Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

RENAL > ACE INHB and Nephrotoxic DRUGS > Flashcards

ACE INHB and Nephrotoxic DRUGS Flashcards

1
Q

Type of drug

Hydroclorothiazide,Clorothiazide,chlorthalidone

A

Thiazide Diuretic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Special use of Thiazide diuretic (2)

A

-Hypertension+osteoporosis
-Hypertension+Kidney stone(Ca++ related)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Thiazide promotes:
excretion :
reabp:

A

-Hypokalemia,Hypocloremia,HYPERTG and HYPERCHOLESTEROL
-Hypercalcemia,Hyperurecemia,metabolic alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Indapamide?

A

-Thiazide diuretic used for patients with Hyper TG and Hyper-cholesterol.
-ONLY thiazide that dosent incr TG and cholesterol in blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

-Torsemide,Bumetanide
-use

A

Loop Diuretics (Furosemide)
-Edematous states, Hypercalcemia (since promotes excretion of Ca++)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

A.E Loop Bumetadine,Furosemide,Tosemide

A

-Ototoxicity
-Sulfa Drug
-metabolic alkalosis
-Hypokalemia
-Hypocalcemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What drug should be carefully adm with Fursemide? (2)

A

-Aminoglycoside(ototoxicity)
-Digoxin (hypokalemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Mannitol type of drug?
-Use for..

A

-Osmotic diuretic
-Intra-occular pressure increased (ACUTE Glaucoma)
-Intra-cerebral pressure increased.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

-Acetezolamide use?
-Adverse effects

A

-High altitude sickness
-Not ACUTE Glaucoma
-Metabolic alkalosis
-Hypokalemia, Precipitation of Ca++-phosphate stones–>alkalanization of pH.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Amiloride use and mechanism.

A

-Direct Enac channel inhb. (K+ sparring diuretic)
-Used for **Diabetus Insipidus relating Lithium. **

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

K+sparring diuretic A.E?

A

-Hyperkalemia
-Nephrolithiasis
-Gynecomastia in MALES(anti-androgenic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Spironolactone + Loop diuretics used in…

A

Congestive Heart Faliure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

ACE INHB+Spironolactone used for…

A

Incr survival in HF.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Patiromer used?

A

Treats HYPERKALEMIA
-Bind K+ in interstine–>incr excretion in feces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Conivaptan and Tolvaptan used

A

-Anti-ADH
-Euvolemic or Hypervolemic Hyponatremia
-A.E:Hypokalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

-Blocks Angiotensinogen to angiotensin 1 (direct renin inhibitor)

A

Aliskiren

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Aliskiren use?

A

-Hypertension, also be used for preventing progression of diabetic nephropathy. Also decr GFR.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Contraindication of Aliskiren.

A

-Given along side ACHE inhb and ARB. Massive decrease in GFR.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Angiotensinogen is made where?

A

Liver.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Characteristics

Ethacrynic acid?

A

-Acts same as Loop diuretic but is NOT sulfa drug
,but is more OTOTOXIC.

21
Q

-ACEH inhb. use (4)
-A.E (4)
-Mecanism action

A

-Hypertension, Protenuria, Diabetic Neuropathy (releives hyperfiltration–>slows down GBM thickening),HF (decr mortality)

-Cough, Angioedema (INCR. Bradykinin–>Contraindicated in C1 Esterase defc.–>Has incr bradykinin), Teratogen, Hyperkalemia, Renal Injury in bilateral renal artery stenosis,incr creatinine

-Dilate both efferent and afferent renal arterioles.

22
Q

If uric acid is increased think of what 2 drugs?

A

Loop diuretics (except etharnic acid) and Thiazide Diuretics

23
Q

What drug?

Adverse effects include hyperGlycemia, hyperLipidemia, hyperUricemia, and hyperCalcemia (hyperGLUC).

A

-Thiazide
-You differentiate with Loop with TG elevation and hyperglycemia which it DOSENT cause.

24
Q
Furosemide Hydralazine Hydroclorothiazide Nitroglycerin Spironolactone
A

-Spironolactone
-Based on the musculoskeletal symptoms and the ECG showing peaked T waves (see next image), this patient has been taking a medication that causes hyperkalemia. Peaked T waves and elongation of the PR interval are important early signs of severe (emergent) hyperkalemia, usually with serum potassium >6 to 7 mEq/L,

25
Q

A 56-year-old man comes to the clinic because of excruciating pain in his right great toe for 2 days. Two weeks ago, he was diagnosed with uncontrolled hypertension and prescribed a new medication. Blood pressure is 135/85 mm Hg. Physical examination reveals an erythematous, warm, and exquisitely tender right great toe.

