteroate synthase

69
Q

common causes of interstitial nephritis

A

the P’s

Pee (diuretics)
Pain free (NSAIDs)
Penicillins and cephalosporins
Proton pump inhibitors
rifamPin
70
Q

acute transplant rejection of a kidney is caused by what type of cells

A

CD8

71
Q

non linear mesangial deposits of IgA in the kidney after a respiratory disease

A

bergers disease

assc with celiac disease

72
Q

chromosome defective in wilms tumors

A

11

deletion of the WT1 tumor suppressor gene

73
Q

what is seen in the urine in a patient with cystinuria

what is the treatment

A 
COLA
cystine
orntithine
lysine
arginine

and the cystine can for hexagonal cystine stones

Tx: urinary alkalizing agents (potassium citrate, acetazolamide), chelating agents (penicillamine, which also treats Cu, Pb and Au tox, but CAUSES membranous nephropathy, didn’t you know?)

74
Q

cola colored urine and orbital edema after being sick

A

post strep GN

hypercellular inflamed glomeruli on HandE, mediated by immune complex deposition, subepithelial humps on EM

75
Q

what cells secrete renin

A

juxtaglomerular cells

76
Q

antihypertensive medication that causes drowsyness and depression without altering electrolytes

A

clonidine, guanfacine

77
Q

obstructive jaundice

what happens to your urine bilirubin levels
what happens to your urine urobilinogen levels

A

urine bilirubin levels rise (conjugated) because the bilirubin in the gall bladder backs up, etc, etc

urine urobilinogen levels DECREASE because the bilirubin cannot get to the gut in obstructive jaundice, where bacteria normally convert bilirubin to urobilinogen

78
Q

what does secretin do

A

increases levels of bicarb in the stomach

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