مدرات البول Flashcards

1
Q

بسم الله الرحمن الرحيم وبه نستعين
فارج الهم كاشف الغم مجيب دعوة المضطرين رحمن الدنيا والاخرة ورحيمهما ارحمنا رحمة تغنينا بها عن رحمة من سواك
تغنينا: فعل مضارغ مرفوع وقعت الجملة الفعلية في محل الصفة ل رحمة وليست في محل جواب الطلب ل ارحمنا

ACEI & NSAIDs # in

A

renal hypoperfusion state

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2
Q

Renal hypoperfusion state casues?

A
Hypovolemia
Extensice dose of loop diretics
Heart failure
Liver cirrhosis
Nephrotic syndrome

ACEI Efferet VC
NSAIDS Afferent VD
Renal Hypoperfusion

Marked decrease in IGP And GFR

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3
Q

Glmerultubular balance?

tubuloglomerulat balance

A

in low GFR there is great reabsoprtion of Na Ca and H2O from tubule decreaisng urine volume

passage of Nacl in high amount to the macula densa decreasing PG synthesis thus decreaing VD of afferents so less GFR

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4
Q

Hypercalcemia and dehydration

A

Casuing vomiting and polyureae and dehydfration decreasing GFR and so increasing Reabsorption of Ca maitain the hypercalacemic state

IV saline to resolve the dehydration decreasing ca reabosortion
Loop direutic preventing reabsotption of Ca from Loop of Henle

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5
Q

CLASSIFICATION OF DIURTEIC ACCORDING TO K?

A
LOSING?
Loop
thiazide
CAEI
OSMOTIC

SPARING?>
Spironolactone , eplrenone
Amiloride , Triametrene

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6
Q

related to its natruretic effect

A

❖ High ceiling: Loop
❖ Moderate: Thiazides
❖ Low: K+ spairing & CAIs

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7
Q

All diureitcs except ? have to reach to the lumen of nephron to act → any defect in the delivery of diuretics to
lumen → ↓ responsee

A

spironolactone

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8
Q

Mannitol (osmotic diuretic): enters through GF. So Mannitol is # in ???because it can’t access to nephron → remain in blood → ?????? (Dilutional hyponatremia, Acute HF,…)

A

acute renal failure

circulatory overload

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9
Q

Loop & Thiazides: enter lumen through ??? → compete with→??

contraindicated in?

A

organic acid secreory system
uric acid secretion

Hyperuricemia and Gout

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10
Q

Amiloride & triamterene: → can be used in Gout??? why

A

enter through organic base secretory system

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11
Q

Loop diuretics: Their access to the lumen in renal failure is decreased due to accumulation of acid waste products in
blood → ↓ diuretic effect (Refractoriness: ↓ effect due to chronic use). Treatment:

A

↑ the dose of loop diuretics قرص ك

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12
Q

Spironolactone: enters to cells of DCT from ??????? to compete with aldosterone on its receptors

A

peritubular capillaries

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13
Q

thiazides + loop diuretic

A

In case of : Hyperplasia in early part of DCT due to chronic use of loop diuretics
to avoid refractoriness

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14
Q

Spironolactone + K losing diuretics

A

To avoid hypokalemia

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15
Q

Loop, thiazides, CAEI acidic drug ?

A

secteted by acid secretory sytem > hyperurecmeia # Gout

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16
Q

Amiloride trimatrine ?

A

secreted by oraginc base secretory system > used in Gout

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17
Q

Thiazides Less effective in RF (↓ GFR & Moderate ceiling). ???????????can be used in renal failure

A

Metolazone

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18
Q

Loop Dose should be increased in case of

A

Renal Failure

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19
Q

Mannitol # in Acute renal failure: can not reach to the lumen →

A

circulatory overload → # in acute renal faliure

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20
Q

. Hypokalemia ليه؟
+: قبل الخط Diuretics❖
decreaing Na reabsorption → ↑ Na+ delivry to the late part of DCT → ↑ Alodosterone → ↑ Na+ exchange with K+ and H+ → hypokalemia and alkalosis.
❖ Thiazides > loop: Part of delivered Na+ by loop diuretic is reabsorbed by early part of DCT before reaching macula densa
❖ Treatment: add

A

spironolactone

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21
Q

Diuretics inhibiting Na+

reabsorption → interfere with reabsorption of electrolytes related to Na+ at the site of action.

