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First Aid > Renal > Flashcards

Renal Flashcards

1
Q

Atrial Natriuretic peptide (ANP) and BNP function on the kidney?

A

constricts EFFerent arterioles

DILATES AFFerent arterioles

thus inc GFR, Diuresis (natriuresis)

MOA: ANP/BNP stimulated to inc volume –> relaxes vascular smooth muscle via cGMP–> inc GFR and Dec renin.

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2
Q

Vasopressin (ADH) effect on kidney

A

water reabsorption

urine concentration

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3
Q

prostaglandins are secreted from? and whtas its affect on kidney

A

paracrine secretion from kidney leading to vasodilation of the AFFerent arterioles to inc RBF. and GFR

no change to FF

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4
Q

what does dopamine secreted from the PCT at high doses due ?

A

acts as a vasoconstrictor

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5
Q

what does dopamine secreted from the PCT in low doses do>

A

promotes natriuresis.

dilates interlobular arteries, AFFerent adn Efferent arterioles –> inc RBF little to no change in GFR.

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6
Q

what is diagnosis

LOW serum Osmolality

Low serum Na

associated with (small cell lung cancer, pulm pathology, head trauma, stroke, cns infections, drugs “cyclophosphamide”)

A

SIADH

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7
Q

in SIADH

you would expect BP, Plasma renin, aldosterone,

to inc, dec, or no change?

A

BP: no change or inc

Plasma RENIN; dec

aldosterone Dec

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8
Q

diagnosis ?

inc urine Volume

dilute urine

HIGH serum osmolarity

LOW urine specific gravity

A

diabetes insipidus

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9
Q

what drug can cause diabetes insipidius by blocking the insertion of Aquaporins into the lumen side stimulated by ADH for water reabsorption.

and how would you treat this?

A

lithium causes it by entering the principle cell.

amiloride (blocks the na channels lithium uses to enter the principle cell)

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10
Q

drugs and other causes that can cause nephrogenic diabetes insipidus by making the kidneys unresponsive to ADH are?

A

lithium

demeclocyline (can treat SIADH)

hypercalcemia

mutation of ADH receptor gene

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11
Q

central DI treatment

A

Intranasal Desmopressin and hydration

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12
Q

Nephrogenic DI

tx

A

1st line = hydrochlorothiazide

causes the pt to become a little dehydrated. thus the PCT will now reabsorb more water

2nd line = indomethacin (it inhibits prostaglandin synthesis decreases RBF –> dec urine output)

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13
Q

the promixal tubue and loop of henle due what to urine

the distal tubule does _____

the collecting tubule____ does what

A

PCT and loop henle concentrate the urine

the DT = dilutes

collecting tubule = concentrates it again

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14
Q

what two electrolyte inbalances can lead to

prolongation of QT interval (widened QRS)

V-Tach, torsades de pointe.

A

HYPOkalemia

HYPOmagnesium

note hyperkalemia can lead to Vtach

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15
Q

what is the Classic ECG finding for

hyperkalemia

hypokalemia?

A

remember: the T waves mirror the K+ levels

HYPOkalemia –> Flattened T waves

really low –> U wave.

Hyperkalemia –> Tall and peaked T waves

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16
Q

____________________ causes K shift OUT of cells–> HYPERKALEMIA

“DO LABSS”

A

lOW insulin ( DKA)

B-blockers

Acidosis

(cells are tryign to correct the acidosis by moving the excess H ions out of the blood by exchanging K ions for H ions

Digoxin (blocks Na/K/ATPase)

Cell lysis (leukemia, _crush injur_y, rhabdomyolysis)

maybe Succinylcholine (inc risk in burns/muscle trauma)

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17
Q

what caues K shift into cells –> HYPOkalemia

A

Insulin

B-agonists

Alkalosis

Cell creation/proliferation

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18
Q

what intervention would correct this finding?

A

1st treatment! IV Caclium to prevent arrhythmias

(does not correct the hyperkalmeia, just stablize)

we need to shift K back into the cells!!!

acute treatment B-agonist (albuterol)

IV bicarb to cause Alkalosis

Dextrose 1st + IV insulin.

you see tall peaked T waves (hyperkalemia)

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19
Q

low serum concentrarton of Mg2+

you would expect?

A

tetany, torsades de points (vtach)

HYPOkalemia,

HYPO calcemia (when [Mg2+] < 1.2 mg/dL)

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20
Q

high Mg2+ (hypermag) you would expect?

A

dec DTRs

llethargy, bradycardia,

hypotension

cardiac arrect

hypocalcemia.

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21
Q

low PO43- (hypophos)

you would expect

A

bone loss,

osteomalacia (adults)

rickets (children)

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22
Q

high serum concentration of PO43- (HYPERphosphatemia) you would expect what findings/ labs

A

renal stones

metastatic calcifcations

hypocalcemia

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23
Q

pt with

polyuria

dilute urine (low specific gravity and osmolality)

water deprivation test –> urine osmolarity does not inc.

whats the diagnosis.

