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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
causes of norma lanion gap metabolic acidosis ## Footnote **HARDASS**
**H**yperalimentation .**A**ddison Disease **R**enal tubular acidosis **D**iarrhea **A**cetazolamide **S**pironolactone **S**aline infusion.
26
causes of **respiriatory alkalosis**
**(hyperventilation)** * **psychogenic​** * **high altitude** * **PE** * **aspirin toxicity (only acutely)**
27
causes of metabolic alkalosis?
**excessive vomiting** **diuretic** * (loss chloirde and the hypocloremia causes alkalosis) or thiazides --\> K excretion **hyperaldosteronism** * triad: hypokalemia, htn, metabolic alkalosis a
28
what type of renal Tubular acidosis **urine** pH \> **5.5** **HYPOkalemia** metabolic acidosis (all RTA have normal anion gap metabolic acidosis)
**type 1 distal** defect in **alpha intercalated cells** in collecting tubule unable to **secrete H+**
29
what type of renal tubular acidosis? ## Footnote **urine ph \< 5.5** **HYPERkalemia**
type **4** hyperkalemic RTA **hypoaldosteronism --\>** hyperkalemia --\> dec NH3 synthesis in PCT --\> dec NH**4**+ (ammonium) excretion
30
what type of renal tubular acidosis ## Footnote **phypokalemia** **hypophosphatemia** **inc bicarb in urine** **urine ph \< 5.5**
type **2** **proximal renal tubular acidosis** **defect in PCT HCO3-** reabsorption --\> inc excretion of bicarb in urine --\> metabolic acidosis.
31
what nerve runs with anterior interoseesous artery?
ant interousseous nerve
32
what nerve runs with posterioro interosseous artery
deep branch of the radial nerve
33
what nerve runs with the **posterior circumflex artery**
**axillary nerve**
34
suprascapular artery runs with what nerve?
suprascapular nerve
35
**deep brachial arter**y runs with?
**radial nerve**
36
**dorsal scapular artery runs with** **lateral thoracic artery** runs with?
**dorsal scaqpular nerve.** **long thoracic nerve**
37
**ulnar artery** runs with **brachial artery** runs with
ulnar nerve **median nerve**
38
**linear pattern** of **IgG** deposition on IF
**Goodpasture disease** **type II HSR**
39
lumpy-bumpy deposits of **IgM, IgM,** and **C3** in the **Mesangium**
**poststreptococcal glomerulonephritis**
40
deposits of **IgA** in the **mesangium**
**IgA nephropathy**
41
**Anti-GBM antibodies** **Hematuria,** **hemoptysis**
Good pasture disease
42
**crescent formation in the glomeruli**
rapidly progressive glomerulonephritis
43
**wire loop appearance** on LM
**lupus nephritis** **(diffuse proliferative glomerulonephritis)**
44
describe what labs and symptoms that are associated with Nephrotic syndrome
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
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
minimal change disesase (Lipoid nephrosis) **LM- normal glomeruli​** (lipid may be seen in PCT cells **EM- effacement (flattening)** of **FOOT PROCESSES**
46
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
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
if you see this image what renal syndrome is it
membranous nephropathy you see **spike and dome** appearance with s**ubepithelial dposits** on LM you see **diffuse capillary and GBM thickening**
48
all the following can cause/ **hep B** **hep C** **Lupus** **Subacute bacterial endocarditis**
**(MPGN**) **membrano-proliferative glomerulonephritis**
49
**subepithelial humps** **decreased C3 levels** **coca colal urine** **+ anti-DNAse B titer**
Post streptococcal GN
50
mesangial deposits of **IgA** **Henoch-Schonlein purpura** **may occur after URI** **AKA berger disease**
Iga nephropathy
51
protein deposits in heart, liver, and kidney apple green birefrinigence associated with multiple myeloma
amyloidosis
52
defect in type **IV collagen** ## Footnote **Cataracts** **Nephritis** **High freequency HEARing loss**
**Alport syndrome** cant see can pee cant hear high C
53
**diffuse proliferative GN** **"wire loop" basement membranes** **Anti-dsDNA ab**
**Lupus nephritis**
54