A

loop diureitcs ↓ Calcium (→Hypocalcemia) and Magnesium (→hypomagnesemia) reabsorption at ascending limb of
loop of Henle

هيبربوتاسيوم = هيبر ماجنسيوم والعكس صحيح reabsoprtion Magnesium ↑ spairing K

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21
Q

Loop dirutics work on ?

Thiazides?

A

Ascending loop of henle

Early part of DCT

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22
Q

lOOP examples?

A

frusemide : renal elmination with variable absorption
bumetanide hepatic elmination
toresmide

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23
Q

ThiaZides Examples/

A

Hydrocholrthalidone short acting
Chlotalidone long acting
Indapampide in HTN
Metolazone in Renal failure

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24
Q

Mechanism of loop

A

decerasing reabsorption of Na / k / 2cl and this leads to loss of Na20 and water
loss of meullary hypertonicity and loss absoprtion of water by medulla
loss of H20 > Na
PG production oVD of afferent and increasing GFR
decreasing the reabsorption of Na from the asecnding loop
#NSAIDS

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25
Q

Thiazaid mechnisms of action ?

A

Decreasing Reabsoption of Na at the early part of DCT and this exretion of Na and H20 > intial hypovolemia> movment of Na from the walls of blood vessels to blood
casuing VD

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26
Q

wHY LOOPS ARE USED IN ACUTE PULMONARY EDEMA/

A

DUE TO VENODILATOR EFFECT

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27
Q

whY USED LOOP IN ACUTE RENAL FAILURE ?

A

INCRSAING RENAL BLOOD FLOW

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28
Q

Thiazid are used in HTN ?

A

due to vasodilator effect

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29
Q

HTN and diretics?

A

loop diretics in hypertienon enephalipoathy
Thiaziade in HTN due to ?
1-intial diretic hypovolemic effect
2-2ry VD effect due to escape of Na from the wall of blood vessels into the blood

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30
Q

Indications of Loop diretics/

A

EEE
Emergency?
1-Acute pulmnary edema due to venodilator effect
2-Hypertensive enchepphalophaty

Edema referactory to other diuretics? 
Heart failure
renal insufficincy
liver ciirhosis
ARF due to increased RBF

Electrolytes DISTURBACNES:
Hypercalacemia : after saline increase gfr decrasing the ca reabsoptiom
Hyperkalemia : decreasing K reabsorption at the loop
the na reaching macula densa and aldosterone exhanging the K with NA causing K excretion
Hypervolemic dilutional hyponaterima : H20»Na
Distal renal tubular acidosis exchnge of H with Na excerting The H+

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31
Q

Hypercalacemia :

and loop

A

after saline increase gfr decrasing the ca reabsoptiom

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32
Q

Hyperkalemia and loop

A
33
Q

Hyperkalemia and loop

A

decreasing K reabsorption at the loop

the na reaching macula densa and aldosterone exhanging the K with NA causing K excretion

34
Q

Hypervolemic dilutional hyponaterima :

A

H20»Na

35
Q

Distal renal tubular acidosis

A

exchnge of H with Na excerting The H+

35
Q

Distal renal tubular acidosis

A

exchnge of H with Na excerting The H+

36
Q

Hert failrure and dirtucs?

A

Loop in acute heart failure

Thiazid in loop refecatriness in congestive heart failure

37
Q

Adverse effects of loops

A
Hypovolenmia L hyptension collapse also thizia
Hypokalemia < thiazide
Hypomagneisuma also thi
Hypocalacemia 
Hyperurecemia also thi
Organs:
ototoxicity 8th cranial nerve
Git upset
intersitial nephritis
Myalgia 
Hypersenesitvity reactions
Refractoriness
38
Q

Thiazaid indication

A

cvs and renal
CVS
Hyper tension due to intial dirtic + 2ry VD effect
Congetice heart failure in loop refreactoriness

Renal :
nephrogein diabitus inspidus by decrasing PGs decasring GFR decreasing urine output

Idipathic calcuiria and ca stones : decreasing the GFR increasing the ca reabosortion

39
Q

Mention adverse effects of the Thiazides?

A

Hypokalemia and alkalosis
HypoMangsisumia
Hyponatreima due to decrease exchangre at early part of distal convoluted tubule
Hyperureicemia due to acid competition
Hypersensitvity
Glucose intolerance potassium out of beta cells decrasing insulin release
Hyperlipidemia
Hepatic encephaloiphathy: NH4TO NH3 CROSSING BBB
impOtenece

40
Q

Mention SPECIAL adverse effects of the Thiazides?

A

Glucose intolerance potassium out of beta cells decrasing insulin release

Hepatic encephaloiphathy: NH4TO NH3 DUE TO ALKALOSIS CROSSING BBB

41
Q

Contraindications of Thiazides?

A

In edema of liver cirrhosis to avoid hepatic encephalopathy

In edema of renal failure cuz it is ineffective in low GFR

42
Q

ethacrynic acid)

A

GIT upset

43
Q

bumetanide)

A

Myalgia (

44
Q

Kinetic refratoriness of the Loops?

A

1- Decrease in intestinal absorption due to decompenstaed heart failure what solve?
IV injection
2-Decreasing plasma protein binding due to nephrophaty or liver cirrhosis?
Mixing the drug with albumin in vitro
3-decerases excretion of diuretic by the acid secretory system due to renal failure due to accumulation of acid metabolites :
increases the dose of Frusemide 5 folds

45
Q

Dynamic refratrincess of loop diuretics?

A

1-Hypertrophy of early part of DCT increasing Na reabosrption > Thiazide
2-Hyperalodsterniusm increasing na exchange with K in distal DCT > Spironolactone aldosterone antagonist

46
Q

1K sparing dirtics
2osmotic
3carobonic anydrase
site of action ?

A

1-DCT
2-PCT and descending limb of loop of henele and Collecting tubule
3-PCT

47
Q

indirect K sparings?

A

Spironloactone and Eplernone
Inhibits aldosternoe preventions of mediator protein synthesis
no synthesis of Na channels of luminal DCT

Used in CHF + LOOP + ACEI
Used in Hyperaldosteronism Edema
Delayed onset (3days)
Long acting

48
Q

Direct K sparing?

A

Amiloride
trimaterene

Short onset
Short acting

Hypokalemia
HypoMagnusmia
Combined with K losing diuretics

49
Q

Adverse effects of Potassium sparing diuretics ?

A

Hyperkalemia
Metabolica acidosis

INDirect spironlocatone Gyncomastia : due to anatgonizing androgen receptors

50
Q

IVI Mannitol Mechanism of Action

?

A

filtration not rabsorped
increasing osmolarity of the urine keepin h20 in tubules
Pereserve Na and kick out h20

51
Q

Mannitol not deffective in Heart failure?

A

due to Na over load edema
and mannitol is preserving agent of Na
decreasing reapsotoptrion of Na < < decreasing reabsorption of H2o
meaining it presreves Na and get rid of H2o

52
Q

Osmotic diretics indications

A

IVI Mannitol is used in
Dehydrating agent for ?
Cerebral edema and icp
Acute glucoma IOP

Prophylaxis in ?- ARF pateint with oliguria caused by trauma or hemolytic reaction

53
Q

Adverse effects of mannitol

A
only if in ARF?
Cirulatory overload
Acute heart failure
Dilutional hyponatremia
Acute pulmonary edema
54
Q

Carbonic anhydrase inhibitors (CAIs)

A
Weak diuretic (most of Na+ lost is 
reabsorbed again in distal nephron)
55
Q

Examples of CAEI

?