A

Diabetes insipidus

then give desmopression

central = urine osmolarity inc

nephrogenic = no change

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24
Q

what causes anion gap acidosis

MUDPILES

A

Methanol (formic acid

Uremia

Diabetic ketoacidosis

Proylene glycol

Iron tablets or INH

Lactic acidosis (think pt thats in shock not perfusing)

Ethulene glycol (–> oxalic acid)

Salicylates (late)

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25
Q

causes of norma lanion gap metabolic acidosis

HARDASS

A

Hyperalimentation

.Addison Disease

Renal tubular acidosis

Diarrhea

Acetazolamide

Spironolactone

Saline infusion.

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26
Q

causes of respiriatory alkalosis

A

(hyperventilation)

  • psychogenic​
  • high altitude
  • PE
  • aspirin toxicity (only acutely)
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27
Q

causes of metabolic alkalosis?

A

excessive vomiting

diuretic

  • (loss chloirde and the hypocloremia causes alkalosis) or thiazides –> K excretion

hyperaldosteronism

  • triad: hypokalemia, htn, metabolic alkalosis

a

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28
Q

what type of renal Tubular acidosis

urine pH > 5.5

HYPOkalemia

metabolic acidosis (all RTA have normal anion gap metabolic acidosis)

A

type 1 distal

defect in alpha intercalated cells in collecting tubule unable to secrete H+

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29
Q

what type of renal tubular acidosis?

urine ph < 5.5

HYPERkalemia

A

type 4 hyperkalemic RTA

hypoaldosteronism –> hyperkalemia –> dec NH3 synthesis in PCT –> dec NH4+ (ammonium) excretion

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30
Q

what type of renal tubular acidosis

phypokalemia

hypophosphatemia

inc bicarb in urine

urine ph < 5.5

A

type 2 proximal renal tubular acidosis

defect in PCT HCO3- reabsorption –> inc excretion of bicarb in urine –> metabolic acidosis.

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31
Q

what nerve runs with anterior interoseesous artery?

A

ant interousseous nerve

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32
Q

what nerve runs with posterioro interosseous artery

A

deep branch of the radial nerve

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33
Q

what nerve runs with the posterior circumflex artery

A

axillary nerve

34
Q

suprascapular artery runs with what nerve?

A

suprascapular nerve

35
Q

deep brachial artery runs with?

A

radial nerve

36
Q

dorsal scapular artery runs with

lateral thoracic artery runs with?

A

dorsal scaqpular nerve.

long thoracic nerve

37
Q

ulnar artery runs with

brachial artery runs with

A

ulnar nerve

median nerve

38
Q

linear pattern of IgG deposition on IF

A

Goodpasture disease

type II HSR

39
Q

lumpy-bumpy deposits of IgM, IgM, and C3 in the Mesangium

A

poststreptococcal glomerulonephritis

40
Q

deposits of IgA in the mesangium

A

IgA nephropathy

41
Q

Anti-GBM antibodies

Hematuria,

hemoptysis

A

Good pasture disease

42
Q

crescent formation in the glomeruli

A

rapidly progressive glomerulonephritis

43
Q

wire loop appearance on LM

A

lupus nephritis

(diffuse proliferative glomerulonephritis)

44
Q

describe what labs and symptoms that are associated with Nephrotic syndrome

A

proteinuria > 3.5 g/day

hypoalbuminemia

edema

inc risk of infection

inc risk of thrombosis

hyperlipidemiab (bc when oncotic pres falls it stimulates the liver to make more lipoprotiens)

45
Q

child presenting with proteinuria > 3.5 g/day

edema w.out inciting event

pitting edema.

on labs 3+ proteinuria, hypoalbuminemia, hyperlipidemia.

what would you expect to see on LM and EM

A

minimal change disesase (Lipoid nephrosis)

LM- normal glomeruli​ (lipid may be seen in PCT cells

EM- effacement (flattening) of FOOT PROCESSES

46
Q

if you see HIV + or sickle cell disease, or heroin abuse.

that is African american or hispanic and nephrotic syndrome.

you expect to see what on LM, IF, EM

A

LM - segmental focal sclerosis and hyalinosis

  • affects less than half of glomeruli, certain regions affected

IF - often negative, but may be + for nonspecific focal deposits of IgM, C3,C1

EM- effacement/dearrangement of foot process similar to minimal change disease

biospy: mesangial collapse w/ sclerosis of some glomeruli

47
Q

if you see this image what renal syndrome is it

A

membranous nephropathy

you see spike and dome appearance with subepithelial dposits

on LM you see diffuse capillary and GBM thickening

48
Q

all the following can cause/

hep B

hep C

Lupus

Subacute bacterial endocarditis

A

(MPGN)

membrano-proliferative glomerulonephritis

49
Q

subepithelial humps

decreased C3 levels

coca colal urine

+ anti-DNAse B titer

A

Post streptococcal GN

50
Q

mesangial deposits of IgA

Henoch-Schonlein purpura

may occur after URI

AKA berger disease

A

Iga nephropathy

51
Q

protein deposits in heart, liver, and kidney

apple green birefrinigence

associated with multiple myeloma

A

amyloidosis

52
Q

defect in type IV collagen

Cataracts

Nephritis

High freequency HEARing loss

A

Alport syndrome

cant see can pee cant hear high C

53
Q

diffuse proliferative GN

“wire loop” basement membranes

Anti-dsDNA ab

A

Lupus nephritis

54
Q

Microscopic hematuria

Pulmonary infiltrates

type II HSR

anti-GBM ab

A

Goodpastures syndrome

55
Q

hematuria and proteinuria

Pulmonary infiltrates

Nasopharyngeal granulomas

C-ANCA

A

Granuomatosis w/ polyangiitis (Wegener’s)

56
Q

proteinuria and edema

podocyte foot process effacement

most common causes of nephrotic syndrome in children

TX corticosteriods

A

Minimal change disease

57
Q

most common cause of nephrotic syndrome in

us adults

hiv pts

blacks and latinos

A

Focal segmental glomerulosclerosis

58
Q

what is the most common tumor of urinary tract system (renal calyces, renal pelvis, ureters and bladder)

A

transitional cell carcinoma (urethelial carcinoma_)

NOT: RCC which is the most common tumor of the kidney itself

59
Q

how does transitional cell carcinoma present

A

painless hematuria

60
Q

what are the risk factors for transitional cell carcinoma?

know these

pnemonic

“Pee SAC:

A

Phenacetin

***Smoking

Aniline dyes

Cyclophosphamide

61
Q

you have a pt that presents with painless hematuria. upon further workup he tells you that hes from the middle east and travels to africa to visit his family. you further work him up and diagnosis him with squamous cell carcinoma of the bladder

what is the most likely strongest risk factor for this patient and how would you treat the cause?

A

Schistosoma haematobium infection

treat with praziquantel

62
Q

most common renal malignancy in early childhood (2-4)

A

wilms tumor

63
Q

most common type of renal stone

A

calcium oxalate

64
Q

type of renal stone associated with proteus vulgaris

A

struvite stones

65
Q

most common primiary renal tumor in adults

A

RCC

66
Q

pt complains of not being able to reach the bathroom in time.

you diagnosis her with urgency incontinence

what is the pathogensis behind this and the tx

A

overactive bladders (detrusor instability*) –> leak with urge to void immediately.

antimuscarinics (oxybutynin.

also (combank) says you can use

antispasmodics (tolterodine)

effects smooth m –> inc bladder capacity, dec uninhibited contraction, ,dec desire to void.

67
Q

outflow incontinence is caused by?

A

incomplete empyting secondary to (detrusor underactivity or outlet obstruction) –>

increased POST VOID RESIDUAL on ultrasound and catheterization!!!!!1

68
Q

in fanconi syndrome. what part of the nephron is defective. and electrolyte disturbances do you expect to see

A

PCT

thus no absorption of glucose, amino acids, bicarbg, phosphate.

69
Q

Bartter syndrome is a reabsorption defect in what part of the nephron?

bartter syndrome is an autosomal_________ mutation of what transporter

A

thick ascending loop of henle

autosomal Recessive mutation iin the NA/K/2Cl cotransporter

70
Q

Bartter syndrome results in what electrolyte abnormalities

A

hypokalemia

metabolic ALKALOSIS .

71
Q

Giltelman syndrome is an autosomal Recessive mut of what part of the nephron and what cotransporter

A

distal convoluted tubule

and

Na/Cl cotransporter

note similiar to thiazides

and less severe than bartter syndrome bc most of the Na reabsorption occurs in early nephron

72
Q

Liddle syndrome results in ________ in the distal collecting tubules due to iinc activity of the epithelial Na channel

A

inc Na reabsorption in the distal collecting tubules

73
Q

liddle syndrome is autosomal____

and causes?

A

htn,

hypokalemia

metabolic Alkalosis

dec Aldosterone.

it presents like hyperaldosteronismb but aldosterone is nearly undetectable.

74
Q

treatment for liddle syndrome?

A

Amiloride which blocks Na reabsorption channels (Enac)

75
Q

Syndrome of Apparent Mineralcorticoid Excess

cortisol tries to be the SAME as aldosterone

is a hereditary def of ____ enzyme

A

11B-hydroxysteroid dehydrogenase

that normally converts

cortisol (active) —> cortisone (nonactive)

76
Q

Syndrome of apparent mineralocorticoid

will present with

A

htn

Hypokalemia

metabolic Alkalosis

low serum aldosterone levels.

77
Q

if a child presents with symptoms characteristic of Syndrome of apparent mineralocorticoid excess (11B hydroxysteroid dedhydrogenase) and you ruled out the inherited cause. what is another possible acquired cause?

A

Glycrrhetinic acid (present in licorice) which blocks the actibity of 11B hydroxysteroid dehydrogenase

78
Q

treatment of Syndrome of apparent mineralocorticoid excess

A

corticosteroids (exogenous corticosteroids dec endogenous cortisol prodcution–> dec mineralocorticoid receptor activation.

79
Q

which renal tubular defect has

hypokalemia and metabolicalkalosis with HYPERCALCIURIA

A

bartter syndrome

80
Q
A

First Aid (15 decks)

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