**Microscopic hematuria** **Pulmonary infiltrates** **type II HSR** **anti-GBM ab**
**Goodpastures syndrome**
55
**hematuria** and **proteinuria** **Pulmonary infiltrates** **Nasopharyngeal granulomas** **C-ANCA**
**Granuomatosis w/ polyangiitis (Wegener's**)
56
**proteinuria** and **edema** ## Footnote **podocyte foot process effacement** **most common causes of nephrotic syndrome in children** **TX corticosteriods**
Minimal change disease
57
most common cause of nephrotic syndrome in ## Footnote **us adults** **hiv pts** **blacks and latinos**
**Focal segmental glomerulosclerosis**
58
what is the most common tumor of **urinary tract system (**renal calyces, renal pelvis, ureters and bladder)
**transitional cell carcinoma** (urethelial carcinoma\_) NOT: RCC which is the most common tumor of the kidney itself
59
how does transitional cell carcinoma present
**painless hematuria**
60
what are th**e risk facto**rs for **transitional cell carcinoma?** know these pnemonic "**P**ee **SAC**:
**P**henacetin **\*\*\*_S_**_moking_ **A**niline dyes _**C**yclophosphamide_
61
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?
***Schistosoma haematobium*** infection treat with **praziquantel**
62
most common renal malignancy in early childhood **(2-4)**
**wilms tumor**
63
most common type of renal stone
**calcium oxalate**
64
type of renal stone associated with ***proteus vulgaris***
**struvite stones**
65
most common primiary renal tumor in adults
**RCC**
66
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
**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
outflow incontinence is caused by?
incomplete empyting secondary to (**detrusor underactivity** or **outlet obstruction) --\>** **increased POST VOID RESIDUAL on ultrasound and catheterization!!!!!1**
68
in fanconi syndrome. what part of the nephron is defective. and electrolyte disturbances do you expect to see
**PCT** thus no absorption of glucose, amino acids, bicarbg, phosphate.
69
**Bartter syndrome** is a reabsorption defect in what part of the nephron? bartter syndrome is an autosomal\_\_\_\_\_\_\_\_\_ mutation of what transporter
**thick ascending loop of henle** autosomal Recessive mutation iin the NA/K/2Cl cotransporter
70
**B**artter syndrome results in what electrolyte abnormalities
**hypokalemia** **metabolic ALKALOSIS .**
71
**G**iltelman syndrome is an **autosomal Recessive** mut of what part of the nephron and what cotransporter
**distal convoluted tubule** ## Footnote **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
**Liddle syndrome** results in ________ in the distal collecting tubules due to i**inc activity of the epithelial Na channel**
inc **Na** reabsorption in the **distal collecting tubules**
73
**liddle syndrome** is autosomal\_\_\_\_ and causes?
**htn,** **hypokalemia** **metabolic Alkalosis** **dec Aldosterone.** it presents like **hyperaldosteronismb** but **aldosterone** is nearly **undetectable.**
74
treatment for **liddle syndrome?**
**Amiloride** which blocks Na reabsorption channels (Enac)
75
**S**yndrome of **A**pparent **M**ineralcorticoid **E**xcess cortisol tries to be the **SAME** as aldosterone is a hereditary def of ____ enzyme
**11B-hydroxysteroid dehydrogenase** that normally converts cortisol (active) ---\> cortisone (nonactive)
76
**Syndrome of apparent mineralocorticoid** will present with
**htn** **Hypokalemia** metabolic **Alkalosis** low serum aldosterone levels.
77
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?
**Glycrrhetinic acid (**present in **licorice)** which blocks the actibity of 11B hydroxysteroid dehydrogenase
78
treatment of Syndrome of apparent mineralocorticoid excess
**corticosteroids** (exogenous corticosteroids dec endogenous cortisol prodcution--\> dec mineralocorticoid receptor activation.
79
which renal tubular defect has **hypokalemia** and metabolic**alkalosis** with **HYPERCALCIURIA**
bartter syndrome
80

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