A

Acetazolamide
Methozolamid
Brizolamide
Dorzolamide

56
Q

Mech of CAEI?

A

Easy!?
Decresing CAE Activity of production of H+ - Decreasing NaHCO3 reabsorption and it is excreted in urine
Alkaline urine
Acidic Blood

57
Q

Methazolamide is preferred

A

Glaucoma: act & chronic. ↓

aqueous humor formation

58
Q

Carbonic anydrase inhibitors indications ?

A

3E A

Emphysema and high altitude sickness
Excretion of acidic drugs as aspirin and barbituates toxicity
Epilipsy
Acute and chronic gluocoma methozolamide

59
Q

Adverse effects of the CAEI ?

A
MRCH
Metabolic acidosis and CNS depression
Refractoriness
Ca Po4 Stones (alkaline urine)
Hypersensitvity
60
Q

Amilordie ant triametrene pereferd than Spironloactone in hyokalmeia/

A

due to ability of daily adjustment of doseage dut to short action and rapid action

61
Q

K-sparing diuretics are combined with K+ losing diuretics (thiazides& loop)

A

To potentiate their diuretic effect & to antagonize their hypokalemic effect (more effective than exogenous K+ & Mg
++ supplement)

62
Q

Spirnolactone preferd in liver cirrhosise ?

A

In liver cirrhosis there is hyperaldosternoism and Spirnolactone and aldostenoe antagonist

Thiazide has minmal effect beacus lost na is reabsorped at the late part of DCT

Spironloactone not casuing Hypokalemia or alkalosis avoding hepatic encephalophathy

63
Q

Loop diuretics can be used in refractory edema of liver cirrhosis only after ?

A

full dose of spironolactone why??? to avoid development

of hypokalemia and alkalosis that may lead to hepatic encephalopathy

64
Q

Carbonic Anhydrase Inhibitors are weak diuretics:

A

because most of the fluids & Na+

lost are reabsorbed again at more distal sites

65
Q

Loop & thiazides diuretics induce hypokalemia:

A

They ↑ Na+ delivered to late part of DCT → excretion of K+ & H+
in exchange with Na+ reabsorption by aldosterone (avoided by adding spironolactone)

66
Q

Vasopressin receptors
• V1A: Vascular → ?
• V2: ?
• V1A & V1B :?

A

Vasoconstriction → control blood pressure
Renal → H20 reabsorption from collecting ducts
CNS receptors

67
Q

(Vaptans) :Vasopressin Receptors Antagonists indications

A

Evlumic hyponateremia L SIADH High aldosterone

Hypervolemic Hyponatremia : Congestive heart failure

68
Q

ACEI & NSAIDS are contraindicated in any cause of ??? to avoid development of acute renal
failure

A

renal

hypoperfusion

69
Q

Lithium (antidepressant) toxicity is enhanced with

A

diuretics (Thiazides & loop)

70
Q

NSAIDs inhibit Prostaglandin (PG) synthesis

A

VC Of aFFRENTS decrasing GFR

71
Q

SIADH:

A

Syndrome of Inappropriate anti-diuretic hormone secretion

72
Q

Hypercalcemia

Hypercalcuria

A

loop

thiazide

73
Q

Hypokalemia

A

amiolride

triametrene

74
Q

Hyperkalemia

A

Loop

75
Q

Hypervolemic Dilutional Hyponatremia

A

Loop

76
Q

Renal tubular Acidosis

A

Loop

77
Q

Alkalosis due to sick sinus syndrome and

emphysema

A

CAEI

78
Q

الحمدلله الذي أنزل علي عبده الكتاب ولم يجعل له عوجا

A