Whats the drug?

A

-Thiazide diuretic

26
Q

-A 75-year-old man is brought to the emergency department with increasing confusion. He has a history of lung cancer and is currently undergoing chemotherapy and radiation therapy. Two weeks ago, he was started on hydrochlorothiazide and enalapril for hypertension. Pulse is 80/min, and blood pressure is 126/78 mm Hg. The physical examination is normal except for disorientation to time and place. Serum studies show a sodium level of 122 mEq/L, potassium of 3.9 mEq/L, and creatinine of 0.9 mg/dL. ADH level is in the low-normal range.

Which of the following describes the most likely mechanism of this patient’s hyponatremia?

Aldosterone inhibition
Decreased glomerular water filtration
Decreased urinary diluting capacity
Hypovolemia
Increased posterior pituitary ADH release
Neoplastic secretion of ADH

A

-Decreased urinary diluting capacity

-Euvolemic hyponatremia will cause hyponatremia without signs of volume depletion or excess, and can be due to SIADH, chronic kidney disease, or thiazides.
Thiazide diuretics may cause hyponatremia by inhibiting NaCl absorption and limiting the ability of the kidney to dilute the urine.

27
Q

ACHE INHB characteristics

A

first-line medications for treating hypertension and heart failure. They are known to cause hyperkalemia, the risk for which is increased when these medications are prescribed along with potassium-sparing diuretics such as spironolactone.

28
Q

53-year-old woman is brought to the emergency department because of nausea and confusion. She has been preparing for a marathon and just finished a 4-hour run in cool weather during which her only intake was water. Medical history is significant for hypertension, well controlled with medication. Pulse is 86/min and blood pressure is 126/82 mm Hg. She is disoriented to time. The remainder of the physical examination is normal. Serum sodium level is 121 mEq/L.

Which of the following is the most likely cause of this patient’s symptoms?

A

-Severe hyponatremia may cause cramping, confusion, and seizures.
-Thiazide diuretics can cause severe hyponatremia, especially in the setting of high water and poor solute intake.
-patients on loop diuretics who have hyponatremia are uniformly hypovolemic (orthostasis, tachycardia, low blood pressure), thiazide-taking patients with hyponatremia usually do not appear hypovolemic. **
-This is because thiazides act in the distal convoluted tubule to reduce sodium reabsorption. This inhibits the generation of a maximally dilute urine (50 mOsm/kg) that normally occurs by the end of this nephron segment. Their minimum urine osmolality may instead be 150 to 200 mOsm/kg. This impaired urine dilution combined with excess water intake and poor solute intake, as seen in this runner, can cause symptomatic hyponatremia**. High ADH levels released during exercise or due to initial volume depletion may contribute as well (see figure). The patients drink excess water, which is why they often do not appear volume depleted.

29
Q

What drug limits diluting capacity of urine?

A

-Thiazide due there action on last area of tubule that reabsp water.

30
Q

Mechanism of Thiazide and causing Hyponatremia?

-Is is usefull to give it in diabetus?

A

-Thiazide diuretics–>by promoting continous Na+ excretion –>continues H2O excretion–>triggers ADH –>water reabsp–>worsening hyponatremia and even worst if you drink lots of water with few Na+ intake.

-NO, causes hyperglycemia.

31
Q

NSAIDS causes (4)

A

-Acute Tubular Necrosis (ischemia)
-Interstitial Nephritis (5 P’S)
-Renal Papillary Necrosis
-Membranous Glomerulonephritis

32
Q

What 2 deugs cause **hypokalemic metabolic alkalosis ** and Why?

A

-Thiazide and Loop Diuretics because as they promote volume loss you will see RAAS activation–> triggers aldosterone to secrte K+ and H+–>Hypokalemia and metabolic alkalosis.

33
Q

57-year-old man is brought to the emergency department after being found with an empty pill bottle at his bedside. He has diffuse abdominal pain. He has a history of depression and past suicide attempts. He also has a history of type 2 diabetes mellitus, currently managed with medication. His vital signs are stable. Laboratory studies show:

Na+: 140 mEq/L
K+: 4.8 mEq/L
Cl–: 100 mEq/L
HCO3–: 18 mEq/L
Glucose: 110 mg/dL
Blood urea nitrogen: 30 mg/dL
Serum creatinine: 3.5 mg/dL

Which of the following is the mechanism of the drug most likely causing this patient’s findings?

Decreases glucagon release
Directly binds insulin receptors
Inhibits gluconeogenesis
Inhibits intestinal α-glucosidases
Triggers insulin release

A

Metformin** inhibits hepatic gluconeogenesis**, increases insulin sensitivity in peripheral tissues, and increases peripheral glucose utilization to help lower the blood glucose level. More specifically, metformin inhibits mitochondrial enzymes (glycerophosphate dehydrogenase and complex I). This mechanism may also contribute to metformin toxicity by increasing the intestinal production of lactate due to increased anaerobic glycolysis and by reducing the hepatic metabolism of lactate (due to decreased gluconeogenesis).

-Promotes acidosis–>decreases HCO-3.

34
Q

What drug?

-Patient with hypertension gicing this drug:then developed

-contraction alkalosis + Hyperkalemia

A

-Loop diuretic
-Also promotes incr Na to DCT by inhibiting Cl-/Na+/K+ transporter in asc. limb.

35
Q

Etarcapnet
-use
-what to check before giving?

A

TNF alpha inhibitor –>important regulator for Granuloma formation–> check for TB before giving
-Used:R.A, psoriasis,ankylosing spondylitis

36
Q

Drugs that cause Pre-Renal azotemia(6)?

A

-NSAIDS, Loop Diuretics, Anticoagulants and Thrombolytics, ACHE Inhb.,Contrast dyes and Arterial vasodilators (Hydralazine)

37
Q

How does thrombolytics cause Pre-Renal azotemia?

A

-By dissolving larger Blood clots and promoting smaller which will obstruct renal arteries–>ischemia,infarct or necrosis

38
Q

Intrisnic Renal AKI drugs ?

A

-ATN:**Aminoglycosides **(Neomycin),Cisplatin and Amphoterecin B
-Interstitial Nephritis: 5P’S (Penincillin-Chephalosporin, PPI(Omeprazole), Diuretics,Rimfampin,NSAIDS)

39
Q

How does aminoglycosides cause AKI?

A

-Accumulation in renal cortex in PCT–>obstruction Blood Flow.

40
Q

Drugs that cause Post-Renal AKI?

A

-Mtx, Acyclovir and Sulfonamides

41
Q

Hemorrhagic cystitis Drugs?

A

Cyclophosphamide,ifosfamide

42
Q

Sevelamer

A

-Binds Phosphate in GI tract.
-CKD patients.

43
Q

Eplerenone??

A

-New spironolactone,without breast enlargement.

44
Q

EPO drug in ESRD A.E??

A

-Hypertension and incr risk Blood Clots
-Excessive RBC formation may cause hypertension.

45
Q

ACHE inhb is teratogenic?

A

-Decr. GFR–>oligohydramnios–>Potter sequence.

46
Q

Where do you use following drugs?
-azoles
-Nystatin
-Amphotericin B

A

-Less serious systemic infections and local infections of fungus–>any fungus.
-Topical use
-Severe systemic fungal infections

47
Q

Use of Nystatin and how does it work?

A

-oral candidiasis (thrush); topical for diaper rash or vaginal candidiasis.
-Binds to ergosterol–>membrane pore formation–>leakage. Same as amphoterecin B.

48
Q

Mayor A.E of amphotericin B?

A

Nephrotoxicity (prevent with hydration).

49
Q

What drug?

Inhibit fungal sterol (ergosterol) synthesis by inhibiting the cytochrome P-450 enzyme that converts** lanosterol to ergosterol.**

AE

A

-Azoles

-Fluconazole for chronic suppression of cryptococcal meningitis in people living with HIV and candidal infections of all types.
Itraconazole may be used for Blastomyces,Coccidioides,Histoplasma,Sporothrix schenckii.
Clotrimazole and miconazole for topical fungal infections.
Voriconazole for Aspergillus and some Candida.
Isavuconazole for serious Aspergillus and Mucor infections.

Inhibit testosterone synthesis–>gynecomastia.

RENAL (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions